Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241107EnglishN2018April14HealthcareA Study of Haemoglobin Level based on Tenofovir given as a First Line Anti Retroviral Therapy in Human Immune Virus Infected Patient English0205Kapildev MondalEnglish Soumabrota DuttaEnglishBackground: Tenofovir has been recently introduced in our country as first line therapy in HIV infection but limited data available on safety profile & tolerability in Indian population of patients. This study focused on change of haemoglobin level due toTenofovir given as a first line anti retroviral therapy in HIV infected patient. Aims of the Study: To show the change of haemoglobin level due to tenofovir in tenofovir based first line anti retroviral therapy in HIV infected patient. Materials & Methods: We studied descriptive & longitudinal study in Art center in Murshidabad medical College & hospital, west Bengal, July 2014 to June 2015.Our study included 107 HIV infected patient (aged 18 years and above) attending Art center, Murshidabad medical College & Hospital who will be started on Tenofovir based 1st line Art (according to NACO guideline) except Pregnant women, patients with serum creatinine >1.2mg/dl & unwilling for consent. Discussion: During this period 10 of them left the study due to lack of follow up. The study population had overall weight gained & increased by haemoglobin at the end of the study. Results: This study shows that tenofovir is well tolerable drug. Tenofovir therapy is associated with mean weight gain and increase in haemoglobin level. Conclusion: Tenofovir therapy is associated with mean weight gain and increase in haemoglobin level. EnglishWeight, Mean, CreatinineIntroduction &Background : Tenofovir recently use in our country as first line therapy in HIV infection but limited data available on safety profile in Indian. The study will focus on change of haemoglobin level due to tenofovir based first line anti retroviral therapy in human immune virus infected patient. Methods: We did approval from Institutional ethics committee and Informed consent from all the study subjects. We studied subjects from July 2014 to June 2015 and followed up upto12 months. We took detailed history  and did physical examinations and baseline investigation  before initiation of Art and subsequently at 2weeks, 1 month, 3 months , 6 months and 12 months of starting of Art. We assessed haemoglobin level before initiation, after 12 months of Art theraphy and different  laboratory tests report. We collected all data and analyzed by using SPSS. Results: This study shows that tenofovir is well tolerated drug in this population of patients with once daily regimen which has improved patients compliance. Tenofovir therapy improves overall general health of the patients. Tenofovir therapy is associated with mean weight gain and increased in haemoglobin level. It is not associated with adverse effect on total leucocyte count, differential leucocyte count, platelet count, serum bilirubin and serum liver enzymes (SGOT, SGPT). Discussion: HIV infection causes significant morbidity and mortality by causing an immune deficient state and patients usually succumb to death from unusual opportunistic infections and malignancies. However HIV infection is a manageable  HAART. We conducted the study involving 107 eligible patients who were followed up for a period of 12 months. During followed up period of 12 months  ten of them left the study. We studied the effect of tenofovir on haemoglobin level on that period. We observed gastrointestinal intolerance which includes anorexia, nausea, vomiting and upper abdominal pain in 12.37% patients at 2 weeks of starting of ART which subsequently relieved with time. Only 4% patients had GI intolerance at 1 month which relieved after few days. We found that there is increment in mean haemoglobin level of total study population from base line value. There was no effect on the total and differential leucocyte count or on the mean platelet count. We found no adverse effect of the drug on liver function (serum bilirubin, SGOT, SGPT did not show any change). The study showed that there is increasing value of mean serum creatinine level of total study population from base line value but mean serum creatinine at the end of study remained within normal reference value. None of the study population developed acute renal failure or feature of proximal renal tubular dysfunction (glycosuria in presence of normal plasma glucose and proteinurea) for which discontinuation of tenofovir required. The pattern of change in serum creatinine level is same in both sex groups. We also found that there was increasing value of mean serum urea level of the total study population from base line value although the value at the end of study remained within normal reference value. We found there is clinical and biochemical  improvement of overall health in general  study of the population probably due to well control of the disease and also the control of opportunistic infection. The study population had overall weight gain at the end of the study Conclusion: Tenofovir increases the level of haemoglobin on that period. This study result reveals improvement of haemoglobin level based on tenofovir given as a first line anti retroviral therapy in human immune virus infected patient. Ethical Considerations :The Institutional Ethics Committee of Murshidabad medical college & hospital approved of our study. Acknowledgement: We are grateful and indebted to respected Principal Sir, MSVP Sir, Deputy Superintendent and Assistant Superintendents for being of help whenever needed. Source of fund: We use from our personal account. Interest of study: there is no conflict of interest for the study Abbreviation TDF-Tenofovir disoproxil fumarate. NACO-National Aids control organization. ART-Antiretroviral therapy. PrEP-Pre-exposure prophylaxis. Sd- Standard deviation. Hb-Haemoglobin. TLC-Total leucocyte count. DLC-Differential leucocyte count. LFT-Liver function test. ALT-Alanine transaminase. HIV- Human Immunodeficiency Virus. SIV- Simian Immunodeficiency Virus. AIDS- Acquired Immunodeficiency Syndrome. AZT -Zidovudine. HAART- Highly active antiretroviral therapy. NNRTI -Non-nucleoside reverse trancriptase inhibitor. Englishhttp://ijcrr.com/abstract.php?article_id=2464http://ijcrr.com/article_html.php?did=24641. Cooper D Ryan, Wiebe Natasha et al. Systematic Review and Meta-analysis: Renal Safety of Tenofovir Disoproxil Fumarate in HIV- Infected Patients. Clin Infect Dis. 2010;51(5):496-505. 2. Bygrave Helen, Ford Nathan, Cutsem van Gilles et al. Implementing a Tenofovir-Based First- Regimen in Rural Lesotho: Clinical Outcomes and Toxicities After Two Years. J Acquir Immune De?c Syndr 2011;56:75-8. 3. Phair J, Palella F. Renal disease in HIV-infected individuals.Curr Opin HIV AIDS. 2011Jul;6(4):285-9. 4. Fernando SK, Finkelstein FO, Moore BA, Weissman S. Prevalence of chronic kidney disease in an urban HIV infected population. Am J Med Sci. 2008;335:89-94. 5. Hall AM, Hendry BM, Nitsch D, Connolly JO. Tenofovir-Associated Kidney Toxicity in HIV-Infected Patients: A Review of the Evidence. Am J Kidney Dis. 2011;57:773-80. 6. Horberg M, Tang B, Towner W, Silverberg M, Bersoff-Matcha S, Hurley L, et al. Impact of tenofovir on renal function in HIV infected, antiretroviral-naive patients. J Acquir Immune Defic Syndr. 2010;53:62–69. 7. Calza L, Trapani F, Tedeschi S, Piergentili B, Manfredi R, Colangeli V, et al. Tenofovir-induced renal toxicity in 324 HIV-infected, antiretroviral-naive patients. Scand J Infect Dis 2011Aug;43(8):656-60. 8. Martinez E, Arranz JA, Podzamczer D, Lonca M, Sanz J, Barragan P,et al. A simplification trial switching from nucleoside reverse transcriptase inhibitors to once-daily fixed-dose abacavir/lamivudine or tenofovir/emtricitabine in HIV-1-nfected patients with virological suppression. J Acquir Immune Defic Syndr. 2009;51:290-97. 9. Longenecker CT, Scherzer R, Bacchetti P, Lewis CE, Grunfeld C, Shlipak MG. HIV viremia and changes in kidney function. Aids 2009;23:1089-96. 10. Ando M, Yanagisawa N, Ajisawa A, Tsuchiya K, Nitta K. Kidney tubular damage in the absence of glomerular defects in HIV infected patients on highly active antiretroviral therapy. 2011 Oct;26(10):3224-. 11. Rebecca Scherzer, Michelle Estrella, Yongmei Li, Steven G. Deeks, Carl Grunfeld and Michael G. Shlipak. Association of tenofovir exposure with kidney disease risk in HIV infection.AIDS2012 Apr 24;26(7):867-75. 12. Woodward CL, Hall AM, Wiliums IG, Madge S, Copas A, Nair D, et al. Tenofovir associated renal and bone toxicity. HIV Med 2009;10:482-7. 13. Weber R, Sabin CA, Friis-Møller N, Reiss P, El-Sadr WM, Kirk O, Dabis F,  Law MG, Pradier C, De Wit S, Akerlund B, Calvo G, Monforte Ad, Rickenbach  M, Ledergerber B, Phillips AN, Lundgren JD. Liver-related deaths in persons infected with the human immunodeficiency virus: the D:A:D study. Arch Intern  Med 2006;166:1632-41. 14. Alter MJ. Epidemiology of viral hepatitis and HIV co-infection. J Hepatol 2006;44:6-9. 15. SorianoV, Puoti M, Peters M, Benhamou Y, Sulkowski M, Zoulim F, Mauss S, Rockstroh J. Care of HIV patients with chronic hepatitis B: updated recommendations from the HIV Hepatitis B Virus International Panel. AIDS2008; 22: 1399-1410. 16. Tenney DJ, Rose RE, Baldick CJ, Pokornowski KA, Eggers BJ, Fang J, Wichroski MJ, Xu D, Yang J, Wilber RB, Colonno RJ. Long-term monitoring shows hepatitis B virus resistance to  entecavir  in  nucleoside-naïve  patients  is  rare through 5 years of therapy. Hepatology 2009;49:1503-14. 17. Price  H,  Dunn  D,  Pillay  D,  Bani-Sadr  F,  de  Vries-Sluijs  T, Jain MK, Kuzushita N, Mauss S, Núñez M, Nüesch R, Peters M, Reiberger T, Stephan C, Tan L, Gilson R. Suppression of HBV  by  tenofovir  in  HBV/HIV  co-infected  patients:  a  systematic review and meta-analysis. PLoS One 2013; 8: e68152.[PMID: 23874527 DOI: 10.1371/journal.pone.0068152] 18. Kitrinos KM, Corsa  A, Liu Y, Flaherty J, Snow-Lampart A, Marcellin P, Borroto-Esoda K, Miller MD. No detectable resistance to tenofovir disoproxil  fumarate  after 6 years of therapy in patients with chronic hepatitis B. Hepatology 2014; 59: 434-42. 19. Rockstroh JK, Bhagani S, Benhamou Y, Bruno R, Mauss S, Peters L, Puoti M,  Soriano V, Tural C. European AIDS Clinical Society (EACS) guidelines for the clinical management and treatment of chronic hepatitis B and C coinfection in HIV-infected adults. HIV Med 2008;9:82-88. 20. Brook G, Main J, Nelson M, Bhagani S, Wilkins E, Leen C, et al. British HIV Association guidelines for the management of coinfection with HIV-1 and hepatitis B or C virus 2010. HIV Med 2010;11:1-30. 21. Soriano V, Tuma P, Vispo E, Labarga P, Fernández JV, Medrano J, Barreiro P. Hepatitis B in HIV patients: what is the current treatment and what are the challenges? J HIV Ther 2009;14:13-18. 22. Benhamou  Y,  Fleury  H, Trimoulet  P, Pellegrin  I, Urbinelli R, Katlama  C, et al. Anti-hepatitis  B virus  efficacy of tenofovir disoproxil fumarate in HIV-infected patients. Hepatology 2006;43:548-55. 23. Zoutendijk  R, Zaaijer HL, de Vries-Sluijs TE, Reijnders JG, Mulder JW,  Kroon FP, et al. Hepatitis B surface antigen declines and clearance  during  long-term tenofovir therapy in patients  coinfected  with HBV and HIV. J  Infect  Dis 2012;206:974:80. 24. Phung BC, Sogni P, Launay O. Hepatitis B and human immunodeficiency virus co-infection. World J Gastroenterol 2014; 20(46): 17360-67. 25. Nelson M, Portsmouth S, Stebbing J, Atkins M, Barr A, Matthews G, et al. An open-label study of tenofovir in HIV-1and hepatitis B virus co-infected individuals. AIDS 2003;17:F7–F10. 26. Kourtis AP, Bulterys M, Hu DJ, Jamieson DJ. HIV- HBV-a global challenge. N Engl J Med.2012;366:1749-52. 27. Matthews GV, Avihingsanon A, Lewin SR, Amin J, Rerknimitr R, et al. A randomized trial of combination hepatitis B therapy in HIV/HBV coinfected antiretroviral naïve individuals in Thailand. Hepatology 2008;48:1062-69. 28. McColl DJ, Margot NA, Wulfsohn M, et al. Patterns of resistance emerging in HIV-1 from antiretroviral-experienced patients undergoing intensification therapy with tenofovir disoproxil fumarate. J Acquir Immune Defic Syndr 2004;37:1340-50. 29. Miller MD, Margot N, Lu B, Zhong L, Chen S-S,  Cheng A, et al. Genotypic and phenotypic predictors of the magnitude of response to tenofovir disoproxil fumarate treatment in antiretroviral-experienced patients. J Infect Dis 2004;189: 837-46. 30. Miller MD, Margot NA, Hertogs K, Larder B, Miller V. Antiviral activity of tenofovir (PMPA) against nucleoside-resistant clinical HIV samples. Nucleosides Nucleotides Nucleic Acids.2001;20:1025–28. 31. Margot NA, Isaacson E, McGowan I, Cheng A, Miller MD. Extended treatment with tenofovir disoproxil fumarate in treatment-experienced HIV-1-infected patients: genotypic, phenotypic, and rebound analyses. J Acquir immune Defic Syndr. 2003;33:15-21. 32. Wainberg MA, Miller MD, Quan Y, Salomon H, Mulato AS, Lamy PD, et al. In vitro selection and characterization of HIV-1 with reduced susceptibility to PMPA. Antivir Ther1999;4:87–94. 33. Larder BA, Stammers DK. Closing in on HIV drug resistance. Nat Struct Biol 1999;6:103–106. 34. Boyer PL, Sarafianos SG, Arnold E, Hughes SH. Selective excision of AZTMP by drug-resistant human immunodeficiency virus reverse transcriptase. J Virol 2001;75:4832–42. 35. Kellam P, Boucher CA, Larder BA. Fifth mutation in human immunodeficiency virus type 1 reverse transcriptase contributes to the development of high-level resistance to zidovudine. Proc Natl Acad Sci USA 1992;89:1934–38. 36. Wainberg MA, White AJ. Current insights into reverse transcriptase inhibitor-associated resistance. Antivir Ther 2001;6( 2):11–19. 37. Santiago ML, Range F, Keele BF, Li Y, Bailes E, Bibollet-Ruche F, et al. Simian immunodeficiency virus infection in free-ranging sooty mangabeys (Cercocebus atys atys) from the Tai Forest, Cote d'Ivoire: Implications for the origin of epidemic human immunodeficiency virus type 2. J Virol.2005;79:12515–27. 38. Stone VE. Strategies for optimizing adherence to highly active antiretroviral therapy: lessons from research and clinical practice. Clin Infect Dis. 200115;33:865–72. 39. Ford N, Calmy A. Improving first-line antiretroviral therapy in resource limited settings. Current Opin HIV AIDS.2010;5:38–47. 8. Brinkman K. Stavudine in antiretroviral therapy: is this the end? AIDS.2009; 23:1727–29. 40. Gallant JE, DeJesus E, Arribas JR, et al. Tenofovir DF, Emtricitabine, and efavirenz vs. zidovudine, lamivudine, and efavirenz for HIV. N Engl J Med. 2006;354:251–60.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241107EnglishN2018April14HealthcareRationale for Palliative Gastrectomy and Metastasectomy in Metastatic Gastric Cancer English0611Abdullah SakinEnglish Makbule TambasEnglish Nurgul YasarEnglish Caglayan GeredeliEnglish Saban SecmelerEnglish Cumhur DemirEnglish Ali AlemdarEnglish Hakan GuvenEnglish Sener CihanEnglishObjectives: Approximately 50% of gastric cancer patients are locally advanced or metastatic staged at the time of diagnosis. In limited metastatic patients, performing surgery is thought to be related to survival benefit. Thus, we evaluated the effect of the surgery on survival in patients with metastatic gastric carcinoma who have been treated and followed-up in our oncology clinic. Methods: Patients with pathologically verified metastatic gastric cancer between 2009-2016 were included in the study.The patients were divided into 3 groups as those who underwent palliative gastrectomy (group A), who underwent simultaneous gastric surgery and metastasectomy (group B), and who underwent no surgery (group C). Results: One hundred and fifty-three patients, including 35 in the group A, 10 in the group B, and 108 in the group C, were included in the study. There was a significant difference between the groups in terms of the mean age of the patients (60,4, 53 and 63, respectively; p=0.016). Median follow-up time was 8±9.6 months. Medianoverall survival (OS) was 20 months in group B, 13 months in group A and 6 months in group C;while OS was found to be significantly increased in surgery groups compared with non-surgery (Group A vs. B, p=0,259; group A vs. C, pEnglishChemotherapy, Gastrectomy, Gastric cancer, MetastasectomyINTRODUCTION Gastric cancer is the fifth most common cancer around the world and is the third most common cause of cancer-related deaths. In 2017, 28,000 new gastric cancer cases and 10,960 gastric cancer-related deaths are expected in the United States(1). At the time of diagnosis, approximately 50% of patients are locally advanced or metastatic while nearly half of non-metastatic patients are eligible for curative surgical treatment(2). Moderate improvements in the gastric cancer prognosis in recent years may adhere to improvements in multidisciplinary treatment modalities, such as improved surgical technique and the use of new chemotherapy regimens(1, 2). Surgical resection of the primary tumor in patients with locally advanced or metastatic disease may provide palliation of symptoms such as nausea, pain, obstruction or bleeding. The results of some studies suggest that palliative gastrectomy may be associated with survival benefit in patients with oligometastatic disease. This benefit, however, has not been seen in all studies (2, 3). We investigated whether surgery provided any survival advantages in patients who were treated and followed-up in our oncology clinic for metastatic gastric carcinoma and underwent palliative gastrectomy, simultaneous gastrectomy and metastasectomy and no surgical intervention. MATERIALS AND METHODS Patients with pathologically verified metastatic gastric cancer between 2009-2016 were included in the study. The clinical characteristics data of patients including age, sex, smoking, comorbidities, type of surgery performed, pathological features, sites of metastases, ECOG performance status, treatment details were obtained retrospectively from patients' medical file. Patients whose data were not accessable and who werw diagnosed with multiple cancer were excluded from the study. The patients were divided into 3 groups as those who underwent palliative gastric surgery at the time of diagnosis (Group A), who underwent simultaneous gastric surgery and metastasectomy at the time of diagnosis (Group B) and who underwent no surgery (Group C). Overall survival (OS) was calculated from the date of diagnosis to the date of death or last contact with patient. Statistical Analysis SPSS 22.0 for Windows program was used for statistical analysis. Descriptive statistics were given as mean, standard deviation, minimum, maximum for numerical variables, number and percentage for categorical variables. The numerical variables in the independent two groups were analyzed by Student t test and Mann Whitney U test if normal distribution condition was provided and not met, respectively. The comparisons of ratios between groups were made with Chi Square Analysis. Monte Carlo simulation was applied when conditions were not met. The survival analyzes were performed with Kaplan Meier Analysis. Determinants for survival were examined by Cox Regression Analysis. Statistical significance level of alpha was accepted as p Englishhttp://ijcrr.com/abstract.php?article_id=2465http://ijcrr.com/article_html.php?did=24651.         Siegel RL, Miller KD, Jemal A. Cancer Statistics, 2017. CA Cancer J Clin. 2017;67(1):7-30. 2.         Jeong O, Park YK, Choi WY, Ryu SY. Prognostic significance of non-curative gastrectomy for incurable gastric carcinoma. Ann Surg Oncol. 2014;21(8):2587-93. 3.         Chen J, Kong Y, Weng S, Dong C, Zhu L, Yang Z, et al. Outcomes of surgery for gastric cancer with distant metastases: a retrospective study from the SEER database. Oncotarget. 2017;8(3):4342-51. 4.         Kodera Y, Fujitani K, Fukushima N, Ito S, Muro K, Ohashi N, et al. Surgical resection of hepatic metastasis from gastric cancer: a review and new recommendation in the Japanese gastric cancer treatment guidelines. Gastric Cancer. 2014;17(2):206-12. 5.         Martella L, Bertozzi S, Londero AP, Steffan A, De Paoli P, Bertola G. Surgery for Liver Metastases From Gastric Cancer: A Meta-Analysis of Observational Studies. Medicine (Baltimore). 2015;94(31):e1113. 6.         Tegels JJ, De Maat MF, Hulsewe KW, Hoofwijk AG, Stoot JH. Improving the outcomes in gastric cancer surgery. World J Gastroenterol. 2014;20(38):13692-704. 7.         Linhares E, Monteiro M, Kesley R, Santos CE, Filho OS, Simoes JH. Major hepatectomy for isolated metastases from gastric adenocarcinoma. HPB (Oxford). 2003;5(4):235-7. 8.         Cheon SH, Rha SY, Jeung HC, Im CK, Kim SH, Kim HR, et al. Survival benefit of combined curative resection of the stomach (D2 resection) and liver in gastric cancer patients with liver metastases. Ann Oncol. 2008;19(6):1146-53. 9.         Tsujimoto H, Ichikura T, Ono S, Sugasawa H, Hiraki S, Sakamoto N, et al. Outcomes for patients following hepatic resection of metastatic tumors from gastric cancer. Hepatol Int. 2010;4(1):406-13. 10.       Dittmar Y, Altendorf-Hofmann A, Rauchfuss F, Gotz M, Scheuerlein H, Jandt K, et al. Resection of liver metastases is beneficial in patients with gastric cancer: report on 15 cases and review of literature. Gastric Cancer. 2012;15(2):131-6. 11.       Rosa F, Marrelli D, Morgagni P, Cipollari C, Vittimberga G, Framarini M, et al. Krukenberg Tumors of Gastric Origin: The Rationale of Surgical Resection and Perioperative Treatments in a Multicenter Western Experience. World J Surg. 2016;40(4):921-8. 12.       Lu LC, Shao YY, Hsu CH, Hsu C, Cheng WF, Lin YL, et al. Metastasectomy of Krukenberg tumors may be associated with survival benefits in patients with metastatic gastric cancer. Anticancer Res. 2012;32(8):3397-401. 13.       Yu P, Huang L, Cheng G, Yang L, Dai G, Ying J, et al. Treatment strategy and prognostic factors for Krukenberg tumors of gastric origin: report of a 10-year single-center experience from China. Oncotarget. 2017;8(47):82558-70. 14.       Hsu JT, Liao JA, Chuang HC, Chen TD, Chen TH, Kuo CJ, et al. Palliative gastrectomy is beneficial in selected cases of metastatic gastric cancer. BMC Palliat Care. 2017;16(1):19. 15.       Kim KH, Lee KW, Baek SK, Chang HJ, Kim YJ, Park DJ, et al. Survival benefit of gastrectomy +/- metastasectomy in patients with metastatic gastric cancer receiving chemotherapy. Gastric Cancer. 2011;14(2):130-8.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241107EnglishN2018April14HealthcareCognitive Functions in Patients of Type 2 Diabetes Mellitus with Peripheral Neuropathy, An Observational Cross Sectional Study Done in India English1217Shubhra BhardwajEnglish Sunita MondalEnglish Rajiv BandhuEnglish Debasish ChaudhuryEnglish Ekta Malik DebnathEnglish Gaurav SwamiEnglish Madhulika MongaEnglish Mukul AdlakhaEnglishBackground: Peripheral neuropathy and cognitive decline both are very common in diabetics but relationship between them is yet unclear. Hence, this study aimed at assessing the cognitive functions in patients of type 2 diabetes mellitus (T2DM) with diabetic peripheral neuropathy (DPN) and compare them with that of patients of T2DM without DPN and apparently healthy controls. Materials and Methods: In this observational cross sectional study eligible T2DM patients were divided into two groups with DPN (25) and without DPN (25) by Nerve conduction velocity (NCV). 25 apparently healthy controls were taken. Cognitive functions were tested by using P300 event related potential. Result: P300 latency on Pz was significantly delayed in the T2DM with DPN as compared to T2DM without DPN (p < 0.05) and controls (p < 0.01). The average latency was also significantly delayed in T2DM with DPN as compared to controls(p < 0.05).A positive correlation between duration of diagnosis of T2DM (r= 0.3339, p= 0.0178*) with P300 Latency Fz was observed. Conclusion: Cognitive functions are impaired in T2DM with DPN. Duration of illness is positively correlated to decline of cognitive functions. EnglishT2DM, DPN, P300, Cognitive functionsINTRODUCTION The term diabetes mellitus (DM) is used for a group of common metabolic disorders that share the common phenotype of hyperglycaemia1. T2DM has assumed more importance due to its attendant long termmicro2‚3 and macro-vascular4 complications.Diabetic peripheral neuropathy (DPN) is one of the most common long term complications of DM. It is progressive and irreversible with an incidence rate of about 50% 5 .T2DM patients are also at increased risk of developing dementia and number of patients of T2DM demonstrating cognitive decline is also on the rise 6 Cognitive impairments can be detected by event related potentials using P300. Cognitive event-related evoked potentials (EREPs) are long-latency potential. P300 is an index of cognitive processing time and has been shown to be prolonged in dementia 7. Conflicting results have been reported regarding the relationship between any association of the long term complications like DPN and cognitive decline. In some studies diabetic patients with DPN have shown a decrease in cognitive and executive functions as compared with those without DPN8‚9. Whereas, no relationship between cognitive functions and neuropathy in diabetic patients was observed in another study10. In India, studies showing correlation between DPN and cognitive decline are scanty. In view of these discordant findings, the fact remains unclear that whether the microvascular complications like DPN provide an early evidence of cognitive decline beyond what is observed in diabetic patients free from such complications. Moreover, development of cognitive dysfunction has an important bearing on the management and further progression of complications in diabetes. Therefore there is a strong need for documenting any such association in T2DM patients. OBJECTIVES: To find out - 1. Differences in cognitive function between T2DM patients with DPN as compared to T2DMpatients without DPN. 2. Relationship between the duration of diagnosis T2DM and cognitive functions.  MATERIAL and METHODS: This present study was an observational cross sectional study carried out in department of Physiology in association with department of Medicine, Lady Hardinge Medical College and associated Smt. Sucheta Kriplani Hospital conducted between November2014 to March2016. The ethical clearance was obtained from the Institutional Ethics committee for Human Research. Written and informed consent was taken from all study participants. The study protocol was carried out as per declaration of Helsinki. Inclusion criteria: For Diabetics-Comprised of 50 new or already diagnosed cases of T2DM either gender (as per ADA criteria 11) in the age group 40 to 60 years. They were then divided into two groups based on presence or absence of DPN (as per minimal criteria given by Tesfaye et al.12 For Controls-v Apparently healthy volunteers in the age group 40 to 60 years which were age, gender, BMI, socioeconomic status (SES) 13 and educational status (ES) matched. Exclusion criteria: Individuals having history of neuropsychiatric illness, type 1 diabetes mellitus14, presence of any significant impairment in communication , pre diabetics 15(as per ADA criteria 11) and  history or examination suggestive  of  any other  risk factors known to cause cognitive impairment . The minimum values of nerve conduction velocity for diagnosing peripheral neuropathy were as follows: Nerve Conduction  Velocity Median motor nerve 7 Median sensory nerve 7 Peroneal nerve 7 Sural nerve 16 54.44 m/sec 36.05m/sec 42.14m/sec 30.5m/sec   Study procedure 1. A detailed history taking and examination was done. For screening the CBC, LFT, KFT, serum electrolytes, blood urea, serum creatinine, chest X ray and ECG were done. Nerve conduction studies were done on all. They were then divided into the following groups Group I a: 25 patients of T2DM with DPN Group I b: 25 patients of T2DM without DPN Group II: 25 apparently healthy individuals as controls 2. Age and anthropometric measurements were recorded. 3. P 300 Recording - Cognitive evoked potential P300 was tested by using a machine SCHWARZER TOPAS EMG neurophysiological measuring system provided by NATUS, Europe. P300 is endogenous or event related potential (ERP) recorded in response to external stimulus or event7. P300 latency was recorded as per standard guidelines17. Patients were asked to report with a clean and oil free scalp18 and to avoid anti-histaminics on the day of testing. The procedure was explained and it was emphasized that he/she should remain alert and still during the test7???????. Gold cup electrodes were applied by 10-20 system for calculating sites for placement 19.Electrode impedance was kept below 10 K ohms7. Auditory stimuli were delivered bilaterally using odd ball paradigm .Target and non target stimuli were used (that comprised 20 % and 80  of total stimuli respectively).Target stimuli (4000 Hz) were presented randomly. Non target stimuli (1000 Hz) appeared at fixed interval of time.7 Intensity of stimuli was kept at 65 dB SPL. STATISTICAL ANALYSIS The data was submitted for statistical evaluation using Graph Pad Prism software version 6.Mean and Standard error of mean (Mean ± SEM) of all the variables were calculated. After testing for normal Gaussian distribution, intergroup comparison was done using ANOVA and Tukey&#39;s post-hoc test was applied for multiple comparisons. Chi square test and Mann - Whitney test were applied as per requirement. Correlation was assessed using the Spearman’s correlation coefficient. RESULTS Table 1 illustrates socio-demographic characteristics of study population. They were age, BMI, WC, sex distribution, SES and ES matched. Table 2 shows the treatments being received by the diabetics of the two groups. There was a statistically significant difference in number of patients receiving Insulin, Metformin and Statins. Table 3 shows -P300 latency on Pz was significantly delayed in the T2DM with DPN as compared to T2DM without DPN (p < 0.05)v and controls (p Englishhttp://ijcrr.com/abstract.php?article_id=2466http://ijcrr.com/article_html.php?did=2466 Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al., editors. Harrison&#39;s principles of internal medicine. 17th ed. New York: McGraw Hill; 2008. Qiu C, Cotch MF, Sigurdsson S, Garcia M, Klein R, Jonasson F, Klein BE, Eiriksdottir G, Harris TB, van Buchem MA, Gudnason V. Retinal and cerebral microvascular signs and diabetes the age, gene/environment susceptibility-reykjavik study. Diabetes. 2008 Jun 1; 57(6):1645-50. Yuan SY, Breslin JW, Perrin R, Gaudreault N, Guo M, Kargozaran H, Wu MH. Microvascular permeability in diabetes and insulin resistance. Microcirculation. 2007 Jan 1; 14(4-5):363-73. Fowler MJ. Microvascular and macrovascular complications of diabetes. Clinical diabetes. 2008 Apr 1; 26(2):77-82. Boulton AJ, Vinik AI, Arezzo JC, Bril V, Feldman EL, Freeman R, Malik RA, Maser RE, Sosenko JM, Ziegler D. Diabetic neuropathies a statement by the American Diabetes Association. Diabetes Care. 2005 Apr 1; 28(4):956-62. Umegaki H. Type 2 diabetes as a risk factor for cognitive impairment: current insights. ClinInterv Aging. 2014 Jun 1;9(9):1011-9. Mishra UK, Kalita J. Clinical Neurophysiology. 2nd Ed. New Delhi:Elsevier ; 2006 Perlmuter LC, Hakami MK, Hodgson-Harrington C, Ginsberg J, Katz J, Singer DE, Nathan DM. Decreased cognitive function in aging non-insulin-dependent diabetic patients. Am J Med. 1984 Dec 31;77(6):1043-8. Ryan CM, Williams TM, Finegold DN, Orchard TJ. Cognitive dysfunction in adults with type 1 (insulin-dependent) diabetes mellitus of long duration: effects of recurrent hypoglycaemia and other chronic complications. Diabetologia. 1993 Apr 1; 36(4):329-34. Dey J, Misra A, Desai NG, Mahapatra AK, Padma MV. Cognitive function in younger type II diabetes. Diabetes Care. 1997 Jan 1; 20(1):32-5. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes care. 2013 Jan 1; 36 (Supplement 1):S67-74. Tesfaye S, Boulton AJ, Dyck PJ, Freeman R, Horowitz M, Kempler P, Lauria G, Malik RA, Spallone V, Vinik A, Bernardi L. Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments. Diabetes care. 2010 Oct 1; 33(10):2285-93. Modified kuppuswamyscale:CPI guidelines:2013 Brands AM, Biessels GJ, De Haan EH, Kappelle LJ, Kessels RP. The effects of type 1 diabetes on cognitive performance A meta-analysis. Diabetes care. 2005 Mar 1; 28(3):726-35. Papanas N, Vinik AI, Ziegler D. Neuropathy in prediabetes: does the clock start ticking early?.Nat Rev Endocrinol. 2011 Nov 1;7(11):682-90. Burke D, Skuse NF, Lethlean AK. Sensory conduction of the sural nerve in polyneuropathy. J NeurolNeurosurg Psychiatry 1974; 37:647-52. Picton TW, Bentin S, Berg P, Donchin E, Hillyard SA, Johnson R Jr, Miller GA, Ritter W, Ruchkin DS, Rugg MD, Taylor MJ Guidelines for using human event-related potentials to study cognition: recording standards and publication criteria.; Psychophysiology. 2000 Mar; 37(2):127-52. Ray K, Chatterjee A, Panjwani U, Kumar S, Sahu S, Ghosh S, Thakur L, Anand JP. Modafinil improves event related potentials P300 and contingent negative variation after 24h sleep deprivation. Life sciences. 2012 Aug 21; 91(3):94-9. Klem GH, Lüders HO, Jasper HH, Elger C. The ten-twenty electrode system of the International Federation. ElectroencephalogrClinNeurophysiol. 1999; 52(3). Ryan CM, Geckle MO, Orchard TJ. Cognitive efficiency declines over time in adults with type 1 diabetes: effects of micro-and macrovascular complications. Diabetologia. 2003 Jul 1;; 46(7):940-8. Worall G, Moulton N, Briffet E: Effect of type II diabetes on cognitive function. J FamPract 1993; 36:639-643. Lawson J, Williams Erdahl D, Monga T, Bird C, Donald M, Surridge D, Letemendia F: Neuropsychological function in diabetic patients with neuropathy. Br J Psychiatry. 1984; 145:263-68. Yamagishi S, Ueda S, Okuda S. Food-derived advanced glycation end products (AGEs): a novel therapeutic target for various disorders. Curr Pharm Des. 2007; 13(27):2832–2836.  Valente T, Gella A, Fernàndez-Busquets X, Unzeta M, Durany N. Immunohistochemical analysis of human brain suggests pathological synergism of Alzheimer&#39;s disease and diabetes mellitus. Neurobiol Dis. 2010;37(1):67–76. Block ML, Zecca L, Hong JS. Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. Nat Rev Neurosci. 2007;.8(1):57–69. Greene DA, Lattimer S, Ulbrecht J, Carroll P. Glucose-induced alterations in nerve metabolism: current perspective on the pathogenesis of diabetic neuropathy and future directions for research and therapy. Diabetes Care. 1985 May 1; 8(3):290-9. Wile DJ, Toth C. Association of metformin, elevated homocysteine, and methylmalonic acid levels and clinically worsened diabetic peripheral neuropathy. Diabetes care. 2010 Jan 1;33(1):156-61. Chen Y, Zhou K, Wang R, Liu Y, Kwak YD, Ma T, Thompson RC, Zhao Y, Smith L, Gasparini L, Luo Z. Antidiabetic drug metformin (GlucophageR) increases biogenesis of Alzheimer&#39;s amyloid peptides via up-regulating BACE1 transcription. ProcNatlAcad  Sci. 2009 Mar 10;106(10):3907-12. Moore EM, Mander AG, Ames D, Kotowicz MA, Carne RP, Brodaty H, Woodward M, Boundy K, Ellis KA, Bush AI, Faux NG. Increased risk of cognitive impairment in patients with diabetes is associated with metformin. Diabetes care. 2013 Oct 1;36(10):2981-7. Hajjar I, Schumpert J, Hirth V, Wieland D, Eleazer GP. The impact of the use of statins on the prevalence of dementia and the progression of cognitive impairment. J Gerontol A BiolSci Med Sci. 2002 Jul 1;;57(7):M414-8. Sparks DL, Sabbagh MN, Connor DJ, Lopez J, Launer LJ, Browne P, Wasser D, Johnson-Traver S, Lochhead J, Ziolwolski C. Atorvastatin for the treatment of mild to moderate Alzheimer disease: preliminary results. Arch Neurol. 2005 May 1; 62(5):753-7. Fassbender K, Simons M, Bergmann C, Stroick M, Lütjohann D, Keller P, Runz H, Kühl S, Bertsch T, Von Bergmann K, Hennerici M. Simvastatin strongly reduces levels of Alzheimer&#39;s disease β-amyloid peptides Aβ42 and Aβ40 in vitro and in vivo. ProcNatlAcad  Sci. 2001 May 8; 98(10):5856-61. Carlsson CM, Nondahl DM, Klein BE, McBride PE, Sager MA, Schubert CR, Klein R, Cruickshanks KJ. Increased atherogenic lipoproteins are associated with cognitive impairment: effects of statins and subclinical atherosclerosis. Alzheimer Dis AssocDisord . 2009; 23(1):11.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241107EnglishN2018April14HealthcarePrevalence of Dental Caries Among Girl Students of Primary School in Buraydah City English1821Kalpana GokulEnglish Samer KasabahEnglish Abrar Mohammed AlrubaianEnglish Atheer Mohammed AlrubaianEnglish Nouf ZahiEnglish Bashayer Al RashidiEnglishBackground: The prevalence of dental caries is high across Saudi Arabia and varied by geographic location. There are very few studies done to assess the prevalence rate of dental caries in Buraydah city. Aim: To determine the prevalence of dental caries among the girl students of primary school in Buraydah, Saudi Arabia Methods: Cross sectional study was done among the girl students of primary school in Buraydah City in the age group of 7-9yrs. The subjects werefrom 3 randomly selectedschools. Sample size was 401. Dentition status was assessed using dft Index for primary teeth and DMFT Index for permanent dentition. Results: The collected data were analysed with IBM. SPSS statistics software 23.0 Version. For the multivariate analysis the Kruskal Walli’s test was used. To find the significance in categorical data Chi-Square test was used. Among the 401 study subjects, caries prevalence was found to be 80.80% in primary teeth and 29% in permanent teeth. Conclusion: The present study reported a high prevalence of dental caries in primary dentition thanpermanent dentition. This implies an urgent need for awareness initiative for preventive dental health behavior and attitudes, which is beneficial for the lifetime. EnglishPrevalence of dental caries, Buraydah, Girl studentsINTRODUCTION: Saudi Arabiais a large, multicultural country. Studies have reported caries prevalence is high in most regions and cities of Saudi Arabia[1]. The national prevalence of dental caries and its severity in children of Saudi Arabia was estimated to be approximately 80% for the primary dentition with a mean dmft of 5.0 and approximately 70% for children’s permanent dentition with a mean DMFT score of 3.5[1]. The current estimates indicate that the World Health Organization (WHO) 2000 goals are still unmet for Saudi Arabian children[1]. Prevalence of dental caries in Buraydah city in particular has been reported only 3 times. Wyne et al reported the caries prevalence was 20.8% for children with primary dentition (mean age 4.0) and 19.7% for children with mixed dentition (mean age 9.7) in 2001[2]. Dosari et al in 2004 reported the dental caries prevalence was 91.2% (mean dmft= 6.35) for 6–7 year olds and 87.9% (mean DMFT = 4.53) for 12–13 year olds [4]. Walid S. Salem et al reported the highest percentage of dental caries in Buraydah city[4] . Dental caries is an infectious disease that can affect children, adults and old people. Dental caries if untreated leads to inflammation of dental pulp and loss of teeth. Almost 50% of tooth loss occurs due to dental caries and its complications[5] Dental caries, though preventable, is the most prevalent oral condition which detrimentally affect different demographic groups and it can have public health impact on oral and systemic health. In view of the very high caries prevalence in school children of Burayadh, it imperative that caries prevalence studies are regularly conducted to determine if there are any changes in the caries prevalence and to monitor the effectiveness of various caries prevention programs. In the light of the above mentioned facts, this cross sectional study has been designed to assess the prevalence rate of dental caries among girl students of primary school in Buraydah City. METHODS: The present cross sectional study has been planned by Buraydah College of Pharmacy and Dentistry to assess the prevalence rate of dental caries among primary school children. Buraydah is the capital of Al-Qassim Region in north central Saudi Arabia in the heart of the Arabian Peninsula. It has a population of 614,093 according to 2010 census. 3 schools have been randomly selected from Buraydah city. All the children from the selected schools were examined. A total of 401 subjects formed the sample size in the age group of 7-9years. Children under long-term medications which affects the oral health and who were physically and mentally challenged, and children who were not willing to participate were excluded from the study. Written informed consent was obtained from the parents of children.  Data Collection was scheduled in the month of December 2016. The clinical examination was carried out in the children&#39;s schools using disposable examination kits and natural light, while child sitting on a chair. Clinical examination included assessment of dental caries using decayed and filled teeth (dft) index by Gruebbel for primary dentition and decayed, missing, and filled teeth (DMFT) index by Klein, Palmer, Knutson for permanent dentition recorded on a structured format. Oral health education was given to the school children in the local language and for those who required treatment, were directed to get it done at Buraydah College of pharmacy and Dentistry. The collected data were analysed with IBM.SPSS statistics software 23.0 Version. To describe  the data, descriptive statistics frequency analysis, percentage analysis were used for categorical variables and the mean and standard deviation (S.D )were used for continuous variables. For the multivariate analysis the Kruskal Walli&#39;s test was used. To find the significance in categorical data Chi-Square test was used. In both the above statistical tools the probability value 0 .05 is considered as significant level. RESULTS: The study sample consisted of 401 subjectsof which 123 (30.7%) subjects were 7 years, 151 (37.7%) were between 8 years and 127(31.7%) were 9 years of age [Table 1].The overall prevalence of dental caries in the present study was found to be 80.80% in primary teeth and 29% in permanent teeth [Table 2and 3] [Graph 1 and 2]. By using Kruskal Walli&#39;&#39;s test the comparison between ages with the total teeth having dental caries in primary teeth show no statistical significance with P = 0.568 > 0.05. [Table 4]. By using Chi-Square test the comparison between ages with the total number of teeth having dental caries in permanent teeth, Crosstabulation shows highly statistical significance with P = 0.0005 Englishhttp://ijcrr.com/abstract.php?article_id=2467http://ijcrr.com/article_html.php?did=2467Dania Ebrahim Al Agili: A systematic review of population-based dental caries studies among children in Saudi Arabia: The Saudi Dental Journal (2013) 25, 3–11 2.         Wyne, A., al-Dlaigan, Y., Khan, N., Caries prevalence, oral hygiene and orthodontic status of Saudi Bedouin children. Indian J Dent Res 12, 194–198; 2001 3.         Dosari, A.M., Wyne, A.H., Akpata, E.S., Khan, N.B., Caries prevalence and its relation to water fluoride levels among schoolchildren in Central Province of Saudi Arabia. Int Dent J 54, 424-428. 2004. 4.         Salem WS, Araby YA ; Significant Caries index in 12-14 years old children in Qassim Area- Kingdom Saudi Arabia. Int. Inv. J. Med. Med. Sci. Vol. 2(1): 12-16.2015 5.         Capelli D , Mobley CC. prevention of in clinical oral care. 1st Edition, stLouis : Mosby: 2008 6.         Awooda EM, Saeed SM, Elbasir EI. Caries prevalence among 3-5 years old children in Khartoum state, Sudan. Innov J Med Health Sci 2013; 3: 42-4.          7.         Naidu R, Prevatt I, Simeon D. The oral health and treatment needs of schoolchildren in Trinidad and Tobago: Findings of a national survey. Int J Paediatr Dent 2006; 16: 412-8. 8.         Sohi RK, Gambhir RS, Veeresha KL, Randhawa AK, Singh G. Assessment of prevalence of dental caries among 5 and 12-year-old schoolchildren in Chandigarh (U.T.), India. Arch Oral Res 2012;8:39–45 9.         Marrs JA, Trumbley S, Malik G. Early childhood caries: Determining the risk factors and assessing the prevention strategies for nursing intervention. Pediatr Nurs 2011; 37 :9-15. 11.       Al-Shammery, A., Caries experience of urban and rural children in Saudi Arabia. J Public Health Dent 59, 60–64;1999  

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241107EnglishN2018April14HealthcareEfficacy of Pemetrexed or Pemetrexed Plus Cisplatin/Carboplatin in Pretreated Patients with Advanced Non–Small-Cell Lung Cancer English2227Nurgul YasarEnglish Caglayan GeredeliEnglishIntroduction: In this study, the efficacy and safety of pemetrexed alone and platinum-pemetrexed combination chemotherapy were evaluated in patients who have demonstrated progression after the first-line treatments in advanced non-small cell lung cancer (NSCLC). Material and Method: 263 patients, who were diagnosed NSCLC in years 2008 - 2014, were assessed retrospectively in single center. Patients were given pemetrexed 500 mg/m2, and the ones receiving combined treatment were given pemetrexed 500 mg/ m2 and cisplatin 75 mg/m2 or carboplatin area under the curve 5 according to the Calvert formula (AUC 5 ) once in every 21 days. Results: One hundred ninety (72%) of the patients had received pemetrexed, seventy three (28%) of the patients had received platinum- pemetrexed. Median PFS (progression-free survival) was 2 months (95% CI, 1. 6 - 2.4 ) for pemetrexed arm versus 4 months (95% CI, 2.6 to 5.3 ) for platinum- pemetrexed arm (p=0.001). The HR ( hazard ration) for disease progression was 0.45 (95% CI, 0.25 to 0.65) in favor of the combination arm (p=0.001). Median OS (overall survival) was 7 months (95% CI, 5.9 - 8 ) for pemetrexed arm versus 10 months (95% CI, 8 to 11.9 ) platinum-pemetrexed arm, respectively (p=0.001). The 1-year survival rate was 24% and 42% for pemetrexed arm and combination arm, respectively. Toxicities in both arm was manageable. Conclusion: Our study has shown that adding platinum compound to second-line pemetrexed chemotherapy significantly increases ORR (overall response rate), PFS and OS in patients with advanced NSCLC after having received first-line platinumbased chemotherapy. EnglishNSCLC, Second line treatment, PemetrexedIntroduction             Lung cancer, estimating for approximately 13% of total cancer cases, pursues one of the major causes of cancer-related death  worldwide with an esti­mated 1.8 million new lung cancer cases occured in 2012(1). Non-small cell lung cancer (NSCLC) accounts for 80-85 % of all lung cancers, and 75%of patients are diagnosed at the advanced stages of disease (2). First-line treatment for  patients with stage IIIB or stage IV NSCLC usually consists of platinum-based doublet chemotherapy was found to produce a survival benefit(3,4). Nonetheless,  disease progression ultimately occurs for most patients and further treatment is reguired.(5). When compared with best supportive care, second-line chemotherapy with docetaxel, pemetrexed or other agents are associated with    (OS) benefit and improvement of quality of life (5,6,7). Pemetrexed, an analogue of folic acid, was approved for first-line, second-line and maintenance  treatmentof advanced NSCLC (4,7). It inhibits three enzymes which necessary for de novo pyrimidine and purine synthesis:thymidylate synthase (TYMS), dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase (4,7). In the first-line setting, pemetrexed/platinum combination  is more effective than gemcitabine/platinum combination for advanced NSCLC patients with adenocarcinoma histologic subtype (4). In the second-line therapy, pemetrexed was associated with more favorable toxicity profile compared with docetaxel and comparable efficacy (median survival of 8.3 months vs 7.9 months)(7).  Combinations of chemotherapy agents have been competent in increasing efficacy over single agents in the first-line treatment(8,9). On the other hand, role of combinations is less clear in the second-line treatment (8,9). In this study, the efficacy and safety of pemetrexed alone and platinum-pemetrexed combination chemotherapy were evaluated retrospectively in patients who were non-responders or who have demonstrated progression after the first-line treatments in local advanced and metastatic NSCLC. Materials and methods We performed a retrospective screening of 263 patients who had pathologically or cytologically confirmed as stage IIIB to IV lung adenocarcinoma in SB Okmeydani Training and Researh Hospital  between November 2008 and May 2014. These patients had failed prior chemotherapy regimen and received pemetrexed alone or platinum-pemetrexed combination chemoterapy rejimens in the second-line setting. Data were collected on baseline characteristics including age, gender, Eastern Cooperative Group (ECOG) performance status (PS),  histology, stage, single agent or combined administration of treatment, third or further-line treatment intake and length of progression-free period after the first-line treatment. Pemetrexed 500 mg/m2 administered as an intravenous (IV) bolus infusion of 10 minutes duration every 3 weeks. Folic acid  and vitamin B12 supplementation was mandatory for all patients.  Dexamethasone   4 mg  tablet, three times a day for 3 days, was administered routinely to prevent allergic reactions.  Cisplatin 75 mg/m2  administration intravenously over a 2-h infusion or carboplatin  area under the curve 5 according to the Calvert formula (AUC 5 ) a 30-min infusion after pemetrexed administration every 3 weeks.              Patients underwent baseline computed tomography (CT) at the beginning of second-line chemotherapy and computed tomography repeated every 2-3 cycles of chemotherapy. Evaluation of treatment response was based on the Response Evaluation Criteria in Solid Tumors (RECIST) (10). Patients achieving complete response and partial response were recognized to be responders. Adverse events (AEs) were classified according to National Cancer Institute Common Terminology Criteria for Advers Events (CTCAE), version 3. statistical analysis The baseline characteristics of the patients were analyzed using descriptive statistics. PFS of second-line chemotherapy was measured from the date of initiation of second-line chemotherapy to the date of disease progression or any cause of death. OS for second-line chemotherapy was calculated from the date of initiation of second-line chemotherapy to the date of death from any cause. The Kaplan-Meier method was used to estimate PFS and OS. The difference between the survival curves of the treatment groups was tested using the log-rank test. In multivariate analysis with the Cox proportional hazards model, including age, gender, ECOG performance status, stage, the length of progression-free period after first- line treatment and the number of course for first and second-line chemotherapy, were used to estimate  for PFS and OS. The chi-square test or Fisher exact test was used to compare the ORRs and adverse events (AEs) between two groups. A two-sided p value of ≤0.05 was considered statistically significant. All statistical analyses were performed using SPSS statistics 17.0 (SPSS, Inc, Chicago, IL). Results             From November 2008 to May 2014, 263 patient files were screened onto this study. The median follow-up period was 7 months (range, 1 to 74 months). Two hundred thirty-seven patients (90%) died during the follow-up. Patients characteristics were listed in Table 1.Two hundred twelve (81%)males and 51 (19%) females were included. Median age at diagnosis was 55 years (range,28-83), 85% had PS of 0 to 1, 91% had stage IV disease, and 94% of the patients were diagnosed with adenocarcinoma. The length of progression-free period after first-line of treatment was 6 months (range, 1- 88 months) for  patient groups. The median time off platinum treatment was 6 months (range, 1 to 49 months) in pemetrexed arm and 7 months (range, 6 to 88 months) in platinum-pemetrexed arm. Median number of courses was five for the first-line setting. One hundred ninety (72%) of the patients had received pemetrexed, seventy three (28%) of the patients had received platinum- pemetrexed as second-line treatment. None of the patients had received pemetrexed as part of first-line treatment. Median number of cycles was four in  patient groups for the second-line treatment. Two patients stopped treatment because of an adverse event. Three percent of patients had a dose reduction for pemetrexed arm, and 4%%of patients  had a dose reduction for platinum-pemetrexed arm. With the exception of hematologic toxicity, fatigue, nasuea and vomiting, the frequency of treatment-related toxicity exceeding CTCAE grade 2 was less than 5% for all categories (Table 2).  Neutropenia (12,5%),  nasuea and vomiting (12%) and fatique (10%) were all more frequently observed in the platinum-pemetrexed arm, significantly (pEnglishhttp://ijcrr.com/abstract.php?article_id=2468http://ijcrr.com/article_html.php?did=2468.Torre LA, Bray F, Siegel R et al.. Global cancer statistics, 2012. CA Cancer J Clin. 2015;65:87–108. 2. Siegel R,Ma J, Zou Z, Jemal . Cancerstatistics, 2014. CA Cancer J Clin.2014 Jan-Feb;64(1):9-29. 3. Schiller JH, Harrington D, Belani CP, et al. Eastern Cooperative Oncology Group. Comparison of four chemotherapy regimens for advanced nonsmall-cell lung cancer. N Engl J Med 2002;346:92–98. 4. Scagliotti GV, De Marinis F, Rinaldi M, et al.; Italian Lung Cancer Project. Phase III randomized trial comparing three platinum-based doublets in advanced non-small-cell lung cancer. J Clin Oncol 2002;20:4285–4291. 5. Shepherd FA, Dancey J, Ramlau R, et al: Prospective randomized trial of docetaxel versus best supportive care in patients with non-smallcell lung cancer previously treated with platinumbasedchemotherapy. J Clin Oncol  2000 ;18:2095-2103. 6. Shepherd FA, Pereira J, Ciuleanu TE, et al: Erlotinib in previously treated non small cell lung cancer. N Engl J Med 2005; 353:123-132 7. Hanna N, Shepherd FA, Fossella FV, et al: Randomized phase III trial of pemetrexed versus docetaxel in patients with non small cell lung cancer previously treated with chemotherapy. J Clin Oncol 2004; 22:1589-1597 8. R, HerndonJ, ListM, et al. Single-agent versus combination chemotherapy in advanced non-small cell lung cancer (NSCLC): a CALGB randomized trial of efficacy, quality of life, and cost-effectiveness. Eur J Cancer 2001; 37: S153–S154.OpenUrl 9.Le ChevalierT, BrisgandD,DouillardJY, et al.Randomized study of vinorelbine and cisplatin versus vindesine and cisplatin versus vinorelbine alone in advanced non-small-cell lung cancer: results of a European multicenter trial including 612 patients. J Clin Oncol 1994; 12: 360–367. 10. Eisenhauer EA, Therasse P, Bogaerts J et al. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). Eur J Cancer. 2009;45(2): 228–47. 11. Azzoli CG, Baker S Jr, Temin S, et al: American Society of Clinical Oncology clinical practice guideline update on chemotherapy for stage IV non–small-cell lung cancer. J Clin Oncol 2009; 27:6251- 6266. 12. Delbaldo C, Michiels S, Syz N, et al: Benefits of adding a drug to a single-agent or a 2-agent chemotherapy regimen in advanced non-small-cell lung cancer: A meta-analysis. JAMA 2004; 292:470-484. 13. Smit EF, Mattson K, von Pawel J, et al: ALIMTA (pemetrexed disodium) as second line treatment of non-small cell lung cancer: A phase II study. Ann Oncol 2003; 14:455-460. 14. Scagliotti GV, Parikh P, von Pawel J, Biesma B, Vansteenkiste J, Manegold C, et al. Phase III study comparing cisplatin plus gemcitabine with cisplatin plus pemetrexed in chemotherapy-naive patients with advanced-stage non-small-cell lung cancer. J Clin Oncol. 2008;26(21):3543–51 15. Zinner RG, Fossella FV, Gladish GW et al. Phase II study of pemetrexed in combination with carboplatin in the first-line treatment of advanced nonsmall cell lung cancer. Cancer. 2005;104(11):2449–56. 16. Di Maio M, Chiodini P, Georgoulias V, et al.Meta-analysis of single-agent chemotherapy compared with combination chemotherapy as second-linetreatment of advanced non-small-cell lung cancer. J Clin Oncol 2009; 27:1836-1843. 17.Smit EF, Burgers SA, Biesma B, et al: Randomized phase II and pharmacogenetic study of pemetrexed compared with pemetrexed plus carboplatin in pretreated patients with advanced non–small-cell lung cancer. J Clin Oncol 2009; 27:2038-2045. 18. Ardizzoni A, Tiseo M, Boni L et al. Pemetrexed versus pemetrexed and carboplatin as second-line chemotherapy in advanced non-small-cell lung cancer: results of the GOIRC 02-2006 randomized phase II study and pooled analysis with the NVALT7trial. J Clin Oncol. 2012  20;30(36):4501-7. 19. Kim YH, Nishimura T, Ozasa H et al. Phase II study of pemetrexed and erlotinib in pretreated nonsquamous, non-small-cell lung cancer patients without an EGFR mutation. Chemotherapy. 2013;59(6):414-9. 20. Yoshimura N, Kudoh S, Mitsuoka S, Yoshimoto N et al.Phase II study of a combination regimen of gefitinib and pemetrexed as first-line treatment in patients with advanced non-small cell lung cancer harboring a sensitive EGFR mutation Lung Cancer. 2015 ;90(1):65-70. 21. Daga H, Takeda K, Okada H et al. Phase I study of nintedanib in combination with pemetrexed as second-line treatment of Japanese patients with advanced non-small cell lung cancer.Cancer Chemother Pharmacol. 2015;76(6):1225-33. 22. Zhou CZ, Qin YY, Xie ZH et al.Efficacy of third-line pemetrexed monotherapy versus pemetrexed combination with bevacizumab in patients with advanced EGFR mutation-positive lung adenocarcinoma Chin J Cancer Res. 2014;26(6):705-10. 23. Vynnychenko I, Bondarenko I, Shparyk Y et al.An open-label, multicenter, randomized phase Ib/II study of eribulin mesylate administered in combination with pemetrexed versus pemetrexed alone as second-line therapy in patients with advanced nonsquamous non-small-cell lung cancer.Clin LungCancer. 2015;16(2):92-9.  24..Choi MK, Hong JY, Chang  et al. Safety and efficacy of gemcitabine or pemetrexed in combination with a platinum in patients with non-small-cell lung cancer and prior interstitial lung disease.Cancer Chemother Pharmacol. 2014;73(6):1217-25. 25.. Heist RS, Wang X, Hodgson L et al; Alliance for Clinical Trials in Oncology.CALGB 30704 (Alliance): A randomized phase II study to assess the efficacy of pemetrexed or sunitinib or pemetrexed plus sunitinib in the second-line treatment of advanced non-small-cell lung cancer J Thorac Oncol. 2014;9(2):214-21. 26. Li S, Zhou F, Ren S, Zhou C et al. 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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241107EnglishN2018April14HealthcareAre the Re-Emerging Diseases a Real Threat Worldwide? English0001Dr. Mohammad Shakil AhmadEnglishMost of the research worldwide confirm that there is an impending threat to the susceptible population – particularly the children and elderly population, from diseases that are deemed to be controlled but are re appearing again with a vengeance. Studies have shown that re-emerging diseases are a result of multiple risk factors like climate change, social determinants of health, inappropriate drug use, frequent travelling, non – compliance among patients etc. Some studies have elaborated specifically on the dynamic relationship between the infective microorganism, the susceptible host and the favorable environment. They have all predicted a pretty interesting scenario of uncontrolled spread and evolution of the infectious diseases that till now were under barricaded control from a barrage of antimicrobials. Projections of mortality and morbidity due to the impending doom of emerging and re-emerging diseases are a stark reality that is getting harder to combat on a day to day basis. The real problem lies with the use of medications without any standard guidelines, particularly in developing and poor countries. The Global outbreak alert and response network initiated by World Health Organization (WHO) to respond early to any reports of infectious outbreak worldwide. Therefore, coming back to the real problem of uncontrolled existing antibiotic use has resulted in multidrug-resistant pathogens, which is so severe that currently for some infections no new drug is being developed to counter it. Even carbapenems, currently the most successful class of antibiotics are reported to be decreasing in effectiveness. The reason this issue is important from the treatment related point of view is that prevention of diseases among the population takes a long time to show effect. This is true of countries where the actual first line of defense against any infection is early diagnosis and treatment. This is because the healthcare machinery is lagging behind in providing effective primary prevention in terms of vaccination, hygiene, environmental pollution control, effective checks for spread of infectious or exotic diseases either within the country or outside and health education. So along with lack of political will there is a laxity in vision for a disease-free future. Currently, we are not even seriously observing the emerging diseases which along with the reemerging diseases continue to occupy the red alert zone among the health agencies worldwide. Apart from having some organization/organizations to continuously monitor the alerts/outbreaks/pandemics worldwide, the individual countries have an obligation to devise means and methods to organize an effective defense against the re-emergence of diseases in an invincible avatar invulnerable to being taken down effectively. A similar observation voiced by Catharine I Paules et al (2017) in her study, who said that research and public health focus on microbes like Zika virus, West Nile virus, Chikungunya virus etc. to avoid the danger of complacency and failure. Lastly, the threat is real, enormous and will get out of control. Devastation at a global scale would merely be an understatement unless we come together to develop a comprehensive and effective health care plan. EnglishMortality,West Nile Virus,WHOMost of the research worldwide confirm that there is an impending threat to the susceptible population – particularly the children and elderly population, from diseases that are deemed to be controlled but are re appearing again with a vengeance. Studies have shown that re-emerging diseases are a result of multiple risk factors like climate change, social determinants of health, inappropriate drug use, frequent travelling, non – compliance among patients etc. Some studies have elaborated specifically on the dynamic relationship between the infective microorganism, the susceptible host and the favorable environment. They have all predicted a pretty interesting scenario of uncontrolled spread and evolution of the infectious diseases that till now were under barricaded control from a barrage of antimicrobials. Projections of mortality and morbidity due to the impending doom of emerging and re-emerging diseases are a stark reality that is getting harder to combat on a day to day basis. The real problem lies with the use of medications without any standard guidelines, particularly in developing and poor countries. The Global outbreak alert and response network initiated by World Health Organization (WHO) to respond early to any reports of infectious outbreak worldwide. Therefore, coming back to the real problem of uncontrolled existing antibiotic use has resulted in multidrug-resistant pathogens, which is so severe that currently for some infections no new drug is being developed to counter it. Even carbapenems, currently the most successful class of antibiotics are reported to be decreasing in effectiveness. The reason this issue is important from the treatment related point of view is that prevention of diseases among the population takes a long time to show effect. This is true of countries where the actual first line of defense against any infection is early diagnosis and treatment. This is because the healthcare machinery is lagging behind in providing effective primary prevention in terms of vaccination, hygiene, environmental pollution control, effective checks for spread of infectious or exotic diseases either within the country or outside and health education. So along with lack of political will there is a laxity in vision for a disease-free future. Currently, we are not even seriously observing the emerging diseases which along with the reemerging diseases continue to occupy the red alert zone among the health agencies worldwide. Apart from having some organization/organizations to continuously monitor the alerts/outbreaks/pandemics worldwide, the individual countries have an obligation to devise means and methods to organize an effective defense against the re-emergence of diseases in an invincible avatar invulnerable to being taken down effectively. A similar observation voiced by Catharine I Paules et al (2017) in her study, who said that research and public health focus on microbes like Zika virus, West Nile virus, Chikungunya virus etc. to avoid the danger of complacency and failure. Lastly, the threat is real, enormous and will get out of control. Devastation at a global scale would merely be an understatement unless we come together to develop a comprehensive and effective health care plan. Englishhttp://ijcrr.com/abstract.php?article_id=2469http://ijcrr.com/article_html.php?did=2469