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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN-0001November30HealthcareUNIQUE APPLICATION OF DATA ENTRY PROCESSES IN LONGITUDINAL MOTOR DEVELOPMENTAL STUDY English0610Amitesh NarayanEnglish U.V. ShenoyEnglish Sailakshmi GanesanEnglish Narayan PrabhuEnglishObjectives: Medical research in longitudinal motor developmental studies brings collection of large data base. Therefore need felt to develop an effective raw data entry method in electronic format using existing software i.e. MS Excel. Methods: 42 infants/children were recruited at the time of birth and were followed up to 36 months of age on Peabody Developmental Motor Scales-2nd edition (PDMS-2) instrument. All 42 subjects had been assessed for 9 times during follow ups at various chronological age points. Total numbers of follow up assessments were 378 i.e. 42 (subjects) × 9 (no. of follow up). Total number of data entry cell required for each subject in this study was approximately 2611. Thus total data entry cell in this study became i.e. 42* 2611 = 109662. Results: Through this process, each child‘s raw data digits i.e. >2600 cells, took only 20 to 30 minutes to enter and processed automatically as summary sheet. This process took 21-22 hours for entry of 109662 raw data digits (i.e. 42* 2611 = 109662) in the electronic format. The entered data in the summary sheet had 99% accuracy. Conclusions: This method is very useful for any number of raw data entries in electronic format in a short span of time for the research works of any type. It is easy and unique, because, it uses very simple concept of formula applications to bring the data entries in a summary sheet, while typing the data in a different sheet of the same MS Excel file, for the ease of typing and data errors verification. This method is cost effective also, since the application software MS Excel is easily accessible. EnglishINTRODUCTION An element of data is an item, idea, concept or raw fact. 1 In motor developmental studies, data should be organized in such a way that we can understand and retrieve them when needed. 2 To understand better about it, we must know what is data? The data is defined as ?representation of facts or concepts or instructions in a formalized manner, suitable for communication, interpretation or processing by manual or electronic means. 1 Data accuracy and data validity are two key principles of data quality. 3 To maintain data quality, health care data must include accuracy, validity, reliability, completeness, legibility, timeliness, accessibility, usefulness and costeffectiveness. 1,4 In recent years, data quality has been an important issue for two basic purposes: 3 a. to promote high standards of patient care, and b. to facilitate accurate and timely dissemination of research data for the statistical analysis. To be useful, the data must be accurate, valid and conform to an expected range of values. Thus it is important that collected data is correct at the point of entry and includes all relevant variables. 3 Since data recording is subject to human error, there is a need to have built-in control measures to eliminate errors, both in manual recording and computer entry. 3 Steps to check the data entry in the research record should be taken at the point of entry, because data accuracy is crucial for analysis purposes. 3 A popular method for data entry is ?Plan, Do, Check and Act? (PDCA) method. 1 The steps involve plan phase, implementation phase, check phase and act phase. 1 Longitudinal developmental studies can provide information that cannot be obtained from crosssectional studies; therefore, they have considerable appeal to research workers. 3,5 Medical research in longitudinal motor developmental studies causes collection of large data base, where data for one or more variables are recorded at more than one point in time. This necessitates that computer systems must have inbuilt edits and validation checks for accurate statistical analysis. 3, 5 Collection of accurate data is only the first step. It is also extremely important that errors are not introduced in the process of converting the data to electronic format. 6 Many studies use doubleentry verification to catch and correct the data entry errors. 6 New technologies are continually being developed to convert raw data to electronic format more efficiently. It is extremely important that data entry software has mechanisms to check the accuracy of entered data at the entry level itself. Some of the newest technologies involve scanning paper forms directly into the computer, or faxing forms to a central data center (where fax machine serves as scanner to convert the data to electronic format). These are efficient data entry system though not cost effective; but it is essential that scanned files are manually checked for accuracy. 6 Data Presentation is also important to ensure the quality of statistics. 3 Commonly all researchers presently type the data in MS Excel manually, whether the data to be entered is less/more without having any other easy options for error verifications. Therefore need felt to develop a cost effective raw data entry method for a longitudinal motor developmental study (having many variables) in to the electronic format using existing software i.e. MS Excel; having all essential properties of new technologies applied for the raw data entry  METHODOLOGY In this longitudinal motor developmental study, 42 infants/children were recruited at the time of birth and were followed up to 36 months of age on Peabody Developmental Motor Scales-2 nd edition (PDMS-2)7 instrument. During ≤12 month‘s period, frequency of assessment was 3 monthly; but from ≥12 months, the same was 6 monthly. Therefore all 42 subjects had been assessed for 9 times during follow ups at various chronological age points. Thus total numbers of follow up assessments were: 42 (subjects) × 9 (no. of follow up) = 378. This process generated massive data digits. At each age point of assessments many variables were obtained for the purpose of statistical analysis of the data i.e. item scores, raw scores, standard scores, age equivalents, percentiles quotients and performance ratings. Therefore total number of data entry cell required for each subject in this study was approximately 2611. So, the total data entry cell in this study became i.e. 42* 2611 = 109662. The need of such large numbers of data digits entry in MS Excel format required us to go through a planned procedure to ensure that entered data must be cross verified for its accuracy before being subjected to statistical analysis. New Data Entry Method: Commonly, research data entered by the researchers needs to be arranged in such a way that it should be easily understood by the statistician in order to understand the study and its variables. In ?MS Excel‘ there is rows and columns and each data gets its entry in one cell. The data stored in cells can be recognized by its cell no. i.e. Column No. x Row No. It helps the data to be recognized easily and detect the errors in the entered data. Generally while entering the data we often follow ?HORIZONTAL‘ wise data entry pattern (because in SPSS software, when the data gets opened through excel format, the naming of variables is automatic for each case), which is very difficult to type i.e. in a single row. If the data is many, we may lose the track of cells and so errors in the data. As a researcher, we faced extreme difficulty during horizontal manner data typing, since there were approximately 2611 cell entries in this study for each subject. Knowing that data entry must happen without any error and there must be an option for easy data retrieval as well as smooth and simple data verification. So, with the help of data entry system manager, we decided that each infant‘s record will be kept separately and a summary file will be derived from each record by using cell number references. Thus first a blank MS Excel file was prepared containing 3 sheets and the sheets were renamed as ?SUMMARY‘, ?DATA‘ and ?TOTAL‘. Their details are explained below: a. SUMMARY Sheet: It contained the format as per the statistical requirements for the data analysis (horizontal wise). e.g. b. DATA Sheet: It contained 239 rows (for raw data variables) and 9 columns (representing 9 age points of recordings), e.g. same way as it is shown below. Each variable was given different cell color to recognize the variables at one stoke, in order to avoid mistakes while entering the data. Also if the data entry is done vertically, it would be very easy to drag one cell to the end, provided the data to be entered is the same. By doing so, it became extremely easy to enter the raw data variables. c. TOTAL Sheet: It contained 6 (rows) x 5 (columns) for 9 test results representing 9 chronological age points of assessments. It is shown below. Finally all the data were transported for each case in SUMMARY sheet through the formula (the cell value which is appeared in the other sheet) E.g. As shown below. Here AK is Column, and 3 is Row. So in cell AK3 formula is stored as =DATA!B311 i.e. in DATA sheet B311 cell value). Through this process, the values stored in other sheets are brought to the SUMMARY SHEET, which is actually required for the statistical use (see appendix-1). RESULTS By this process, each child‘s raw data (>2600 cells) took only 20 to 30 minutes to enter and processed automatically as SUMMARY SHEET, which is actually required for the statistical analysis (see appendix-1). The SUMMARY SHEET contains data of all children in one place. Through this mechanism total raw data digits, i.e. 42* 2611 = 109662, took 21-22 hours for entry in the electronic format. The accuracy of entered data was verified manually by creating a PDF file print physically of each case (see appendix-2). The entered data in the SUMMARY SHEET had 99% accuracy. DISCUSSION The process adopted in this study for raw data entry is unique and cost effective, as MS EXCEL is commonly used application software. Simple formula concepts were applied in this study to bring the data together as SUMMARY SHEET in horizontal orientation (while typing the data in vertical orientation or in tabular form) (see appendix-1). By this process, large number of raw data digits could easily be converted in to the electronic format in short span of time, with 99% accuracy (with options for data error verification), for statistical analysis purposes. This would be a very useful concept for senior or junior level individual researchers, as it can save their lots of time required for data typing, and help in preventing data digit errors during data entry. CONCLUSIONS This method is very useful for any number of raw data entries in electronic format in a short span of time for the research works of any type. It is easy and unique, because, it uses very simple concept of formula applications to bring the data entries in a summary sheet, while typing the data in a different sheet of the same MS Excel file, for the ease of typing and data errors verification. This method is cost effective also, since the application software MS Excel is easily accessible. ACKNOWLEDGEMENT Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Authors also wish to acknowledge Mr. K. A. Shenoy of Sri Venkateshwar Computer Camp, Car Street, Mangalore for giving this concept and preparing the MS Excel format files. Englishhttp://ijcrr.com/abstract.php?article_id=1859http://ijcrr.com/article_html.php?did=18591. Abdelhak M, Grostick S, Hankin MA, Jacobs E. Health Information: Management of a Strategic Resource. Philadelphia, WB Saunders Company, 1996. 2. Davis N, Lacour M. Introduction to information technology. Philadelphia, WB Saunders, 2002. 3. Improving data quality: A guide for developing countries. World Health Organization. World Health Organization 2003. Regional office for the western pacific, United Nations Avenue, 1000 Manila, Philippines. ISBN 92 9061 050 6 4. Donabedian A. quality assessment and assurance: unity of purpose, diversity of means. Inquiry: 25, 1988: 173–195. 5. Roche AF, Guo S. Methods and analysis issues in longitudinal studies of growth. Wright State University School of Medicine. http://www.amstat.org/sections/srms/procee dings/papers/1988_024.pdf. 6. Whitney CW, Lind BK, Wahl PW. Quality assurance and quality control in longitudinal studies. Epidemiol Rev. 20 (1), 1998: 71-80. 7. Folio MR, Fewell RR. Peabody Developmental Motor Scales: Examiner‘ Manual. 2nd ed. Austin, Tex: PRO-ED. Inc; 2000
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN-0001November30HealthcareDIABETIC CARDIOVASCULAR COMPLICATIONS AND DYSLIPIDEMIA: A HOSPITAL BASED CROSS SECTIONAL STUDY IN NORTHWEST INDIA English1115Sharma AshishEnglish Agrawal ApurvaEnglish Sharma AnitaEnglishAim: To investigate the strength of association of each parameter of deranged lipid profile with diabetic cardiovascular complications Methods: This was a hospital based cross sectional study which included 150 diabetic patients who visited shree krishna hospital from May 2008 to April 2009. Lipid profile of all the patients was estimated by fully autoanalyser, cardiovascular complications assessed by Echo-cardio graphic changes and Electro cardiogram (ECG) changes. Results: The prevalence of dyslipidemia is higher in diabetic population in our study. Serum cholesterol >240 mg/dl was seen in 14%, serum triglycerides >160 mg/dl was seen in 43.33 %, raised LDL (low density lipoproteins) >130 mg/dl in 35.33 %, VLDL (very low density lipoproteins) >40 mg/dl in 25.33% and low levels of HDL (high density lipoproteins)EnglishDyslipidemia, Type II Diabetes, Cardiovascular complicationsINTRODUCTION Diabetes Mellitus and its associated complications have become a public health problem of considerable magnitude. Cardiovascular disease (CVD) is the most prevalent complication and is associated with excess morbidity and mortality in diabetic patients. (1)The etiopathogenesis of the longterm complications of diabetes is not fully understood and controversies exist about why they occur in some patients and not in others. (2) Though role of dyslipidemia in the development of diabetic complications is well known but data regarding individual parameter of deranged lipid profile are lacking. Various risk factors act synergistically for the development of cardiovascular complications in type II diabetes and the contribution of individual risk factor is yet to be clearly identified and quantified. (3) Thus the present study aimed to assess the effect of dyslipidemia on cardiovascular complications in western India. MATERIAL AND METHODS Study population In this hospital based cross-sectional prospective study, total 150 type II diabetic patients attending diabetic clinic and medicine OPD at shree krishna hospital, PSMC, karamsad during May 2008 to April 2009 were included. Patients were confirmed for diabetes by clinical and biochemical diagnosis based on American Diabetes Association revised criteria. (4) Approval from the institutional ethics committee was taken prior to study. The patients included in the study were informed about the study in brief, in their local language, and then written consent was taken from them. Study design Diabetic patients were evaluated for presence of cardiovascular complications which was assessed by either Electrocardiogram or Echocardiographic changes. Lipid profile was done by fully-auto analyzer (ERBA -XL-300). Triglyceride level was estimated by GPO (trinder) method. (5) Total cholesterol was estimated by CHOD-POD method (6), while HDL estimation was done by phosphotungustic method. (7) Blood glucose was estimated by glucose oxidase method (8) and glycosylated hemoglobin by immunoturbidometric method. (9) Estimated values of total cholesterol >240 mg/dl, serum triglycerides >160 mg/dl, HDL 130 mg/dl and VLDL >40 mg/dl were considered as abnormal. Statistical analysis Means or proportions for baseline clinical and laboratory characteristics were computed for subjects with and without cardiovascular risk. Ttest was used to compare means and chi square test was used to compare proportions. Significance tests were two tailed and p-values less than 0.05 were considered statistically significant. Multiple Logistic regression analysis was used to assess effect of individual variable in the development of cardiovascular complication of diabetes. RESULTS The details of demographic profile of the study population revealed that the mean age of the study population was 60.4 years, with average duration of diabetes 9.7 years. Mean fasting blood sugar was 161.9 ± 51.7 mg/dl and mean glycosylated hemoglobin was found to be 8.2 %. Mean serum cholesterol was 182.9 ± 50 mg/dl, serum HDL was 40.6 ± 13.2 mg/dl, serum LDL was 110.3 ± 41.3 mg/dl, serum VLDL was 35.8 ± 23.8 mg/dl and serum triglyceride (TG) was 175.8 ± 110 mg/dl. Data regarding lipid profile showed that out of 150 patients, hypertriglyceridemia is most common abnormality in diabetic patients, followed by high level of LDL and VLDL. Serum TG levels were high (>160 mg/dl) in 43.33 % patients, while high LDL level (>130 mg/dl) were found in 35.33% patients. Comparison of means revealed that duration of disease, serum cholesterol, serum LDL, serum VLDL and serum triglyceride levels were significantly associated with the cardiovascular complication, with p value < 0.05. While age of patients, serum HDL levels, fasting blood sugar levels (FBS) and PP2BS levels did not have statistically significant association with cardiovascular complication. (Table-1) Use of statins in diabetic patients was found to be significantly associated with reduction of cardiovascular complications. Sex of the patients, glycosylated hemoglobin levels and smoking were not found to be significantly associated with the risk of cardiovascular complications, with p values more than 0.05. (Table-2) On application of multiple logistic regression and after adjusting all the variables mutually, only serum LDL level was found to be significantly associated with the development of cardiovascular complication in diabetes patients with approximately a threefold increase in the  risk of cardiovascular complications (OR 2.7, 95% CI 1.5613 to 4.8532). (Table-3) DISCUSSION The present study showed the prevalence of dyslipidemia in diabetic population of west India comprising rural population. Dyslipidemia is an established risk factor for CAD in patients with type II diabetes, (10, 11) which include low HDL levels, raised triglycerides and raised LDL levels. LDL is a major determinant of atherosclerosis in patients with diabetes, results are consistent with study of R.P. Agrawal et al, in which changes in LDL particle composition such as density, oxidation potential and glycation, render even normal LDL levels as highly atherogenic. (3) The Strong Heart Study, which was an American Indian population based study, concluded that each 10 mg/dl increase in LDLcholesterol corresponded to a 12% increase in cardiovascular risk. (12). Similar information was also observed in present study, in which LDL-cholesterol was the most important independent variable in the model used for multivariate analysis, while from baseline data of the United Kingdom Prospective Diabetes Study (UKPDS), Stratton IM et al revealed that both decreased HDL and elevated LDL predict CHD. (13) There were some limitations in the present study, sample size was small and it was a hospital based study, so can‘t represent whole population. There is a need to perform such studies on larger and community based population. CONCLUSION In conclusion, the results of our study showed that in type 2 diabetes population of western India, estimated cardiovascular risk correlated with abnormal lipid profile, especially high serum levels of LDL. These data could explain the failure of intensive glycemic control in reducing cardiovascular events observed in diabetic patients. Duration of disease also had strong impact on diabetic complications. Patients on hypolipidemic drugs had an inverse relationship with the development and progression of cardiovascular complications, while patient‘s age, sex, and smoking behavior did not show statistically significant asssociation. More studies are required for development of appropriate preventive and treatment strategies to reduce diabetic cardiovascular complications. ACKNOWLEDGEMENT We acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. We are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Englishhttp://ijcrr.com/abstract.php?article_id=1860http://ijcrr.com/article_html.php?did=18601. Schalkwijik CG, Stehouwer CDA. Vascular complications in diabetes mellitus: the role of endothelial dysfunction. Clin Sci 2005;109:143-59. 2. Zimmet P, Alberti KGMM, Shaw J. Global and societal implications of the diabetes epidemic. Nature 2001 Dec 13;414:782-7. 3. Agrawal RP, Sharma P, Pal M, Kochar A, Koachar DK. Magnitude of dyslipedemia and its association with micro and macro vascular complications in type 2 diabetes: a hospital based study from Bikaner (Northwest India). Diabetes Res Clin Pract 2006;73:211-4. 4. American Diabetes Association. Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 2004; 27:s5-s10. 5. McGowan MW, Artiss JD, Strandbergh DR, Zak B. A peroxidase-coupled method for the colorimetric determination of serum triglycerides. Clin Chem 1983; 29:538-42 6. Richmond W. Preparation and properties of cholesterol oxides from nocardia sp. and its application to the enzymatic assay of total cholesterol in serum. Clin Chem 1973;19:1350-6. 7. Rifal N, Warnick GR editors. Laboratory measurement of lipids, lipoproteins and apolipoproteins. Washington DC: American Association of Clinical Chemistry (AACC) press; 1994 p. 21 – 42. 8. Trinder P. Determination of Glucose in blood using glucose oxidase with an alternate oxygen acceptor. Ann Clin Biochem 1969;6:24–7. 9. Trivelli LA, Ranney HM, Lai HT. Hemoglobin components in patients with diabetes mellitus. N Engl J Med 1971;284:353-7. 10. Adult Treatment Panel. Third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III) final report. Circulation 2002;106(25):3143-421. 11. Berthezène F. Diabetic dyslipidaemia. Br J Diabetes Vasc Dis. 2002;2(1):S12–7. 12. Stamler J, Vaccaro O, Neaton JD, Wentworth D. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the multiple risk factor intervention trail. Diabetes Care 1993;16:434–44. 13. Stratton IM, Adler AI, Neil HAW, Matthews DR, Manley SE, Cull CA et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ 2000;321:405–12.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN-0001November30TechnologyDEVELOPMENT OF AN EXPERT SYSTEM FOR DIAGNOSIS OF BEARING FAULTS OF ROTATING MACHINERY WITH A CASE STUDY ON BOILER FEED PUMP English1624G. Durga PrasadEnglish B.Raghu KumarEnglish K.V.RamanaEnglish B.S.K.SundaraEnglish Siva RaoEnglishIn this paper an attempt has been made to develop an expert system called VIBMASTER to help the plant maintenance persons in diagnosing the cause of excessive vibration at the bearing supports of a rotating machinery. In the expert system a data base has been compiled from Standards, Journals, Handbooks and Rules from Maintenance Manuals related to maintenance engineering and management. The transfer of knowledge from these sources into the expert system for diagnosis is achieved with knowledge engineering procedures using if and then rules. The developed software tool can identify the fault(s) using vibration characteristics like velocity, speed of machine and signatures. The proposed system has been developed on Microsoft Windows environment and is written in Microsoft Visual Basic and Visual C++. To validate, the expert system is tested with the data collected at the bearing supports of a Boiler Feed Pump of a Boiler Feed Pump train of a large utility thermal power plant.  EnglishExpert System, Fault Diagnosis, Boiler Feed Pump Train.INTRODUCTION Condition monitoring is a technique which enables the maintenance engineer to detect the incipient failure with ease and confidence in advance. Out of the number of condition monitoring techniques available, Vibration based monitoring is the best and early indicator of a machine‘s health [1, 2, 3]. Diagnostic process is a process of locating the exact cause(s) for fault or failure. Since a machine has many components and is highly complex, diagnosis of a machine fault usually requires technical skill and experience. It also requires extensive understanding of the machine‘s structure, operation and general concepts of diagnosis. This requires an expert engineer to have a domain specific knowledge of maintenance and knows the ?ins and outs‘ of the system. In normal situation, the expert is either too busy with some other tasks or a specific component expert is not available at all or the expert left the organization [4]. It is necessary to develop an expert system to carry out the diagnosis process with the help of a non-expert. In the recent past, various approaches have been used to produce expert systems. Among them, the rule-based diagnostic expert system is the most promising [5, 6, 7]. To guide the diagnosis, expert systems rely on an inference engine to derive the conclusions from the knowledge base. The inference engine checks all heuristic rules in the knowledge base based on backward chaining, forward chaining, or mixed modes of chaining. If the inference engine finds that any premise clause is unknown during the rule-checking process, the inference engine generates a query to ask the user. For improving search efficiency, Vranes et al [9] proposed a best-first search strategy based on fault probability information. The nodes with high fault probability components are generated and checked first, followed by those with lower fault probability. However, fault probability information is not the only criterion to determine the priority of each node. The other criteria such as the difficulty of fault diagnosis and the symptoms should be considered. Liu and Liu [8] proposed a new search strategy to enhance the efficiency of the diagnostic process for air compressor troubleshooting. A diagnostic tree is constructed based on the functions and connectivity of the air compressor devices. A fuzzy multiple attribute decision making method for a single user is used to determine the priority of each node in the tree. Then, the priorities of devices control the diagnostic process. However, the expert system for air compressor troubleshooting lacks generality. In addition, there might be more than one fault diagnosis expert and they may have different opinions about the importance of each criterion. Hence, a fuzzy group multiple attribute decision making method seems more appropriate for this problem [10, 11]. An efficient Expert System for Machine Fault Diagnosis (EMFDES) has been developed via a fuzzy group multiple attribute decision making method to overcome the diagnosis inefficiency problem, mentioned above. EMFDES is a hybrid expert system that combines an expert system and a fuzzy group multiple attribute decision making [12] method. Reddy CM[13] mentioned about the use of advanced techniques such as Artificial Intelligence. He further stated that these techniques provide a range of tools that allow successful condition monitoring and fault diagnosis systems to build and deploy efficiently. Gale KW and Walton J[14] described the evaluation of an expert system for condition monitoring of hydraulic control systems in hot steel strip finishing mill. The system integrates real time LABVIEW data acquisition with GENSEM G2 expert system running on windows. MISHRA.C and Muncherji.S [15] discussed about an expert system development at Tata steel, Jamshedpur for wear debris analysis. The system guides analyst through a step by step procedure and records all observations regarding presence of different types of wear particles. The system also offers the diagnostic and corrective actions. Depold HR and Gass FD [16] depicted the application of expert systems for gas turbine. These systems integrate data, furnish diagnosis, provide prognosis for planning maintenance action. METHODOLOGY In the present work Data files are created, based on data bank, giving emphasis to vibrational velocity, to tag the offensive vibration source. The domain is established by incorporating Codes and Standards as per ISO–2372, stipulating the limiting velocity for trouble free operation based on RPM of rotor which is supported by bearings. The source code is developed in C++ with #.net as back up for graphic visualization. Fig.1 gives the Flow Chart.   The following templates are designed as primary data to be given as input to the expert system. 1. Field data collection 2. Machine parameters 3. Tri-axial Measurements 4. Harmonics of peaks The expert system facilitates the following ? Bearing fault diagnosis in terms of tri axial measurements ? Bearing fault diagnosis in terms of signature analysis ? Vibration trouble shooting guide lines for bearings. ? Probable causes of faults and the remedial measures to be taken up The expert system facilitates the identification of existing fault with ease by simply giving velocity measurements along vertical, horizontal and axial directions along with harmonics of speeds at which peaks are observed, as input. The proposed system also suggests the remedial measures to bring down the intensity of offensive vibration to ensure trouble free operation. Options are provided to select a particular type of bearing and / or gear to diagnose the fault specifically. Case Study Fig. 2 shows the line diagram of a Boiler Feed Pump train under investigation. It is supported by 10 journal bearings. The motor drives the Booster Pump which runs at a speed of 1440rpm. The Boiler Feed pump (BFP) is run by the output shaft of a gear coupling. The speed of BFP shaft is 5220rpm. It is proposed to validate the expert system by measuring vibration intensity at the key point 9 and 10, related to BFP. Table 1 shows the recorded values at these key points in the month of June, 2011.   Application of Expert System In the developed expert system, ?VIBMASTER?, the velocity values are given at the appropriate screen. Figs. 4 and 5 shows the Input and Out Put screens. From Fig 5 it is clearly evident that the fault is due to soft footing. The remedial measures suggested are to check for distortion of base frame or deterioration of grouting giving raise to soft footing. After proper reinforcement of the base the subsequent measurement indicated a velocity of 7.20mm/sec, at bearing 10 along horizontal direction. At bearing 9 the vibration velocity is well within the limit along 3 directions. The velocity intensity is exceeding the limiting value along horizontal direction at bearing 10 and the reason can be attributed to soft footing [17].   CONCLUSIONS This paper describes the development of a vibration based expert system, VIBMASTER, which enables operators of rotating machinery, to solve vibration problems. The developed expert system validated with experimental data taken at the bearings of BFP of a large utility thermal power palnt. The expert system is used to provide the information possible to avoid or reduce the vibration intensity in the absence of expert. It is suitable to monitor and diagnose 18 different probable faults in any rotating machinery. The proposed expert system is developed to diagnose and suggest the remedial measures for rotating machinery. ACKNOWLEDGEMENTS The authors are thankful to the Naval Science and Technological Laboratories, Visakhapatnam for funding the project and also Vijayawada Thermal Power Station, Vijayawada for their support to carry out the validation of expert system. Englishhttp://ijcrr.com/abstract.php?article_id=1861http://ijcrr.com/article_html.php?did=18611. Farrar, C.R. and Doebling, S.W., (1999). ?Damage detection II: field applications to large structures‘. In: Silva, J.M.M. and Maia, N.M.M. (eds.), Modal Analysis and Testing, Nato Science Series. Dordrecht, Netherlands: Kluwer Academic Publishers. 2. Al-Najjar, B., (1994). ?A new vibration based approach for monitoring rolling element bearing‘. In Nordic Conference on Vehicle and Machine Vibration, Goteborg, Sweden. 3. Al-Najjar, B., (1996). ?TQMain; a common database for total quality maintenance. An approach for continuous reduction in costs of quality products.‘ J. Quality. in Maintenance Engineering, Vol 2(3), p 2-20. 4. Patel, S.A and Kamrani.A.K. (1996), Intelligent decision support system for diagnosis and maintenance of automated systems, ?Computers Industrial Engineering?, 30(2), p 297 – 319. 5. P. Burrell and D. Inman (1998),?An expert system for the analysis of faults in an electricity supply network: problems and achievements?, Computers in Industry, 37, pp. 113–123. 6. J. H. Bradley and R. D. Hauser (1995), ?A framework for expert system implementation?, Expert Systems with Applications, pp. 157– 167. 7. J. Liebowitz (1995), ?Expert systems: a short introduction?, Engineering Fracture Mechanics, 50, pp. 601–607. 8. S. C. Liu and S. Y. Liu (2001), ?An efficient expert system for air compressor troubleshooting?, Expert Systems, 18, pp. 203–214. 9. S. Vranes, M. Stanojevic and V. Stevanovic (1996), ?BEST-based expert diagnostic system for the aluminum industry?, Computers in Industry, 32, pp. 53–68. 10. S. J. Chen, and C. L. Hwang (1992), ?Fuzzy Multiple Attribute Decision MakingMethods and Applications?, SpringerVerlag. 11. C. C. Hon, Y. Y. Guh, K. M. Wang and E. S. Lee (1996) ?Fuzzy multiple attribute and multiple hierarchical decision making?, Computers with Mathematical Applications, 32, pp. 109–119. 12. S. C. Liu and S. Y. Liu (2003),?An Efficient Expert System for Machine Fault Diagnosis? The International Journal of Advanced Manufacturing Technology?, 21, pp, 691 – 698. 13. Reddy CM (1991), ?Expert Systems for condition monitoring, fault diagnosis and control?, IEEE colloquium on condition monitoring for fault diagnosis, London. 14. Gale KW and Walton J (1995), ?A real time expert system for condition monitoring Hydraulic control systems in hot steel strip finishing mill?, Journal of Systems and control Engineering, Vol 213, No.5. 1 5. Mishra C and Muncherji S (1996), ?Expert system for wear debris analysis? – A powerful tool for condition monitoring. Proceedings of 14th world conference on NDT, Vol 2 , New Delhi. 16. Depold HR and Gas FD (1999), ?The application of Expert systems and Neural networks to Gas turbine Prognostics and Diagnostics?. ASME Journal of Gas turbines and Power, Vol. 121, No.4. 17. B.Raghu Kumar, K V Ramana and K Mallikharjuna Rao (2009), ?Condition monitoring and fault diagnosis of a boiler feed pump unit?, Journal of Scientific and Industrial research, Vol.68, pp 789 – 793.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN-0001November30HealthcarePRENATAL STUDY OF HISTOGENESIS OF HUMAN LATERAL GENICULATE BODY English2532Indira Devi BEnglish Raju SugavasiEnglish Sujatha MEnglish Sirisha BEnglishObjectives: The lateral geniculate body in human fetuses of different gestations. The Present study is to determine the apperance of the number of laminae and to observe the types of cells present in different laminae at different gestations. Methods: The present work is the result of study of lateral geniculate bodies in human fetuses, which are obtained from local government hospitals. Age of the fetuses ranged from 20-40 weeks. The age of fetuses is judged by CR lengths. The photo graphes of slides are taken by SAMTRON‘computer having a closed circuit camera and an adapter fixed to ?LYNX‘ (LAWRENCE AND MAYO) trinocular research microscope after the routine histological procedures. Result: Histo genisis of lateral geniculate body is of different propotions at different gestations of embryonic life. In the present study at 20 wees of gestation bipolar cells are abundantly seen and laminar differentiation has not seen. At 24 th week of geststion the laminar differentiation has started.all 6 laminae are visible by at 33 weeks of gestations.varied diameters of rounded neurons are seen with predominance of multipolar neurons have been observed at 38 weeks of gestation. Multipolar cells are visible at 40 weeks of gestation in all 6 laminae. Conclusion: in the present study all 6 laminae are differentiated at 33 week of gestation. During 20 to 40 weeks of gestation the predominance of cells present in laminae differentiated from rounded to multipolar neurons. EnglishINTRODUCTION In view of, interesting changes that occur in the cytoarchitecture of lateral geniculate body, an attempt has been made to notify its histogenesis in human fetuses of different gestations. The lateral geniculate body is a part of the visual pathway. It is a small, ovoid, ventral projection from the posterior thalamus. The lateral geniculate nucleus is an inverted, somewhat flattened, U-shaped nucleus and is laminated. Its internal organization is usually described on the basis of six laminae, although seven or eight may be present. The laminae are numbered 1 to 6, from the innermost ventral to the outermost dorsal. Laminae 1 and 2 consist of large cells, the magnocellular layers, whereas layers 4 to 6 have smaller neurones, the parvocellular laminae. The apparent gaps between laminae are called the interlaminar zones. The lateral geniculate nucleus receives major afferent inputs from the retina. The contralateral nasal hemiretina projects to laminae 1, 4 and 6, whereas the ipsilateral temporal hemiretina projects to laminae 2, 3 and 5. The efferent fibres from the lateral geniculate nucleus pass principally to the primary visual cortex (area 17) in the banks of the calcarine sulcus. It is possible that additional small projections from interlaminar zones pass to extrastriate visual areas in the occipital lobe [1] . MATERIALS AND METHODS The present work is the result of study of lateral geniculate bodies in human fetuses. 50 human fetuses have taken up and all the fetuses belong to gestational age group of 20 – 40 weeks. The age of fetuses is judged by CR lengths. The foetal brains have been fixed by injecting 10% formalin into the vessels of umbilical cord and through anterior fontanelle. The cranial vaults have been removed by using a bone cutter, hand saw and scissors. The dural folds have been removed to expose the cerebral hemispheres. The brains have been severed at the lower end of medulla oblongata. It has been observed that most of foetal brains have not hardened, most probably foetal brains are having less neuroglial tissue.The piamater has been removed. The optic tracts are traced backwards to view the lateral geniculate bodies. After the fixation, tissue processing, and sectioning the microphotographs of sections stained with haematoxylin and eosin were studied on a ?SAMTRON‘ computer having a closed circuit camera and an adapter fixed to ?LYNX‘ (LAWRENCE AND MAYO) trinocular research microscope. The stained sections were examined with 10x and 40x magnifications. The closed circuit camera with adapter is attached to one of the eye pieces of trinocular microscope. With manipulation of the fine adjustment of camera as well as that of microscope, pictures having magnifications of 10x and 40x have been obtained with good resolution on computer screen and this has been utilized for taking microphotographs of various sections. The lateral geniculate body in human fetuses of different gestations is further studied, to view the number of laminae and observe the types of cells present in different laminae. RESULTS Microscopic Observations: Lateral geniculate body is of different proportions at different gestations of the embryonic life. Most of the neurons in it are rounded to oval to multi polar. The density of the neurons as well as congregation of neurons changed as the gestations of fetuses increases. Before 20th week, bipolar cells are abundant. However, a few multi polar cells are also seen. 20 weeks of gestation: The proportion of bipolar and multi polar cells is 4:1. No clear laminar pattern is seen. There is aggregation of the rounded neurons into nuclear groups. However, definite nuclear groups are not clearly seen. Division of magnocellular and parvocellular components of lateral geniculate body is also not clear. Supporting glial cells are abundant. 24 weeks of gestation: Laminar pattern is still not clear, Neuron density is distinctly more. The number of multi polar neurons has increased. Differentiation of parvocellular and magnocellular regions has begun. Axodendritic synapsis started appearing. There is increased density of glial cells simultaneously. Increased vascularity is also seen, confirming the increased cellular activity. 33 weeks of gestation: 6 laminae are visible (Fig.no.01). Each lamina is separated by a white band that indicates the synaptic zone in between the cells of the different lamina. The first lamina is concave and cells are small, multi polar cells, the density of the cells is less. The second lamina is having higher density of multipolar cells. The cell nuclei are closely packed. In the synaptic zone round to oval cells are present, these are called koniocytes or konio (k) cells. Third lamina is thicker than that of the first and second lamina. Cells are widely distributed throughout entire length of the lamina. Most of the cells are still rounded. The density of multi polar cells is less. The glial cells are also more. The width of the fourth lamina is less than that of the third lamina. Cells are widely distributed. Cell nuclei are small and rounded. Multi polar cells are also seen, but minimal in number.The fifth and sixth lamina are clearly demarcated like the rest of the laminae. The cells of the fifth lamina are multipolar and rounded. Similarly, in the sixth lamina also the cells are multipolar and rounded. 38 weeks of gestation: A well developed 6 layerd lateral geniculate body with predominance of multipolar cells of varied diameter with very minor density of rounded neurons has been observed (Fig.no.02).The conversion of rounded neurons into multipolar neurons will be taking place henceforth. Koniocytes are clearly seen in between the laminae. 40 weeks of gestation: All the 6 laminae are clearly seen.Each of the lamina is studded with multipolar neurons (Fig.no.03). Koniocytes are also seen in between the laminae. No increase in the width of the lamina is seen. DISCUSSION Lateral geniculate nucleus is a thalamic station in the projection of visual pathway from retina to primary visual cortex. The topographic organization and the study of neurons have been extensively taken up in non human primates by Polyak (1953) [2], Kaas et al (1972) [3], Malpeli and Baker (1975) [4]. The lateral geniculate body is organized into six layers, each of which receive input from either the contralateral or ipsilateral eye and contains a retinotopic map of lateral hemifield. Out of six layers, the dorsal layers contain small neurons where as the ventral two layers contain large neurons. Hence, the distinction of the two regions of dorsal parvocellular and ventral magnocellular components has been observed by Wiesel and Hubel (1966) [5], Creutzfeldt et al (1979) [6], Maunsell (1993)[7] . The development of the human lateral geniculate body is remarkably similar to that of Rhesus monkey (Rakic, 1977) [8]. The lateral geniculate body is displaced and rotated infero lateral to the thalamus because of late growth of pulvinar around the 24`Th week of intra uterine life and the lateral geniculate body has come to lie along the ventro lateral border of the thalamus. The characteristic laminar pattern has been observed over a period of 3 weeks, beginning around 22 weeks of gestation. Caudal part of the lateral geniculate body laminates first (Hickey and Guillery 1979) [9] . In the earlier studies, it was found out that the lateral geniculate body became apparent at 14weeks, light microscopically (Dhamayanti N, S. Wadhwa and V. Bijlani, 1988) [10].At 16 weeks, the nucleus attained the maximum size and was found to be having two parts, the larger part closely associated with sub thalamus another less distinct part among the optic tract fibres. At 18 to 20 weeks, the appearance of the lateral geniculate nucleus is similar as at 16 weeks.At 22 weeks the nucleus was situated rostrally. Saini K, Kretz R and Rager G (1987) [11] described three types of neurons, these are multipolar radiate, bi tufted and intermediate types. The dendrites of these neurons are confined to one lamina only. Multi laminar neurons with multipolar radiate, bi tufted and intermediate types of dendrites have also been described by them. Inter laminar neurons whose cell bodies and dendrites are confined to a single inter laminar zone have also been described. The lateral geniculate nucleus (LGN) is the principal thalamic relay to the visual cortex (area 17), and its neurons have similar morphological characteristics in both monkey and man, as identified by Golgi impregnation (de Courten C, Garey LJ, 1983) [12]. Hitchcock PF, Hickey TL (1980) [13] stated that the development of the human lateral geniculate nucleus is remarkably similar to that described for the rhesus monkey (Rakic, 1977). The development of the lateral geniculate nucleus has been studied systematically in Nissl preparations from a series of cats (Kalil R) [14] that ranged in age from newborn to adult. In addition, preliminary observations are reported at two stages of fetal development. It was found that laminae develop in the lateral geniculate nucleus near the time of birth and continue to differentiate during the first postnatal week. During development the major axis of the lateral geniculate rotates approximately 180 degrees in the sagittal plane. The rotation begins prenatally and is not completed until after the twentieth postnatal week. In the human lateral geniculate nucleus (LGN) anatomical studies have revealed a similar organisation compared with the macaque in lateral geniculate nucleus (LGN) terms of laminar pattern. The layout of the representation of the visual field, however, is less well understood, because its study has historically been restricted to postmortem anatomical analysis of degeneration patterns after retinal or cortical lesions (Rönne, 1910 [15] , Juba and Szatmári, 1937 [16], Highresolution functional magnetic resonance imaging (fMRI) at 3 T in humans has been utilized to derive a detailed account of the retinotopic organisation of the lateral geniculate nucleus (LGN). The results of researchers reveal a close correspondence in the topographic organisation of the macaque and human lateral geniculate nucleus (LGN) and support accounts of a constant magnification from the retina through the cortex. CONCLUSION In the present prenatal histological study At 20 weeks gestation bipolar cells are abundantly seen. Formation of nuclear groups is observed. Division of magnocellular and parvo cellular components has not taken place. Differentiation of parvocellular and magnocellular regions has started at 24 weeks there is increased density of neurons and glial cells. All 6 layers are visible by 33 weeks. The first lamina is concave and is present towards the hilum. The first and second laminae of the lateral geniculate body have closely packed with multipolar cells at 33 weeks of gestation. The density of glial cells is more in 3`rd lamina with round cell nuclei. The 5`Th and 6`Th laminae are not clearly distinguished, with predominance of multipolar neurons. Varied diameters of rounded neurons are seen with predominance of multipolar neurons is observed at 38 weeks of gestation. All 6 layers are well developed. All the neurons are of 6 laminae are multipolar at 40 weeks of gestation. ACKNOWLEDGEMENTS I express my deep sense of gratitude to Dr. B. Narasinga Rao professor and HOD of Anatomy and Padmini for well support through out this work, and colleagues for their proper guidance, precious suggestions and priceless encouragements to accomplish my work. I am very much greatful to the research scholars and so many authors whose efforts have helped me to update my knowledge of Anatomy and continue this work. I am thankful to my co authors for contribution of their efforts to this work. Englishhttp://ijcrr.com/abstract.php?article_id=1862http://ijcrr.com/article_html.php?did=18621. Standring S. Grays Anatomy. The Anatomical basis of clinical practice. 40 Th ed. Edinburg. Elsevier Churchill Livingstone ; 2008. (21): p. 314 - 315. 2. Polyak S, Santiago Ramon y Cajal and his investigation of the nervous system. J Comp Neurol. 1953: 98: 3 - 8. 3. Kaas JH, Guillery WR, Allman JM, Some principles of organization in the dorsal lateral geniculate nucleus. Brain Behav Evol. 1972; 6: 253 - 299. 4. Malpeli JG, Baker FH. The representation of the visual field in the lateralgeniculate nucleus of Macaca mulatta. J Comp Neurol. 1975: 161: 569 - 594 5. Wiesel TN, Hubel DH. Spatial and chromatic interactions in the lateral geniculate body of the rhesus monkey. J Neurophysiol. 1966: 29: 1115 - 1156. 6. Creutzfeldt OD, Lee BB, Elepfandt A. A quantitative study of chromatic organisation and receptive fields of cells in the lateral geniculate body of the rhesus monkey. Exp Brain Res. 1979: 35: 527 - 545. 7. Maunsell JH, Merigan WH. How parallel are the primate visual pathways? Annu Rev Neurosci. 1993: 16: 369 - 402. 8. Rakic P. Prenatal development of visual system in rhesus monkey, Phil Trans R Soc Lond, 1977; B278:245. 9. Hickey TL, Guillery RW. Variability of laminar patterns in the human lateral geniculate nucleus. J Comp Neurol. 1979: 183: 221 - 246. 10. Bijlani V, Wadhwa S. Cytodifferentiation and developing neuronal circuitry in the human lateral geniculate nucleus. Int J Dev Neurosci. 1988; 6 (1): 59 - 75. 11. Saini K, Kretz R, Rager G. Classes of neurons in relation to the laminar organization of the lateral geniculate nucleus in the tree shrew, Tupaia belangeri. J Comp Neurol. 1987 May 1;259(1):31 – 49. 12. de Courten C, Garey LJ. Morphology of the neurons in the human lateral geniculate nucleus and their normal development. A Golgi study.Exp Brain Res. 1982 ;47(2):159 - 71. 13. Hitchcock PF, Hickey TL. Prenatal development of the human lateral geniculate nucleus, J Comp Neurol. 1980 Nov 15; 194(2): 395 - 411. 14. .Kalil R. Development of the dorsal lateral geniculate nucleus in the cat. J Comp Neurol 1978:No15; 182(2): 265 - 91. 15. RonneH Pathologisch-anatomische untersuchungen über alkoloische intoxikationsamblyopie. Arch Ophthalmol. 1910: 77: 1 - 95. 16. Juba A, Szatmári A. Ueber seltene hirnanatomische befunde in fällen von einseitiger peripherer blindheit. Klin Monatsbl Augenheilkd. 1937: 99: 173 - 188.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN-0001November30General SciencesPHYTOCHEMICAL SCREENING AND ANTIMICROBIAL ACTIVITY OF CHLORELLA VULGARIS BEIJERINCK English3338Jayshree Annamalai English Jayashree Shanmugam English Thangaraju NallamuthuEnglishAim: In the last few decades, increased resistance of bacterial strains to drugs including antibiotics has been a major factor for increasing morbidity, mortality and healthcare costs to bacterial infections. With this concern, effort has been made to investigate the phytochemicals and antibacterial potency of chloroform, acetone, ethanol and aqueous extract from Chlorella vulgaris Beijerinck (Chlorellaceae). Method: Mass cultivation of algae was carried out in outdoor and chloroform, acetone, ethanol and aqueous extracts were extracted directly from the biomass. The extracts were subjected to phytochemical screening and antimicrobial activity against test organisms; E.coli, P.vulgaries, S.aureus, P.aeruginosa and B.subtilis by agar well diffusion assay and Minimum Inhibitory Concentration of all the four extracts were determined. Result: Phytochemical screening revealed the presence of alkaloid, flavonoid, phenol, tannin, terpenoids, saponin and glycosides. Acetone and ethanol extracts were potential antimicrobial agent when compared to chloroform and aqueous extracts. Aqueous extract showed very less inhibitory potency against test organisms. Conclusion: Daily supplementation of food with C. vulgaris Beijerinck will not only nourish in the body growth but it will also serve as immense source to defend against bacterial infection. EnglishChlorella vulgaris, mass cultivation, phytochemicals, agar well diffusion, Minimum Inhibitory Concentration.INTRODUCTION Chlorella vulgaris Beijerinck is a single-celled fresh-water algae super-food and is thought to be one of the planet&#39;s earliest life-forms. Since the 1960&#39;s Chlorella has been popular in Japan as a multi-supplement taken to maintain health through optimal nutrition. It is the most researched of all the algae. Initially research was focused on improving our understanding of photosynthesis, but since the 1970s the health benefits of Chlorella have been documented in vast collection of studies1 . Chlorella users report to experience more energy, improved physical appearance and protection from disease and illness. Infectious diseases are the leading cause of death world-wide and antibiotic resistance has become a global concern2 . The clinical efficacy of many existing antibiotics is being threatened by the emergence of multidrug-resistant pathogens3 . Many infectious diseases have been known to be treated with herbal remedies throughout the history of mankind. Unmatched availability of chemical diversity among natural products either as pure compounds or standardized plant extracts, provide unlimited opportunities for new drugs to lead in pharmaceutical industries. With an urgent need to discover new antimicrobial compounds, there is also need for the developing novel mechanisms of action for new and re-emerging infectious diseases4 . In recent years, marine natural product search has yielded a considerable number of drug candidates5 . The chemical compounds responsible for the antibacterial activity in algae have been variously identified as bromophenols, carbonyls, halogenated aliphatic compounds, terpenes, isoprenylated and brominated hydroquinones, as well as phlobatannins6 . In this regard, the present study is focused on the phytochemical analysis and antibacterial potency of chloroform, acetone, ethanol and aqueous solvent extracts of Chlorella vulgaris Beijerinck. MATERIALS AND METHODS Culturing and collection of algal mass C.vulgaris Beijerinck (Chlorellaceae) was cultured in Bold Basal medium (BBM) and incubated for 15 days at 24 ± 1 ºC in a thermostatically controlled room and illuminated with cool inflorescence lamps (2000 lux in a 12: 12 h L/D) regime. The log-phase culture was used as feeder culture for outdoor cultivation and was carried out at terrace in wide mouthed plastic tubs by inoculating 1500 mL of culture in 15.0 L of medium; pH was adjusted to 8.5. Biomass was harvested and collected after 15 days. Preparation of algal extract Ten gram of collected fresh algal biomass which was equal to 1g of dried weight7 was completely homogenized and soaked (w/v; 1:10) in 100 ml of chloroform, acetone, ethanol and water; and kept for 72 hours. This process was repeated until the extracted solvent became colorless except with that of water. The extracts were pooled together, filtered through Whatman no. 40 and chloroform, acetone, ethanol extract were condensed under vacuum at 50?C using rotary evaporator while water extract was lyophilized. The condensed chloroform, acetone, ethanol extracts were dried at room temperature and stored in an air tight amber vial at 4?C while aqueous extract was stored in desiccator, until further analysis to determine phytochemicals and antimicrobial activity against test organisms. Phytochemical screening Standard phytochemical test8 was carried out on the chloroform, acetone, ethanol and aqueous extracts of C.vulgaris Beijerinck to determine presence of Alkaloids, steroids, flavonoids, phenols, tannin, terpenoids, saponin and glycosides. Antimicrobial susceptibility studies Inhibition of microbial growth was tested by agar well diffusion assay. Standard aseptic microbiological methods were followed throughout this antibacterial study. Bacterial inoculums were prepared as per 0.5 McFarland standard9 with test organisms that were procured from the Microbial Type Culture Collection (MTCC) and Gene Bank, Chandigarh ,India includes: Escherichia coli MTCC -1687, Proteus vulgaries MTCC-742, Staphylococcus aureus MTCC -96, Pseudomonas aeruginosa MTCC -1688 and Bacillus subtilis MTCC -441 in Muller Hinton broth (MHB). Dried crude chloroform, acetone, ethanol and aqueous extracts were dissolved in 100% Dimethyl Sulfoxide (DMSO) at mg/mL concentration. From this 25 μL, 50 μL, 75 μL and 100 μL extracts were used to load in agar wells. Agar well diffusion assay Antimicrobial activity of chloroform, acetone, ethanol and aqueous extract of C.vulgaris Beijerinck was determined by agar well diffusion technique10 using Muller Hinton agar. Bacterial culture of 108 cells/mL was swabbed on sterile agar surface and well was cut using cork borer of 9 mm diameter. Wells were loaded with different extracts, negative control DMSO and positive control, Streptomycin (50 μL at mg/mL in sterile water). Loaded plates were incubated at 37?C for 24 hrs and after incubation, diameter of inhibition zone was measured in mm using ruler and experiment was repeated thrice. Minimum Inhibitory Concentration (MIC) MIC of chloroform, acetone, ethanol and aqueous extract of C.vulgaris Beijerinck was determined by the standard method11. Nutrient broth was prepared and sterilized using autoclave. One mL of the prepared broth was dispensed in to the test tubes numbered 1-9. A stock solution containing 25 mg/mL of each extract was prepared. Then 1 mL of the solution was dispensed into the tubes numbered 1. Subsequently, from tube 1, serial dilution was carried out and 1 mL from tube 1 was transferred up to tube number 7 and 1 ml from the tube 7 was discarded. Tube 8 was control for sterility of the medium and tube 9 for viability of the organisms. An overnight culture (inoculums) of each of the test organism was prepared in sterile nutrient broth. 1 mL of the inoculum was transferred into each tube from tube 1 to tube 9 with exception of tube 8, to which another sterile nutrient broth was added. The final concentration of the algal extract in each of the test tubes numbered 1-7 after dilution 25, 12.5, 6.25, 3.125, 1.563, 0.78 and 0.39 mg/mL, were incubated at 37°C for 24 hrs and examined for growth. The last tube in which growth failed to occur was the Minimum Inhibitory Concentration tube. RESULT Preliminary phytochemical screening of chloroform, acetone, ethanol and aqueous extract of C.vulgaris Beijerinck revealed the presence of alkaloids, flavonoids, phenol, tannins, terpenoids, saponins and glycosides (Table 1). Antimicrobial activity All the four extracts of C.vulgaris Beijerinck; chloroform, acetone, ethanol and aqueous extract exhibited varying degree of antimicrobial activities against test microorganisms, E.coli, P. vulgaries, S. aureus, P. aeruginosa and B. subtilis (Table 2, 3, 4, 5, 6). S. aureus showed low susceptibility to all the four extracts whereas E. coli was showed moderate susceptibility to acetone and ethanolic extract. Wide range of antimicrobial activity was exhibited by all the extracts between the range 50-100 µg/mL. The Minimum Inhibitory Concentration of acetone, ethanol, chloroform and aqueous extract of Chlorella vulgaris in this study against the test organisms ranged between 25 to 1.5 mg/mL (Table 7). Ethanol extract was more potential in inhibiting test bacteria at minimum concentration when compared to other extracts. DISCUSSION The variation in the presence and absence of phytochemicals with respective solvents attributed to the solubility of the active component in different solvents12. To a large extent, the chronological growth phase, percentage humidity of the harvested material, situation and time of harvest, and the method of extraction were possible sources of variation for the chemical composition, toxicity and bioactivity of the extracts13 . It was observed that antibacterial effectiveness increased with increasing concentration of extracts and higher concentrations of antimicrobial substances shows appreciable growth inhibition to microorganisms14 . B.subtilis showed susceptibity to acetone and ethanol extract. Though chloroform exhibited low antimicrobial activity against most test organisms, it showed potential inhibitory activity against P.aeruginosa. Aqueous extract showed low antimicrobial activity when compared to other extracts. Acetone and ethanol extract are potential antimicrobial agents, effectively inhibiting the growth of B. subtilis, P.vulgaris and P.aeruginosa. Although the positive control, streptomycin showed significant growth inhibitory activity on all the bacteria tested, chloroform extract was found to be more effective on P.aeruginosa at concentration of 100 µg/mL (Table 2) while the ethanolic extract was found to show similar activity against S.aureus at same concentration (Table 4).Antimicrobial agents with low activity against an organism have a high MIC while a highly active antimicrobial agent gives a low MIC. Tannins, alkaloids saponins and phlobatannins have been reported for their antibacterial and antiviral activity15. Furthermore, alkaloids and saponins are classes of compounds that are known to be effective for the treatment of syphilis and other venereal diseases16. The presence of these constituents has been reported to account for the exertion of antimicrobial activity by plants17 . CONCLUSION After evaluating the phytochemicals and antimicrobial potency of different extracts of C.vulgaris Beijerinck, it can be concluded that C.vulgaris Beijerinck, not only serve as extreme food supplement, beside it is good wound healer, antioxidant and from the above study it is a good antimicrobial agent also. Further studies can be carried out to isolate the pure compound responsible for antimicrobial activity. ACKNOWLEDGEMENT The authors acknowledge and thank for the support provided by Prof. R. Rengasamy, Director, Centre for Advanced Studies in Botany, University of Madras, India. Authors also acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are grateful to authors/ editors/ publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Englishhttp://ijcrr.com/abstract.php?article_id=1863http://ijcrr.com/article_html.php?did=18631. Tsukada O, Kawara T, Miyachi S. Mass culture of Chlorella in Asian countries. In: Mitsui AS, Miyachi A, SanPietrp S, Tamure, editors. Biological Solar Conversion. Academic Press, New York; 1977. p. 363- 365 2. Westh H, Zinn CS, Rosdahl VT. An international multicenter study of antimicrobial consumption and resistance in Staphylococcus aureus isolates from 15 hospitals in 14 countries. Microb Drug Resist 2004; 10: 169-176. 3. Bandow JE, Brotz H, Leichert LIO. Proteomic approach to understanding antibiotic action. Antimicrob Agents Chemother 2003; 47: 948-955. 4. Rojas R, Bustamante B, Bauer J. Antimicrobial activity of selected Peruvian medicinal plants. J Ethnopharmacol 2003; 88: 199- 204. 5. Haefner, B. Drugs from the deep: marine natural products as drug candidates. Drug Discovery Today 2003; 8: 536–544. 6. Glombitza LW. Antibiotics from algae. In: marine algae in pharmaceutical science. Walter de Gruyter. Berlin 1979; 303-342. 7. Keivan Z, Saeed T, Iraj N, Zahra R, Forough Y, Samin S et al. In vitro antitumor activity of Gracilaria corticata (a red alga) against Jurkat and molt-4 human cancer cell lines. AJB 2010; 9(40): 6787-6790. 8. Trease GE, Evans WC. A Textbook of Pharmacology. 13th ed. London: Ballieria Tindall Ltd; 1989. p. 83,685. 9. Bauer AW, Kirby MDK, Sherras JC, Trick M. Antibiotic susceptibility testing by standard single disc diffusion method. American journal of clinical pathology 2003; 45:4-496. 10. Perez C, Paul M, Bazerque P. An Antibiotic assay by the agar well-diffusion method. Acta Bio Med Exp 1990; 15: 113-115. 11. Wariso, BA. and Ebong, O. 1996. Antimicrobial activity of Kalanchoe pinnaata (Ntiele. Lam) pers. W. Afr. J. Pharm. Drug Res. 12: 65-68. 12. Ekpo MA, Etim PC. Antimicrobial activity of ethanolic and aqueous extracts of Sida acuta on microorganisms from skin infections. Journal of Medicinal Plants Research 2009; 3(9), 621-624. 13. Felix MT. Medical Microbiology. Churchill Livingstone 1982; (Publishers): London, UK. 14. Kurosoki F, Nishi A. Isolation and antimicrobial activity of the phytoalexin–6- methoxymellein from cultured carrot cells. Phytochemistry 1983; 22(3): 669-672. 15. Enzo AP. Traditional plants and herbal remedies used in the treatment of diarrheal diseases. Mode of action, quality, efficacy and considerations. In: Ahmad I, Aqul F, Qwaiss M, Modern Phytomedicine Turning Medicinal Plants into Drugs. WILEY-VCH Verlag GMBH and Co. KGQA. Weinheim 2007; p: 248-260. 16. Sofowora A. Medicinal Plants and Traditional Medicines in Africa. Chichester John Wiley and Sons New York. 1993; p 97- 145. 17. Clark WS. Antimicrobial activities of phenolic constituents of Magnolia grandiflora L. Journal of Pharmaceutical. Science 1981; 70: 951-952.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN-0001November30HealthcareAPPENDICITIS IN THE ELDERLY - A MICROANATOMICAL PERSPECTIVE English3944A. AnandEnglish D. RavichandranEnglishBackground of the study: The appendix lies in the junction between small and large intestine. It is highly vascular and rich in lymphoid follicles and forms a part of Gut Associated Lymphoid Tissue (GALT). With advancing age, the diameter of the lumen and lymphoid follicles supposedly get reduced. Therefore appendicitis is less common in the elderly population and more common in the young and adolescents. Aim and Objective: To study the micro anatomical features of appendix in terms of presence of luminal diameter and lymphoid tissue in the walls of human vermiform appendix.Methodology: 54 post appendectomy specimens belonging to the age group of 40 – 80 years were utilized for the present study. The specimens were subject to routine histological study Results and Conclusion: The entire specimen (100%) showed histological evidence of presence of lumen and lymphoid tissue contrary to the conventional teaching. Englishappendix, lymphoid tissue, appendicitisINTRODUCTION The inflammation of the Human vermiform appendix always poses a challenge to the surgeon in spite of numerous technological and surgical advancements in the field of gastrointestinal surgery. The Human vermiform appendix is regarded as a specialized structure rather than as a vestigial organ 1 . Many factors contribute to the causative aspect of acute appendicitis; however the obstruction to the lumen by a facecloth is cited to be the commonest cause2 . In later decades of life the lumen is partially of wholly obliterated whereas it is widely patent in early childhood 3 . More so as age advances the lymphoid follicles in the walls of the vermiform appendix also undergo degeneration and is replaced by scar tissue. Since in the elderly the lumen of the appendix is either partially or fully obliterated and there is a reduction in the distribution of lymphoid tissue in the appendicular walls, logically there should be no inflammation of the organ in the older age group. The life expectancy has increased when compared to the previous century. Therefore the incidence of appendicitis in the elderly age group is on the rise4 . Undiagnosed appendicitis can lead to rupture of appendix which in turn will give rise to perforation and peritonitis. To our knowledge review of literature showed a dearth of histological studies proving the luminal obliteration and decrease of lymphoid follicles in the older age group. Therefore the present study is undertaken to introspect the state of lumen and lymphoid tissue in the elderly population from a micro anatomical point of view and its possible role in the pathogenesis of acute appendicitis. MATERIALS AND METHODS Specimen tissues of vermiform appendix was collected from patients undergone appendicectomy between the age group ranging from 44 years to 79 years over a period of three years after due clearance from the Institutional ethical committee and informed consent from the patient. The patients were elaborated about the reason for surgery and the procedure of surgery. They were explained about the significance of appendix and its functions. The process of histological sectioning was explained in common language. The significance of the study was also explained to them. They were assured of confidentiality and non-disclosure of identity. The total number of cases of elderly persons in the series was 54. Out of this 2 specimens belonged to female patients and 52 belonged to male patients. Persons undergoing negative appendicectomy and cases of gangrenous appendicitis were excluded from the purpose of study. The obtained specimen tissues were processed and stained with hematoxylin and eosin and were observed under microscope for the presence of appendicular lumen and aggregations of lymphoid follicles. DISCUSSION The incidence of acute appendicitis in adolescents is 20%5 . Few other authors have reported that the life time risk of acute appendicitis is 7%2 . Acute appendicitis is more common in adolescents and young adults5 The pathogenesis of appendicitis is associated with obstruction (due to a faecolith) in majority of cases (50 to 80%)2 . Other causes include impaction due to a gall stone, tumor or ball of worms. This is usually the outcome of increased intraluminal pressure and retention of contents which allows acute suppuration to occur3 . However less commonly, in some number of cases the inflammation is not associated with luminal obstruction and the pathogenesis of the inflammation is not known. When inflammation of the appendix exceeds its confines there is a significant increase in the rate of mortality5 This has been attributed to the atypical presentation of appendicitis due to physiological changes and disease manifestation in the elderly population1 According to conventional teaching and prescribed standard texts, the lumen of the human vermiform appendix is either partially or fully obliterated in old age. In a study on Bangladeshi people, Rahman MM (2008)6 reported a progressive decrease in the weight of the appendix with age. The maximum luminal diameter was observed in the age group of 21-35 years and the minimum luminal diameter was noted in the elderly age group (56-70 years)6,7. The presence of lymphoid follicles in the walls undergo a significant reduction in the elderly which invariably leads to a delayed or decreased immune response2,8 All these factors, reduced luminal diameter, decreased lymphatic follicle and its replacement by fibrous tissue have been attributed to a reduction in the incidence of acute appendicitis in the elderly. Therefore the diagnosis of appendicitis in the elderly age group is difficult to make and it carries a significantly increased risk of mortality and complications9 In the present study the samples were collected from patients aged above 40 years. All the specimens (n= 54) showed presence of appendicular lumen and aggregation of lymphoid follicles in the walls irrespective of the age distribution (44yrs – 79 years, the mean age being 64 yrs). The presence of the lumen and aggregation of lymphoid follicles in all the cases (100%) is contrary to the conventional and established teaching. CONCLUSION In summary, in the present series the authors did not observe any case with obliteration of appendicular lumen, reduction or absence of lymphoid aggregations in the walls of the appendix in elderly age group. These findings in the present study indicate that the human vermiform appendix still is an enigma and cannot be taken lightly by surgeons with regards to its age. In elderly persons with pain abdomen the appendicitis should be also included as a probable cause since, the morbidity and mortality associated with this condition at this age is significantly higher. However the authors recommend future studies with a larger sample size to establish our findings. ACKNOWLEDGEMENTS The authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Englishhttp://ijcrr.com/abstract.php?article_id=1864http://ijcrr.com/article_html.php?did=18641. Peter L Williams and Warwick. Gray‘s Anatomy In: Splanchnology. 36th ed; Churchill Livingstone, Edinburgh; 1986: 1353 - 1354 2. Chen Liu. Robbins and Cotran Pathologic Basis of Disease in: The Gastrointestinal Tract. 7th ed; Elsevier, Philadelphia; 2007: 870 - 872 3. Neil R Borley. Gray‘s Anatomy, The Anatomical Basis of Clinical Practice In: Abdomen and Pelvis. 40th edn; Churchill Livingstone, Spain; 2008: 1142 – 1144 4. Sanda RB, Seliem SI, Omar E, Ashraf S. Perforated appendicitis in a septuagenarian. Ann Afr Med 2011;10:249-51 5. Charles V. Mann. Bailey and Love‘s Short Practice of Surgery In: The Vermiform Appendix. 22nd ed; ELBS, London; 1995: 828- 841 6. Rahman MM, Khalil M, Khalil M, Jahan KM, Shafiquazzaman M, Parvin B. Mass of the Vermiform Appendix in Bangladeshi People. J Banglades Soc Physiol. 2008 Dec; (3): 8-12 7. Bhide SA, Waderkar KV, Koushik SA. Peyer‘s patches are precocious to the appendix in human development. Dev. Immunol. 2001; 8(2):159 – 66. 8. Datta AK. Essentials of Human Anatomy. Part – I. 6th ed. Calcutta: Current Books International. 2007. P.228-30 9. Gurleyik G, Gurleyik E. Age-related clinical features in older patients with acute appendicitis. Eur J Emerg Med 2003;10:200-3
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN-0001November30TechnologyEXPERIMENTAL ANALYSIS OF THE EFFECT OF FIN GEOMETRY ON HEAT TRANSFER RATE THROUGH THE REFRIGERATOR CONDENSER English4551G. Kiran KumarEnglishA refrigerator is a machine which attains and maintains the temperature of a space below that of surroundings by transferring heat from the space to be cooled to the surroundings with the help of a compressor. Majority of the refrigerators works on the vapor compression refrigeration system which consists of components like compressors, condensers, expansion valve and evaporator. The performance of the system depends on the performance of all the components of the system. A condenser is a heat exchanger where the refrigerant is first desuperheated and then the saturated vapor condenses into liquid state. This is an important part of the refrigeration cycle without which the refrigerant cannot be recycled. In general all the domestic refrigerators have naturally air cooled condensers. Heat transfer from suchcondensers can be increased by the extended surfaces called fins. The rate of heat transfer through condenser depends on fin material, spacing between the fins, geometry of the fins and it‘s thermal conductivity. This experimental work focuses on the effect of condenser fin geometry on the performance of the condenser. Experiments are conducted with circular and rectangular cross sectional fins fabricated to the condenser of 165 lts capacity refrigerator. Heat transfer rate through the condenser is calculated for different fin geometries. EnglishINTRODUCTION A condenser is a heat exchanger is which desuperheating of high temperature vapor changes the phase from vapor to liquid and sub cooling of condensate occurs. The condenser is an important device used in the high pressure side of a refrigeration system. Its function is to remove heat of hot vapor refrigerant discharged from the compressor. The hot vapor refrigerant consists of the heat absorbed by the evaporator and the heat of compression added by the mechanical energy of the compressor motor. The heat from the hot vapor refrigerant in a condenser is removed first by transferring it to the walls of the condenser tubes and then from the tubes to the condensing or cooling medium. The cooling medium may be air or water or a combination of the two. An air cooled condenser is one in which the removal of heat is done by air. It consists of steel or copper tubing through which the refrigerant flows. The size of tube usually ranges from 6mm to 18mm outside diameter, depending upon the size of the condenser. Generally copper tubes are used because of its excellent heat transfer ability. The condensers with steel tubes are used in ammonia refrigerating systems. Majority of the domestic refrigerators uses the natural convection air cooled condenser. In the present work refrigerator uses the natural convection air cooled condenser. In natural convection air cooled condenser, the heat transfer from the condenser coils to the air is by natural convection. As the air comes in contact with the warm condenser tubes, it absorbs heat from the refrigerant and thus the temperature of air increases. The warm air being lighter, rises up and cold air from below rises to take away the heat from the condenser. This cycle continues in natural convection air cooled condensers. This paper is an experimental approach to increase the heat transfer through the condenser with different fin geometry . If the condenser is having circular fins the heat transfer through the condenser is less. Because of it small surface area. On the other hand if the condenser is having rectangular fins the heat transfer through the condenser is more, because of its more surface area. PRESENT WORK: The procedure for the present work is as follows. In vapor compression refrigeration system basically there are two heat exchangers. One is to absorb the heat which is done by evaporator and another is to reject the absorbed heat in the evaporator to the surroundings. The work focuses on more heat transfer through the condenser. This is only possible either by providing a fan or extending the surfaces. The extended surfaces are called fins. The rate of heat transfer through the condenser depends upon the number of fins and fin geometry attached to the condenser. The present work investigates the rate of heat transfer through the condenser using different fin geometry. In the present domestic refrigerator of the condenser fins are circular and rectangular are used and compared. In order to know the performance characteristics of the vapor compression refrigeration system pressure and temperature gauges are installed at each entry and exit of the component. Experiments are conducted on different fin geometry of the condenser. All the values of pressures and temperatures are tabulated. The domestic refrigerator selected for the present work has the following specifications. Capacity of refrigerator - 165liters Refrigerant used - R134a Compressor - 1/7 HP Hermetically Capacity sealed. Condenser Length - 8.5m Diameter - 6.5mm Evaporator Length - 7.62m Diameter - 6.5mm Capillary tube Length - 2.128m Diameter - 0.8mm   Calculations and analysis: Where P1 = Compressor suction pressure P2 = Compressor discharge pressure P3 = Condensing pressure P4 = Evaporator pressure T1 = Compressor suction temperature T2 = Compressor discharge temperature T3 = Condensing temperature T4 = Evaporator temperature Analysis of the condenser: Thermal analysis in the heat exchangers can be done in two ways. 1. LMTD Method (Logarithmic Mean Temperature Difference) 2. NTU Method ( Number of Heat transfer Units) LMTD Method is useful when the inlet and outlet fluid temperatures of condenser and air are known. NTU Method is useful when the heat exchanger is designed for the particular mass flow rate. For the given conditions LMTD Method is suitable. LMTD Method: In a heat exchanger, the temperature of the heating and cooling fluids do not in general, remain constant, but vary from point to point along the length of the heat exchanger. Since the temperature difference between the two fluids keeps changing, the rate of heat transfer also changes along the length of the heat exchanger as shown. The rate of heat transfer can be calculated from the relation Q = U A ?T Since ?T changes from point to point in a heat exchanger, we propose to use ?Tm, a suitable mean temperature difference between the two ends of a heat exchanger. The rate of heat transfer can be rewritten as Q = U A ?Tm Where ?Tm = Log Mean Temperature Difference (LMTD) A = surface area of condenser in m2 = ΠDL ?Tm = (?T1-?T2)/ln (?T1/?T2) Where ?T1 = Th1-TC1 ?T2 = Th2-TC2 Th1 =Refrigerant temperature at Condenser inlet Th2 = Refrigerant temperature at Condenser outlet Tc1 = Air temperature at the condenser inlet Tc2 = Air temperature at the condenser outlet Where U = overall heat transfer coefficient in w/m2 k Ao = outside tube Area in m2 Ai = inside tube Area in m2 hi = convective heat transfer coefficient of R-134(a) in W/m2 k ho = convective heat transfer coefficient of Airin w/m2 k = 10 W/m2 k ro = outside radius of pipe in m ri = inside radius of pipe in m K = thermal conductivity of copper in W/m-k If Ao = Ai the above equation can be reduced to U = 1/ (1/ hi + 1/ ho) Properties of R-134(a) are taken at bulk mean temperature of condenser with different fin geometry. Bulk mean temperature of condenser can be calculated by = (Condenser inlet temp. + Condenser outlet temp.)/2 In order to calculate convective heat transfer coefficient of R-134(a) the following steps are to be followed and the convection is of forced convection pipe flow with respect to refrigerant. ReD = (ρVD)/μ Pr = (μ Cp)/K Where ReD = Reynolds number ρ = Density of R-134(a) in kg/m3 V = Velocity in m/sec = 3 to 4 m/sec D = Diameter of the pipe in m μ = Viscosity in pa-s Cp = specific heat in J/kg K K = thermal conductivity in W/m K Forced convection correlations in turbulent pipe flow are given by Dittus-Boelter NuD = 0.023ReD 4/5 Prn NuD = hiD/K Where D= Diameter of the pipe = 6.5x10-3m Pr = Prandtl number n = 0.4 for heating of the fluid and 0.3 for cooling of the fluid The Dittus-Boelter equation is valid for  0.7< Pr < 160 and Red  >10000 The Dittus-Boelter equation is good approximation where temperature differences between bulk fluid and heat transfer surface are minimal .Nusselt number: In heat transfer at boundary (surface) within a fluid, the Nusselt number is the ratio of convective to conductive heat transfer across (normal to) boundary. Named after Wilhelm Nusselt, it is a dimensionless number. A Nusselt number is close to one for slug or laminar flow. It varies for turbulent flow. For forced convection, the Nusselt number is generally a function of the Reynolds number and prandtl number, or Nu = f (Re, Pr). Calculation of overall heat transfer coefficient Condenser coil dimensions: Outer diameter of tube = 6.5mm Inner diameter of tube = 6mm For Test -1 Refrigerant temperature at condenser inlet = 56.20C Refrigeranttemperature at condenser outlet =45.80C Air temperature at the condenser inlet = 33.20 C Air temperature at the condenser outlet = 34.20 C For Test -2 Refrigerant temperature at condenser inlet = 68.50C Refrigeranttemperature at condenser outlet =38.50C Air temperature at the condenser inlet = 31.20 C Air temperature at the condenser outlet = 32.20 C Calculations: Inside heat transfer coefficient for condenser coil Sizes of tube: Outer diameter of tube = 6.5mm Inner diameter of tube = 6mm For Test -1 Condenser entering temperature = 56.2 0 C Condenser leaving temperature = 45.8 0 C Air temperature at the condenser inlet = 33.20 C Air temperature at the condenser outlet = 34.20 C Mean temperature = (56.2 +45.8)/2 = 56 0C Mean temperature = 560C at this temperature properties of From R-134a are From R-134a refrigerant property tables ρ = 1073.0 kg/m3 D = 6.5 X 10-3 m μ = 146.1 X 10-6 pa-.s V = 3.5 m/s K = 67.6x 10-3 W/m k Cp= 1.621 x103 J/kg k ReD = (ρvD)/ μ = (1073x3.5x6.5 X 10-3 )/ 146.1X 10-6 = 1.67x105 Pr = (μ Cp)/K = (146.1 x10-6 x1. 621x103 )/ (67.6x10-3 ) = 3.503 NUD = 0.023ReD 4/5 Prn = 0.023x (1.67 x105 ) 4/5 x (3.503)0.3= 504.932 NuD = hiD/K 516.514 = (hi 6.5 X 10-3 )/ 67.6x10-3 hi = 5251.29 W/m2 k U = 1/ (1/ hi + 1/ ho) = 1/(1/5251.29 + 1/10) = 9.981 W/m2K ?Tm = (?T1-?T2)/ln(?T1/?T2) =(23-11.6)/ln(23/11.6) =16.650 c ?T1 = Th1-TC1= 56.2-33.2 = 230 C ?T2 = Th2-TC2 = 45.8-34.2 = 11.60 C ?Tm = (23-11.6)/ln(23/11.6) = 16.654oC Q =Heat transfer rate through the condenser = U A ?Tm Q= 9.998xπx6.5x10-3 x8.5x16.654 = 28.84 W For Test- 2 Q=Heat transfer rate through the condenser Q = U A ?Tm Q=9.981X6.5X8.5X10-3X17.43=30.19W RESULTS AND CONCLUSIONS Referring to fig.5 it is seen that the rate of heat transfer through the condenser is maximum for the rectangular fin geometry when compared to the circular fin geometry of the condenser. In the existing system condenser fin geometry is circular. When compared with the rectangular fin geometry of the condenser the present work produces the following results. Heat transfer rate is increased by 4.68% For the rectangular fin geometry when compared to the circular fin geometry. This is because of rectangular plate fins have more surface area. The Refrigerator condenser performance can be enhanced with the help of Rectangular plate fin geometry of the condenser Where ?Tm = log mean temperature difference. Condenser entering temperature = 56.2 0 C Condenser leaving temperature = 45.8 0 C Air temperature at the condenser inlet = 33.2 0 C Air temperature at the condenser outlet = 34.20 C Analysis of the condenser: Thermal analysis in the heat exchangers can be done in two ways. 1. LMTD Method (Logarithmic Mean Temperature Difference) 2. NTU Method ( Number of Heat transfer Units) LMTD Method is useful when the inlet and outlet fluid temperatures of condenser and air are known. NTU Method is useful when the heat exchanger is designed for the particular mass flow rate. For the given conditions LMTD Method is suitable. LMTD Method: In a heat exchanger, the temperature of the heating and cooling fluids do not in general, remain constant, but vary from point to point along the length of the heat exchanger. Since the temperature difference between the two fluids keeps changing, the rate of heat transfer also changes along the length of the heat exchanger as shown. The rate of heat transfer can be calculated from the relation Q = U A ?T Since ?T changes from point to point in a heat exchanger, we propose to use ?Tm, a suitable mean temperature difference   Properties of R-134(a) are taken at bulk mean temperature of condenser with different fin geometry. Bulk mean temperature of condenser can be calculated by = (Condenser inlet temp. + Condenser outlet temp.)/2 In order to calculate convective heat transfer coefficient of R-134(a) the following steps are to be followed and the convection is of forced convection pipe flow with respect to refrigerant.   n = 0.4 for heating of the fluid and 0.3 for cooling of the fluid The Dittus-Boelter equation is valid for 0.7< Pr 10000 The Dittus-Boelter equation is good approximation where temperature differences between bulk fluid and heat transfer surface are minimal.   Nusselt number: In heat transfer at boundary (surface) within a fluid, the Nusselt number is the ratio of convective to conductive heat transfer across (normal to) boundary. Named after Wilhelm Nusselt, it is a dimensionless number. A Nusselt number is close to one for slug or laminar flow. It varies for turbulent flow. For forced convection, the Nusselt number is generally a function of the Reynolds number and prandtl number, or Nu = f (Re, Pr). Calculation of overall heat transfer coefficient Condenser coil dimensions: Outer diameter of tube = 6.5mm Inner diameter of tube = 6mm   RESULTS AND CONCLUSIONS Referring to fig.5 it is seen that the rate of heat transfer through the condenser is maximum for the rectangular fin geometry when compared to the circular fin geometry of the condenser. In the existing system condenser fin geometry is circular. When compared with the rectangular fin geometry of the condenser the present work produces the following results. Heat transfer rate is increased by 4.68% For the rectangular fin geometry when compared to the circular fin geometry. This is because of rectangular plate fins have more surface area. The Refrigerator condenser performance can be enhanced with the help of Rectangular plate fin geometry of the condenser. Englishhttp://ijcrr.com/abstract.php?article_id=1865http://ijcrr.com/article_html.php?did=18651. Abu Madi M. Johns, R.A and Heikal M.R (1998).Performance chracteristics correlation for round tube and plate finned heat exchangers, int J.Refrigeration.Vol.21(7),pp.507-517. 2. Achaichia,A and Cowel ,T.A (1998).Heat transfer and pressure drop characteristics of flat tube and louvered plate fin surfaces ,Exp .Thermal fluid sci.Vol 1(2),pp.147-157. 3. Chang,W.R Wang C.C Tsi W.c and Shyu, R.J(1995)Air side performance of louver fin heat exchanger,4 th ASME/JSME Thermal Engineering Joint Conference.Vol.4,pp.467-372. 4. Du, Y.J and Wang CC (2000).An Experimental study of the Airside performance of the superslit Fin-andTube Heat exchangers.Int.J.Heat mass transfer,Vol.43,pp.4475-4482 5. Gray.D.L and Webb, R.L(198^)Heat Transfer and Frictio Correlations for plate Finned-Tube Heat Exchangers having plain fins ,proceeding 8 th International journal of Heat transfer conference,Vol.6,pp.2745-2750
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18TechnologyDESIGN AND ANALYSIS OF COMPACT CPW-FED UWB ANTENNA FOR WIRELESS COMMUNICATION APPLICATIONS English5258D. UjwalaEnglish B.T.P.MadhavEnglish J. RajanikanthEnglish B.JyothiEnglish B.HarishEnglish H.M.RameshEnglishFor the exchange of high data rate information, wide band antennas are needed and their usage increased tremendously now a days. A compact antenna of size 22mm x 26mm x 1.6mm is proposed with serrated radiating patch and ground fed by Coplanar Waveguide Feedline (CPW). The proposed antenna concedes a wide bandwidth from 3.2 GHz to 10.8 GHz with return loss less than -10dB, VSWR less than 2 and has Omni directional radiation pattern with good radiation efficiency in the operating bandwidth. The proposed antenna is simulated using FEM based Ansoft HFSSv13 and the results are analyzed. EnglishCoplanar Waveguide, UWB antenna, VSWR, Omni directional pattern, Radiation efficiencyINTRODUCTION Ultra wideband communication systems have incurred great attraction in wireless world. Recently, a tremendous attention has been focused on these UWB communication systems since they are capable for exchanging high rate information. The Federal Communication Commission allocated a bandwidth from 3.1 GHz to 10.6 GHz for UWB systems [1] in 2002. The major challenges in the design of UWB antenna are Compact size, Omni directional pattern and stable gain along with wide bandwidth [2] and high speed data rate. The UWB antenna provides secured signal transmission, immunity to interference and low power consumption. UWB antennas are integrated in systems where band notch characteristics are needed [3-4]. Parasitic elements added to the antenna provide broad bandwidth but increases size of antenna [5]. The planar monopole antennas [6-8] are better for UWB applications due to compact size and static radiation pattern. UWB antennas can be implemented with microstrip line [9] or CPW [10]. The CPW antennas are useful for microwave and millimeter applications since they offer low profile and ease of integration with circuits. Few other applications of UWB antenna are position location and tracking, automotive sensors, collision avoidance sensor in vehicles etc. In this paper, we have proposed a planar monopole antenna with CPW feed with a wide bandwidth from 3.2 GHz to 10.8 GHz. It provides nearly Omni-directional pattern, high radiation efficiency and approximately stable gain. ANTENNA STRUCTURE:The geometry of the proposed CPW-fed antenna is shown in Figure 1. The antenna is printed on a FR4 substrate with dielectric constant εr=4.4, loss tangent δ=0.02 and thickness h=1.6mm. The serrated radiating patch consists of three rectangles of lengths L1, L2, L3 and widths W1, W2, W3 respectively. The ground plane is a combination of three rectangles of lengths L4, L5, L6 and widths W1, W2, W3 respectively on either side of CPW feed line. The gap between the radiating patch and ground plane is d=2mm. The antenna is fed by a 50? CPW line with a feed line length Lf, strip width W and gap G. The various configuration parameters of the antenna are L1=20mm, L2=15mm, L3=12mm, L4=8.15mm, L5=5.65mm, L6=4.15mm, W1=8mm, W2=2mm, W3=2mm, Lf=12mm, d=2mm, G=0.35mm, W=3mm, h=1.6mm, εr=4.4 RESULTS AND DISCUSSIONS The Return Loss is less than -10dB from 3.2 GHz to 10.8 GHz as shown in Figure 2 and resonates at three frequencies 3.92 GHz, 6.24 GHz and 10.08 GHz whose return losses are -33dB, -17dB and - 16dB respectively.  Figure 3 shows the VSWR plot and it is less than 2 in the operating bandwidth. Figure 4 is a Gain versus Frequency plot with a maximum gain of 4.1dBi at 8 GHz and gain is approximately stable in the operating bandwidth. Figure 5 shows E-Field, H-Field and Surface current distributions on the patch and ground of the antenna at 3.92 GHz, 6.24 GHz and 10.08 GHz. Figure 6 shows the Mesh Plots on the patch and ground of the antenna at 3.92 GHz, 6.24 GHz and 10.08 GHz. For each mode, there are two orthogonal planes in the far field region. One designated as E-plane and the other designated as H-plane. The far zone electric field lies in the E-plane and the far zone magnetic field lies in the H-plane. The patterns in these planes are referred to as the E and H plane patterns respectively. Figure 7 shows the co-polarization and cross-polarization radiation patterns in E-Plane and H-Plane at 3.92 GHz, 6.24 GHz and 10.08 GHz respectively. Figure 8 shows the contour plots for different values of theta versus phi.   Table 1 shows antenna output parameters like Peak Gain, Peak Directivity, Radiated Power, Radiated Efficiency etc at three resonant frequencies at 3.92 GHz, 6.24 GHz and 10.08 GHz. Table 2 shows radiated field data at Phi and Theta angles at those three resonant frequencies. CONCLUSION A Compact CPW-fed UWB antenna for wireless applications is designed and analyzed using Ansoft HFSS vs.13. Antenna resonates at three frequencies 3.92 GHz, 6.24 GHz, 10.08 GHz. The antenna exhibits Omni-directional radiation pattern in H-Plane and quasi Omni-directional pattern in E-Plane. It is observed that cross polarization is less than co-polarization in E and H Planes. ACKNOWLEDGEMENTS We would like to express our gratitude towards the Management and Department of ECE, K.L.University for their support during this work. Englishhttp://ijcrr.com/abstract.php?article_id=1866http://ijcrr.com/article_html.php?did=18661. FCC, First report and order in the matter of revision of part 15 of the Commission&#39;s rules regarding ultra-wideband transmission systems, FCC, Washington, DC, ET-Docket 98- 153, 2002. 2. K.L. Wong, Compact and broadband microstrip antennas, Wiley, Hoboken,NJ 2002. 3. G. M. Zhang, J. S. Hong, B. Z. Wang, Q. Y. Qin, J. B Mo, and D. M. Wan, ?A novel multi folded UWB antenna fed by CPW,? J. of Electromagn. Waves and Appl., Vol. 21, No. 14, 2109-2119, 2007. 4. Shi-Wei qu, Jia–Lin Li, and Quan Xue, ?A band notched ultra wide band printed monopole antenna,? IEEE Antennas Wireless Propa. Lett., vol. 5, pp. 495-498, 2006. 5. K. F. Jacob, M. N. Suma, R. K. Raj, M. Joseph and P. Mohanan, ?Planar branched monopole antenna for UWB applications,? Microw. Opt. Technol. Lett., Vol. 49, no. 1, pp 45-57, Jan. 2007. 6. Y. J . Cho, K. H. Kim, D. H choi, S. S. Lee and S. O. Park, ?A miniature UWB planar monopole antenna with 5-GHz band rejection filter and time domain characteristics,? IEEE trans. Antennas Propag., vol.54, pp. 1453-1460, Mar. 2006. 7. W. S. Lee, D. Z. Kim, K. J. Kim and Y. W. Yu, ?Wideband planar monopole antenna with dual band–notched characteristics?, IEEE trans. Antennas Propag., vol.54, no. 6, pp. 2800-2806, Jun. 2006. 8. Reza Zaker, Changiz Ghobadi and Javad Nourinia, ?Novel modified UWB planar monopole antenna with variable frequency band-notch function?, IEEE Antennas Wireless Propag. Lett.,, vol. 7, pp. 112-114, 2008. 9. Jen-Yea Jan, Liang-Chih Tseng, "Small Planar Monopole antenna With a Shorted Parasitic Inverted- L Wire for Wireless Communications in the 2.4, 5.2 and 5.8 GHz Bands," IEEE Trans. Antennas and Propagation, vol. AP-52, no. 7, pp. 19031905, July 2004. 10. Jon II Kimker and Yong Jee, ?Design of Ultra wideband Coplanar waveguide-fed LIshape planar monopole antennas?, IEEE Antennas Wireless Propag. Lett.,, vol. 6, pp. 383-387, 2007.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareEFFECT OF RESPIRATORY ENDURANCE TRAINING ON PULMONARY FUNCTION TEST English5964Muneeb JehanEnglish Shaikh MohsinEnglish Mohamed Irshad AhmadEnglish Jabbar AfjalEnglish Pasha ArifEnglishBackground: Respiratory endurance focuses on increasing respiratory muscle resistance with the use of regular endurance training exercise and to prevent respiratory disabilities leading to respiratory failure.Aim: to study the effect of respiratory endurance training exercise on lung volumes and lung capacities in young healthy human adults. Methods: Research was conducted on 60 health young adults including randomly selected 31 males and 29 female students of Osmania medical college of Hyderabad (India), studying in final year of graduate program. They were made to exercise 30 minutes thrice a week for 3 times a day for 16 weeks. Research was conducted at post graduate physiology research lab during January- March 2005. Results: Lung Capacities were compared pre test and after a completion of 16 weeks of respiratory endurance training in young health subjects of age group 18-30 yrs. Mean weight was 59 kg and mean height was 160 cm, while the mean body surface area was 1.59 m2. Pulmonary  function tests were conducted and determined on these subjects by using Medspirer. First phase of recordings were done before starting of the exercise training and second phase recordings were done at the end of 16 weeks. The following parameters were recorded: Forced Vital Capacity, Forced expiratory volume at 1 second, Maximum Voluntary volume, Inspiratory reserve volume, Vital Capacity and Endurance Test Time). All the parameters have shown significant increase in the second phase when compared to the first phase. Our study has shown that the Pulmonary Function Tests values are higher after exercise training. Conclusion: Mechanical efficiency leads to increase in skeletal muscle strength which finally increases respiratory airflow meaning increase in all pulmonary function tests. Englishrespiratory endurance, respiratory muscles, lung capacities, pre test and post testINTRODUCTION Pulmonary ventilation is generally known to have a linear relationship with oxygen consumption at different levels of exercise. Oxygen consumption is also known to increase the resting state and intense exercise. Lung function parameters tend to have a relationship with lifestyle such as regular exercise and nonexercise1, 2. Endurance results from an increase in intensity of work performed in a given unit of time. Work may be intensified by raising the cadence as experiences in running faster or by increasing the resistance against which the muscles contract as experienced in lifting heavier weight. This principle provides the rationale for all progressive resistance exercise program. Endurance is the ability to withstand fatigue, or the ability of the body to withstand the stresses set by prolonged activity which produces fatigue. Endurance includes aerobic endurance, anaerobic endurance and muscular endurance. These types of endurance are closely related within the unity of human organism. The effectiveness of each to some extent is dependent upon others and the development of each type compliments the effectiveness of the others, aerobic endurance also known as general endurance or stamina is the general ability to withstand fatigue of entire organism in the presence of sufficient supply of oxygen over a pronged period. It involves the ability to resist fatigue under conditions where oxygen intake and oxygen requirements for activity are kept at a steady and equal level. This quality is called cardiovascular endurance and .circulo-respiratory endurance is most evident in work of medium intensity involving the entire organism. Endurance exercises stimulate the mobilization and oxidation of fatty acids to plasma which are delivered to skeletal muscle for fuel. Endurance training leads to increase in plasma epinephrine and non epinephrine concentration, basal plasma insulin concentration increases after exercise training. Lung function tests provide qualitative and quantitative evaluation of pulmonary function and are therefore of definitive value in the diagnosis and therapy of patients with cardiopulmonary disorders as well as those with obstructive and restrictive lung disease3,4. The parameters used to describe lung function are the lung volumes and lung capacities. While the various lung volumes reflect the individual‘s ability to increase the depth of breathing the capacities is simply a combination of two or more lung volumes. Exercise when performed regularly has benefits on the various systems of the body. Regular exercise has a favorable influence on cardiovascular functions and also lung functions. Pulmonary function tests measure lung volumes and capacities. Our research focuses on magnitude of the role of endurance development in respiratory muscle and its effect of lung volume and lung capacities. This should be put in practical application on bed side clinics in respiratory care centers and cardio thoracic surgical wards and centers dealing with neuromuscular disorders. The ultimate goal is to prevent respiratory failure, which may occur in such disorders and to offer the subject a quality of life, with better physical capabilities. The present study was carried out to know the effect of long term stress in the form of exercises and sports activities, on Pulmonary Function Tests. MATERIAL AND METHODS A quasi experimental study was conducted on randomly selected 60 healthy young adults between January to march 2005, which included 31 male 29 female individuals in the age group of 18-30 years from Osmania Medical College, Hyderabad (India). Study group comprises students of Osmania medical college and it was conducted at post graduation research laboratory of Osmania medical college, Hyderabad. The subjects were made to exercise for 30 minutes thrice a week for three times a day, for a period of 16 weeks. Candidates were involved in the research after taking informed, verbal and written consent. All subjects were informed about the procedure and demonstration of the procedure was done for incentive spirometer and Med-spirer. Basic anthropometric measurements were recorded before the start of the research and data were analysed using SPSS version 17.0. Lung volumes and capacities were measured according to established methods with the use of spirometer and Medspirer at two different phases. 1st phase recorded before the start of the exercise containing baseline data and 2nd phase was recorded at the end of respiratory endurance training involving physical exercise at the end of 16th week. Subjects suffering from hypertension, Diabetes, any respiratory tract infections or lung diseases, recent heart attack and smokers were excluded. The pulmonary function testing was done on Medspirer (automated pulmonary function analyser), which is an advanced microprocessor based on computerized pulmonary function testing device. Method of determining lung volumes using med spirer: Data such as height, weight, age, sex and temperature were fed to the Medspirer before recording the lung functions; the subject was made to sit in a comfortable position and the nose clip was put on the nose. A clean mouth piece was placed in breathing tube. The subjects were then asked to take a single maximum inspiration and exhale fully and rapidly with maximum effort before finally removing the mouth piece. The E key was kept pressed throughout this forced expiration. This was repeated three times and the best of the three readings were recorded. This manoeuvre also recorded FEV, PEFR, FEF 25-75 % and FEV simultaneously and same way other lung volume too  Precautions taken while conduction research: 1. Care was taken to give through instruction and demonstrations regarding the performance of the tests, records were taken after being fully satisfied. 2. Due care was also taken to avoid operational error on the part of observer and to maintain uniformity as far as possible. 3. The machine was calibrated at the start and in between while the research was going on, to check for accuracy, linearity and resistance. 4. Aseptic precautions including the use of KMNO4 solution for cleaning the mouth piece before and after the use were strictly adhered to. Below mentioned parameter were evaluated with the use of Medspirer. FVC – Forced vital capacity FEV – Forced expiratory volume FEV1- Forced expiratory volume in 1 sec FEV1/FC % - forced expiratory volume to forced vital capacity section FEF 25-75 % - Mean forced expiratory flow during middle half of FVC PEFR- peak expiratory flow rate FEF 25 % - Forced expiratory flow after 25 % of FVC has been expired FEF 50 % - Forced expiratory flow after 50 % of FVC has been expired FEF 75 % - Forced expiratory flow after 75 % of FVC has been expired FIVC- Forced Inspiratory vital capacity PIFR – Peak Inspiratory flow rate FIF 50 % - Forced expiratory flow after 50 % inspired FVC Other parameters includes MVV – Maximum Voluntary Ventilation ETT – Endurance Test Time RESULTS Lung Capacities were compared pre test and after a completion of 12 weeks of respiratory endurance training in young healthy 60 subjects (31 males and 29 females) of age group 18-30 yrs using incentive spirometer and Medspirer. Mean weight was 59 kg and mean height was 160 cm, while the mean body surface area was 1.59 m2 . There was not a significant difference between male and female lung parameters. Table 1 present baseline lung volume measurement which was recorded before the start of the exercise and table 2 represents lung volumes measured at the end of respiratory endurance training. When both the recordings are compared it showed a significant difference. Forced vital capacity (FVC) (2.15 l pretest while 2.85 l post test), Forced Expiratory volume at 1 second (FEV1) (2.15 l pretest while 2.61 l post test), Maximum Voluntary volume (MVV)( 88 lit/min pretest while 118 lit/min post test), Inspiratory reserve volume (IRV)( 1995 ml pretest while 2571 ml post test), Vital Capacity (VC)(2035ml pretest while 2571 ml post test) and Endurance Test Time (ETT)(28 seconds pretest while 36 seconds post test) were recorded and found highly significant at the end of endurance training exercise. Results from the present study showed significant difference in the lung function parameters of male and female subjects pre-test and post-tests. DISCUSSION Here regular physical activity causes many desirable physical, physiological and psychological changes in an individual consequently raising his level of fitness. Possible explanation for this could be regular forceful inspiration and expiration for prolonged period during training leads to strengthening of the respiratory muscles. This helps the lungs to inflate and deflate maximally. This maximum inflation and deflation is an important physiological stimulus for the release of surfactant5 . McCurdly and Larsen (1940) in their studies, working with trained subjects and untrained controls have shown that trained subjects had significantly higher vital capacity as compared to untrained6 . A study by Pansare MS showed one month training is sufficient to bring about increase in Pulmonary Function Test7 . One of the important outcome of this respiratory endurance exercise is to have its beneficial effects in cardiovascular and respiratory systems. Physical training programme of 8 months is necessary to bring about improvement in Cardio-respiratory function8 .Which is very much in relation to our research findings having a significant difference in pulmonary function test after implementing respiratory endurance training. CONCLUSION Results from the present study strongly suggest that the intensity or severity of the sports engaged in by the students probably determines the extent of strengthening of the respiratory muscles with a resultant increase in the lung volumes and that way chronic exercise may cause an increase in the respiratory function which could be due to increased development of respiratory musculature incidental to physical training. ACKNOWLEDGEMENT Author acknowledges the immense help received from the scholars whose articles are cited and included in references of this manuscript. The author is also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Englishhttp://ijcrr.com/abstract.php?article_id=1867http://ijcrr.com/article_html.php?did=18671. Wassreman K, Gitt A, Weyde I, Eckel HE. Lung function changes and exercise-induced ventilator responses to external restive loads in normal subjects. Respiration 1995, 62 (4), 177-84. 2. Twick 1W, Staal BJ, Brinknian MN, Kemper HC, Van Mechelen W. Tracking of lung function parameters and the longitudinal relationship with lifestyle. Eur, Resp. J. 1998, 12 (3), 627-34. 3. Beirnan, MJ, Miuman C.: Ventilatory muscle training improves exercise capacity in COPD patients, 1980, AmResp Dis. 121; 273-9. 4. Robinson EP, Kjeldqard JM. 1 Improvement Inventilatory muscle function with running. J. Appl. Physiol 1982, 52, 1400— 1405. 5. Hildebrean JN, Georice I, Clements JA. Surfactant release in exercised rat lung stimulated by air inflation. Journal of Applied Physiology.1981, 51: 905-910. 6. Mc Curdly JH, Larson A. The Validity of circulatory respiratory measures as an index of endurance condition in swimming. Research quarterly.1940, 31: 3-11. 7. Pansare MS, Pradhan SG, Kher JR, Aundhkar UG, Joshi AR. Study of effect of exercise on Physical fitness tests and Pulmonary function tests in tribal girls of Maharashtra. Netaji Subhas National Institute of Sports Edition. 1930, 3 (4): 39-43. 8. Y J Cheng et al., Effect of physical activity on exercise test and respiratory function. Br J Sports Med 2003; 37:521–528.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18General SciencesCORONAL MASS EJECTIONS, STORMS IN SOLAR WIND PLASMA PARAMETERS IN RELATION WITH INTENSE GEOMAGNETIC STORMS English6577P.L. VermaEnglishCoronal mass ejections (CMEs) are the most energetic solar events in which large amount of solar plasma materials are ejected from the sun into heliosphere and are widely recognized as being responsible to generate disturbances in solar wind plasma parameters, interplanetary shocks and intense geomagnetic storms in the magnetosphere of the earth. I have studied intense geomagnetic storms (Dst ? - 100nT) observed during the period of 2001-2006, with halo and partial halo coronal mass ejections associated with X-ray solar flares and interplanetary shocks which are interplanetary manifestations of coronal mass ejections. I have found that 77.78% intense geomagnetic storms are associated with halo and partial halo coronal mass ejections. The association rate of intense geomagnetic storms with halo and partial halo coronal mass ejections are found 74.29% and 25.71% respectively. Further I have observed that intense geomagnetic storms which are associated with coronal mass ejections are also associated with X ray solar flares of different categories. The association rate of B-class, C-class, M-class and X-class X-ray solar flares are found 11.43%, 28.57%, 40.00%, and 20.00% respectively. From the study of intense geomagnetic storms with storms in solar wind plasma parameters, I have determined positive co-relation between magnitude of intense geomagnetic storms and peak values and magnitude of associated storm in solar wind plasma parameters with co-relation co-efficient 0.42 between magnitude of intense geomagnetic storms and peak values of associated storms in solar wind plasma velocity, 0.41 between magnitude of intense geomagnetic storms and magnitude of associated storms in solar wind plasma velocity , 0.792 between magnitude of intense geomagnetic storms and peak values of associated storms in interplanetary magnetic field, 0.787 between magnitude of intense geomagnetic storms and magnitude of associated storms in interplanetary magnetic field. Positive co-relation has also been found between magnitude of IMF and magnitude of solar wind velocity with correlation coefficient 0.54 and 0.53 between Maximum IMF and maximum solar wind velocity. EnglishIntense Geomagnetic Storms. Halo and Partial Halo Coronal Mass Ejections. Interplanetary Shocks, Storms in Solar Wind Plasma Parameters.INTRODUCTION Geomagnetic storms are the significant perturbations of the earth‘s magnetosphere that occur when the interplanetary magnetic field (IMF) turns southward (Bz classes of geomagnetic storms [3] recurrent and non recurrent have been studied by Londi and Moreno [4] with coronal mass ejections and they have concluded that CMEs which are associated with enhanced solar soft X ray emission, are responsible for large fraction of geomagnetic storms. Crooker and Cliver [5] have concluded that the non-recurrent geomagnetic storms are caused by coronal mass ejections and coronal holes / streamer, ensemble. I.G. Richardson et al [6] have determined that intense geomagnetic activity often associated with CME related structure and intense geomagnetic storms are produced by Coronal Mass Ejection at any stage of the solar cycle. Lyatsky and Tan. [7] have studied geomagnetic storms with disturbances in solar wind plasma parameters. They have concluded that the averaged disturbances in solar wind, responsible for generating geomagnetic storms, are associated with compression of ambient solar wind plasma and interplanetary magnetic field ahead of a high speed plasma flow. The magnetic field strength and plasma density start to increase, several hours before geomagnetic storm onset; however, the negative IMFBz start to increase approximately 4or 5 hours after the maximum variation in plasma and IMF By. Michalek and Gopalswamy et al [8] have concluded that only fast halo CMEs with space velocity higher than 1000 km/s and originating from the western hemisphere close to the solar center could cause intense geomagnetic storms. Magnetic clouds, interplanetary shocks, ejecta are the interplanetary manifestations of coronal mass ejections. Zhang and Burlaga [9] have studied geomagnetic storms with magnetic clouds and found that magnetic clouds can produce geomagnetic storms with the larger storms being associated with shock related clouds. The time of onset of the geomagnetic activity coincides with the arrival of magnetic clouds when the magnetic field is oriented southward at the cloud onset and it occurs later during the cloud when the magnetic field is oriented northward at the cloud onset.Richardson.et al. [10] have investigated geomagnetic storm with coronal mass ejections, they have determined that Intense geomagnetic storm are produced by coronal mass ejections at any stage of solar cycle. Shrivastava [11] has examined the solar origin of the geoeffective CMEs and their interplanetary effects, namely, solar wind speed, interplanetary shocks and the southward component of the interplanetary parameters. They have found that full halo CMEs associated with strong flares and originating from a favorable location, i.e. close to the central meridian and low and middle latitudes, are the most potential candidates for producing strong ram pressure at the earth‘s magnetosphere and hence intense geomagnetic storms. Gopalswamy et al [12] have studied geoeffectiveness, speed, solar source and flare association of a set of 378 halo coronal mass ejections (HCMEs) of solar cycle 23 (1996- 2005). They have found that the disk halos are followed by strong geomagnetic storms, limb halos are followed by moderate storms and back side halos are not followed by significant storms. They have concluded that disk halos and limb halos CMEs are very much effective in producing geomagnetic storms. Verma et al [13] have studied geomagnetic storms Dst < - 50nT observed during the period of 1997- 2006, with halo and partial halo coronal mass ejections associated with X-ray solar flares of different categories and concluded that halo and partial halo CMEs associated with X ray solar flares are most potential candidates for production of geomagnetic storms. In this investigation I have studied intense geomagnetic storms observed during the period of 2001to 2006 with coronal mass ejections and disturbances in solar wind plasma parameters (solar wind plasma velocity and interplanetary magnetic field ) to know the real cause of intense geomagnetic storms . Data and Analysis In this investigation hourly Dst indices of geomagnetic field have been used over the period 2001 to 2006 to determine onset time, maximum depression time, and magnitude of geomagnetic storms. This data has been taken from the NSSDC omni web data system which has been created in late 1994 for enhanced access to the near earth solar wind, magnetic field and plasma data of omni data set, which consists of one hour resolution near earth, solar wind magnetic field and plasma data, energetic proton fluxes and geomagnetic and solar activity indices. The data of CMEs and shocks have been taken from the list of shocks derived by PM/MTOF group from the SOHO observations, shocks arrival derived by the IPS group from ACE observations, shock arrival derived by WIND group from WIND observations SOHO, LASCO, CME catalogue which consists all CMEs manually identified since 1996 from large angle and spectrometric coronagraph(LASCO)onboardard(SOHO) (http://umtof.edu/pm/shocks.html,www.lmsal.c om/cgidiaposon/www_getcme_list_sh,htpp://p wg.gsfc.nasa.gov/wind/current_listIPS.html). The solar wind plasma parameter data has also been taken from NSSDC omni web data system RESULTS The association between intense geomagnetic storms (Dst < –100nT) and coronal mass ejections (CMEs), interplanetary shocks and disturbances in solar wind plasma parameters for the period 2001to 2006 are given in Table No.1. From the data analysis it is observed that 35 out of 45 (77.78%) intense geomagnetic storms are found to be associated with halo and partial halo coronal mass ejections. The association rate of halo and partial halo coronal mass ejections have been found 74.29 and 25.71% respectively. We have also determined that the coronal mass ejections, which are related to intense geomagnetic storms, are also related to the Xray solar flares of different categories. Out of 35 associated CMEs, 07 (20.00%) are related with X-class, 14 (40.00%) are related with Mclass, 10 (28.57%) are  Geomagnetic storm observed on 31.03.01 Onset time 31(04) in dd(hh) and magnitude, -379 nT, Shocks- Start time 31(00) in dd(hh). CMEs- Start time 28 (01.27) in dd(hh) and type- H. Solar flare- Start time28 (02) in dd(hh) and Class- M-17. Maximum jump in Geomagnetic storm observed on 11.04.01 Onset time 11(15) in dd(hh) and magnitude, -269 nT. Shocks- Start time 11(14) in dd(hh). CMEs- Start time 09 (15.54) in dd(hh) and type- H. Solar flare- Start time09 (15) in dd(hh) and Class- M-79. Maximum jump in solar wind velocity= 732km/s Magnitude of jump in solar wind velocity = 233km/s Maximum jump in IMF =34.5nT Magnitude of jump in IMF= 30.1nT. Geomagnetic storm observed on 05.11.01 Onset time 05(19) in dd(hh) and magnitude= -297 nT. Shocks- Start time 06(02) in dd(hh). CMEs- Start time 04 (16.35) in dd(hh) and type- H. Solar flare- Start time04 (16) in dd(hh) and Class- X-10. Maximum velocity Geomagnetic storm observed on 24.11.01 Onset time 24(06) in dd(hh) and magnitude -223 nT. Shocks- Start time 24(05) in dd(hh). CMEs- Start time 22 (20.30) in dd(hh) and type- H. Solar flare- Start time22 (20) in dd(hh) and Class- M-38. Maximum jump in solar wind velocity velocity= 946km/s. Magnitudeof jump in solar wind velocity =504km/s. Maximum jump in IMF =56.9 nT. Magnitude of jump in IMF= 51.2nT.   Geomagnetic storm observed on 28.10.03 Onset time 28(06) in dd(hh) and magnitude, -384 nT. Shocks- Start time 28(02) in dd(hh). CMEs- Start time 27 (08.30) in dd(hh) and type- P. Solar flare- Start time 27 (08) in dd(hh) and Class- M-27. Maximum jump in   Geomagnetic storm observed on 20.11.03 Onset time 20(02) in dd(hh) and magnitude, -461 nT. Shocks- Start time 20(07) in dd(hh). CMEs- Start time 18 (08.05) in dd(hh) and type- H. Solar flare- Start time 18 (09) in dd(hh) and Class- M-45. Maximum jump in solar wind velocity=703km/s Magnitudeof jump in solar wind velocity =262km/s. Maximum jump in IMF= 55nT. Magnitudeof jump in IMF =48.1nT. Geomagnetic storm observed on 07.11.04 Onset time 07(20) in dd(hh) and magnitude, -376 nT. Shocks- Start time 07(02) in dd(hh). CMEs- Start time 04 (09.54) in dd(hh) and type- H. Solar flare- Start time 04 (09) in dd(hh) and Class- C-63. Maximum jump in solar wind velocity =730km/s Magnitude of jump in solar wind velocity =386km/s. Maximum jump in IMF =47.8nT. Magnitude of jump in IMF =38.8nT.   Geomagnetic storm observed on 15.05.05 Onset time 15(05) in dd(hh) and magnitude, -293 nT. Shocks- Start time 15(02) in dd(hh). CMEs- Start time 13 (17.12) in dd(hh) and type- H. Solar flare- Start time 13 (16) in dd(hh) and Class- M-80. Maximum in solar wind velocity= 959km/s Magnitudeof jump in solar wind velocity =545km/s. Maximum jump in IMF =54.2nT. Magnitude of jump in IMF =48.4nT.   Geomagnetic storm observed on 24.08.05 Onset time 24(08) in dd(hh) and magnitude , -219 nT. Shocks- Start time 24(06) in dd(hh). CMEs- Start time 22 (01.31) in dd(hh) and type- H. Solar flare- Start time 22 (01) in dd(hh) and Class- M-26. Maximum jump in   found to be related with C-class and 04 (11.43%) are found to be associated with B class X-ray solar flares. From further analysis it is observed that majority of these intense geomagnetic storms are also related to the interplanetary shocks and the related shocks are forward shocks. I have 45 intense geomagnetic storms in our list in which 38 intense geomagnetic storms (84.44%) have been found to be associated with interplanetary shocks. From the study of intense geomagnetic storms with solar wind plasma parameters i.e. Jump in solar wind velocity (JSWV) and jump in interplanetary magnetic field we have determined positive co-relation between magnitude of intense geomagnetic storms and peak values and magnitude of associated storm in solar wind plasma parameters with corelation co-efficient 0.42 between magnitude of intense geomagnetic storms and peak values of associated storms in solar wind plasma velocity, 0.41 between magnitude of intense geomagnetic storms and magnitude of associated storms in solar wind plasma velocity , 0.792 between magnitude of intense geomagnetic storms and peak values of associated storms in interplanetary magnetic field, 0.787 between magnitude of intense geomagnetic storms and magnitude of associated storms in interplanetary magnetic field. From the study of disturbances in solar wind velocity and interplanetary magnetic field, it is observed that these two parameters are closely related. We have found positive correlation between magnitude of jump in solar wind velocity and magnitude of jump in interplanetary magnetic field with correlation coefficient 0.54 between these two events. Positive correlation has also been found between peak value of solar wind velocity and peak value of interplanetary magnetic field with correlation coefficient 0.53 between these two events. Further I have analyzed all the intense geomagnetic storms having storm magnitude ≤-200nT (severe geomagnetic storms) and the results are shown with the figure 7-15. From the analysis of severe geomagnetic storms .I have observed that all the geomagnetic storms are associated with halo and partial halo coronal mass ejections. The association rates of halo and partial halo coronal mass ejections have been found 88.88% and 11.12% respectively. Further these CMEs have been found to be related with XRay solar flares .All severe geomagnetic storms have been found to be associated with interplanetary shocks. I have also observed that all severe geomagnetic storms are associated with higher jump and peak values of associated disturbances in solar wind plasma parameters. CONCLUSION From our study 35 out of 45 intense geomagnetic storms < -100nT have been identified as being associated with coronal mass ejections and 90% of them are related to X-ray solar flares (CMEs). 38 out of 45 (84.44%) are identified as being associated with interplanetary shocks. These results are suggesting that the X-ray solar flares related coronal mass ejections associated with shocks is very much effective in producing major geomagnetic storms. The positive correlation between magnitude of intense geomagnetic storms and peak values and magnitude of solar wind velocity and interplanetary magnetic fields suggest that disturbances in solar wind parameters play crucial role in producing intense geomagnetic storms. Positive corelation between magnitude of IMF and magnitude of solar wind velocity and peak value of interplanetary magnetic field and peak value of interplanetary magnetic field suggesting that intense geomagnetic storms ,disturbances in interplanetary magnetic field and solar wind velocity are closely related . Further I have inferred that geomagnetic storms Dst < - 200 nT which are defined as severe geomagnetic storms are associated with higher jump and peak values of associated disturbances in solar wind plasma parameters including interplanetary magnetic field and interplanetary shocks .All severe geomagnetic storms are associated with X-ray solar flares .It is concluded that the severe geomagnetic storms are caused by coronal mass ejections associated with X –ray ray solar flares and related to interplanetary shocks . ACKNOWLEDGEMENT The author would like to thank Prof. P.K Shukla, S.K.Nigam and B.P.Chandra for valuable suggestions. The author is grateful to OMNIWEB and SOHO data group whose data have been used in this study. Englishhttp://ijcrr.com/abstract.php?article_id=1868http://ijcrr.com/article_html.php?did=18681. Gonzalez W.D. and B.T. Tsurutani planet, space sci. 35, 1101, 1987 2. Gonzalez W.D, J. Geophys Res. 99, 5771, 1994. 3. Cliver E.W EOS, Trans, AGU 76(8) 75, 1995. 4. R. Londi and G. moreno, J. Geophys Res. 103 No A5 20 20,553.1998. 5. E.W. Cliver J. Geophys Res. 99 23 , 383, 1994. 6. I.G. Richardson J. Geophys Res 105 No A8 18 703, 2000. 7. Lysatsky.W.and Tan.W.J. Geophys.Res. Vol 108,No A3,1134,2003 8.Michalek,Gopalswamy.G.,Lara.N.Yashiro. S.space weather Volume 4,Issue 10,2006. 9. Zhang.G.Burlaga.L.F.J.Geophys.Res.Vol.9 3.page 2511-2518 1998. 10. Rechardson I.G. E.W.Cliver.H.V.Cane. J.Geophys.Res.Vol. 105 18, 203, 2000. 11. Shrivastava.N.J.Geophys.Res.Vol. 109: A10, 103, 2004. 12. Gopalswamy.N.Yashiro.S.Akiyama.S.J.Gr ophys.Res.Vol.112.A06, 112, 2007. 13. Verma P.L. Tripathi A.K. & Sharma, Sushil J. Plasma Fusion Res. SERIES, Vol. 8 221, 2009.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareASSESSMENT OF GINGIVAL CREVICULAR FLUID LEPTIN LEVELS IN OBESE AND NON-OBESE INDIVIDUALS WITH AND WITHOUT CHRONIC PERIODONTITIS English7888Priyanka.K.CholanEnglish P.HarinathEnglish Pradeep K. ReddyEnglish C.S Anand MohanEnglishAim and Objectives: Leptin, a multifunctional adipokine and pleiotrophic hormone produced by the adipose tissue plays a significant role in pathogenesis of periodontitis. The purpose of this study is to compare the gingival crevicular fluid (GCF) leptin levels in obese and non-obese individuals with and without Chronic Periodontitis and to lend greater clarity to the role of leptin as a reliable biomarker for Periodontitis. Materials and Methods: Sixty subjects were divided into 4 groups of 15 each based on the clinical evaluation and body mass index (BMI) – Group I (obese with healthy periodontium), Group II (non-obese with healthy periodontium), Group III (obese with chronic periodontitis) and Group IV(nonobese with chronic periodontitis). GCF samples (by microcapillary pipettes) were collected to estimate the levels of leptin using enzyme linked immunosorbent assay (ELISA) kit Results: The mean GCF leptin levels in Group I is 715 ± 71pg/ml, Group II is 503 ± 230 pg/ml, Group III is 346 ± 82 pg/ml and Group IV is 137 ± 40 pg/ml. It proved that Group I and II had significantly higher leptin concentrations than Groups III and IV (pEnglishGCF, Leptin, Obesity, PeriodontitisINTRODUCTION Periodontitis is a polymicrobial and multifactorial infection characterized by a destructive inflammatory processes that leads to loss of tooth-supporting tissues. Although disease progression is episodic in nature at a tooth site level, the risk of developing periodontal disease is principally patient-based rather than site-based. While microorganisms are the primary etiologic agent in periodontitis, current research attributes tissue destruction as a consequence of an exaggerated host immune response.1,2 Obesity is associated with a state of chronic low level inflammation, which is characterized by abnormal cytokine production and activation of pro-inflammatory signaling pathways. Adipose tissue is not only a reserve passive organ but also a metabolically active endocrine organ releasing adipokines including Leptin, Adiponectin, Resistin, Visfatin, Serum retinol binding protein (RBP4) and various other cytokines.3 Leptin (Ob), a product of the ob gene is a 16 kDa non-glycosylated peptide hormone, synthesized mainly in adipocytes and in minor quantities by placenta, T cells, osteoblasts and gastric epithelium. It regulates weight control and modulates other physiological functions, such as regulation of neuroendocrine, reproductive, hematopoietic systems, and bone remodeling. It has been classified as a cytokine as it shows structural similarities to the long chain helical cytokine family [interleukin (IL)- 6]4 and during inflammation, leptin expression is altered in a manner similar to the cytokine response to infection and injury. Though it has been suggested that leptin modulates the host response by enhancing pro-inflammatory cytokine production and phagocytosis by macrophages,5 other studies have elucidated its anti-inflammatory role also.6,7 Very few studies address the problem of altered leptin levels in periodontal health and disease. Though there are no adipocytes in gingiva, studies by Johnson and Serio et al 20018 and Karthikeyan and Pradeep et al 20079 revealed that ?leptin concentration is higher in the healthy gingiva compared to diseased gingiva.? It may be due to the entrapment of leptin within gingiva by diffusion from microvasculature. Since, leptin has a role in inflammatory response,3 an increase in leptin level in healthy gingiva may be a host defense mechanism10. However, during gingival inflammation its concentration is decreased due to expansion of vascular network, which possibly increases the net rate of leptin removal from the gingival tissues and could raise serum leptin levels. Elevated serum leptin concentration have been suggested as a risk factor for cardiovascular disease by promoting atherosclerosis and enhancing calcification of arterial walls.11,26 Leptin levels and the role of Leptin in the pathogenesis of periodontitis is still a matter to be addressed and debated. Hence, this study is designed to 1) Assess the concentration of human leptin in GCF during periodontal health and disease 2) To find out the possible association between BMI and leptin levels 3) To explain it‘s potential role in the initiation and progression of periodontal disease. MATERIALS AND METHODS Patient selection A total of 60 adult patients, aged 21-48 years, who reported to the Department of Periodontology (SRM Dental College and Hospital, Chennai, India) were selected and randomly allocated to the 4 different groups of 15 each. Based on the Plaque index, CPITN index, radiograph evidence of bone loss and body mass index, according to the chart of the World Health Organization 200212 patients were categorized into four groups. BMI was computed as weight in kilograms divided by square of height in meters. Group I (obese with healthy periodontium) consisted of 15 patients who had clinically healthy gingiva with no evidence of bone loss and clinical attachment loss ie CAL=0 and BMI >30 kg/m2 Group II (non-obese with healthy periodontium) consisted of 15 patients who had clinically healthy gingiva with no evidence of bone loss and clinical attachment loss ie CAL=0 and BMI30 kg/m2 . Group IV (non-obese with chronic periodontitis) comprised 15 patients who showed clinical signs of gingival inflammation with loss of attachment and radiographic evidence of bone loss and BMI < 25kg/m2 . Furthermore, the participants were systemically healthy, without taking any medications affecting the periodontal status, and had received no periodontal therapy in the preceding 6 months. Exclusion criteria includes: aggressive forms of periodontitis; smoking; alcoholism; pregnancy and lactating women. Written informed and verbal consent was obtained from all recruits and the ethical clearance was obtained from the institutional ethical committee. GCF sample collection Prior to GCF collection, the Supragingival plaque was scored. The test site for GCF sample collection in chronic periodontitis groups (III and IV) was selected based on the highest scored sites in the oral cavity ie the site with maximum attachment loss. In the healthy groups (Group I and II), to standardize site selection, sampling was predetermined to be from the mesio-buccal region of the maxillary first molar. The test site selected, was air dried, isolated with a cotton roll and supragingival plaque was removed without contacting the marginal gingiva. From each test site, GCF samples were obtained before probing by placing a black color-coded 1–5 µL calibrated volumetric microcapillary pipettes (Sigma Aldrich Chemical Company USA) extracrevicularly (unstimulated) for 5-20 minutes. A standardized volume of 1 µL was collected, using the calibration on the micropipette. Test sites from which no GCF could be obtained, and the micropipette which was contaminated with blood and saliva, were excluded from the study. The GCF collected was immediately transferred to a plastic vial and frozen at -70°C until the time of assay. Principles of Leptin assay The assay was performed using the leptin Elisa kit (Biosource International Inc., Camarillo, CA, USA). The manufacturer&#39;s instructions were strictly adhered to and each plate was checked before use to ensure the calibration curve measured leptin standards (0–1000 pg/mL) within the stated limits of the assay. The assay uses monoclonal antibodies (MAbs) directed against distinct epitopes of human leptin. The samples were run in duplicate. Standards and samples react with the capture monoclonal antibody (MAb 1) coated on the microtiter well and with a monoclonal antibody (MAb 2) labelled with horseradish peroxidase (HRP) forming a sandwich : coated MAb 1 - human leptin - MAb 2 - HRP. Bound enzyme-labelled antibody is measured through a chromogenic reaction. Absorbance of the substrate color reaction was read on an enzyme-linked immunosorbent assay (ELISA) reader using 450 nm as the primary wavelength. The optical density values obtained with the known samples were used to calculate the quantity of leptin in the other samples. Assay procedure 50 μl of each calibrator, control, and sample was pipetted into the appropriate wells in the microtitre plate. 100 μl of anti-Leptin-HRP Conjugate and then 50 μl of Incubation Buffer was pipetted into all the wells and incubated for 2 hours at room temperature, on an horizontal shaker set at 700 ± 100 rpm. The liquid was apirated from each well. The plate was washed four times by: dispensing 0.4 ml of BioSource Wash Solution into each well and then aspirating the content of each well. 100 μl of Chromogenic Solution was pipetted into each well within 15 minutes following the washing step. The plate was incubated for 30 minutes at room temperature on an horizontal shaker set at 700 ±100 rpm, avoiding direct sunlight. 200 μl of Stop reagent was pipetted into each well. Absorbances was read at 450 nm and 490 nm (reference filter: 630 or 650 nm) within 3 hours and results calculated. Statistical analysis The Kruskal Wallis one way ANOVA test was used to calculate the P- value and the P value < 0.05 was considered statistically significant. The Mann Whitney U test followed by Bonferroni Correction method was employed to identify the significant groups at 5% level. The Spearmans Rank Correlation Coefficient was calculated to assess the relationship between the various clinical parameters and leptin levels in each study group.   The mean PI and CPITN index in group III (2.57 ± 0.34) (4.1 ± 0.3) and group IV (2.37 ± 0.38) (3.9 ± 0.3) are significantly higher than the mean PI and CPITN index in group I (0.66 ± 0.30) (1.4 ± 0.6) and group II (0.58 ± 0.24) (1.2 ± 0.7) (pEnglishhttp://ijcrr.com/abstract.php?article_id=1869http://ijcrr.com/article_html.php?did=18691. Genco RJ: Host responses in periodontal diseases: current concepts, J Periodontol 63:338, 1992. 2. Birkedal-Hansen H. Role of cytokines and inflammatory mediators in tissue destruction. J Periodont Res 1993;28:500– 510 3. McCauley LK, Nohutcu RM. Mediators of periodontal osseous destruction and remodeling: principles and implications for diagnosis and therapy. J Periodontol 2002;73:1377–1399 4. Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L. and Friedman, J. M. Positional cloning of the mouse obese gene and its human homologue. Nature 372, (1994) 425–342 5. Ahima, R. S. and Flier, J. S. (2000) Leptin. Annual Review of Physiology 62, 413–437.  6. Gabay C, Dreyer MG, Pellegrinelli N, Chicheportiche R, Meier CA. Leptin directly induces the secretion of interleukin-1 receptor antagonist in human monocytes. J Clin Endocrinol Metab 2001; 86: 783-791. 7. Xiao E, Xia-Zhang L, Vulliemoz NR, Ferin M, Wardlaw SL: Leptin modulates inflammatory cytokine and neuroendocrin responses to endotoxin in the primate. Endocrinology 2003, 144:4350-4353. 8. Johnson RB, Serio FG. Leptin within healthy and diseased human gingiva. J Periodontol 2001; 72: 1254–1257. 9. Karthikeyan BV, Pradeep AR. Leptin levels in gingival crevicular fluid in periodontal health and disease. J Periodont Res 2007; 42: 300–304 10. Santos-Alvarez J, Goberna R, SanchezMargalet V. Human leptin stimulates proliferation and activation of human circulating monocytes. Cell Immunol 1999; 194: 6–11. 11. Sarraf P, Frederich RC, Turner EM, Ma G, Jaskowiak NT, Rivet DJ 3rd et al. Multiple cytokines and acute inflammation raise mouse leptin levels: Potential role in inflammatory anorexia. J Exp Med 1997; 185:171-175. 12. World Health Organization (2000) Obesity: Preventing and Managing the Global Epidemic. WHO Obesity Technical Series 894. Geneva: World Health Organization. 13. Catherine M.E Champagne, William Buchannan, Michael S Reddy, John S Preisser, James D Beck and Steven Offenbacher, Potential For Gingival Crevice Fluid Measures As Predictors Of Risk For Periodontal Diseases. Periodontology 2000, Vol. 31, 2003, 167–180 14. Agnello D, Meazza C, Rowan CG, Villa P, Ghezzi P, Senaldi G et al. Leptin causes body weight loss in the absence of in vivo activities typical of cytokines of the IL-6 family. Am J Physiol 1998; 275: R913– R919. 15. Sanna V., A. Di Giacomo, A. La Cava, R.I. Lechler, S. Fontana, S.zappacosta and G. Matarese. Leptin surge precedes onset of autoimmune encephalomyelitis and correlates with development of pathogenic Tcell responses. J. Clin. Invest.2003; 112:1821. 16. Ottonello L, Gnerre P, Bertolotto M, Mancini M, Dapino P, Russo R, Garibotto G, Barreca T, Dallegri F: Leptin as a uremic toxin interferes with neutrophil chemotaxis. J Am Soc Nephrol 2004, 15:2366-2372. 17. Martin-Romero C, Sanchez-Margalet V: Human leptin activates PI3K and MAPK pathways in human peripheral blood mononuclear cells: possible role of Sam68. Cell Immunol 2001, 212:83-91. 18. Gabay C, Dreyer MG, Pellegrinelli N, Chicheportiche R, Meier CA. Leptin directly induces the secretion of interleukin-1 receptor antagonist in human monocytes. J Clin Endocrinol Metab 2001; 86: 783-791. 19. Takeda, S., Elefteriou, F., Levasseur, R., Liu, X., Zhao, L., Parker, K. L., Armstrong, D., Ducy, P. and Karsenty, G. Leptin regulates bone formation via the sympathetic nervous system. Cell 2002; 111: 305–317. 20. Gordeladze JO, Drevon CA, Syversen U, Reseland JE. Leptin stimulates human osteoblastic cell proliferation, de novo collagen synthesis and mineralization: Impact on differentiation markers, apoptosis and osteoclastic signaling. J Cell Biochem 2002;85:825-836. 21. Yesim Bozkurt F, Yetkin Ay Z, Sütcü R, Delibas N, Demirel R. Gingival crevicular fluid leptin levels in periodontitis patients with long term and heavy smoking. J Periodontol 2006; 77: 634-640  22. Alfano MC. The origin of gingival fluid. J Theor Biol 1974; 47:127-136. 23. Pashley DH. A mechanistic analysis of gingival fluid production. J Periodontal Res1976;11:121-134 24. Yamagishi, S. I., Edelstein, D., Du, X. L., Kaneda, Y., Guzma, M. and Brownlee, M. Leptin induces mitochondrial superoxide production and monocyte chemoattractant protein-1 expression in aortic endothelial cells by increasing fatty acid oxidation via protein kinase A. The Journal of Biological Chemistry 2001: 276, 25096–25100 25. Michael, W. A., McMahon, A. D., Packard, C. J., Kelly, A., Shepherd, J., Gaw, A. and Sattar, N. Plasma leptin and the risk of cardiovascular disease in the West of Scotland Coronary Prevention Study (WOSCOPS). Circulation 2001;104, 3052– 3056. 26. Parhami, F., Tintut, Y., Ballard, A., Fogelman, A. M. and Demer, L. L.Leptin enhances the calcification of vascular cells artery wall as a target of leptin. Circulation Research 88, 2001, 954–960.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18General SciencesBIOLOGICAL ACTIVITY AND ANALYTICAL CHARACTERIZATION OF BARBITURIC ACID English89100Vijaya Laxmi SEnglish Janardhan BEnglish Rajitha BEnglishEarlier literature reports imply that this scaffold is having activity on central nervous system. According to the present studies it has become an attractive target for the development of drugs, which hold variety of biological activities. Derivatives of barbituric acid have attracted the attention of researchers in synthetic organic chemistry, as well as medicinal chemistry, for a long time as a result of their exceptionally diverse biological activity. Present review highlights the importance of the barbituric acid in the present context. EnglishBarbituric acid, Biological activity, Spectral studies, X-ray Crystallography, Dye properties.1 INTRODUCTION Barbituric acid (BA) is documented as the parent compound of the barbiturate drugs. (Fig.1). It is used in the production of riboflavin, Nembutal, and Phenobarbital.1-2 This class of compounds has been extensively used in medical and biological studies for many years, the best known of which is their sedative action in the central nervous system3 (CNS). It was demonstrated that some barbituric acid derivatives have new and very interesting biological activities that stand apart from previous medical utilization of barbituric acid derivatives.4 However it is a precursor to barbituric acid derivatives widely been used in the manufacturing of plastics,5 textiles,6 polymers,7 and pharmaceuticals,8-9 dental materials,10 water thinned or oil-based inks,11 and as polymerization catalysts.12 In view of the above observations it is worthwhile to make a brief review on it. 2 Barbiturates 2.1 Chemistry of Barbiturates Barbituric acid an organic compound of the pyrimidine family,13 chemically called as 2,4,6 trioxopyrimidine, a class of compounds with a characteristic six-membered ring structure composed of four carbon atoms and two nitrogen atoms. Compounds possessing the C2=O group are known as oxybarbiturates, and those having a C2=S group are known as thiobarbiturates. The thiobarbiturates generally have higher lipid solubilities than their corresponding oxybarbiturates. The α-carbon has a reactive hydrogen atom and is quite acidic, variety of barbituric acid drugs were synthesized by employing Knoevenagel condensation. Their biological activities varied when substituent‘s introduced on two Nitrogen atoms and 5th position of barbituric acid. (Fig. 2) 2.2 Synthesis of Barbituric acid Several synthetic methods are available in the literature. In 1862, A. V. Baeyer accidentally discovered the barbituric acid, by combining urea and malonic acid on condensation reaction.14 2.3 Synthesis of Barbiturate drugs Barbituric acid condense smoothly with aldehydes under moderate conditions,15-17 yielding 5-ylidene.The presence of low electron density at the C-5 position in the exocyclic C=C bond, owing to conjugation with the carbonyl groups in the 4 and 6-positions, causes the nucleophilic addition reaction. Several literature procedures were reported for the Knoevenagel condensation of substituted benzaldehydes and barbituric acid.18-19 Jursic20 performed the condensation of barbituric acid substituted benzaldehydes in excess of methanol solution without adding any external acid or base catalyst. Uncatalysed Knoevenagel condensation of barbituric acid and substituted benzaldehydes in aqueous medium at room temperature was reported by Mohit L. et al. 21 Solvent-free Knoevenagel condensations of barbituric acid under solid state, synthesis was achieved by Gerd Kaupp et al.22 2.4 Tautomerism Barbituric acid exists in the solid state in the trioxo structure as shown by X-ray23-24 and 14NNQR25 methods. NMR investigation of the oxohydroxy equilibrium also indicates that only the oxo form is present in a solution in anhydrous DMSO.26, 27 BA exist as single molecular species in the gas phase with trioxo tautomers being the most stable. This conclusion was reached on the basis of calculated tautomer energies and FT-IR spectra.28 Igor Novak et al. have used G3MP2B3 method to calculate Gibbs free energies of the two possible tautomers established that keto tautomers are more stable than enols by 36.8 and 36.7 kJ/mol, respectively.29 Recently Michale R.Chierothi et al. reported that by griding a commercial sample of Barbituric acid in its trioxo form for 24 h, a new compound has been isolated. The new phase has been identified as trihydroxy isomer. 30 Ab inito and density functional theory (DFT) methods were used to study the tautomers of barbituric acid in the gas phase and in a polar medium, this method was concluded that the triketo form of barbituric acid is found to be the most stable form in the gas phase and in solution. Tautomers, which are partially, enolized forms, have higher dipolemoments in gas phase are stabilized in polar medium.31 2.5 Spectral studies on Barbituric acid UV-Vis, IR spectra, Raman spectroscopy, NMR and Mass spectrometry details for BA discussed by Jacek T. Bojarski et.al.32 2.6 X-ray studies Crystallographic data show that barbiturates generally have low symmetric crystal systems, i.e., monoclinic or sometimes triclinic. Sadad Al-Saqqar et al. reported the X-ray diffractometric analysis of barbituric acid (1,4)- dioxane solvate confirmed the two nitrogen atoms of the acid act as hydrogen donors to two oxygen atoms, each from a different molecule of (1,4)-dioxane.33 (Fig.3.) Maria Victoria Roux et al. reported the calorimetric, computational, and powder Crystallographic Study of barbituric acid 34 and Single crystal X-ray Crystallographic study has been done for the compound 5,5dimethyl Barbituirc acid.35 Crystallization of Polymorphs of Phenobarbital was reported by Neslihan Zencirci et al.36 Mechanically Induced Phase Change in Barbituric acid was achieved by Michele R. Chierotti, et al. By grinding a commercial sample of barbituric acid in its trioxo form (polymorph II, 99%) for 24 h, a new compound has been isolated. The new phase has been identified as the trihydroxyl isomer. 2.7 Thermogravimetric analysis and Thermophysical Study According to Alexandre Berlin et al. made thermogravimetric characteristics of barbituric acid and its derivatives they indicates the degrees of hydration as well as the range of stabilities of the anhydrous compounds. The decomposition of barbital has also been made to study the effect of alkyl substituent‘s in the 5 position on the decomposition. The differential thermal analysis for dilituric acid showed a sharp exotherm at 190o indicating a violent explosion.37 Manuel Temprado et al. reports a differential scanning calorimetry (DSC) study of some of the barbituric acid derivatives.38 Electron paramagnetic resonance study of thermal decomposition of barbituric acid can be studied by J. N. Herak et al. the structures of the detected radicals in the decomposition of the barbituric acid derivatives suggest that there are various ways of decomposition of these substances. In all the analyzed compounds a loss of the substituent group R1 or R2 is detected. The loss of R1 or R2 is not necessarily decomposition for all the molecules other competitive decomposition pathways are possible. These experiments undoubtedly prove that in thermal decomposition of molecules free radicals may be found.39 4 Dyes Many Barbituric acid derivatives such as Thiobarbituric acid and its derivatives also been used in the synthesis of dyes and pigments or intermediates in the preparation of Dyes.40,41 Barbituric acid has been used as disperse dyes with strong fluorescent and as yellow organic pigments,5 and investigated as stain developers for the identification of nucleic acids.42 Isidor greenwald investigated that by the addition of alcohol to a mixture of solutions of barbituric acid, picric acid and sodium hydroxide, a red precipitate is obtained.43 The barbituric acid group present in the yellow and orange iso indolinone and azo pigments provides hydrogen bonding within these pigment systems giving them good durability but this still falls short of the standard required for automotive quality. The synthesis, characterisation and properties of some polycyclic barbiturate pigments are described. The pigments have been tested as colourants for plastic and paint and the results of lightfastness, heatfastness and contact bleed tests are reported by D. Thetford et al. results suggest that only the barbiturate pigments with large aromatic moieties such as the pyren-1-yl and fluoren-2-yl substituent‘s have good lightfastness properties at reduced shades in plastics.5 Novel heterocyclic disazo barbituric acid dyes were synthesized and solvatochromic properties were studied (Fig.4. and Fig.5.) The effects of varying the pH and solvent on the absorption of the dyes substituted with electronwithdrawing and electron-donating groups at their o-, m-, and p-position were examined in detail.44 Some other literature reports also well documented about the dyes properties of the barbituric acid.45-475 Biological Activities of Barbituric acid Barbiturates are 6-oxo derivatives of uracil, a component of the nucleic acids. This similarity may be important since barbiturates have been found to associate preferentially with adenine2 analogous to the uracil-adenine binding in nucleic acids. The strong interaction observed between barbiturates and adenine led to the suggestion that the barbiturates exert their biological activity by specifically binding and inactivating a variety of molecules containing adenine, including coenzymes and adenosine 5‘triphosphate,48 they bind to specific regions of various receptors e.g. to GABA, nicotinicacetylcholine (nAChR) or BK channel receptors which are all ligand-gated ion channels,49 the binding to the GABA receptor requires that C5 substituted by alkyl or aryl groups. The substitution enhances lipid solubility and facilitates transport of BA towards their enzyme targets.29 5.1. CNS Depressant activity It is important to note that Barbituric acid itself has no CNS activity. Barbituric acid ring as well as the C(5) lipophylic side chains known to be necessary for CNS activity. CNS activity obtained by substitution certain alkyl, alkenyl or aryl groups on pyrimidine ring structure. Edwared. Smmissm et al. reported the synthesis of Acyloxy alkyl barbiturates as Potential LongActing Central Nervous System Depressants.50 (Fig.6.) Recently José D. Figueroa-Villar et al. investigated the synthesis of a new family of barbiturates, 5-chloro-5-benzylbarbituric acids using a simple efficient synthetic method from aromatic aldehydes and barbituric acid, followed by reduction and chlorination with trichloroisocyanuric acid in vivo evaluation with mice showed that these compounds are having tranquilizing activity. The obtained data clearly indicate that the most active compounds are those with substituent‘s at the ortho position51 (Fig.7.) 5.2. Antiinflamatory activity A novel series of barbituric acid derivatives were identified as selective inhibitors of α4β7- MAdCAM (mucosal addressin cell adhesion molecule-1) and investigated the structure– activity relationships of the barbituric acid for their ability to inhibit the interaction between α4β7 and MAdCAM out of all the synthesized compounds 3-indolyl barbituricacid derivative (Fig.8.) exhibited potent activity at 0.06 (μM), 3-indolyl was identified as an important pharmacophore component.52 A series of 1,3- diphenylharbituric acid derivatives has been prepared and evaluated for antiinflammatory activity by means of the Randall-Selitto test,53 and the pleural effusion method, the compounds are found to be toxic and less active than phenylbutazone by the testing procedures used. 1,3-diphenyl-5-(3- methyl-2-butenyl)barbituricacid (Fig.9.) was identified as the most potent member of the series.54 5.3. Anti cancer activity By combining indole and barbituric acid, new hybrid molecules were designed and synthesized. Evaluations of these molecules over 60 cell line panel of human cancer cells.   From all the synthesized compounds 5-((1-allyl1H-indol-3yl)methylene)pyrimidine2,4,6(1H,3H,5H)-trione (Fig.10.) and 5-((1-allyl1H-indol-3yl)methylene)- 1,3dimethylpyrimidine-2,4,6(1H,3H,5H)-trione (Fig.11.) has shown significant anticancer activity. Dockings of these active molecules in the active sites of COX-2, thymidylate synthase and ribonucleotide reductase indicate their strong interactions with these enzymes.55 5- benzyl (Fig.12.) and 5-benzylidene (Fig.13.) derivatives useful in Uridine Phosphorylase inhibitors in cancer theraphy. Inhibition of Uridine Phosphorylase of these compounds equal to or greater than that of their acyclouridine counterparts.56 Various Barbituric acid derivatives which are having significant anticancer activities were reported in the literature. 57, 58 5.4. Anti Bacterial Activity Ayoob Bazgira et al. described a one-pot and efficient method for the synthesis of pyrazolo [4&#39;,3&#39;:5,6]pyrido[2,3-d]pyrimidine-dione (Fig.14.) derivatives by condensation reaction of barbituric acids, 1H-pyrazol-5-amines and aldehydes under solvent- free conditions. All the products were evaluated for antimicrobial activity.   Almost most of the compounds exhibited good to excellent antibacterial activity against all the tested strains.59 Huacan Song et al. reported the synthesis and antimicrobial activity of 5-(4- hydroxybenzylidene)-dihydro-2- thioxopyrimidine-4,6(1H,5H)-dione (Fig.15.) and 5-(4-hydroxybenzyledene)pyrimidine2,4,6(1H,3H,5H)-triones (Fig.16.) and found to be most potent inhibitors with IC50 value of 14.49 μM and, 13.98 μM respectively.60   5.5. Antituberculosis activity Recently we reported the synthesis of novel barbiturates and thiobarbiturate analogs of Furano chromene carbaldehydes and dihydropyranochromenes and evaluated for their antitubercular activities against Mycobacterium tuberculosis H37RV, and cytotoxicity (CC50) in the VERO cell MABA assay. The results indicate pyranochromene analog showed good antitubercular activity (IC90: 5.9 µg/mL) and cytotoxicity (CC50: 14.27 µg/mL). antitubercular activity of 5-(6,10-Dimethyl-4,8-dioxo-4,8- dihydropyrano[3,2-g]chromen-3-yl)methylene)- pyrimidine-2,4,6(1H,3H,5H)trione (Fig.17.) was superior to the antituberculosis drug, pyrazinamide (PZA; IC90: >20 µg/mL).61   5.6. Analgesic activity In Analgesics 1 Julius A. Vida et al. reported the synthesis of 5-substituted 5- propionoxybarbituric and evaluated for analgesic activity. One compound, 5- propionoxy-5-(1-phenylethy1)barbituric acid, (Fig.18.) displayed better analgesic activity than codeine orally and had half the analgesic potency of morphine when administered subcutaneously.62 In Analgesics 2 same authors (Julius A. Vida et al.) synthesized the acyloxy, trialkylsilyloxy, triphenylsilyloxy, and tosyloxy derivatives of 5-(1-phenylethy1)barbituric acids from all the synthesized compounds 5-acetoxy5-(l-phenylethyl)barbituricacid (Fig.19) and 5- cyclopropylcarbonyl-oxy-5-(lphenylethyl)barbituricacid (Fig.20.) exhibited better analgesic activity than codeine orally.63   5.7. Protein Tyrosine Phosphatase Inhibitor protein tyrosine phosphatase are key regulators of the phosphorylation of proteins involved in cellular signal transduction pathways. New series of barbituric acid derivatives synthesized and evaluated protein tyrosine phosphate inhibitory activity. 5-(2,4bis(4- (trifluoromethyl)benzyloxy)benzylidene)pyrimid ine-2,4,6(1H,3H,5H)-trione (Fig.21.) was proved most potent with an IC50 value of 10μM. 64   5.7. Protein Tyrosine Phosphatase Inhibitor protein tyrosine phosphatase are key regulators of the phosphorylation of proteins involved in cellular signal transduction pathways. New series of barbituric acid derivatives synthesized and evaluated protein tyrosine phosphate inhibitory activity. 5-(2,4bis(4- (trifluoromethyl)benzyloxy)benzylidene)pyrimid ine-2,4,6(1H,3H,5H)-trione (Fig.21.) was proved most potent with an IC50 value of 10μM. 64   5.9. Anti Diabetic activity Peroxisome proliferator-activated receptor (PPAR) belongs to the nuclear hormone receptor (NHR) superfamily.1 Three subtypes, PPARα, PPARγ and PPARδ, for this receptor has been identified and found to be important targets for the treatment of type 2 diabetes, dyslipidemia, atherosclerosis. Etc66 A new series of PPARγ ligands based on barbituric acid (BA) has been designed for virtual screening and molecular docking. Out of the total 14 molecules, 6 were found to bind to the murine PPARγ with IC50 ranging from 0.1 to 2.5 μM as compared to reference standard, pioglitazone (IC50 = 0.7μM).67 Lijuan Chen et al. evaluate the protective effect and the mechanism of the novel agonist of PPARγ on NAFLD model using one of the compounds, 68 5-(4- (benzyloxy)benzylidene)pyrimidine2,4,6(1H,3H,5H)-trione (Fig.23.) Same authors in another report synthesized forty-four novel barbituric and thiobarbituric acid derivatives against non-alcoholic fatty liver disease (NAFLD) This disease is closely associated with insulin resistance and metabolic syndromes including obesity, type II diabetes.   From all the synthesized compounds four compounds were found to increase the expression of adiponectin and lower the leptin level in 3T3-L1 adipocytes at respective concentration of 10 μM. Among them, N(Pyridin-2-yl)-2-(4-((2,4,6- trioxotetrahydropyrimidin-5(6H)- ylidene)methyl)phenoxy)acetamide (Fig.24.) showed the most efficacious and orally active molecule for reducing fat deposition against non-alcoholic fatty liver disease.69 6 ACKNOWLEDGEMENTS Authors would like to thank the IICT and CFRD Hyderabad for providing the library facility to complete the literature review. 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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareUNUSUAL SUTURAL BONE AT PTERION - A CASE REPORT English101103Raju SugavasiEnglish Sujatha. MEnglish Indira Devi. BEnglish Sirisha. BEnglishSutural (wormian) bones are accessory bones which occur within the cranial sutures and fontanelles. Sutural bones of the cranial vault are formations associated with insufficient rate of suture closure and regarded as epigenetic and hypostatic traits. The Pterion is the H shaped suture present at the junction between Frontal, Parietal, Greater wing of sphenoid and Temporal bone at lateral side of skull. We are reporting a case of unusual large sutural bone at left side of the pterion region in an adult skull. Knowledge of this variation is very important for, radiologists, orthopedic surgeons, neurosurgeons and anthropologists. EnglishPterion, Sutural Bone, Pterion ossicle and Epipteric bone.INTRODUCTION Sutural bones are small irregular bones generally found at cranial sutures. Additional ossification centers may occur in or near sutures, which may give rise to isolated sutural bones. Sutural bones are irregular in shape, variable in size and number, from skull to skull. The Pterion is the H shaped suture present at the junction between Frontal, Parietal, Greater wing of sphenoid and Squamous part of Temporal bone. Pterion corresponds to the site of antero lateral (Sphenoidal) fontanelle on the neonatal skull [1] . Sutural bone which is occasionally present at pterion is called as pterion ossicle or epipteric bone or flower‘s bone [2, 3] . Case report During the routine osteology demonstration classes for undergraduate medical students we observed a single sutural bone on the left side of the pterion. This variant sutural bone which is found at the junction between Frontal, Parietal, Greater wing of sphenoid and Squamous part of Temporal bone is large in size, rhomboidal in shape and unilateral (FIGURE : 01). The other side of skull is found to be normal. DISCUSSION Studies by Bergman et al (1988) [4] reveal that nearly 40% of skulls have sutural bones in the vicinity of the lambdoid suture and The next most common is the epipteric bone found near the anterolateral fontanelle. According to El– Najjar et al (1977) [5], the presence of sutural bones may be regulated by genetic factors. Sutural bones are found to be single or multiple. Burgener et al (1997) [6] observed a higher incidence of multiple sutural bones in congenital disorders like osteogenesis imperfecta, cretinism, cleidocranial dysostosis, progeria, rickets etc. Various studies on Indians showed a higher incidence of epipteric bone. According to Saxena et al (1988) [7] the incidence rate of epipteric bone in Indian skulls was 11.79 %. Satheesha nayak. B et al (2008) [8] showed three sutural bones at right pterion and Hussian Sahib. S et al (2010) [9] showed the presence of two sutural bones at right side and two cases of single unilateral sutural bones on left side. Studies by Nair et al (2011) [10] showed that the gross incidence of epipteric bones at pterion was 6% and the percentage of single large epipteric bone was more when compared to the small multiple epipteric bones. Their studies also showed that the epipteric bones were more on right side than on left side. According to Pryles C V et al (1979) [11], the presences of such variant sutural bones are usually associated with cranial and central nervous system anomalies. Ersoym M et al (2003) [12] suggested that the presence of epipteric bones at pterion region may cause complications while performing Burr holes during neuro-surgeries. CONCLUSION This article reviews the clinical importance of unusual occurrence of sutural bone at the pterion. We are reporting a case of unusual single large sutural bone on the left side pterion in an adult skull. Presence of such sutural bones at pterion region may be mistaken for fracture of skull. The knowledge of this variation is useful for radiologists, orthopedic surgeons. Complications while performing Burr holes during neuro surgeries can be avoided with this knowledge. ACKNOWLEDGEMENTS The authors are greatful to Dr. G. Kanchana latha, Professor and HOD of Anatomy and, Dr.P.Udaya Kumar. We would like to thank academic staff for their proper guidance, and encouragements. I am very much greatful to the research scholars and so many authors whose efforts have helped me to update my knowledge of Anatomy.   Englishhttp://ijcrr.com/abstract.php?article_id=1871http://ijcrr.com/article_html.php?did=18711. Standring S. Gray‘s Anatomy. The Anatomical basis of clinical practice. 39th ed. Edinburg. Elsevier Churchill Livingstone. 2005; 27: p.486. 2. Malhothra VK, Tewari PS, Pandey SN, Tiwari SP. Interparietal bone. Acta Anat. (Basel). 1978; 101: 94 – 96. 3. Das S, Suri R, Kapur V, Anatomical observations on os inca and associated cranial deformities. Folia Morphol. 2005; 64: 118 – 121. 4. Bergman RA, Affifi AK, MIyauchi R. Skeletal Systems. Cranium. In: Compendium of human Anatomical Variations. Baltimore. Urban and Schwarzenberg. 1988; 197 – 205. 5. El-Najjar M, Dawson GL. The effect of artificial cranial deformation on the incidence of wormian bones in the lambdoidal suture. Am.j.Phys.Anthropal.1977; 46: 155 – 160. 6. Burgener FA and Kormano M. Bone and Joint disorders, Conventional radiologic differential diagnosis. New York: Thieme Medical Publishers, 1977; P.130. 7. Saxena SK, Chowdhary DS, Jain SP. Interparietal bones in Nigerian Skulls. J. Anat. 1986; 144: 235 – 237. 8. Satheesha Nayak B, Soumya KV. Unusual sutural bones at Pterion. International Journal of Anatomical variations.2008; 1: 19 – 20. 9. Hussain Saheb S, Haseena S, Prassana LC. Unusualwormian bones at PterionThree Case Reports. J Biomed Sci and Res.Vol 2 (2). 2010; 116 – 118. 10. Nair S, Gour KK, GN Trivedi, Budhiraja V, Rastogi. Morphological study of Epipteric Bones in North Indian Skulls. Int J Cur Bio Med Sci. 2011; 1 (4): 166 – 168. 11. Pryles CV, Khan AJ. Wormian Bones. A Marker of CNS Abnormality. Am. J. Dis. Child. 1979; 133: 380 – 382. 12. Ersoy M, Evliyaoglu C, Bozkurt MC, Konuskan B, Tekdemir I, Keskil IS. Epipteric Bones in the Pterion may be a Surgical Pitfall. Minim. Invasive Neurosurg. 2003; 46: 363 – 365.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareSTUDY OF SYMPTOMATOLOGY OF UTERINE LEIOMYOMAS WITH DEGENERATIVE CHANGES English104107Ramesh B.HEnglish Shashikala PEnglishA clinical and pathologic study of 314 patients with uterine leiomyomas revealed no significant relationship between the presenting symptoms and degenerative changes in the tumors. Some form of degeneration was demonstrated in 44% of specimens. Correlation of symptomatology with the type of degenerative change showed that the hyaline change was the commonest type associated with each symptom or group of symptoms; whereas the other types of degeneration occurred at random. The commonest associated pathology contributing to symptomatology includes adenomyosis (39.22%), followed by follicular cyst in 24.11% of patients and endometrial hyperplasia in 57 cases. EnglishLeiomyoma; degenerative changes; symptomatology.INTRODUCTION Uterine leiomyomas is the most common benign neoplasm of the female reproductive tract1,2 . Though ulterine leiomyomas are common, it is difficult to obtain much information regarding clinical and pathological aspects of it in Indian literature3 . The exact incidence is difficult to assess as most of the patients do not come to the hospital unless and until there is presence of progressive symptoms of some duration4 . Unfortunately their symptomatology continues to be variable5 . Leiomyomas can undergo various secondary changes including hyaline degeneration, cystic change, myxoid, infection, necrosis, calcification and rarely ossification6, 7 . This is a clinicopathological study of degenerative changes in leiomyomas and to correlate any specific symptoms associated with any particular type of degeneration. MATERIAL AND METHOD This is a prospective study consisting of 314 cases of leiomyomas , which included three myomectomies collected over a period of 2 yrs at J.J.M Medical college, Davangere,Karnataka. The clinical details were extracted from the records of patients treated. All tissues were embedded in paraffin and stained with hematoxylin and eosin. RESULTS Of the 314 specimens studied, associated degenerative changes were seen in 136 leiomyomas (43.3%). Hyaline changes in the commonest form of degeneration were seen in 131 (41.71%) of leiomyomas. Grossly the mean size of these leiomyomas was 4.8cms. Cystic change was seen in 3.5% of cases. Myomas with mucoid degeneration (1.91%) also result in cystic change. Fatty and Myxoid change was seen in 2 cases each (0.64%). Out of 7 patients (2.22%) with calcareous degeneration, 4 were detected grossly and 3 showed microscopic foci of calcification. Leiomyoma with haemorrhage was observed in 2 cases, which included a case of red degeneration, occurred in absence of pregnancy. Necrosis was found in 2 cases (0.64%). Leiomyoma with infection and infarction was detected microscopically in one case each (0.32%).There was no case of sarcomatous degeneration in the present study. Menorrhagia was the only representing symptom in 67 patients, but 50% of these showed no evidence of degeneration. Menorrhagia associated with abdominal mass occurred in 108 patients, and in 57.4% of these had some form of degeneration. Of the 40 patients with pain abdomen, 15 patients presented with degenerative changes, when pain associated with other symptoms degenerative change occurred in 56.3% of 110 patients. Of the 10 patients with abdominal mass, 6 patients showed degenerative changes and when the complaint of mass was associated with other symptoms, degenerative change was found in 58.3%. Mass/Vagina was the presenting compliant in 33 cases and White discharge per vagina(WDPV) in 24 cases of which 3 cases each had some form of degenerative changes.Of the 11 patients presenting with pressure symptom like Bladder disturbances and backache, 2 patients showed degenerative changes. Of the 5 patients with fever, 3 patients showed degenerative changes. Proliferative phase was found in 150 cases (48.23%) followed by secretary phase in 95 cases (30.54%), endometrial hyperplasia in 57 cases (18.34%) and atrophic in only 9 cases. Adenomyosis was associated with leiomyomas in 122 (39.22%) patients followed by follicular cyst in 75 patients (24.11%). DISCUSSION Degenerative changes was observed in 43.31% of leiomyomas in our study.Persaud & Arjoon (1970) found secondary changes in 65% of leiomyomas while Reddy & Malathy(1963) found secondary changes present in all leiomyomas (325 cases)4, 7 . Hyaline change (41.71%) is the commonest form of degeneration seen in leiomyomas4,7,8,9,10.The mean size of leiomyomas with hyaline change was 4.8 cms, which is in accordance with Shaw (1971), states that some degrees of hyaline degeneration present in all leiomyomas more than 4 cms diameter11 . Persaud & Arjoon4 (1970) & Reddy & Malathy (1963,)7 reported low incidence of fatty change1,6, similar to the low incidence of present study(0.64%). Reddy & Malathy (1963, 2.5%), Torpin et al (1942, 2.4%) & Persaud & Arjoon (1970, 7.0%) found low incidence of calcification in their respective studies4,7 . Cystic change in present study (3.5%) is comparable to Norris & Zaloudek (1981, 4%) & Persaud & Arjoon7,9 (1970, 4%). Myomas with mucoid degeneration (1.91%) is low,when compared to Persaud & Arjoon7 (1970) who reported higher incidence of 5.36%.Myxomatous degeneration in leiomyomas is considered to be rare,while Persaud & Arjoon (1970) reported higher incidence of 12%7 . Leiomyoma with haemorrhage was reported in 2 cases in our study, while Norris & Zaloudek (1981)9 observed in 11% of cases. Rosario pinto (1968, 1.2%), Persaud & Arjoon (1970, 3.3%) and Reddy & Malathy (1963, 2.5%) found low incidence of red degeneration without pregnancy4,7,8. Harshmohan et al (2003) reported 0.55% of incidence of ossification in leiomyomas10 . Sarcomatous change in leiomyomas is rare. Incidence of leiomyomas with this change varies from 0.04% to 0.5% in different studies done over many decades7,12 . The symptomatology continues to be variable. Many patients presented with more than one symptom13 . Menorrhagia (46.07%) was the commonest clinical symptom as noted by various studies 7, 8, 13. Menorrhagia does not occur in every case, but when the growths are deep intramural or submucous, it is a constant symptom. Increased blood loss often cause severe anaemia.Excessive bleeding may be from increased surface of the endometrium or from thickened polypoidal endometrium. Multiple intramural growths by hindering effective uterine contractions result in prolonged & profuse loss12. Dysmenorrhoea due to irregular uterine contractions12 found in 22.29% of cases. Mass per Abdomen in the present study in comparable to Rosario pinto (1968, 17.7%) studies8 .White discharge per vagina (WDPV) in our study in majority of cases was caused by excessive mucus secretion from the hyperplastic endometrium12 . Bladder disturbances (1.27%) were due to cervical fibroids or those arising from lower part of the body getting impacted into the pelvic cavity elongate & distort the urethra & displace the bladder upwards12 . Majority of patients with fatty change, calcification, cystic change, mucoid & myxoid change do not cause any symptoms and are diagnosed only after removal by operation or at postmortem12 . Red degeneration is considered to be more common in pregnancy when it may produce severe pain often accompanied by vomiting and pyrexia12. It is however difficult to give an accurate estimate of the incidence of red degeneration in pregnancy since surgical intervention is not always required and pathologic confirmation cannot therefore be obtained7 . Red degeneration in fibroid is usually associated with pregnancy though absence of pregnancy does not exclude red degeneration4 . It would thus appear that red degeneration is not as severe in the non-pregnant as in the pregnant patient7 . Adenomyosis , follicular cyst and endometrial hyperplasia were some of the commonly associated pathological lesions which may also contribute to the symptomatology3,8 . CONCLUSION Hyaline change was the commonest degenerative change associated with each symptom or group of symptoms ; whereas the other types of degeneration occurred at random.Associated pathology may also contribute to the symptomatology. Majority of leiomyomas being symptomless and especially when small & progress slowly. There appears to be no relationship between the presenting symptoms and the type of degeneration. Symptomatology and severity usually depend on the size and location of leiomyomas rather than degenerative changes. ACKNOWLEDGEMENT Authors acknowledge the immense help received from the scholars whose articles are cited and included in reference of this manuscript. The authors are also grateful to authors/editors/publishers of all those articles, journal and books from where the literature for this article has been reviewed and discussed. Englishhttp://ijcrr.com/abstract.php?article_id=1872http://ijcrr.com/article_html.php?did=18721. Parker WH. Etiology, symptomatology and diagnosis of uterine myomas. Fertil Steril. 2007;87:725–736. 2. Iftikhar R. Modes of presentation of leiomyoma of uterus. Pakistan Journal of Surgery. 2008; 13: 117-20. 3. Novak R.E, Jones G.S, and Jones H.W. Novaks Text Book of Gynecology. 7th Edition. 1966:319-354. 4. Reddy D.B and Malathy P.M. Fibromyoma uterus. J. of Obstet. & Gynecol. of India. 1963; 13:54-60. 5. Chabra S, and Ohwri Neenu. Leiomyomas of uterus. A clinical study. J. of Obstet. & Gynaecol. Of India. 1993; 43: 436-439. 6. Bhattacharya N, Banerjee AK, Sengupta J. Ossification of leiomyoma. J Indian Med Assoc. 1998;96:99 7. Persaud V, Arjoon PD. Uterine leiomyoma: incidence of degenerative change and a correlation of associated symptoms. Obstet Gynecol. 1970;35:432-6. 8. Pinto RY. Uterine fibromyomas. J. of Obstet. & Gynaecol. 1968; 18:101-107. 9. Zaloudek C and Norris H.J. Mesenchymal Tumours of uterus. Blaunstein‘s Pathology of Female Genital Tract. 3rd Edit b. Springer-verlag. New York. 1987; 374-402. 10. Mohan H, Punia RS, Kumar S, Jain P and Handa U. Ossification in uterine leiomyomas. The internet Journal of Gynecology and Obstetrics. 2003; 2. 11. Padubidri VG and Daftary SN. Howkins & Browne. New Growths of uterus. Shaws text book of Gynaecology, 10th Edn. : Churchill livingstone, New Delhi. 1989;399-427. 12. Masani MM. New growths of cervix and uterus. Text book of Gynaecology. 6th Edition. Bombay Popular. Prakashan. 1971;313-417. 13. Vollenhoven BJ, Lawrence AS, Healy DL. Uterine fibroids: a clinical review. Br J Obstet Gynaecol 1990; 97:285-298
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareA COMPARATIVE STUDY OF OBJECTIVE STRUCTURED PRACTICAL EXAMINATION WITH CONVENTIONAL PRACTICAL EXAMINATION English108112D. RavichandranEnglish R. ShankarEnglish Varun MalhotraEnglishBackground and Aim of the Study: The Objective Structured Practical Examination (OSPE) recommended by medical educationists is a new concept in practical assessment. However, this tool of practical evaluation is not widely used in our country. The validity of the examination is improved in OSPE as this tool tests both the process and the product with much importance to individual competency 1,5. Presently OSPE is used as a formative assessment tool in some medical colleges. Nationwide very few studies had been conducted on OSPE, so this study aimed at comparing the OSPE with conventional examination pattern. Methodology: The study was conducted in the department of Anatomy, VMKV Medical College, Salem, Tamil Nadu, India. 1st year MBBS students of total 100 were included in the study. All the 100 students were made to face both the conventional pattern of examination and OSPE. The mean marks obtained by the students by conventional and OSPE method was analysed by a paired student T test. A well-structured questionnaire was administered to the same students and a feedback was got about the process of OSPE. Results : The marks obtained by the students in conventional method was comparatively less when compared to the marks obtained through OSPE type. This difference was found to be statistically significant (pEnglishOSPE, Conventional exams, Assessment, FeedbackINTRODUCTION Practical assessment of students in the medical curriculum needs a better tool which is reliable, uniform and has a capacity to differentiate between different categories of students1,2. The Objective Structured Practical Examination (OSPE) recommended by medical educationists is a new concept in practical assessment 1 . The term OSPE was introduced in the year 1975 as a modification of the Objective Structured Clinical Examination (OSCE) used for evaluation of pre and preclinical subjects2, 3 . However, this tool of practical evaluation is not widely used in our country. The All India Institute of Medical Sciences has standardized this method4 . The validity of the examination is improved in OSPE as this tool tests both the process and the product with much importance to individual competency 1, 5. Presently OSPE is used as a formative assessment tool in some medical colleges. Currently a modification of OSPE called as SOSPE (Semi-Objective Structured Practical Examination) is also being followed in some medical schools2, 6 . Aim and objective: The aim of the present study was to compare the scores obtained by medical students in OSPE and Traditional or Conventional Practical Examination in the subject of Anatomy. To get the students feedback for Objective Structured Practical Examination process. METHODOLOGY The study was conducted in the department of Anatomy, Vinayaka Missions Medical College, Salem, Tamil Nadu, India. All the first year MBBS students (n=100) were included in the study For those 100 students a surprise conventional method of anatomy practical examination was conducted on a chapter (head and neck) where they wrote their recent theory internal assessment. The conventional examination comprised of spotters in gross anatomy and histology and viva voce in osteology, embryology and radiology. The same set of students also faced the new Objective Structured Practical Examination type of practical examination a week later, and as earlier this time also it was a surprise test. The Objective Structured Practical Examination had five sections namely dissection spotters, histology slides, embryology, osteology and surface anatomy. Each section had 3 stations out of which 1 was an observer station and 2 were response stations. The time allotted for each station was 2 minutes. Both the examinations were conducted for a total of 50 marks. The mean marks obtained by the students by conventional and Objective Structured Practical Examination method was analysed by a paired student T test. In addition a well-structured questionnaire was administered to the same students and a feedback was got about the process of Objective Structured Practical Examination. The results of the feedback was analysed with SPSS 16.0. RESULTS The results of the comparison of marks obtained in conventional practical test with OSPE are presented in Table 1. The results of the feedback obtained from the students are presented in the Table 2. The marks obtained by the students in conventional method was comparatively less when compared to the marks obtained through OSPE type. This difference was found to be statistically significant (pEnglishhttp://ijcrr.com/abstract.php?article_id=1873http://ijcrr.com/article_html.php?did=18731. Aarti Sood Mahajan, Nilima Shankar, O.P. Tandon. The Comparison of OSPE with Conventional Physiology Practical Assessment. JIAMSE Vol: 14: No 2 2. Hasan S, Malik, Hamad A, Khan H, Bilal M. Conventional/Traditional Practical Examination (CPE/TDPE) Versus Objective Structured Practical Evaluation (OSPE)/Semi Objective Structured Practical Evaluation (SOSPE). Pak J Physiol 2009; 5 (1); 58-64 3. Harden, R.M and Gleeson, F.A. Assessment of clinical competence using an objective structured clinical examination (OSCE). Medical Education. 1979; 13: 41-54 4. Nayar, U. Objective structured practical examinations. In: R.L. Bijlani and U. Nayar (Eds)Teaching Physiology, Trends and Tools. All India Institute of Medical Science. New Delhi. 198; 151-159 5. Ananthakrishnan N. Objective structured clinical/practical examination (OSCE/OSPE). JPGM 1993; 39 (2): 82-4 6. Gitanjali B. The other side of OSPE. Indian J Pharmacol 2004; 36: 388-9 7. Newble, D.I and Swanson, D.B. Psychometric characteristics of the objective structured clinical examination. Medical Education. 1988; 22: 325 – 334 8. Nayar, U., Malik, S.L. and Bijlani, R.L. Objective structure practical examination: a new concept in assessment of laboratory exercise in preclinical sciences. Medical Education. 1986; 20: 204-209 9. Praveen R Singh, Raksha Bhatt, Suman Singh. Perceptions Towards Implementation of OSPE as an assessment tool in anatomy for undergraduates at a rural medical college in Western India. National Journal of Basic Medical Sciences. 2010;VolII Issue 1, 54- 60. 10. Watson A R, Houston I B, Close G C. Evaluation of an objective structured clinical examination. Arch Dis Child 1982;57: 390- 392 11. Smith L J, Price D A, Houston I B. Objective structured clinical examination compared with other forms of student assessment. Arch Dis Child 1984;59:1173- 1176.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareREHABILITATION IN POST-CHEMOTHERAPEUTIC UNSTABLE ARTHRITIC SHOULDER- A CASE REPORT English113119Roopa DanaitEnglish Asawari PeterEnglishPost-chemotherapy shoulder complications are common. They result in long term functional impairment and disability. The following case is of a woman who was diagnosed with bilateral shoulder joint arthritis (Right>left) post lumpectomy of the left breast. Her symptoms started a year after she was put on anastrozole. Patient started complaining of multiple joint pains involving the shoulder joints, bilateral hip and knee. She was asked to undergo shoulder replacement if disability persisted. Physiotherapy was suggested and she was treated with aggressive strengthening both for treating pain and improving function. Post treatment patient gave a visual analogue score of 6 on 10 on the right and 5 on 10 on the left as compared to pre-treatment scores of 8 on 10 bilaterally. Patient now had mild difficulty in cooking as compared to moderate previously and moderate difficulty in overhead activities, making bed, grooming and dressing. There was a subjective improvement of 50% in the activities of daily living which was previously not being done or severely limited. Considering the above findings strengthening can be cautiously suggested for improving function in patients with breast cancer on chemotherapy. Englishcancer, arm and functionINTRODUCTION Breast cancer is now becoming one of the most common causes of death in females from developing countries.1 Treatment of breast cancer involves a host of modalities namely; pharmacological, radiotherapy and surgery.2 Surgical procedures include mastectomy and breast conservation surgery (lumpectomy). Lumpectomy is done in early breast cancer cases and may be accompanied by removal of lymph nodes. In lumpectomy the tumor is resected along with small amount of surrounding unaffected tissue. This procedure is generally followed by chemotherapy and radiotherapy especially if there is involvement of lymph nodes.3Chemotherapy has been shown to reduce recurrence of breast cancer and improve survival rates in hormone receptor dependent breast cancer.4 Chemotherapy has been associated with various complications. Shoulder disability due to pain and dysfunction is a common complication of treated early breast cancer cases.5 Pain in these cases is multifactorial.3 Shoulder pain and dysfunction may be due to surgery especially if it involves lymph node excision or chemotherapy. Among chemotherapy options Aromatase Inhibitors (AIs) have been found to improve disease free survival when used as an adjuvant hormonal therapy but patients put on AIs have shown a higher incidence of joint pains and myalgias. These symptoms in most cases last till the patient is on therapy and subside thereafter and no association has been found between pain induced due to AIs and arthritis.6,9 There are a wide range of physical and pharmacological treatment options that can be given to patients who are on adjuvant therapies to manage the effects associated with breast cancer and its treatment. Studies have discussed in detail management of breast cancer with exercise therapy in general and found a positive influence of physical activity on physical function and psychology.2,7 The following report is a case of a lady who had undergone a lumpectomy and was still on anastrazole which is an Aromatase Inhibitor. She complained of joint related symptoms but also had coexisting ultrasonographic changes consistent with arthritis and showed signs of shoulder instability. Our aim was to find out if strengthening and lifestyle changes improved symptoms associated with AI administration in a lady having co-existing osteoarthritis and shoulder instability. We hypothesized that the pain arising from the shoulders was typically AI induced, exacerbated an already existing arthritis and would improve when managed with exercises. History: A 67 year old lady visited the physical therapy department with a complaint of pain in bilateral shoulder joint right more than left and difficulty in doing overhead activities. Pain started 3 years back first in the left and then in the right shoulder. An ultrasound examination showed right supraspinatus calcific tendinitis and right subscapular tendinitis with gross joint effusion. A bone scan done at the same time showed changes suggestive of arthritis. The patient visited the author‘s outpatient department a week later. She presented with continuous sharp pain more in the right shoulder, which was deep in nature accompanied by dull aching pain in the arm and forearm. Pain in bilateral shoulders measured 8 on a 10 point visual analogue scale, was aggravated by shoulder movements and relieved by cessation of activity and rest. The patient also complained of a feeling of instability and a clicking sound on all the shoulder movements. The patient complained of moderate difficulty in cooking and an inability to do overhead activities such as taking objects from the closet above shoulder level and drying clothes. She had severe difficulty in upper body dressing, grooming and making her bed. Past history: Four years ago the patient underwent a lumpectomy of the left breast followed by local radiotherapy over a period of two months. The radiotherapy was followed by four cycles of chemotherapy with cyclophosphamide and docitaxel. A year after the surgery she approached a physician with symptoms of pain in the left shoulder and left knee during which she was diagnosed as having multidirectional instability of the left shoulder with secondary osteoarthritis. The right shoulder started showing symptoms a year after she was put on anastrozole. Physiotherapy was taken for the same which consisted of moist application, selfassisted shoulder mobilization and static quadriceps for knee with partial relief in symptoms. The patient was a known case of hypertension and diabetes with good glycemic control as shown by routine blood investigations and she was on amylodipine, metformin and nabivolol as well as calcium and vitamin B supplementation. Recreational and personal history: The patient had been a recreational badminton player till her late 40‘s. She gave a family history of early onset of osteoarthritis. Her left shoulder was lax and had subluxed on many occasions and she had relocated it on her own.The patient admitted to having restricted her social activities since the surgery. She complained of lack of appetite, fatigue and projected a negative outlook towards life in general and treatment in particular. Physical Examination: On observation the right shoulder was found to be depressed. Atrophy of all three fibers of deltoid, supraspinatus and infraspinatus was noted. Hollowing of supraclavicular and infraclavicular fossa bilaterally was also seen. On palpation of the shoulder joint margins tenderness was elicited. Tenderness was also noted in the muscles of the upper arm and forearm bilaterally. The sulcus sign was present. Cervical range of motion was full and painless in all directions. Beighton‘s criteria for hypermobility showed a score of 1 out of 9. Sensory testing over the upper limb dermatomal area was normal and active range of motion was grossly limited in all directions with extension being better than all other ranges. Active movement was accompanied by apprehension, a clicking sound and altered scapulohumeral rhythm which was predominant on the left due to a greater available range of motion. Initiation of movement was difficult. Winging was present bilaterally on doing a wall push up. A faradicgalvanic test was done to rule out any local motor nerve lesion. No other special tests were done. Consent form was understood and duly signed by the patient. Treatment: Day1- day 10 1. Electrical stimulation was started for the deltoid (all three fibres), supraspinatus and infraspinatus. 2. Gentle low load muscle setting exercises for rotator cuff and deltoid was initiated in supine. Initially 2 sets of 10 repetition was started and progressed to 3 sets of 10 repetition each. 3. Scapular strengthening was started as retraction exercises using thera tube 4. Core strengthening was started with training for transverse abdominis activation. No significant post treatment soreness was observed. Day 11- 3 weeks 1. Rhythmic stabilization was initiated using medicine ball against the wall for mediolateral and anteroposterior direction 2. Wall push ups were instituted 3. Eccentric exercises for shoulder flexion and abduction in supine and sitting respectively were started up to 90? as free exercises and subsequently with half kilogram weight. 4. Alternating isometrics were given at different ranges of flexion within pain free range 5. Shoulder isometrics were continued 6. End of two weeks rhythmic stabilization was started in ranges where poor motor control was demonstrated. 3 weeks onwards: After 2 weeks the patient was given a home program after supervising the exercises to be done in two sittings. 1. Isometric strengthening submaximal intensity was given against the wall 2. Wall push ups were continued 3. Pulley exercises with one kilogram weight were given up to 90? flexion and abduction in standing. A makeshift simple pulley was set up in the patient‘s home environment to enable her to continue these exercises. 4. One kilogram weight was given for rotator strengthening with focus on external rotators in side lying. A follow up was done after one month and the prescribed load was increased by half kilogram. The protocol given above was applied only on the right shoulder and left shoulder was treated with conventional treatment consisting of isometrics and moist packs in the initial stages followed by strengthening with weighted pulleys. Post treatment Examination: Post treatment the patient gave a visual analogue score of 6 on 10 on the right and 5 on 10 on the left as compared to pre-treatment scores of 8 on 10 bilaterally. Patient now had mild difficulty in cooking as compared to moderate previously and moderate difficulty in overhead activities, making the bed, grooming and dressing. There was a subjective improvement of 50% in the activities of daily living which was previously not being done or severely limited. DISCUSSION Post-treatment results showed improvement in both strength and range of motion in both the shoulders. There was a reduction in pain as measured on visual analogue scale. Our patient had more symptoms of the shoulder on the opposite side of breast surgery. Shoulder disability on the side of breast surgery has been previously observed and documented5 . Pain in the operated side shoulder has been positively correlated with chemotherapy although no significant correlation was found with radiotherapy exposure.8We hypothesized that the severe symptoms on the uninvolved side shoulder might have been due to already existing arthritis which was exacerbated by AI induced arthralgia.9This has been known to occur due to depletion in estrogen levels due to AI.9One study stated that previous chemotherapy and treatment with anastrozole were major risk factors for development of joint disorders. 10Evidence also shows that rotator cuff muscle weakness is a direct consequence of breast cancer and instability can occur as a result of its fatigue or failure to stabilize.11,12This explains the dynamic instability noted in this case. Cervical radiculopathy, rotator cuff tendinitis, arthritis and complex regional pain syndrome are few of the common complications of breast cancer and its treatment. 11Bone metastasis were ruled out by quarterly mammography and bone scan.Cervical radiculopathy was ruled out on cervical examination and so was complex regional pain syndrome (CRPS) as most of the mandatory criterions for CRPS were not fulfilled. Patient satisfied all criteria of articular pain which included instability, crepitation and pain on shoulder movement.9,13Considering this as a case of AI induced arthralgia with shoulder joint arthritis and instability caused due to rotator cuff weakness; we commenced her treatment with electrical stimulation as the first line of treatment. Electrical stimulation can have an analgesic effect and is effective in gaining early ranges of motion14 in patients having problem initiating movement.15Isometrics were started to prevent further atrophy and reflex inhibition that was a major factor in decreased active range.16Rhythmic stabilization was given to improve joint stability and neuromuscular control during active movements.16,17Scapular strengthening was started to enhance the distal component to work on a more stable proximal component. This was followed by rotator cuff strengthening to improve dynamic control and endurance, enough to suffice for daily activities.16Painful eccentric strengthening has been proved to be effective for severe chronic subacromial impingement cases.18The authors thought of trying the same for this case since she had a problem in eccentric control. Along with the above, the patient was given feedback on the progress, advice on posture and ways to deal with her negative thoughts. Clinical Message: The results of this case report imply that a combination of isometric and isotonic strengthening can help in short term gain in strength and lost range of motion in breast cancer patients who were/are on chemotherapy. Further research can focus on long term effects of strengthening. ACKNOWLEDGEMENTS Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. The authors would like to acknowledge the cooperation of the patient and her family during entire process of treatment and editing of manuscript. We would also like to thank Dr Bhamini Rao for helping us out with manuscript editing Englishhttp://ijcrr.com/abstract.php?article_id=1874http://ijcrr.com/article_html.php?did=18741. Jemal A, Freiddie B, Mellisa C, Jacques F, Elizabeth W, David F. Global cancer statistics. CA Cancer J Clin 2011; 61:69-90. 2. Mutrie N, Campbell A, Whyte F, McConnachie A, Emslie C, Lee L, Kearney N, Walker A, Ritchie D. Benefits of supervised group exercise program for women being treated for early breast cancer: pragmatic controlled trial [online first]. BMJ 2007. 3. Jung BF, Ahrendt GM, Oaklander AL, Dworkin RH. Neuropathic pain following breast cancer surgery: proposed classification and research update. Pain 2003; 104: 1-13. 4. Burstein H, Griggs J. Adjuvant hormonal therapy for early stage breast cancer. Surg Oncol Clin N Am 2010; 19: 639-647. 5. Lauridsen MC, Overgaard M, Overgaard J, Hessov IB, Cristiansen P. Shoulder disability and late symptoms following surgery for early breast cancer. Acta Oncol 2008; 47(4). 6. Qamar K, O‘Dea A, Priyanka S. Musculoskeletal adverse events associated with adjuvant aromatase inhibitors. Jour of oncology 2010. 7. Courneya S, Mackey J, Mckenzie D. Exercise for breast cancer survivors. The physician and sports medicine 2002; 30 (8). 8. Hack T, Cohen L, Katz J, Robson L, Goss P. Physical and Psychological Morbidity After Axillary Lymph Node Dissection for Breast Cancer. Journal of Clinical Oncology 1999; 17(1):143. 9. Thorne C. Management of arthralgias associated with aromatase inhibitor therapy. Current Oncology 2007; 14 Suppl 1.  10. Sestak I, Cuzick J, Sapunar F, Eastell R, Forbes J, Bianco A, Buzdar A. Risk factors for joint symptoms in patients enrolled in the ATAC trial: a retrospective, exploratory analysis. The Lancet Oncology 2008; 9(9): 866-872. 11. Stubblefield MD, Custodio CM. UpperExtremity Pain Disorders in Breast Cancer. American Academy of Physical Medicine and Rehabilitation 2006; 87(3). 12. Tytherleigh Strong G, Hirahara A, Miniaci A. Rotator cuff disease [abstract]. Curr Opin Rheumatol 2011; 13: 135-45 13. Phillips A, Polisson RP. The rational initial clinical evaluation of the patient with musculoskeletal complaints [abstract]. Am J Med1997;103:7S–11S 14. Rushton DN. Electrical stimulation in the treatment of pain. Disability and Rehabilitation 2002; 24(8): 407-415. 15. Baker L, Parker K. Neuromuscular electrical stimulation of the musclessurrounding the shoulder. Physical Therapy 1986; 16(12). 16. Wilk K, Macrina L, Reinold M. Nonoperative rehabilitation for traumatic and a traumatic glenohumeral instability. North American journal of sports physical therapy 2006; 1(1). 17. Lephart SM, Warner JJP, Borsa, PA, Fu FH. Proprioception of the shoulder joint in healthy, unstable, and surgically repaired shoulders. J Shoulder Elbow Surg. 1994; 3:371-380. 18. Jonsson P, Wahlstrom P, Ohberg L, Alfredson H. Eccentric training in chronic painful impingement syndrome of the shoulder: results of a pilot study. Knee Surg Sports Traumatol Arthrosc(2006); 14: 76– 81.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18General SciencesROLE OF CHAPERONES IN BACTERIAL PATHOGENICITY - A NEW THERAPEUTIC STRATEGY English128140Balagurunathan REnglish Shanthi JEnglishThere is an upsurge in the resistance pattern of bacterial pathogens demanding new therapeutic targets to keep in pace with the infectious organisms. This review discusses harnessing the virulence factors of microorganisms as drug targets that are produced to cope with demanding and rapidly changing environments during establishment in the host. It would be promising to develop small molecule inhibitors targeting specifically the stress proteins, so-called molecular chaperones that assist the protein folding machinery. There are several natural products that bind specifically to components of the chaperone machinery of microbial pathogens have been identified. Many successful pathogens have developed robust haperone systems to conquer the stressful environments in the host environmental challenges, such as oxidative bursts that are often triggered in response to infection. Heat shock proteins are also linked for the emergence of drug resistance and hence targeting sites unique to the bacterial pathogens can be exploited for therapy, chaperons are already viewed as targets for many human ailments like protein aggregation diseases and cancer. This review discusses new insights in exploiting bacterial chaperones as drug targets and their role in pathogenicity. EnglishHsp/HSP, heat shock protein; HspR, heat shock protein receptor; Csr1, cellular stress response protein; Cpx, extra cytoplasmic stress.INTRODUCTION Molecular chaperones from bacteria to humans are a highly conserved class of proteins and represent a significant proportion of the total protein content of all living cells. Many heat Shock Proteins function as molecular chaperones and perform important functions in protein folding, unfolding or translocation, assembly and disassembly of protein complexes, in reversing polypeptide unfolding, preventing protein aggregation, and repairing proteins that have been damaged or misfolded by stress (Craig, 1996). Under normal conditions, molecular chaperones are present at low concentrations in cells, but under stress conditions they accumulate to high levels (Kohler et al., 2002) and therefore enable cells to survive. Thus, chaperones are important in both normal and stressed cells. During infection, the molecular chaperones production increases in both pathogen and host cells [Steinhoff et al., 1994). When entering the host from the environment, a pathogen is confronted with several changes, some of which under stress due to temperature, pH and pO2 and changes the natural host resistance mechanisms, phagocytes receptor). Manipulation of either of these factors alters heat shock response and also influences bacterial virulence (Gophna and Ron, 2003). In the case of Helicobacter pylorus, survival in human gastric mucosa requires it to withstand constantly fluctuating environments and low pH conditions. H. pylori responds to environmental changes by modulating a regulator of heat shock protein genes called Csr1 (cellular stress response protein1; hspR is one of the genes modulated by Csr1). Consistent with the possibility that pathogens regulate stress responses to effective virulence, and H. pylori mutant for the csr1 gene showed attenuated infection in a mouse model indicating that genes involved in stress tolerance are critical for H. pylori virulence (Barnard et al., 2004). However, in Mycobacterium tuberculosis, inactivation of hspR and the overexpression of Dna K cause an enhanced clearance of the bacterium in the mouse model of tuberculosis (Gupta et al., 2008). It appears that increased synthesis of DnaK primes the immune system early during infection possibly resulting in increased bacterial clearance. This example indicates that mere overexpression of heat shock proteins may not always confer virulence to bacteria as in the case with induction of heat shock proteins by fluoroquinolones in E.coli correlated well with DNA relaxation but not with cell death (Tohru Mizushima, 1997). Thus the timing and possibly the magnitude of expression needs to be regulated for their cytoprotective effects. One of the best known examples of the role of heat shock proteins in bacterial pathogenesis is Listeria monocytogenes infection in host macrophages. After being phagocytosed into the host, Listeria can be digested upon fusion of the phagosome with an endosomal compartment. However, the bacteria rely on a member of Hsp100 family called ClpC to overcome this consequence. Expression of ClpC in the phagosome allows Listeria to be released from the phagosome into the host cytoplasm where it undergoes multiplication (Nair et al., 2000). Experiments with a clpC deletion strain of Listeria showed accumulation of the bacteria in phagosomes resulting in a significant reduction of bacterial load in a mouse model of infection. While the precise mechanism by which ClpC mediates bacterial exit from the phagosome is not known, it is possible that its interaction with phagosome membrane proteins may be involved. In Brucella suis, Campylobacter jejuni and Salmonella enterica serovar Typhimurium, deletion of DnaK results in compromised growth in macrophages or inability to colonize mice (Konkel et al., 1998). The role for another member of Hsp100 family, ClpB, was shown in Francisella tularensis infection of macrophages. ClpB was essential for F. tularensis to replicate in target organs and cause pathogenesis in mice (Melbom et al., 2008). These studies clearly indicate that intracellular pathogens rely upon their endogenous chaperone machinery to survive and establish an infection within their hosts. Besides these examples there are several reports that suggest a role for bacterial chaperones at the cell surface, as adhesions for invading the host cell or in signaling the immune system. Both the Hsp60 and Hsp70 classes of chaperones have been implicated in this role. In addition, there are also examples where bacteria have found ways to recruit or target host chaperones to enhance bacterial growth and overcome host defense (Henderson et al., 2006). It is apparent that bacteria have mainly exploited their heat shock protein functions to cope with host defense mechanisms triggered in response to infections; additional roles in invasion and multiplication have also been suggested in some of the cases. Antibiotic stress for the induction of chaperones Resistance to antibiotics typically occurs as a result of drug inactivation or modification, target alteration or reduced accumulation associated with decreased permeability and/ or increased efflux. The majority of these mechanisms of resistance depend on the rapid over expression of different kinds of protein (Peleg et al., 2008). Challenge of S. aureus with cell wall-active antibiotic initiates an extensive program of gene and protein expression. A large number of genes, including ones encoding proteins involved in cell wall metabolism and stress responses were up regulated by oxacillin, Dcycloserine or bacitracin. This response may represent the transcriptional signature of a cell wall-stress stimulon induced in response to cell wall-active agents. An insertional inactivation in the middle of DnaK, a member of the cell wall stress stimulon, using a kanamycin resistance gene, in S. aureus strains RN450, SH1000, and COL resulted in mutants that grew poorly at temperature above 45°C (Utaida, 2003). DnaK increased more than fourfold after 60 min of exposure to a subinhibitory concentration of antibiotic, and GroEL levels doubled. Furthermore, Acinetobacter baumannii cells pretreated for 30 min at 45°C had an increased ability to survive antibiotic exposure compared with cells pretreated at physiological temperatures. These results suggest that the chaperones DnaK and GroEL could play an important role in the stress response caused by streptomycin in A.baumannii. (Karen Cardoso, 2010). In S. aureus, the Hsp100/Clp ATPases have been extensively studied and they have been shown to play important roles in stress tolerance, intracellular replication in eukaryotic epithelial cells, biofilm formation, expression of extracellular toxins, and pathogenicity in a murine model of infection (Chatterjee et al., 2005). The lack of a functional DnaK reduces oxacillin and methicillin tolerance in S. aureus. The mutation in DnaK had increased the susceptibility of methicillin-resistant strain COL to the cell-wall-active antibiotics oxacillin and methicillin. In the case of the methicillinsusceptible strain SH1000, deletion of DnaK did not reduce the oxacillin MIC, but it had led to a significantly reduced survival after oxacillin treatment. The decreased oxacillin MIC of the DnaK mutant of strain COL, and the decreased persistence of the DnaK mutant of strain SH1000, suggested that protein damage does occur as a result of challenge with cell-wall active antibiotics, and that DnaK plays a role in dealing with these damaged proteins. In Staphylococcus aureus, a mutation in the DnaK gene increased the susceptibility of the methicillin-resistant strain COL to the antibiotics oxacillin and methicillin (Singh et al., 2007). In S. aureus, HSPs are thought to be involved in responses to antibiotics because they are induced when the cell wall is subjected to antibiotic stress (Utaida et al., 2003). HSPs are up regulated at the transcriptional and translational levels by different kinds of antibiotic and that this up regulation could improve the ability of the cell to cope with stress caused by antimicrobials and perhaps acts simultaneously with the antibiotic resistance machinery to maintain cell survival. Some studies have suggested that the role for HSPs in the bacterial stress response due to antibiotics. Yamaguchi et al., 2003 demonstrated that the chaperones DnaK and GroEL have an effect on the antimicrobial activity of the fluoroquinolone, levofloxacin in E. coli and briefed that chaperones might contribute to quinolone resistance because they sequester the aggregates that accumulate in cells exposed to fluoroquinolones. Furthermore, mutations in the DnaK, GroEL and Lon genes increased bacterial susceptibility to levofloxacin. Recent studies have demonstrated that sub inhibitory concentrations of the antimicrobials gentamicin and tobramycin induced a set of genes that affect the interaction of Pseudomonas aeruginosa with host cells, including the gene encoding Lon protease, which is known to play a role in protein quality control (Marr et al., 2007). Sparfloxacin induces DnaK and GroEL proteins, the major heat shock proteins of E. coli, in a dose-dependent manner. A large number of genes, including ones encoding proteins involved in cell wall metabolism and stress responses were up regulated by oxacillin, D-cycloserine or bacitracin. Penicillin dose-dependently increased clpL levels but decreased pbp2x levels, because ClpL is induced by heat shock and other stresses (Kwon et al., 2003), pneumococcal survival seems to depend on competition between the amounts of ClpL and PBP2x. Low-level stress may induce ClpL and increase cell resistance to penicillin compared to normal cells and hence low-level stress could improve pneumococcal survival. This implies that treatment with cell wall-active antibiotics results in damage to proteins. These changes in gene expression can be viewed as an attempt by the organism to defend it against the antibacterial activities of the agents. The molecular chaperone DnaK has been shown to be induced by a variety of stresses including cell wall-active antibiotic stress, suggesting its potential role in response of bacteria to stresses. Pilus biogenesis and host pathogenesis Colonization is not a single event but rather a dynamic process that involves panoply of changes in both the bacterium and host alike as a result of attachment. (Mulvey et al.,1998) have recently found during interactions between type 1-piliated E. coli and host superficial epithelial bladder cells glycoproteins, pili shortened to an average length of 0.12 to 0.01 mm compared to broth culture where they were 1 to 2 mm long. The mechanism by which this apparent shortening occurs remains unknown, but retraction of the pilus upon attachment has been suggested as one possible means (Mulvey et al., 1998). Scanning and high-resolution electron microscopy has shown that type 1 pili can mediate direct and intimate bacterial contact with the uroplakin coated bladder epithelium. Environmental conditions in the urinary tract presumably favor the expression of pili at critical points during the pathogenic cascade (Lim et al., 1998). Interestingly, pilus assembly leads to the activation of Cpx (extra cytoplasmic stress), which in turn would serve to reinforce the commitment to make pili by activating periplasmic assembly factors and maintaining the phase variation in ON state. This would ensure that daughter cells remain piliated in order to facilitate the colonization of the epithelium and persistence in the urinary tract. In addition, host–pathogen interactions in the urinary tract activate a cascade of innate defenses, such as an increase in the production of nitric oxide that may induce the periplasmic stresses (Mumtaz et al., 2000) and lead to an activation of Cpx. The activation of Cpx via pilus biogenesis and host–pathogen interactions serves to reinforce the commitment to produce pili, facilitating colonization of the urinary tract. In addition, Cpx may control the expression of a number of other virulence factors, putative CpxR binding sites upstream of genes encoding hemolysin, cytotoxic necrotizing factor and type 1 pili (Hung et al., 1996). Thus, environmental factors that activate pilus expression may indirectly activate additional virulence factors due to the induction of Cpx by OFF-pathway subunits. In this way, Cpx may tie up the expression of virulence factors to pilus biogenesis, which may be part of a mechanism in which microbial colonization is linked to the expression of new genes important in the pathogenic cascade and establishment in the host. The type 1 pilus adhesin FimH binds to mannose-containing receptors expressed by many host cell types and is a significant virulence determinant in the development of bladder infections (Thankavel, 1997). It has been shown that uropathogenic E. coli and K12 strains expressing type 1 pili can invade cultured human bladder epithelial cells, whereas nonpiliated strains or piliated strains lacking the FimH adhesin cannot. Thus, FimH may function like the invasin of Yersinia pseudotuberculosis and the internalin of Listeria monocytogenes (Parida, 1998). Once internalized, type 1-piliated E. coli cystitis isolates, but not their K12 counterparts, are able to proliferate and survive within the host cell. Thus the elucidation of the molecular mechanisms of pilus mediated bacterial attachment to host cells and the consequent pathogenesis offers the opportunity to develop new methods of prevention and treatment for many bacterial diseases. Drug targeting based on the mechanism of the chaperone –usher system Strategies for inhibition of pilus biogenesis are based on three different points of the processes of pilus biogenesis and adhesion: inhibition of chaperone-subunit complex formation; inhibition of chaperone-subunit interaction with the usher; and inhibition of adhesion to the host receptor. P and type 1 pili are responsible for the early onset and persistence of UPEC-caused urinary tract infections (UTIs) by mediating attachment to the kidney epithelium (P pili) or attachment and invasion of the bladder epithelium cells (type 1 pili), respectively. They are assembled by the conserved chaperone/usher (CU) pathway, responsible for the biogenesis of more than 100 surface organelles in many other important human pathogens (Yersinia, Salmonella, Shigella, and Haemophilus). The activity of a family of bicyclic 2-pyridones, termed pilicides, was evaluated in two different pilus biogenesis systems in uropathogenic Escherichia coli. A group of antibacterial agents called ?pilicides? (pyridinones derivatives) was designed based on the crystallographic data of both PapD and FimC chaperones and their complexes (Svensson et al., 2001). Pilicides blocks the process of pilus biogenesis by binding to three possible binding sites in FimC or PapD. Inhibition of the latter interaction is particularly promising as it is the only one to have been convincingly established (Pinkner et al., 2006). Pilicides targeting this site, by inhibiting pilus biogenesis, have been shown to interfere with bacterial attachment and biofilm formation. Finally, anti-adhesive compounds targeted against the adhesive sub-units like antiadhesin antibodies have been shown to block bacterial adhesion (Langermann, 2000), thus paves the way to antimicrobial vaccine development strategies. Pilicides block pilus biogenesis by preventing chaperone-subunit complexes from interacting with the outer membrane usher (Pinkner et al., 2006). Rationally designed small compounds inhibit pilus biogenesis in uropathogenic bacteria. The crystal structure of a pilicidechaperone complex indicates that the pilicide binds to a conserved hydrophobic patch on strands F1, C1 and D1 on the back of the Nterminal domain of the pilus chaperone (Pinkner, et al.2006). So far, efforts at developing pilicides have focused on inhibiting the periplasmic chaperone proteins of the chaperone usher pathway in uropathogenic E. coli (UPEC). Bicyclic 2-pyridones and N-substituted amino acid derivatives have been shown to competitively inhibit binding of chaperones to pilin subunits by surface plasmon resonance (Svensson et al., 2001). In vitro, bicyclic 2- pyridones have also been shown to inhibit hemagglutination and biofilm formation in laboratory and clinical E. coli strains, and ex vivo they have been shown to inhibit adhesion of the bacteria to bladder carcinoma cells by 90%. It has been suggested that pilicides may have broad-spectrum of activity due to the conservation of both chaperone structure and the chaperone-usher pathway (Lee, et al., 2003). This is suggested as an alternative and attractive approach to meet the vital needs in developing new anti infective agents. The pilicides were designed to mimic the C-terminal part of the fimbrial subunits and to bind to FimC or PapD thus blocking the chaperone from binding to the pilus subunits in the periplasm. Another interaction site of these pilicides has been shown to be at the surface of the chaperone involved in the interaction with the usher, thus blocking subunit delivery. In addition to rationally designed small synthetic molecules, natural compounds are also screened for their activity against adhesion. Proanthocyanidines, a component of cranberry juice represents one of the most well known natural products used to block adhesion of uropathogenic E. coli in the bladder. Coating of abiotic surfaces with isolated group II capsule polysaccharides of E. coli has been shown to drastically decrease adhesion and biofilm formation and may be used for new strategies to reduce biofilm formation on medical devices (Valle, 2006). Heat shock protein as antibody triggers and potential vaccines: Analysis of immune responses to bacteria in the 1970s enabled scientists to identify what was termed as ?common antigen? in many bacterial species. Patients infected with Mycobacterium tuberculosis or Mycobacterium leprae exhibits significant antibody responses to a 65-kDa antigen which was identified as the molecular chaperone Cpn60. It has now been established that a number of molecular chaperones from bacteria and protozoan parasites (Cpn60, Hsp70, and Hsp90) are (i) potent immunogens, (ii) active immunomodulators, and (iii) inducers of cross-reactive immunity and autoimmunity (Van Eden et al., 2005). The mammalian immune system recognizes the molecular chaperones of infecting parasites as strong immunological signals, which is surprising in view of the significant homology between host and parasite proteins. The Cpn60 (Hsp65) protein of M. tuberculosis has also proven to be an extremely powerful immunomodulator that is able to protect against a number of experimental autoimmune diseases in rodents, including diabetes. Members of the hsp70 family in other parasites and bacteria have proved to be immunogenic in both humans and experimental animals. For example, the hsp70 of Schistosoma mansoni shows about 85% homology with human hsp70, yet the majority of infected animals and humans develop antibodies to the S. mansoni protein (Hedstrom et al., 1987). The antibodies are directed towards the nonconserved sequences of the protein and can distinguished between infection with S. mansoni and that with S. japonicum (Scallon, 1987). Antibodies produced against malarial hsp70 proteins are directed mainly at nonconserved epitopes (Peterson, 1988), although a minor component also reacts with human hsp70 (24). Infection with Brugia malayi stimulates antihsp70 antibodies that react predominantly with epitopes specific to the Brugia protein, but there is some cross reactivity with hsp70 molecules from S. mansoni and Plasmodium falciparum (Selkrik et al., 1989). A 75-kDa protective antigen of Chlamydia trachomatis has also been identified as a member of the hsp70 family, and human antibodies react primarily with non conserved epitopes of the protein. Therefore, members of the hsp70 family from a wide range of parasites and bacteria are strong B-cell antigens, stimulating antibodies directed mainly towards the nonconserved regions of the protein. There is a variable degree of cross-reactivity with hsp70 proteins of other species and a minimal response to human hsp70, consistent with the need to preserve self tolerance. In the case of M. leprae hsp70, the dominant antibody response is directed to the C-terminal region. Hsp60 has been found to be a common antigen of many bacterial pathogens including species of Pseudomonas, Mycobacterium, Borrelia, Salmonella, Legionella, Coxiella and Rickettsia (Shinnick, 1991). In Borellia burgdorferi, there are two HSP60 of molecular masses 60 and 66 kDa which have been implicated in developing autoimmune pathologies such as arthritis (Carreiro et al 1990). HSP60 class of proteins serves as an immunodominant targets of α, ß and γ, δ classes of T-lymphocytes and have been used to provoke immunological protection against Mycobacterium and Legionella (Silva and Lowrie, 1994). It has been postulated that since HSP60 is highly conserved, the host may frequently encounter this antigen through infection with various other microorganisms there by constantly boosting the immune response to HSP (Kaufmann et al 1991). Chimeric pili/fimbriae with inserted antigenic sequences can be used as effective and safe recombinant vaccines, application of atypical fimbriae Saf for design of Salmonella vaccine components of the Salmonella atypical fimbriae (Saf) are investigated for inclusion in a Salmonella vaccine. Vaccination with purified Dr fimbriae reduces mortality associated with chronic urinary tract infection due to E. coli bearing Dr adhesin (Pawel Goluszko, 2005). Purified E. coli Dr fimbrial antigen to vaccinate C3H/HeJ mice against an experimental urinary tract infection due to a homologous strain bearing Dr adhesion had demonstrated reduced mortality in the vaccinated animals. Antipneumococcal DnaK antiserum did not cross react with DnaK homologues in E.coli, staphylococcus aureus and human cells and hence may be a good candidate as a vaccine (Hamel et al., 1997). Still, the role Dna K in pathogenesis remains unknown. The difference between gram positive, and gram negative bacteria, suggests that the regulation mechanism of heat shock response of gram positive bacteria (especially DnaK function of gram positive bacteria) is quite different than E.coli and other gram negative. CONCLUSION The new paradigm for antimicrobial therapy should redefine the goal of balance in favor of the host enabling to control infection, rather than complete in vivo killing of a pathogen by the drug itself. Though some virulence inhibitors such as pilicides and T3SS inhibitors have the potential to target a wider spectrum of bacteria, new approaches have to be designed to understand how bacteria cause disease. As antibiotic resistance continues to evolve and the need for new antimicrobials continues to grow therapeutics that target in vivo essential gene functions, all the more compelling. Pilicides, by blocking chaperone and usher functions, have the potential to inhibit pili formation in a broad spectrum of pathogenic bacteria to prevent critical host–pathogen interactions necessary for many diseases. There are hundreds of diverse cell-surface virulence organelles that are assembled by the chaperone–usher pathway in important bacterial pathogens. Because all chaperones have a conserved structure and mechanism of action, it is reasonable to propose that pilicides likely have broad-spectrum activity. These pilicides represent an example of selective, low-molecular-weight, nonpeptidic virulence-determinant inhibitors (Gauthier et al., 2005; Hung et al., 2005). Immunization with a FimH-based vaccine reduces bladder colonization by uropathogenic E. coli by 99% in a mouse cystitis model and suggested adhesinbased vaccines may be effective in preventing both urinary tract and other bacterial infections. Understanding the molecular events involved in the biogenesis of these organelles will be crucial for the development of novel therapeutic strategies. Elucidating common themes in these pathways will be a prerequisite for any efforts targeted towards developing a therapeutic strategy with broad-spectrum activity. Targeting bacterial virulence or disrupting the interaction between the host and the pathogen are attractive options and should be explored. The identification of those processes that occur following attachment will undoubtedly open up further avenues of therapeutic possibilities, as we come closer to understanding how hostpathogen interactions lead to the expression of bacterial genes that are important in pathogenesis. Besides having high sequence homology Hsps can be used as protective vaccines. The design of new drugs can be based on either mimicking the conformation of known ligands or on the structure of the peptide-binding domain of the receptor. The IgG repertoire during intravesical bacille Calmette- Guerin (BCG) immunotherapy in superficial bladder patients includes antibodies to GroEL and Hsp70 but not to DnaK (Zlotta et al., 1997) exploiting the functional differences between bacterial DnaK and the analogous human Hsp70. This finding emphasizes the significant structural and functional differences between mammalian Hsp70 and the corresponding bacterial DnaK and supports our findings and hypothesis that antibacterial peptides can inactivate DnaK (bacterial Hsp70) without binding to Hsp70 (human) and affecting its normal functions. Drosocin, pyrrhocoricin, and apidaecin, representing the short (18-20 amino acid residues) proline-rich antibacterial peptide family, originally isolated from insects, were shown to act on a target bacterial protein in a stereospecific manner. Radicicol represents the first non –benzoquninone ansamycin antifungal inhibitor of Hsp90. It is thus worth investing both effort and cost effective in antivirulence inhibitor research. In this effort, structural biology allied with improved computational tools provides a powerful platform for rational chemical design and thus, should help fulfill our antibiotics development goals in the very near future. In conclusion microorganisms have smartly harnessed utilization of host‘s unfavorable environment by several molecular mechanisms, increased induction of genes coding for stress proteins and deletion of these genes resulted in attenuation of their growth within the host. Inhibitions of these factors are attainable by pharmacological new lead compounds that function directly by binding and inhibiting HSPs are under clinical trials are cited in literatures. ACKNOWLEDGEMENT The author (R.B) thanks the Vice-Chancellor and Registrar of Periyar University for their support and encouragement while preparing the manuscript. Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Competing interests: None declared. 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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareINTENSIVE CARE UNIT: A BREEDING GROUND FOR ANTIBIOTIC RESISTANT BACTERIA English141148Silpi BasakEnglish Monali N. RajurkarEnglish Ruchita O. AttalEnglish Sanjay Kumar MallickEnglishObjective: The present study was undertaken to detect the prevalence of multiple antibiotic resistant bacteria isolated from ICU patients and to study their antibiotic susceptibility profile. Method: The organisms were isolated from different clinical specimens and antibiotic susceptibility tests were done as per Clinical Laboratory Standard Institute (CLSI) guideline. The different tests for detection of Methicillin Resistant Staohylococcus aureus (MRSA) and Gram negative bacilli producing Extended spectrum beta-lactamases(ESBL), AmpC β-lactamases and Metallobetalactamases(MBL) were performed by standard methods. Results: A total number of 240 bacterial strains were studied. Out of which 105(43.8 %) were Gram positive isolates and 135(56.2%) were Gram negative isolates. 57(54.3%) MRSA strains were isolated. Amongst Gram negative isolates 29(21.5%) strains were only ESBL; 13(9.6%) only AmpC β-lactamase, 18(13.3%) both ESBL and AmpC β-lactamase and 21(15.6%) were MBL producers. 19 MBL producing strains were resistant to all antibiotics studied as per CLSI guideline. Conclusion: Accurate detection of multidrug resistant bacteria by any Clinical Microbiology Laboratory should be done for prompt and effective antimicrobial therapy to ICU patients and successful management of infections. EnglishMRSA, Multidrug resistant organisms.INTRODUCTION Intensive care units (ICUs) are unique patient care areas where severely ill patients are housed together in an environment of multiple invasive devices, drug resistant micro-organisms and few trained health care workers, especially in developing countries. Though ICU represents only 5% of the hospital beds, 25% of Hospital acquired infections occur in ICUs1 . In ICU patients the mortality ranges from 11% for surgical site infections (SSIs) to 20% for bloodstream infections (BSIs)2 . Though Carbapenems, Vancomycin and Linezolid are reserved antibiotics and are used as a last resort for treating severe infections with multiple drug resistant bacteria but bacteria have developed resistance to these drugs also. The ICUs are breeding ground of several drug resistant micro-organisms e.g. Methicillin Resistant Staphylococcus aureus (MRSA), newer B-lactamases i.e. Extended Spectrum BetaLactamases(ESBL), AmpC β-lactamase and Metallobetalactamases(MBL) producing Gram negative bacilli, Vancomycin resistant Enterococci (VRE), Vancomycin resistant Staphylococcus aureus (VRSA) and Vancomycin intermediate sensitive Staphylococcus aureus (VISA) etc. ICUs usually have a higher prevalence of infection with Multidrug Resistant Organisms (MDRO) than do non-ICU settings. MDROs are defined as micro-organisms predominantly bacteria, that are resistant to one or more classes of antimicrobial agents. The key to success in controlling infections in ICU patients are prompt and accurate detection of these microorganisms.3 Hence, the present study was undertaken to detect the prevalence of multiple antibiotic resistant bacteria isolated from ICU patients and to study their antibiotic susceptibility profile. In this study simple phenotypic methods for detection of MRSA and newer β-lactamases were used, which can be routinely and easily carried out in any Clinical Microbiology Laboratory. MATERIAL AND METHODS A total number of 240 bacterial strains isolated from clinical samples of ICU patients were studied from January 2008 to January 2011 and were identified by conventional methods4 . The clinical samples collected were blood, endotracheal tube aspirate, pus and wound swab, urine, urinary catheter tip, body fluids etc. Antibiotic sensitivity testing was done by using Kirby Bauer disk diffusion method according to Clinical Laboratory Standard Institute (CLSI) guidelines5 . All antibiotic disks and culture media used were procured from HiMedia Pvt Ltd.(India). Staphylococcus aureus strains were tested for Methicillin resistance by using Cefoxitin (30 µg) disc as per CLSI guidelines5 . Inducible Clindamycin resistance was detected by D-Zone test as per NCCLS guideline 20046 . To detect VRE, VRSA and VISA, Vancomycin disk were put and for confirmation Vancomycin E test strip (AB biomeriux) was used4 . In 135 Gram negative bacterial isolates antibiotic susceptibility test was done with Ceftazidime, Cefotaxime, Cefoxitin, Cotrimoxazole, Aztreonam, Ciprofloxacin, Amikacin and Imipenem as per CLSI guideline5 . In Gram negative bacterial isolates, for detection of ESBL producing strains combined disk method using Ceftazidime (CA 30 μg) and Ceftazidime-Clavulanic acid (CAC 30/10 μg) disk for Enterobacteriaceae as per CLSI guideline and for Pseudomonas aeruginosa combined disc using Piperacillin (Pc 100μg) and Piperacillin-Tazobactum (PIT 100/10μg) was used. Confirmation of ESBL production was determined by ESBL E-test strip (AB Biomeriux)4 . ? ESBL DETECTION For ESBL detection, Combined disk method and ESBL E-test were used. Combined disk method Broth cultures of test strains adjusted to McFarland 0.5 standard and inoculated on Mueller Hinton(MH) agar plates. Ceftazidime (CAZ) 30 µg and Ceftazidime plus Clavulanate (CAC) 30µg plus 10µg were used. After overnight incubation at 370C increase in zone diameter of ≥5mm with CAC disk as compared to CAZ disk alone was considered positive for ESBL detection. ESBL E-test4 Lawn culture of test strain was done on a MH agar plate and ESBL E-test strip was placed. After overnight incubation at 370C, MIC ratio of ceftazidime/Ceftazidime Clavulanic acid (TZ/TZL) ≥ 8 or deformation of ellipse or phantom zone present was considered positive for ESBL production. DETECTION OF AmpC β- LACTAMASE For detection of AmpC β-lactamase producing stains substrate inducer combination of Imepenem(10 μg) / Ceftazidime(30 μg) disks and for confirmation disk potentiation test using 3 aminophenyl boronic acid (100 μg/ml) was used7 . Confirmatory test : Disk potentiation test Two ceftazidime(30µg) disks with centre to centre distance of 30mm were placed on lawn cultured MH plate. 3-aminophenylboronic acid (APB) was dissolved in DMSO at a concentration of 100mg/ml. 10µl of this APB solution was added to one of the ceftazidime disk. After overnight incubation at 370C, an increase in zone size of ≥5mm around the Ceftazidime - APB disc compared to ceftazidime only disk was recorded as a positive result. ? DETECTION OF METALLOBETALACTAMASES (MBL) All Imipenem resistant strains were tested for MBL production by disk potentiation (DP) test using Imipenem and Imipenem-EDTA disk and were confirmed by MBL E test strip (AB biomeriux)8,9 . Disk Potentiation Test (DP): The IMP-EDTA combined disk test was performed for detection of metallobetalactamases. Test strains (turbidity adjusted to 0.5 McFarland standard ) were inoculated on to MH agar plate. Two imipenem disk (10 µg) were placed on the plate wide apart and 10 μl of 50mM zinc sulphate solution was added to each of the imipenem disks. Then 10µl of 0.5M EDTA solution was added to one of the disk and the plates were incubated at 350 C for 16-18 hrs.If the increase in inhibition zone with the Imipenem and EDTA disk was ≥7 mm than the imipenem disk alone, it was considered as MBL positive. MBL E-Test : Confirmatory test: The MBL E-test was done and interpreted using test strains and Quality control strains according to manufacturer‘s instructions. Overnight broth culture of test strain (turbidity adjusted to 0.5 McFarland standard) was used to inoculate MH agar plate. The MBL E-test strip was put on that inoculated MH plate with a sterile forceps and plates were incubated at 370C for 18-20 hrs. After incubation, MIC ratio of Imipenem /Imipenem-EDTA (IP/IPI) of ≥8 or deformations of ellipse or phantom zone indicate MBL production. The Candida albicans strains were detected by growth on Sabouraud‘s Dextrose agar (SDA), Gram‘s staining, germ tube formation, chlamydospore formation, growth on CROME agar and Hi-Candida identification kit. The antifungal drug sensitivity test with Fluconazole and Voriconzole for Candida albicans was done as per CLSI guideline10 . The control strains used in this study were Staphylococcus aureus ATCC 25923, Enterococcus faecalis ATCC 29212, Escherichia coli ATCC 25922, Klebsiella pneumoniae ATCC 700603, Pseudomonas aeruginosa ATCC 27853 and Candida albicans ATCC 90028. RESULTS Out of 240 bacterial stains isolated from ICU patients, 105 (43.8%) were Gram positive cocci and 135 were Gram negative bacilli. From 2 ICU patients Candida albicans was isolated. Maximum number of bacterial strains isolated were from Neonatal ICU (NICU) 123(51.3%), followed by Medicine ICU (MICU) 58(24.2%), Paediatrics ICU (PICU) 32(13.3%) and Operation theater ICU (OT ICU) 27(11.3%). The prevalence of MRSA, ESBL, AmpC, both ESBL and AmpC and MBL producing strains from different ICUs is shown in Figure 1. Amongst 96 Staphylococcus aureus strains isolated, 57 (59.4%) were MRSA and most of the MRSA strains 44(77.2%) were isolated from blood. All (100%) MRSA strains were resistant to Penicillin and sensitive to Vancomycin and Linezolid. 20(35.1%) MRSA strains were resistant to 08 antibiotics commonly used for treating Staphylococcal infections as per CLSI guideline5 . Amongst 57 MRSA isolates, resistance to Ciprofloxacin, Erythromycin, Clindamycin and Pristinamycin was found to be 51(89.5%), 46(80.7%), 26(45.6%) and 39(68.4%) respectively. 11(19.3%) and 14(24.6%) MRSA strains were even resistant to rifampicin and mupirocin respectively. 19(33.3%) MRSA strains belonged to iMLSB phenotype i.e. inducible Clindamycin resistant. Out of 5 Coagulase negative Staphylococci isolated 2 (40%) were Methicillin resistant but 4 Enterococcus faecalis strains isolated were Vancomycin sensitive. Amongst 135 Gram negative bacterial isolates 57(42.2%) were Pseudomonas aeruginosa, 30(22.2%) were E.coli, 43(31.9%) were Klebsiella pneumoniae and rest 5(3.7%) include others i.e. Proteus vulgaris(2), Citrobacter freundii(1), Acinetobacter baumanii(2). 29(21.5%) were only ESBL producers 13(9.6%) were only AmpC β-lactamase producers, 18(13.3%) were both ESBL and AmpC producers and 21(15.6%) strains were MBL producers. 19(90.5% ) MBL producing strains were resistant to all 08 antibiotics used as per CLSI guideline5 and 2 were only sensitive to Amikacin. Confirmation of MBL production by E-test is shown in Figure 2. Out of 21 MBL producing strains 12(57.1%) strains were Pseudomonas aeruginosa. Maximum 7(53.8%) strains producing AmpC β-lactamases were Klebsiella pneumoniae and 11(37.9%) ESBL producing strains were E.coli. All (100%) MBL producing strains were sensitive to Polymyxin B. Amongst 18 strains producing both ESBL and AmpC β-lactamase, 7(38.9%) were resistant to all 8 antibiotics used as per CLSI gudeline5 , but were sensitive to Imipenem and Amikacin. None of the MBL producers also produced ESBL or AmpC β- lactamase. 143 (59.6%) bacterial strains were isolated from blood samples, followed by 27(11.3%) from endotracheal tube aspirate. In 2 cases, Candida albicans was isolated from blood and from urine respectively. Candida albicans was isolated on two repeat culture from the same sample. The two Candida albicans strains were sensitive to fluconazole and Voriconazole10 . DISCUSSION According to World Health Organization(WHO) guidelines, 2002 more than 1.4 million people at any time suffer from Health care associated infections (HAI)11. The highest rates of HAIs occur in ICUs, and the crude mortality rates of HAI in the ICUs of the developed countries range from 12 to 80%12. Though no nationwide surveillance data are available, Rosenthal et al in 2006 had reported that the rates of HAI in ICUs range from 12.3% in few ICUs in India to 88.9% in a Turkish ICU13. The ICUs are the highest consumers of antimicrobials in any Health care set up. Moreover, ICUs have an unusually high rate of antimicrobial resistance14 . Antibiotic resistance in ICU acquired infections is responsible for increase in mortality, morbidity and prolonged hospital and ICU stay15 . Ventillator-associated pneumonia (VAP), Cather-associated urinary tract infection(CAUTI), Catheter-related bloodstream infections(CRBSIs), Surgical site infections(SSI), Clostridium difficile-associated diarrhoea(CDAD), Paranasal sinusitis especially maxillary sinusitis are common infections occurring in ICUs. In the present study, out of 23 bacterial strains isolated from urine, 13(56.5%) were isolated from CA-UTI. To consider CA-UTI, no minimum time period for which the catheter is to be in place is required16 . CA-UTI account for 30-40% of health care associated infections17. Richards et al had reported that 95% of UTI cases in hospitals are catheter associated18 . Our hospital is a tertiary care hospital, which is situated in a rural set-up and patients from surrounding villages of Vidarbha and the adjoining states come to our hospital for treatment. Lack of awareness, indiscriminate use of antibiotics before attending the hospital, might be the contributory factors for high prevalence of MRSA and Gram negative bacilli with production of newer β-lactamases i.e. ESBL, Amp C and MBL production, leading to multiple drug resistant organisms. Infection in the ICU patients can be successfully managed by prompt institution of effective antimicrobial therapy. But in an era of multidrug resistance, selecting the appropriate antibiotic is a significant challenge. Thus, every health care set up with ICU facility must have Clinical Microbiology Laboratory where different organisms isolated can be studied for antimicrobial resistance mechanisms and prompt communication of urgent Microbiology reports, help to modify the antimicrobial prescribing guidelines. ?Bundled approach or interventions‘ comprise of ?small straightforward set of best practices‘ which should primarily aim at the prevention of cross transmission and control or elimination of reservoirs or sources of infection should be followed. These ?Bundled approach when followed collectively can significantly reduce infection rates and improve patient‘s outcome in ICU19. Standard precautions, contact precautions, antimicrobial stewardship programmes etc., SMART i.e. (Specific, Measurable, Achievable, Relevant and Time bound) objectives and educating the health care workers, especially the nursing staffs are need of the hour19. Proper hand hygiene between every patient contact itself reduces the infection rate. Hence to conclude, detection of multidrug resistant bacteria by simple phenotypic methods should be done by any Clinical Microbiology Laboratory for effective antimicrobial therapy to ICU patients. Active efforts should be taken by all health care personnel to prevent antibiotic resistance as WHO has already mentioned ?‘No action today, No cure tommorow‘‘. ACKNOWLEDGEMENTS The authors highly acknowledge Datta Meghe Institute of Medical Sciences (MS), India for funding this project.Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/editors/publishers of all those articles, journals and books from where literature of this article has been reviewed and discussed. Englishhttp://ijcrr.com/abstract.php?article_id=1877http://ijcrr.com/article_html.php?did=18771. Eggimann, P. and D.Pittet. Infection control in the ICU. Chest. 2001;120:2059-93. 2. Klevens, R.M. , Edwards J.R. , Richards Jr. C.L. et al. Estimating health care-associated infections and deaths in U.S. hospitals, Public Health Rep. 2007;120:160-6. 3. Siegel J.D., E. Rhinehart, M. Jackson and L. Chiarello. Management of Multidrug Resistant Organisms in Health care settings. The Health care Infection control Practices Advisory Committee.CDC, Department of Health and Human Services, USA. 2006;1-73. 4. Washington C.W. Jr., Stephen D.A., William M.J., Elmer W.K., Gary W.P., Pant C.S., Gait L.W. Koneman‘s color Atlas and Textbook of Diagnostic Microbiology. 6th ed. Lippincott Williams and Williams USA. 2006. 5. Clinical and Laboratory Standards Institute (CLSI). Performance Standards for Antimicrobial disk diffusion tests; Approved standards. 9th ed. CLSI Document M2- M9.Wayne PA: Clinical and Laboratory Standards Institute. 2006. 6. National Committee for Clinical Laboratory Standards. Performance standards for 146 International Journal of Current Research and Review www.ijcrr.com Vol. 04 issue 07 April 2012 antimicrobial susceptibility testing; 14th Informational supplement. M100-54. Wayne PA : NCCLS. 2004. 7. Yagi T., J. Wachino, H. Kurokanz and S.Suzuki et al. Practical methods using boronic acid compounds for identification of class C B-lactamase producing Klebsiella pneumoniae and Escherichia coli. J. of Clin Microbiol. 2005;43(6):2551-8. 8. Attal, R.O., S. Basak, and S.K. Mallick. Metallobetalactamase producing Pseuodomonas aeruginosa: An emerging threat to clinicians. Journal of Clinical and Diagnostic Research. 2010;4:2691-6. 9. Walsh, T.R., A. Bolmstrom, A. Quarmstorm and A.Gals . Evaluation of a new E test for detecting metallobetalactamases in clinical testing J. Clin. Microbiol. 2002;40:2755-9. 10. Clinical and Laboratory Standards Institute (CLSI). Antifungal disk diffusion susceptibility testing of yeasts ; Approved guideline M-44 A, CLSI, USA. 2006. 11. WHO: Guidelines on Prevention and Control of Hospital Associated Infections. World Health Organisation. South East Asian Region. Geneva: WHO. 2002. 12. Vincent, J. L. Nosocomial infections in adult intensive care units. Lancet. 2003;361:2068-77. 13. Rosenthal, V.D., D.G. Maki and R. Saloman et al. Device associated nosocomial infections in 55 intensive care units of 8 developing countries. Ann. Intern. Med. 2006;145:582-91. 14. Kollef M.H. Time to get serious about antimicrobial susceptibility testing; 14th Informational supplement. M100-54. Wayne PA : NCCLS. 2004. 7. Yagi T., J. Wachino, H. Kurokanz and S.Suzuki et al. Practical methods using boronic acid compounds for identification of class C B-lactamase producing Klebsiella pneumoniae and Escherichia coli. J. of Clin Microbiol. 2005;43(6):2551-8. 8. Attal, R.O., S. Basak, and S.K. Mallick. Metallobetalactamase producing Pseuodomonas aeruginosa: An emerging threat to clinicians. Journal of Clinical and Diagnostic Research. 2010;4:2691-6. 9. Walsh, T.R., A. Bolmstrom, A. Quarmstorm and A.Gals . Evaluation of a new E test for detecting metallobetalactamases in clinical testing J. Clin. Microbiol. 2002;40:2755-9. 10. Clinical and Laboratory Standards Institute (CLSI). Antifungal disk diffusion susceptibility testing of yeasts ; Approved guideline M-44 A, CLSI, USA. 2006. 11. WHO: Guidelines on Prevention and Control of Hospital Associated Infections. World Health Organisation. South East Asian Region. Geneva: WHO. 2002. 12. Vincent, J. L. Nosocomial infections in adult intensive care units. Lancet. 2003;361:2068-77. 13. Rosenthal, V.D., D.G. Maki and R. Saloman et al. Device associated nosocomial infections in 55 intensive care units of 8 developing countries. Ann. Intern. Med. 2006;145:582-91. 14. Kollef M.H. Time to get serious about infection prevention in the ICU. Chest. 2006;130:1293-6. 15. Kollef M.H. and V.J. Fraser. Antibiotic resistance in the intensive care unit. Ann. Intern. Med. 2001;134:298-314. 16. Gould, C V, Umscheid C.A. and Agarwal R.K. et al.HI.AAC/CDC Guideline for Prevention of Catheter Associated Urinary Tract Infection.HICPAC,2009. Available at: http://www.cdc.gov.nhsn/pdfs/pscManual/tp sc CAUTIcurrent.pdf.(Online) 17. Johnson J R, M.A.Kuskowski and T.J.Wilt. Systematic review: Antimicrobial urinary catheters to prevent catheter-associated urinary tract infection in hospitalized patients. Ann Intren Med. 2006;144:116-26. 18. Richards M., J. Edwards, D. Culver and R. Gaynes. Nosocomial infections in medical intensive care units in the United States. National Nosocomial Infections Surveillance System. Crit. Care. Med. 1999;27:887-92. 19. Lachman P. and S. Yuen. Using care bundles to prevent infection in neonatal and pediatric ICUs. Curr. Opin. Infect. Dis. 2009;22(3):224-8.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-524147EnglishN2012April18HealthcareEFFECT OF OZONE ON HUMAN ELECTROCARDIOGRAM English149154Sonali S. SakhareEnglish B. H. PawarEnglishThis paper presents the effect of ozone on the electrocardiogram. The electrocardiogram (ECG) is a test that records the electrical activity produced by the heart. The ECG can pick up abnormalities of heart rhythm and can give us information on whether the heart is enlarged or working under strain. Ozone thus plays a key role in the temperature structure of the Earth&#39;s atmosphere. We record the ECG of human being at normal conditions. After that person is seating inside the chamber. The temperature inside the chamber can be increased by heating lamp. Then long breathing can be carried out for ten minutes at higher temperature. Again record the ECG‘S at higher temperatures. It is found that the Heart Rate becomes increases in higher temperatures. EnglishElectrocardiogram(ECG), heart rate, ozone.INTRODUCTION A. Ozone Ozone is very rare in our atmosphere, averaging about three molecules of ozone for every 10 million air molecules. In spite of this small amount, ozone plays a vital role in the atmosphere. Ozone is mainly found in two regions of the Earth&#39;s atmosphere. Most ozone (about 90%) resides in a layer that bA. Ozoneegins between 10 and 17 kilometers above the Earth&#39;s surface and extends up to about 50 kilometers. This region of the atmosphere is called the stratosphere. The ozone in this region is commonly known as the ozone layer. The remaining ozone is in the lower region of the atmosphere, which is commonly called the troposphere. Ozone is a gas that forms in the atmosphere when 3 atoms of oxygen are combined (03). It is not emitted directly into the air, but at ground level is created by a chemical reaction between oxides of nitrogen (NO), and volatile organic compounds (VOC) in the presence of sunlight. Ozone has the same chemical structure whether it occurs high above the earth or at ground level and can be "good" or "bad," depending on its location in the atmosphere. The ozone molecules in the upper atmosphere (stratosphere) and the lower atmosphere (troposphere) are chemically identical, because they all consist of three oxygen atoms and have the chemical formula O3. However, they have very different roles in the atmosphere and very different effects on humans and other living beings. At the Earth&#39;s surface, ozone comes into direct contact with life-forms and displays its destructive side (hence, it is often called "bad ozone"). Because high levels of ozone are toxic to living systems. Stratospheric ozone (sometimes referred to as "good ozone") plays a beneficial role by absorbing most of the biologically damaging ultraviolet sunlight (called UV-B), allowing only a small amount to reach the Earth&#39;s surface. The absorption of ultraviolet radiation by ozone creates a source of heat, which actually forms the stratosphere itself (a region in which the temperature rises as one goes to higher altitudes). Ozone thus plays a key role in the temperature structure of the Earth&#39;s atmosphere. B. Electrocardiogram (ECG) The electrocardiogram (ECG) is a noninvasive test that is used to reflect underlying heart conditions by measuring the electrical activity of the heart. By positioning leads (electrical sensing devices) on the body in standardized locations, information about many heart conditions can be learned by looking for characteristic patterns on the ECG. An electrocardiogram can tell a lot about your heart and how it is working. A healthy person&#39;s electrocardiogram has a certain pattern. When there are changes in that pattern, then there is a problem with your heart. For example, during a heart attack, the EKG machine records the changing pattern of the heart&#39;s electrical activity. C. Heart rate Heart rate is the number of heartbeats per unit of time, typically expressed as beats per minute (bpm). Heart rate can vary as the body&#39;s need to absorb oxygen and excrete carbon dioxide changes, such as during exercise or sleep. The measurement of heart rate is used by medical professionals to assist in the diagnosis and tracking of medical conditions. It is also used by individuals, such as athletes, who are interested in monitoring their heart rate to gain maximum efficiency from their training. The R wave to R heart rate (HR) is readily calculated from the ECG as follows: HR = 1,500/RR interval in millimeters, HR = 60/RR interval in seconds, or HR = 300/number of large squares between successive R waves. In each case, the authors are actually referring to instantaneous HR, which is the number of times the heart would beat if successive RR intervals were constant. However, because the above formula is almost always mentioned, students determine HR this way without looking at the ECG any further. Wave interval (RR interval) is the inverse of the heart rate. MATERIALS AND METHODS On detail history, all subjects were nonalcoholic, non-smokers, not taking any drug and were having similar dietary habits, physical and mental activities in working and home atmosphere. They were subjected to clinical examination and found healthy. Data on physical characteristics was obtained such as age, height, weight, diet, hemoglobin. The some normal human being where selected for study. ECG leads are attached to the body while the person lies flat on a bed or table. Leads are attached to pre-defined positions. A small amount of gel is applied to the skin, which allows the electrical impulses of the heart to be more easily transmitted to the ECG leads. First of all we record the ECG at normal condition. Then the person is seating inside the chamber. The temperature inside the chamber can be increased by heating lamp. The temperature can be measured by thermometer. Again record the ECG at higher temperature. Lastly interpret ECG in different conditions. RESULTS Present study was a case-control study. There were 15 subjects above 30 years of age of both sexes. Here we present result of two subjects. The first ECG recorded (shown in ECG 1) shows the normal ECG of First subject. He is vegetarian. The weight is fifty nine and hemoglobin is 11.5. The second ECG (shown in ECG 2) shows the effect Heart rate at high temperature. The third ECG recorded (shown in ECG 3) shows the normal ECG of second subject. He is vegetarian. The weight is fifty and hemoglobin is 12.5. The Fourth ECG (shown in ECG 4) shows the effect Heart rate at high temperature. This shows tremendous change in ECG. In both the subject heart rate at higher temp goes on increases as compare to the normal ECG. Thus we have to maintain ozone level so that temperature in the atmosphere can be maintained. DISCUSSION To the best of our knowledge no study has been carried out showing effect of ozone on parameters at different temperature. Environmental conditions and variety of behavioral factors such as stress, anxiety, affective and attitudinal dispositions of the individual influence the cardiovascular responses. Ground-level ozone is created near the Earth&#39;s surface by the action of daylight UV rays on a group of pollutants called ozone precursors. There is a great deal of evidence to show that ground level ozone can harm lung function and irritate the respiratory system. Exposure to ozone and the pollutants that produce it is linked to premature death, asthma, bronchitis, heart attack, and other cardiopulmonary problems. CONCLUSIONS A number of investigations indicate that change in heart rate has emerged as a new risk factor for mortality in cardiovascular mortality in human beings. 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