Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Notice: Undefined index: issue_status in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 142

Notice: Undefined index: affilation in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 195

Notice: Undefined index: doiurl in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 198

Warning: Cannot modify header information - headers already sent by (output started at /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php:195) in /home/u845032518/domains/ijcrr.com/public_html/downloadarchiveissuexml.php on line 234

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareINCIDENCE OF VARIOUS FUNGAL SPECIES IN OCULAR INFECTIONS English0103Amrita BajpaiEnglish Rajesh BarejaEnglish Munesh SharmaEnglish Vashishth MishraEnglish Hiba SamiEnglishBackground: The fungi are significant pathogens causing ocular infections due to their frequent involvement and difficulty in establishing definitive diagnosis. The present study was aimed to detect various fungal and bacterial agents that can cause ocular infections. Material & Methods: An ophthalmologist collected the corneal scrapping that was smeared onto two slides and stained with Gram’s stain and mounted with 10% KOH (potassium hydroxide) for microscopic examination. Material collected was inoculated directly onto 5% sheep’s blood agar in the form of ‘C’ streak, Sabouraud dextrose agar (SDA), and sent to the Microbiology department for further processing and identification of causative agent. Results: Out of three hundred and sixty samples, ten cases were found to be fungal culture positive. Aspergillus species were accounting for 40% cases followed by Curvularia species (30%), Alternaria species (1%), Fusarium species (1%) and Scytalidium dimidiatum (1%). Conclusion: Fungal infection is a life threatening condition, which needs early diagnosis and treatment to save the patient’s eye. EnglishKeratitis, Corneal scrapping, KOH, SDAIntroduction Leber, in 1879, first time described the fungal infection of the cornea, mycotic keratitis [1]. Since then it has been recognized as a major public health problem in the tropical parts of many developing nations including India [2-4]. The etiological cause for keratitis may vary at different geographical locations [5]. Many fungal genera have been implicated in keratomycosis, like Aspergillus, Fusarium, Curvularia, Alternaria, Penicillium and Bipolaris species. According to World Health Organization (WHO) about 1.5 to 2.0 million new cases of monocular blindness in developing country every year is due to corneal ulceration and corneal ulcer is the second most common cause of blindness after cataract in developing country [6,7]. Fungal infection is a life threatening condition that needs early diagnosis and treatment to save the patient’s eye. In view of this context, the present study was conducted to find out various fungal and bacterial agents that can cause ocular infections. Material and Methods This prospective study was carried out in a tertiary care hospital during March 2015 to June 2016. The ethical clearance from the ethical committee of the institute was taken to conduct the study. Three hundred and sixty samples of corneal scrapping from clinically suspected cases of corneal ulcer were subjected to bacterial and fungal examination. An ophthalmologist examined all the patients in the eye OPD and ward. A corneal scrape was performed by an ophthalmologist using a sterile 21 gauge needle, or sterile bard parker blade (No.15), following the instillation of 4% lignocaine (lidocaine). Scrapping material was taken from edge and base of ulcer [8]. Corneal material obtained from scraping was smeared onto two slides, which were stained with Gram’s stain and mounted with 10% potassium hydroxide (KOH) for microscopic examination respectively. Also material was inoculated directly onto 5% sheep’s blood agar (BA) in the form of ‘C’ streak, Sabouraud dextrose agar (SDA), and sent to the Microbiology department for further processing and identification. If there was sufficient specimen of corneal scraping, then it was inoculated on BHI (brain heart infusion) broth and CA (chocolate agar). Inoculated BA, CA plates and BHI broth were incubated at 37°C for 7 days, and discarded after seven days if no growth was observed. Inoculated SDA tubes were incubated at 25°C and 37°C for four weeks. Inoculated tubes were checked once in first week and then twice in every week for maximum period of 3 weeks. Bacteria were further identified using routine biochemical identification tests and selective media [9]. Fungi were identified according to the macroscopic appearance of cultures on SDA and microscopic appearance in LPCB (lactophenol cotton blue) mount [10]. Results Three hundred and sixty specimens of corneal scrapping from clinically suspected cases of corneal ulcer were subjected to bacterial and fungal examination. Of these, ten cases were found to be fungal culture positive. Among the culture positive specimens, Aspergillus species were accounting for 40% cases followed by Curvularia species (30%), Alternaria species (1%), Fusarium species (1%) and Scytalidium dimidiatum (1%). All the specimens that were found positive in 10% KOH mount were positive for fungal culture also. None of the bacteria were isolated from bacterial culture. Discussion Fungal infections kill at least 1,350,000 patients with or following AIDS, cancer, TB and asthma as well as causing untold misery and blindness to tens of millions more worldwide [11]. Blindness caused by fungal infection of the eye affects over 1 million adults and children globally because the tools are not available for rapid diagnosis and treatment [11]. In 2006, CDC, state and local health departments, and the Food and Drug Administration (FDA) investigated a large, multistate outbreak of Fusarium keratitis associated with a specific type of contact lens solution, which was later withdrawn from the market [12-14]. In the present study, Aspergillus species were found to be positive in 40% cases. Aspergillus species (56.42%) were also repoted the common cause of fungal keratitis by Sherwal et al. [15]. A study from South India also repoted the Aspergillus species as the common causitive organism of fungal keratitis [16]. Several other reports from Nepal, Bangladesh and India have also shown Aspergilus species as most common isolate in fungal keratitis [17-19]. Another study from North India showed the prevalence of Aspergillus species (41%) in fungal keratitis that was concordant to this study [20]. The Aspergilus species is most common pathogen for fungal keratitis, probably, because it is resistant to hot and dry conditions [5]. In the current study, Curvularia species were found to be positive in 30% cases and was the second most common cause of fungal keratits. Some other authors also reported the Curvularia species, second most common cause of fungal keratits [15,16]. Curvularia species (29%) were second common isolate found in the another study done in North India [20]. Some studies in south India have reported Fusarium species to be more common than Aspergillus species [16, 21]. In the present study, Fusarium species were present in only 1% of the total positive cases. Fusarium species have also been found to be the principal fungal pathogen in Florida, Paraguay, Nigeria, Tanzania, Hong Kong, and Singapore [5]. Aspergillus species predominate in Northern India, Nepal, and Bangladesh [22-24]. This phenomenon may be explained by differences in climate and the natural environment. Conclusion The causative fungi of keratomycosis are ubiquitous organisms and are responsible for 6 to 53% of all the corneal infections worldwide [25]. The use of PCR can yield quick results, confirming the diagnosis of mycotic keratitis within a few hours, but in a developing country like India where more than 65% people are from rural area cannot afford the cost of PCR. Direct microscopic examination of KOH mounts appeared as a rapid, reliable, inexpensive and highly sensitive diagnostic method that would facilitate the institution of early antifungal therapy before the culture results became available to limit the ocular morbidity and other complications. 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. Conflict of interest: Nil Source of funding: Self financed / Nil Englishhttp://ijcrr.com/abstract.php?article_id=177http://ijcrr.com/article_html.php?did=177 Abad JC, Foster CS. Fungal keratitis. Int’l Ophthalmol Clin 1996; 36: 1-15. Agarwal V, Biswas J, Madhavan HN, Mangat G, Reddy MK, Saini JS, et al. Current perspectives in infectious keratitis. Indian J. Ophthalmol 1994; 42: 171-2. Gunawerdena SA, Ranasinghe KP, Arseceuleratne SN, Scimon CR, Ajello L. Survey of mycotic and bacterial keratitis in Sri Lanka. Mycopathologia 1994; 127: 77-1. Hagan M, Wright E, Newman M, Dolin P, Johnson G. Causes of suppurative keratitis in Ghana. Brit J Ophthalmol 1995; 79: 1024-8. Leck AK, Thomas PA, Hagan M, Kaliamurthy J, Ackuaku E, John M, et al. Aetiology of suppurative corneal ulcers in Ghana and south-India, and epidemiology of fungal keratitis. Br J Opthalm 2002; 86: 1211-5 Whitcher JP, Srinivasan M, Upadhyay MP. Corneal blindness: a global perspective. Bull World Health Organ vol 2001; 79(3): 214-1. Nayak N. Fungal infections of the eye - laboratory diagnosis and treatment. Nepal Med Coll J 2008; 10(1): 48-3. Srinivasan M, Gonzales CA, George C, Cevallos V, Mascarenhas JM, Asokan B, et al. Epidemiology and etiological diagnosis of corneal ulceration in Madurai, south India. Br J Ophthalm 1997; 81: 965-1. Collee, JG, Fraser AG, Marmion BP, Simmons A. Tests for the identification of Bacteria. Mackey and McCartney practical Medical Microbiology, New Delhi, India: Elsevier 2006; 131-9. Fisher F, Cook NB. Fundamentals of diagnostic mycology. Saunders, Philadelphia, PA. 1998; 13-4. www.gaffi.org/global-plague-how-150-people-die-every-hour-from-fungal-infection Chang DC, Grant GB, O'Donnell K, Wannemuehler KA, Noble-Wang J, Rao CY,  et al. Multistate outbreak of Fusarium keratitis associated with use of a contact lens solution. JAMA 2006; 296: 953-3. CDC. Update: Fusarium keratitis—United States, 2005-2006. MMWR 2006; 55: 563-4. CDC. Fusarium keratitis—multiple states, 2006. MMWR 2006; 55: 400-1. Sherwal BL, Verma AK. Epidemiology of ocular infection due to bacteria and fungus – a prospective study. J Med Edu Res 2008:10(3); 127-1. Kuniomoto DY, Sharma S, Garg P, Gopinathan U, Miller D, Rao GN. Corneal ulceration in the elderly in Hyderabad, south India. Br J Ophthalmol 2000; 84: 54-9. Yeh DL, Stinnett SS, Afshari NA. Analysis of Bacterial culture in infectious kerititis 1997-2000. Am J Opthalmol 2006; 142; 1066-8. Dunlop AA, Wright ED, Holader SA, Nazrul I, Jussain R, McClellan K, et al. Suppurative corneal ulceration in Bangladsh. A study of 142 cases examining the microbiological diagnoses, clinical and epidermological feature of bacterial and fungal keratitis. Aust NA J Opthalmol 1994; 22: 105-10. Mahajan VM. Ulcerative keratitis: An analysis of laboratory data in 674 cases. J Ocul Ther Surg 1985; 4: 138-1. Chowdhary A, Singh K. Spectrum of Fungal Keratitis in North India. Cornea 2005: 24(1); 8-15 Gopinathan U, Garg P, Merle F, Sharma S, Sreedharan A, Rao GN. The Epidemiological Features and Laboratory Results of Fungal Keratitis: A 10-Year Review at a Referral Eye Care Center in South India. Cornea 2002: 21(6); 555-9. Chander J, Sharma A. Prevalence of fungal corneal ulcers in northern India. Infection 1994; 22: 207–9. Upadhyay MP, Karmacharya PC, Koirala S, Tuladhar NR, Bryan LE, Smolin G, et al. Epidemiologic characteristics, predisposing factors, and etiologic diagnosis of corneal ulceration in Nepal. Am J Ophthalmol 1991; 111: 92-9. Williams G, McClellan K, Billson F. Suppurative keratitis in rural Bangladesh: the value of gram stain in planning management. Int Ophthalmol 1991; 15:131–5. Thomas P. Mycotic keratitis - an underestimated mycosis. J Med Vet Mycol 1994; 32: 235–6.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareAUDITORY PLASTICITY AND COCHLEAR IMPLANTS IN CHILDREN- A REVIEW English0409Muhammed AyasEnglish Hakam YaseenEnglish Ahmed Munzer AlwaaEnglishAim: The review article is aimed at highlighting the importance of Auditory Plasticity for the positive outcomes in cochlear implantation, which is intrinsic to the critical age period. Method: Various electronic databases such as PubMed/ Medline, Science Direct, CINHAL etc. were used to extract the articles. The keywords used for the search engine were ‘auditory plasticity’, ‘deprivation’, and ‘cortical re organization’,‘ cochlear implants’. Discussion: The current review suggests that auditory plasticity is important in achieving proper wiring of acoustic sensation in the congenial hearing loss cases. Critical age period for the intake of new information and learning occurs before 3.5 years of age and post critical period the language learning is delayed. Conclusion: Auditory plasticity and its related functions are critical in influencing the outcome after the CI in children. The advent of electrophysiology into clinical research has paved a path breaking journey in understanding the complex processing of auditory signals in the primary and secondary cortical areas. EnglishAuditory Plasticity, Auditory Deprivation, Cortical Reorganization, Cochlear Implants INTRODUCTION Auditory plasticity is defined as the functional and structural changes occurring in the auditory cortex during the normal course of development. The ability of the auditory system to enhance the auditory sounds in the auditory cortex is pivotal for the successful speech perception in humans. The auditory plasticity is intrinsic to the critical age period, which defines the age period during which the neuronal and other functional developments occur in the brain for the normal wiring in the auditory system [1]. The interest in the research prospects in auditory plasticity has reached its prime since last two decades due to the introduction of the cochlear implants (CI) for the severe to profound hearing loss individuals. The success of the CI was determined based on the outcome in auditory and speech development in cochlear implantees. Poor outcome on CI was initially attributed to the performance of the implant or the speech processer used by the person. Little was known on the auditory plasticity and the effect of auditory stimulation in the auditory cortex, until technological advances allowed researchers to drive deep into the system of the complex auditory processing using fMRI, PET, and evoked potential studies. Researchers in the field of auditory plasticity believe, a lot more intense research is required to unravel the mystery that presents in the primary auditory cortex; which in turn facilitates the hearing impaired to respond and process the complex speech signals. The advent of electrophysiological measures has paved a path-breaking journey to understand the auditory development, auditory plasticity and critical age period in humans. A bulk of studies in literature on the critical age period and auditory plasticity was done on animals, especially rats and rodents [2,3,4]. The results were later extrapolated into human research. The basic research question that intrigued most of the researchers is that, if the deprived auditory cortex responded to the electrical stimulation through the CI or not .Also, if the poor outcome in CI patients was related to the reorganization of auditory cortex due to the long-standing auditory deprivation. They also researched if the other senses have taken over the functional areas of the auditory system. Such a set of complex research questions requires extensive research studies that would primarily focus on using non-invasive methods. This method being cost effective for the researchers is expected to create ripples in the field of auditory plasticity and CI. MATERIAL AND METHODS A detailed literature review was carried out to review the auditory plasticity and cochlear implants in children with respect to the outcome based in CI children. The review was focussed mainly on the following 4 areas; (a) auditory deprivation on the auditory cortical development and critical age period; (b) functional and metabolic changes in the auditory cortex due to auditory deprivation; (c) Electro physiological evidence in auditory plasticity after CI;(d) auditory decoupling hypotheses; (e) cortical reorganization and cross modal plasticity. The literature search was done independently by the author. Various electronic databases such as PubMed/ Medline, Science Direct, CINHAL etc. were used to extract the articles. The keywords used for the search engine were ‘auditory plasticity’, ‘deprivation’, and ‘cortical re organization’,‘ cochlear implants’ The extracted articles were further screened to segregate the  four key areas of the aim of the current review. RESULTS All the extracted electronic articles were categorised according to the five core areas namely (a) auditory deprivation on the auditory cortical development and critical age period; (b) functional and metabolic changes in the auditory cortex due to auditory deprivation; (c) Electro physiological evidence in auditory plasticity after CI;(d) auditory decoupling hypotheses; (e) cortical reorganization and cross modal plasticity. Journals which are printed in English as a primary language as been wetted for the review. The final articles were reviewed independently by the authors. DISCUSSION The aim of the current review article is to update on the auditory plasticity and its effect on post cochlear implantation in children. The reviewed articles on the specific areas were measured on the above mentioned four key areas and discussed in detail further. Auditory deprivation and critical age period       Auditory plasticity is intrinsic to the critical age period, and defines the ability of the auditory systems to undergo certain plastic changes that may be irreversible in nature. These changes may not be retrained in later life. During this period the human brain undergoes various structural and functional changes through the natural course of development [5]. The development of sound detection and localisation along with other segmental and suprasegmental features in speech are all wired during this period.This period prepares the humans to face the competitive acoustic world through the normal course of action. Any disturbance in the natural development of the central auditory system or the auditory cortex may result in the tonotopic changes in the auditory system. This shall subsequently alter the acoustic image in the auditory cortex [6]. Therefore, the accurate and precise flow of acoustic signals during the early years of life is critical in wiring and strengthening the auditory centres in the auditory cortex. Gaps in this flow may lead to the auditory derivation, which will in turn stall the normal auditory development. The arguments advocating the development of auditory function during the critical period is well established in the literature and enormous studies have been done on rats to identify its effects and further the results were extrapolated to understand the human nature [7, 8]. One of the recent studies by Kral [3] states that initial post-natal exposure to the auditory system in rats is critical in developing the auditory plasticity in them, as the auditory centres were highly sensitive during this period compared to the other centres in the brain. Therefore, the initial acoustic stimulation would enhance the overall wiring of the auditory cortex .This would encapsulate the functioning of the later stages. Study done by Meridith and Allamn [4], in rats proved that the initial post-natal auditory stimulation during the first 13 days changes the sound representation in the auditory systems. However, if the system is exposed post 30 days, no differences in the representation of the acoustic image were found. This supports the notion that lack of early auditory stimulation would lead to the auditory deprivation [9, 10]. The outcome of all these experiments directs to an important fact that the early acoustic exposure is critical for the auditory cortical development in rats during the early days of life. It is believed that attenuation or blockages of ongoing acoustic signal in the auditory system will misalign the wiring of auditory afferent development in children during the critical period [11]. These facts have been well explained in various studies by the authors with examples of long-standing middle ear pathology- Otitis media in children. These children have shown potential decline in various auditory processing tasks and have shown poor academic performance. Such lack of exposure incidents have later progressed to auditory processing disorders in children. Thus, reaffirming the fact that any disturbance in the incoming signals during the critical age period would affect the normal course of auditory development. Kral and Sharma [12] reported that in hearing impaired children with lack of acoustic stimulation, there is a disassociation of the primary auditory cortex from that of higher cortical centres in the brain. This was predominantly observed in children who were implanted late and found to be having poor outcome from the CI. They believe that the normal cortical development is simply based on the stimulus driven learning. Thus, lack of stimulation during the early years of life would end up in auditory deprivation. Rewiring of such areas during the rehabilitation in children post cochlear implantation would therefore be an enormous task. The effect of auditory deprivation is enormous and plays an important role in determining the outcome from any form of habillitation/rehabilitation, be it through hearing aids or cochlear implants. During the early learning period, an exposure to a new stimulus would largely reorganise the acoustic representation in the brain [13, 14]. In this process both cortical and subcortical regions play a significant role. The rewiring of the system to understand the acoustic features and later categorize into the environmentally important sounds is essential for the overall representation of the acoustic image in the brain [15]. This processing is easily done in the plastic brain in young children than in those who have crossed the critical age period. Functional changes in the auditory cortex Auditory deprivation will lead to various changes in the alignment of the auditory cortex and central auditory nervous system (CANS). The lack of stimulation is expected to disassociate the morphological structure .It also brings about various other metabolic changes in the system which is essential for the synaptogenesis and maturation of the higher order centres. The resulting alterations due to auditory deprivation include changes in the volume of neurons in the spiral ganglion, changes in the neuronal projections in the CANS and auditory cortex, the regulation of intracortical and thalamocortical neural activities, pruning in pyramidal cells, decoupling of cortico- cortical neural fibres and so on [3,16]. These changes will have detrimental effects on the auditory function and relate to the auditory rewiring or reorganisation. The excitatory and inhibitory changes due to auditory deprivation are profound as they are expected to play a major role in synaptic pruning and for the accurate transmission of the acoustic sensation to the brain.  All these factors need to be taken into account prior to the cochlear implantation in children, especially congenial hearing loss cases. During the early years of life, the auditory cortex and CANS undergoes various developmental changes, one such process is the synaptogenesis. Synapses undergo continuous development and disappear after few days. These continual processes in the central auditory pathway and the auditory cortex are traced using various functional measures for better comprehension [17]. It is believed that in cats, during the initial months, synaptogenesis occur in the auditory cortex. In deaf animals during the same period there was a delay noticed of approximately 2 months. This in turn proves the notion that lack of auditory stimulation shall lead to functional changes in the auditory system. This substantiates the need for early identification and stimulation through cochlear implantation in the congenital hearing loss individuals. This rewiring of the auditory system would also have a pronounced decrease in the synaptic plasticity in the auditory cortex, followed by changes in the excitatory and inhibitory function in the auditory cortex [11, 18]. Such molecular level changes hugely relied on the input signal from the peripheral structures. The lack of auditory streaming of signals would eventually enhance the strengthening of visual cortical functions. The changes in the interplay between the cortico cortical structures will also affect the processing of acoustics signals into the brain. It is a proven phenomenon that the perceptual skills are purely dependent on the interaction between the top down and bottom up process. Such a complex interaction allows the individuals to understand the highly time varying speech sounds in various complex situations. Electrophysiological evidence on Auditory plasticity after Cochlear implantation The ability of the auditory system to continuously process the acoustic signal is integral for the normal speech and language development in humans. Such an auditory capacity requires integration of multiple systems of acoustic cues, which humans constantly adjust according to the behaviour and environmental needs. Cochlear implants are one of the most advanced forms of hearing restoration currently available for the hearing-impaired individuals. Electrophysiology/evoked potentials (EP) have been constantly used in the diagnosis and monitoring of the cochlear implant outcome in children and adults. One of the recent themes of research using EP is focussed on the maturation of auditory function in children with cochlear implants. Due to the increased demand for evidence based clinical research, cochlear implant outcome measures are majorly utilized with the addition of EPs, mainly cortical auditory evoked potentials (CAEPs). These potentials are generated from the primary auditory cortex in response to an acoustic stimulus, predominantly the speech stimulus. The first peak in CAEP, P1, can be used as the biological marker for cortical auditory processing and maturational aspects as studied by Sharma and Dormon [1]. They have done enormous research in the maturation of P1 in children with hearing impairment and also post CI. Their research states that children who are identified early and done with CI would show greater development of cortical auditory processing compared to those who have done CI after 9 years. These results are again supportive of the much-debated critical age period for children to learn the language through auditory mode.  Cardon et al [19] studied the central auditory maturation in children with ANSD using CI and reported that the children who were implanted before 2 years showed normal P1 latencies compared to the group which was implanted after 2 years. They believed that in children with ANSD, the sensitive period would be much shorter than that of hearing impaired children. Thus, suggesting the clinical importance of CAEP. The varied interest in the application of EPs in CI patients dates back to early 2000. A series of studies have been conducted by various researchers to underpin the developmental course in auditory cortex by monitoring the latency measures of various peaks [17]. Similar line of studies was conducted by Sharma and Colleagues [1,8,20] by comparing the P1 latencies in various groups of children. In fact, they have done large-scale studies on children to prove their basic research question of using P1 as a biological marker for auditory processing in children. Interestingly, these studies also highlighted the CI candidacy, during the process of monitoring the cortical maturation after hearing aid amplification in children. The breakthrough research finding was that some children who were fitted with hearing aids would not show any change in P1 latencies even after 6 months of continuous stimulation. This could eventually lead to the conclusion that acoustic amplification is barely helpful and these children can be considered for CI, if the other parameters are supportive. The use of CAEPs also helped the clinician to objectively quantify the aural rehabilitation outcomes after cochlear implantation. In some children the development of P1 would go through the natural process [1]. However, the following negative trough would be concordant with the neural strengthening between primary and secondary cortex. This shed light into the possible dent in speech perception in CI children as against speech detection after CI. These changes in the cortical structure are thought to be due to the auditory deprivation. Further, the central auditory plasticity needs to be rewired with continuous stimulation through CI. The underlying mechanisms for the rapid changes in P1 latencies are not clear. Yet, it is believed that the structural resynchronization of granular layers in the auditory cortex with improved neuronal firing could be attributed as a reason for the rapid development. The studies done in animals [2, 3]   have reported that, during the early days of stimulation there is rearrangement of cortical functioning occurring in the deaf cats.  These evidences when extrapolated into humans, advocate that in young children the cortical stimulation after CI would enhance the cortico cortical structures. Major rewiring would thus occur due to the rapid stimulation in the auditory cortex. However, these measures are interpreted with caution, as it requires in depth analysis with much more research.  Certain sections of researchers believe that the synaptic plasticity is the key in the development of auditory cortical function in the auditory cortex. Kral and Eggermont [18] reported that there is massive increase in synaptic connections during the post-natal period and continues to develop until 4 years of age. This is considered as synaptic overshoot. Therefore, during this period the development is intrinsically regulated. Any alteration before 4 years of age will thus have a major impact on the potential development. This could be a probable explanation for the sensitive period and cortical maturation in children who were implanted before 4-5 years of age. The same declined in children who were implanted after 5 years. Auditory plasticity is thus age dependent; however, certain sections of researchers still believe that it can be rewired even after the sensitive period. Auditory decoupling hypothesis In congenital hearing loss subjects, a long-standing perception remains that after the sensitive period, the cortical activation would be degraded. In a break through research, Kral et al [5] reported that in congenitally deaf white cats, the sensitive period is approximately first 4 months. During this period acoustic stimulation would show some amount of activation in the auditory cortical region. However, after the sensitive period, the auditory stimulation shows degraded responses in supragranular and infraganular layers in the auditory cortex. The  delay in the activation seen at the supra granular layer level and absence of infraganular layer indicates the incomplete developmental process .This affects the free flow of signal to top down and bottom up region, which could be attributed to the lack of synaptogenesis during the post sensitive period. As a result, they reported that there would be functional decoupling of the primary auditory cortex from that of the higher order cortical regions for acoustic processing. It is also believed that this functional decline in processing would have a detrimental effect in strengthening of the sub cortical auditory pathways. If these results could be extrapolated to humans, then it is imperative that the children who are implanted post sensitive period would show functional decline in the various cortico-cortical structures in the auditory cortex. Also, its effects could be seen in the sub cortical development after the implantation. All these results eventually point at the functional outcomes of CI in children. It was also reported that the human auditory cortex would maintain a rudimentary capacity in processing the incoming acoustic signal, even in the absence of primary auditory stimulation[18]. However, the delay or lack of acoustic stimulation would lead to the under development of the higher order cortical structures that are responsible for the primary auditory processing. It will also reduce the speed at which signals are corresponded to the auditory areas in the brain. Overall, these functional declines in the system would deteriorate the rapid development of the combined bottom up and top down processing .As a result of the decoupling, the other sensory areas in the brain would strengthen their territory, eventually rendering it difficult to rewire after the sensitive period. This could be a prime reason to justify the poor outcomes and poor auditory processing seen in children who are implanted post sensitive period. The functional coupling of all these areas is integral for linguistic learning. The decoupling of higher order cortical areas would result in poor speech processing skills in young children after the sensitive period [21]. Thus, substantiating that the auditory plasticity is intrinsic to the time period of learning, especially in congenial hearing loss children. Cortical reorganization and cross modal plasticity It is a proven theory that the sensitive period is critical in normal development of auditory processing in humans. Late implanted children after sensitive period would show delayed representation of the acoustic image in the CANS and auditory cortical areas. This could due to the lack of early stimulation in the auditory cortex and consequent reorganization of cortical function. To prove this significant phenomenon of cortical reorganization in children, Gilley et al [15] studied the EEG responses for the stimulus /ba/ in normal hearing, early and late implanted children. They found that in normal hearing children, there was normal activation of superior temporal sulcus and inferior temporal gyrus. Similar near normal activation was seen in children who were implanted before 3.5 years of age, which is considered as cut off duration for the sensitive period. Interestingly, post sensitive period implanted children showed certain activation areas in the anterior temporal cortex, insular areas etc., that are considered as the multi modal areas in the brain. In addition, activation was seen in visual cortical regions justifying the notion that during the post sensitive period, cortical areas undergo various changes functionally and reorganization of the areas takes place [20]. The impact of cortical reorganization in CI children was an interesting area of research for many researchers. It will be interesting to figure how the already re organized areas in the brain would accommodate the new incoming auditory stimulation. The speculation is that the auditory areas in the brain would have already been wired to other senses predominantly visual function [22].If such a takeover has occurred, then the new input signal would face competition to find its place in the cortical regions. Such an action would enhance the already reorganized brain to adopt new forms of plasticity to accommodate the new signal. There are various studies done in these areas, to assess the effect of auditory mode of stimulation versus combined auditory –visual stimulation in late implanted children. Bergerson [23] reported that, children who are implanted before the age of 4 yeas showed better responses for the auditory mode alone experiment and those who were implanted after 4 years relied more on the combined auditory visual mode. These results are in conjunction with the earlier theory that cortical reorganization hampers the learning period for the late implanted children. Also, it was reported that in cases with congenital hearing loss, the auditory cortex was activated for visual input signal for the location of the objects in space. Thus, underlining the cross modal plasticity that occurs during the post sensitive period [4]. CONCLUSION To conclude, auditory plasticity and its related functions are critical in influencing the outcome after the CI in children. Various studies in literature have pin pointed the impact of sensitive period in auditory and linguistic learning in congenital hearing loss children. The advent of electrophysiology into clinical research has paved a path breaking journey in understanding the complex processing of auditory signals in the primary and secondary cortical areas. Lack of auditory stimulation in the early years would lead to the cortical decoupling and the cortical re organization. Taken together, auditory plasticity serves a unique form of function that would allow the brain to rewire the incoming signal after the implantation. This subsequently allows them to learn the new world of sounds. Research in this area of unravelling the mystery behind the cortical plasticity and sensitive period is still naive. The unprecedented increase in the CI in children in recent years has paved way for more research in coming years for better understanding of the sensitive period. Further research is also warranted to study how auditory plasticity could be detrimental to obtain good outcomes after CI in children. ACKNOWLEDGEMENTS  Authors acknowledge the immense help received from the scholars whose articles are cited and included in the 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 gathered, reviewed and discussed. Englishhttp://ijcrr.com/abstract.php?article_id=178http://ijcrr.com/article_html.php?did=178 Sharma A, Dorman MF. Central auditory development in children with cochlear implants: clinical implications. Adv Otorhinolaryngol. 2006; 64:66–88. Kotak VC, Takesian AE, MacKenzie PC, Sanes DH. Rescue of inhibitory synapse strength following developmental hearing loss.PLoSOne.2013; 8:1-8. Kral A. Auditory critical periods: a review from system’s perspective. Neurosci . 2013; 247: 117–133. Meredith MA, Allman BL. Early hearing-impairment results in crossmodal reorganization of ferret core auditory cortex. Neural Plast. 2012; 12: 1-13. http://dx.doi.org/10.1155/2012/601591 Kral A, Tillein J, Heid S, Klinke R, Hartmann R. Cochlear implants: cortical plasticity in congenital deprivation. Prog Br Res.2006; 157:283–13. Campbell J, Sharma A. Cross-modal re-organization in adults with early stage hearing loss.PLoSOne.2014; 9,2:1-8. Chen Z, Yuan W. Central plasticity and dysfunction elicited by aural deprivation in the critical period. Frontiers in neural ciricuts. .2015;26,9: doi: 10.3389/fncir.2015.00026 Sharma A, Gilley PM, Dorman MF, Baldwin R. Deprivation-induced cortical reorganization in children with cochlear implants. Int J Audiol. 2007; 46: 494–99. Gilley PM, Sharma A, Mitchell TV, Dorman MF. The influence of a sensitive period for auditory-visual integration in children with cochlear implants. Restor Neurol Neurosci. 2010; 28, 2: 207–18. Whitton JP, Polley DB. Evaluating the perceptual and pathophysiological consequences of aural deprivation in early postnatal life: a comparison of basic and clinical studies. J Assoc Res Otolaryngol. 2011;12:535-47 Wingfield A, Peelle JE. The effects of hearing loss on neural processing and plasticity.  Front Syst Neurosci. 2015; 35: 9.  doi: 10.3389/fnsys .201 5. 00035 Kral A, Sharma A. Developmental neuroplasticity after cochlear implantation. Trends Neurosci. 2012;  35:111–22 McDonald JJ, Störmer VS, Martinez A, Feng W, Hillyard SA. Salient sounds activate human visual cortex automatically. J Neurosci. 2013; 33, 21: 9194–01. Kral A, Hubka P, Tillein J. Strengthening of Hearing Ear Representation Reduces Binaural Sensitivity in Early Single-Sided Deafness. Audiol Neurootol. 2015;20:7–12 Gilley PM, Sharma A, Dorman M, Martin K. Abnormalities in central auditory maturation in children with language-based learning problems. J Clin Neurophysiol. 2006; 117, 9: 1949–56. Mowery TM, Kotak VC, Sanes DH. Transient hearing loss within a critical period causes persistent changes to cellular properties in adult auditory cortex. Cerebral Cortex. 2015; 25:2083-94.  doi: 10.1093/cercor/bhu013 [Epub ahead of print]. Eggermont, J. J., Ponton, C. W. Auditory-evoked potential studies of cortical maturation in normal hearing and implanted children: correlations with changes in structure and speech perception. Acta Otolaryngol. 2003; 123, 2: 249–52. Kral A, Eggermont JJ. What’s to lose and what’s to learn: development under auditory deprivation, cochlear implants and limits of cortical plasticity. Br Res Rev. 2007.  56: 259–69. Cardon G, Campbell J, Sharma A. Plasticity in the developing cortex, evidence from children with sensorineural hearing loss and auditory neuropathy spectrum disorder. J Am Acad Audiol. 2012; 23:1-16. Sharma A, Nash AA , Dorman M. Cortical development, plasticity and reorganization in children with cochlear implants. J Commun Disord. 2009; 42:272–79. Ruíz LE, Pico T, Pérez-Abalo MC, Hernández C, Bermejo S. et al. Cross-modal plasticity in deaf child cochlear implant candidates assessed using visual and somatosensory evoked potentials. Medicc rev. 2013; 15: 16–22. Doi: 10.1590/s1555-79602013000100005. Mao YT, Pallas, SL. Cross-modal plasticity results in increased inhibition in primary auditory cortical areas. Neural Plasticity. 2013; 13:1-18. http:// dx.doi.org /10.1155/ 2013/ 530651 Bergeson TR, Pisoni DB, Davis RA. Development of audiovisual comprehension skills in prelingually deaf children with cochlear implants. Ear Hear, 2005; 26, 2: 149–4.  

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareCLINICOPATHOLOGICAL AND IMMUNOPHENOTYPIC CHARACTERISTICS OF EWINGS SARCOMA FAMILY OF TUMORS: SPECIAL EMPHASIS ON ROLE OF FRIEND LEUKEMIA INTEGRATION - 1(FLI-1) ANTIBODY AND OCCURRENCE OF TUMOR ON RARE SITES English1016Alka MittalEnglish Jayanti MehtaEnglish Kalpana MangalEnglish Alpana JainEnglish Neetu AgarwalEnglish Madan Kumar SolankiEnglishObjective: Ewings sarcoma /Primitive neuroectodermal tumor (ES/PNET) is one of the aggressive malignant round cell tumors affecting mainly children and adolescents. This study aimed to emphasize the role of FLI-1 antibody along with CD99 in diagnosing ES/PNET and to keep this tumor in differential diagnosis even at some rare sites. Material and Method: This descriptive and retrospective study was conducted from January 2014 – May 2016 and included 58 patients of ES/PNET. Histopathological and IHC findings were reviewed and the diagnosis of ES/PNET was confirmed. The tumors were further categorized into classic Ewings, PNET and atypical subtypes. Panel of IHC markers included vimentin, CD99, FLI-1, PanCK, LCA, Desmin, Myogenin, NSE, Synaptophysin, S100 and Chromogranin. Results: Clinical Findings- We studied 58 patients of ES / PNET of whom 63% (37/58) were males, 37% (21/58) were females. The age ranged between 3- 65 years (mean 20 years). Histological Findings: 57% of cases (33/58) exhibited classic morphology, 40% (23/58) were classified as PNET. There were only two cases of atypical Ewings sarcoma including large cell and Clear cell variant. Immunohistochemical Findings: Strong membranous CD99 expression was seen in 100%, FLI -1 nuclear staining in 85% , NSE in 50%, S100 in 30%, Synaptophysin in 10% and EMA in 2% (1/58) cases. All other markers included in the panel were negative. Tumor on Rare Sites: 10 Cases were of primary extradural spinal PNET, 1 intramedullary spinal, 2 brain parenchyma, 2 nose and nasopharynx , and one rare case of urinary bladder. Conclusion: Clinical details, histomorphology and IHC includingCD99 and monoclonal FLI-1antibodies may help in supporting diagnosis of EFT if cytogenetic and FISH techniques are not available at any centre. EnglishEwings sarcoma, Primitive neuroectodermal tumor, CD99, FLI-1v  Immunostaning for NSE was seen in 50% cases, S100 in 30% cases and Synaptophysin in 10% cases. EMA was focally positive in clear cell variant (Figure 7). All other markers included in the panel were negative (table 2). Discussion This series comprised patients of Ewings sarcoma / PNET of all ages who were enrolled and treated in a tertiary care center, Jaipur, Rajasthan. There was male preponderance and the mean age was 20 years. The most common sites of involvement were bone of both upper and lower extremities. The patients presented most often with swelling followed by pain, some have fever and limbs weakness which is in accordance with other studies10. Histomorphogically the incidence of classic type was the most common followed by PNET and atypical variants, which is similar to a study done by Folpe et al11. In our study we had only 2 cases of atypical Ewing’s sarcoma which is quite less as compared to one study12and quite similar to other study done by Priya D et al. in which they found 4 cases of atypical Ewing’s sarcoma out of total 51 cases of EFT studied13. These entire EFT show strong membranous CD99 Positivity. The differential diagnosis that could be considered for Ewings sarcoma with CD99 positivity included lymphoblastic lymphoma, poorly differentiated synovial sarcoma, small cell osteosarcoma, rhabdomyosacoma, desmoplastic small round cell tumor (DSRCT) small cell carcinoma and merkel cell carcinoma14. As CD-99 has not proven to be specific marker for EFT despite initial promise, we included other quite specific marker for EFT that is FLI-1. FLI-1 was positive in 85% cases including atypical Ewings sarcoma. Nuclear staining was considered positive with positive endothelial cell nuclei and a subset of lymphocytes serving as internal control. Results are similar to study done by Llombart bosch et al in 2001, they found FLI-1 expression in 84% (16/19) cases of Ewings sarcoma family of tumors out of 48 studied cases of small round cell tumors15. Our results are slightly higher to study done by Folpe AL in 200016.He studied 132 cases of CD99 positive mimics of Ewing’s  sarcoma/ primitive neuroectodermal tumors  including 41 cases of Ewings sarcoma. He found FLI-1 positivity in 71%  cases of EFT (29/41) and 88% cases of lymphoblastic lymphoma (7/8), rest all were found to be negative.    Introduction Ewings sarcoma/Primitive neuroectodermal tumor (ES/PNET) is one of the aggressive malignant small round cell tumors that may arise virtually anywhere but is most common in bone, deep soft tissue of extremities and parenchyma. This tumor was first reported in 1918 by Arthur Purdy stout as ulnar nerve tumor1. Three years later in 1921 James Ewing reported a round cell neoplasm calling it a “diffuse endothelioma of bone “in the radius2.The soft tissue Ewing’s sarcoma was first described in 1975 by Angervall and Enzinger3.Seemayer and colleagues described Peripheral neuroectodermal tumors (PNET) arising in soft tissues at the same time4.In 1979, Askin and coworkers described the malignant small cell tumor of the thoracopulmonary region (Askin tumor) similar to PNET5. With the advent of IHC, cytogenetic and molecular  techniques it is universally accepted that these tumors shared identical features and these were designated as ES/PNET family of tumors(EFT) 6,7.70-80% of cases show morphology of classic Ewings sarcoma and up to 20% show atypical features including large cell, spindle cell, sclerosing, clear cell, vascular or admantinoma like patterns8. Diagnosis of PNET was considered when homer wright rosettes were seen or when any two different neural markers were positive according to criteria proposed by Schmidt et al9. A panel of immunomarkers  such as vimentin, CD99, FLI-1, Desmin, Myogenin, Leucocyte common antigen (LCA), cytokeratin (CK) ,Neural markers like non specific enolase (NSE) ,S100,Chromogranin  and Synaptophysin are usually used to distinguish various small round cell tumors.CD99(MIC2) has not proven to be specific for Ewings sarcoma family of tumors despite initial promise. Approximately 90% of EFT have a specific t (11; 22) (q24; q12) that results in fusion of the EWS and FLI-1 protein; hence we included both CD99 and FLI-1 in the panel. Although molecular testing is gold standard but many centers still do not have this facility, hence IHC plays an important role in differentiating these tumors. The aim of our study was to analyse the clinicopathological and immunophenotypic characteristics of 58 cases of Ewing’s sarcoma/ primitive neuroectodermal tumors from tertiary care centre in Jaipur, Rajasthan with special emphasis on role of FLI-1 protein, and occurrence of tumors at some rare sites. Material and Method This descriptive and retrospective study was conducted from January 2014 – May 2016 and included 58 patients of ES/PNET. Clinical details were collected from the case files. Clinical features such as age, sex, site of involvement, radiological findings, and soft tissue extension were evaluated. The paraffin blocks of all cases were retrieved. Histopathological and immunohistochemical (IHC) findings were reviewed and the diagnosis of ES/PNET was confirmed. The tumors were further categorized into classic Ewings, PNET and atypical subtypes. Diagnosis of PNET was considered when Homer Wright or Flexner Wintersteiner rosettes were seen or when any two different neural markers were positive. Atypical Ewings sarcoma was labeled when cells were large pleomorphic with coarse chromatin, prominent nucleoli and absent rosettes.   Panel of IHC markers included vimentin, CD99, FLI-1, CK, LCA, Desmin, Myogenin, NSE, Synoptophysin, S100, and Chromogranin. Additional IHC markers like glial fibrillary acidic protein (GFAP), INI-1, terminal deoxyneotidyl transferase (Tdt) etc. were also included according to site of lesion and differential diagnosis. IHC analyses for all above markers were done on 4µ thick section taken on tissue bond coated slides by immunoperoxidase method with respective antibodies as per manufactures instructions. Antigen retrieval was done by the heat induced epitope retrieval method in diva decloaker chamber by using citrate buffer (PH 6.0) after tris buffer wash. Endogenous peroxidase was blocked by hydrogen peroxide solution. Sections were incubated with primary antibody for 1 h 30 min. Biocare’s HRP polymer is applied as secondary antibody and 3’3 diaminobenzidine as chromogen substrate. Appropriate positive and negative controls were included. Results Clinical details                                                                                                           This retrospective and descriptive study included 58 patients of ES / PNET of whom 63% (37/58) were male, 37 %( 21/58) were female. The age ranged between 3- 65 years (mean age 20 years).   Most common site of involvement was skeletal in 61% (35/58), followed by soft tissue in 29% (17/58) and parenchyma of rare sites in 10% (6/58) cases. Rare sites included 10 cases of primary extradural spinal PNET, 1 case of intramedullary spinal, 2 cases of brain parenchyma, one case of nose, nasopharynx and urinary bladder each (Table 1). The most common bones involved were of upper and lower extremities followed by iliosacral region. The patients presented with local swelling as most common complaint followed by pain, fever, weakness of limbs and pathological fracture. Localized disease at presentation was seen in 29% (17/58) cases whereas locally advanced disease was seen in 15% (9/58) cases. Soft tissue extension was noted in 74 % ( 20/27) of osseous cases. Follow up related to recurrence, metastasis and treatment history was available in very few patients hence not included in this study. Histological Characteristics 57% of cases (33/58) exhibited classic morphology (Figure1). Microscopically tumor shows solidly packed, lobular pattern of strikingly uniform round cells with high N/C ratio. The individual cells have a round to ovoid nucleus with a distinct nuclear membrane, fine chromatin and 2-3 inconspicious nucleoli. The cytoplasm was ill defined scanty, pale, clear and sometime vacuolated. Neoplastic cells were positive for PAS and digested with D-PAS indicating accumulation of glycogen. Some of the cases showed darker crushed spindled cells. The number of mitotic figures varied from 1 per 10 HPF to 7 per 10 HPF. Most of the cases showed necrosis. 40% (23/58) cases were classified as PNET characterized by presence of rosettes (figure 2). Most of the rosettes contain a central solid core of neurofibrillary material (Homer Wright rosettes) rarely rosettes contain a central lumen or vesicle (Flexner Wintersteiner rosettes).  There were only two cases of atypical Ewings sarcoma in the present study showing large cell and clear cell variant. Large cell variant was seen in nasopharynx and clear cell variant was noted in spinal cord. In large cell variant, cells were large, pleomorphic with coarse chromatin, prominent nucleoli and absent rosettes (figure 3).Large areas of necrosis were also seen. In clear cell variant, tumor cells had abundant clear cytoplasm with small round cell morphology (figure 4). Immunohistochemical Findings All of the cases (58/58) studied showed strong membranous CD99 expression (figure 5) and cytoplasmic Vimentin. FLI -1 nuclear staining was noticed in 85% cases (49/58) (Figure 6).   Previous study done on FLI-1 was by using polyclonal antibody. Rossi et al17used monoclonal antibody and found 100% positivity for FLI-1 in EFT cases(15/15).We also used polyclonal  antibody that is why positivity rates were lower in our study. NSE was expressed in50% and S100 in 30% which was similar to previous study done by Kavalar et al18, where NSE and S-100 were expressed in 66.6% and 25.4% cases respectively. We had 10 cases of primary intraspinal PNET at our centre .All of our cases were extradural. A case study done by Sundar Venkataraman found that only 19 cases of primary intraspinal PNETs have been reported to date19.To best of our knowledge we had half of this data at our centre within such a short time duration. One interesting case at this location was atypical Ewings sarcoma with ciear cell type showing focal EMA positivity.EMA positivity highlights the epithelial differentiation in the EFT. Previously many studies were done on expression of broad spectrum of AE1/AE3 antibody showing positivity rates ranging from 20% to 40% 20,21. Machado et al in 2011 studied 415 genetically confirmed ESFT, for expression of CK, EMA and CEA. They found 19.2 %, 6.6% and 20.8% positive cases for these antibodies respectively22. We had 2 cases of primary intracranial peripheral PNET (pPNET). The IHC panel included GFAP, EMA, CD-99, FLI-1, CD-34, synaptophysin, INI-1, NSE and MIB-1 score. The cases were positive for CD-99, FL-1and NSE. MIB-1 labeling index was 6% and 45% respectively (Figure 8). PNET at any site show variable but generally high MIB-1 score varying from 0-85%.23 These cases are different from CNS PNET in the clinical behavior, treatment, prognosis, IHC and molecular genetic study.24 We had one case of primary intramedullary spinal PNET in 12 year old male child at D11-L2 label. Bone scan and MRI brain were done to know any other site of primary tumor. Both investigations did not reveal any evidence of tumor elsewhere and a diagnosis of primary intramedullary spinal PNET was made. The diagnosis of such a tumor is very crucial as management strategies are relatively unclear and have a poorer outcome as compared to other primary intramedullary spinal tumors25. We had one another interesting case of primary PNET of urinary bladder in 31 year old female patient. These are extremely rare and to our knowledge only 12 cases have been reported so far in the English literature26. We had other two interesting cases of nasal cavity and nasopharynx in40 and 10 year old male patients respectively. It is very rare in head and neck region and accounts for only 2-3% of all the cases27. Conclusion Clinical details, histomorphology and IHC including CD99 and monoclonal FLI-1antibodies may help in supporting the diagnosis of EFT even in absence of cytogenetic and FISH techniques. EFT should be kept in differential diagnosis of all malignant small round cell tumours even at rare sites.   Acknowledgment Authors wish to express and convey their sincere thanks and gratitude to all those who helped for completion of this research article. 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 author’s /editors/ publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Authors acknowledge that we did not get any grants for this study; required funds were generated by ourselves. The Authors declare and acknowledges that we have no conflict of interest.       Englishhttp://ijcrr.com/abstract.php?article_id=179http://ijcrr.com/article_html.php?did=179 Stout AP. Tumor of the ulnar nerve. Proc NY: Path Soc 1918; 18:2. Ewing J. Diffuse endothelioma of bone. Proc NY Path Soc 1921; 7:17-24. Angervall L, Enzinger FM. Extraskeletal neoplasm resembling Ewing’s sarcoma. Cancer 1975; 36:240-51. Seemayer TA, Thelmo WL, Bolande RP, et al. Peripheral neuroectodermal tumors. Perspect pediatr pathol.1975; 2:151. Askin FB, Rosai J, Sibley RK et al. Maligrant small cell tumor of the thoracopulmonary region in childhood: a distinctive clinico-pathologic entity of uncertain histogenesis. Cancer 1979; 43:2438. Dehner LP. Primitive neuroectodermal tumor and Ewing’s sarcoma. AmJ Surg Pathol. 1993; 17:1. Dehner LP. The evolution of the diagnosis and understanding of primitive and embryonic neoplasm in children: living through an epoch. Mod Pathol.1998; 11:669. Wu HT, Govender D. Ewings sarcoma family of tumors: unusual histological variants and immunophenotypic characteristics. Diagn histopathol 2012; 18:348-55. Schmidt D, Herrmann C, Jurgens H, Harms D. Malignant peripheral neuroectodermal tumor and its necessary distinction from Ewing’s sarcoma: A report from the kiel pediatric tumor registry. Cancer 1991; 68:2251-59. Hoffman C, Ahrens S, Dunst J, Hillman A, Winkelmann W, Craft A, et al, Pelvic Ewing sarcoma: A retrospective analysis of 241 cases. Cancer 1999;85:869-77. Folpe AL, Goldblum JR, Rubin BP, Shehata BM, Liu W, Dei Tos AP et al. Morphologic and immunophenotypic diversity in Ewings sarcoma family of tumors: A study of 66 genetically confirmed cases.Am J Surg Pathol 2005;29;1025-33  Liombart-Bosch A, Machado Navarro S, Bertoni F, Bacchini P, Alberghini M, et al. Histological heterogeneity of Ewings sarcoma. virchows Arch 2009;455:397-411. D Priya, Rekha V Kumar, L Appaji, B S Aruna Kumari, M Padma, Prasanna Kumari. Histological diversity and clinical characteristics of Ewing sarcoma family of tumors  in children: A series from a tertiary care center in south India2015;52:331-35. Enzinger, Weiss SW, Goldblum JR. Ewing’s sarcoma/PNET tumor family and related lesions. In:Schmitt W editor. Soft tissue tumors, 5th ed. Philadelphia: Elsevier Publisher;2008.p.945-87. Llombart-bosch A navarros: Immuno histochemical detection of EWS and FLI-1 Proteins in Ewings sarcoma and PNET: comparative analysis with CD-99 (MIC-2) expression: Appl immunohistochem mol morphol 2001:9(3):255-60. Folpe AL., Hillc E, Parham D M, Oshea PA, Weiss S W. Immunohisto-chemical detection of FLI-1 protein expression : a study of132 round cell tumors with emphasis on CD-99 positive mimics  of Ewings sarcoma/ PNET. AMJ Surg pathol 2000 Dec, 24 (12):1657-62. Rossi S, Orvieto E, Furlanetto A,et al. Utility of the immunohistochemical detection of FLI-1 expression in round cell and vascular neoplasm using a monoclonal antibody. Mod Pathol2004;17:547-52. Kavalar R, Pohar MZ, Jereb B, Cagran B, Golouh R. Prognostic value of immunohistochemistry in the Ewing’s sarcoma family of tumors. Med Sci Monit 2009;15:442-52. Venkataramann S, Pandian C, Kumar A S. Primary spinal primitive neuroectodermal tumor-a case report. Ann Neurosci2013;20:80-82. Collini P, Sampietro G, Bertulli R, Casali PG, Luksch R, Mezzelani A, et al. Cytokeratin immunoreactivity in 41 cases of ES/PNET confirmed by molecular  diagnostic studies. Am J Surg Pathol 2001;25:273-4. Elbasshier SH,Naazarina AR,Looi LM,Cytokeratin immunoreactivity in Ewing sarcoma/primitive neuroectodermal tumor.Malays J Pathol2013;35:139-45. Machado I, Navarro S, Lopezz-Guerrero JA,Alberghini M,Picci P,Liombart-Bosch A. Epithelial marker expression does not rule out a diagnosis of Ewing’s sarcoma family of tumors. Virchows Arch2011;459:409-14. Louis DN, Ohgaki H, Wiestle OD, Cavenee WK. WHO classification of tumours of the central nervous system. 4th ed. IARC: Lyon; 2007. P141-6 Kiranchand V,Alugolu R,Megha S U,Anirrudh K P.Primary intracranial peripheral PNET-Acase report and review of literature. Neurology India 2014;62:669-673.  Harbhajanka A, Jain M, Kapoor K S. Primary spinal intramedullary primitive neuroectodermal tumor. J Pediatr Neurosci.2012;7:67-69. Quadri SSS, Bheeshma B, Ravi Jahgirdas, Shymala N, Sundari devi T, Kumar OS. urinary bladder primitive neuroectodermal tumor/Ewing’s tumor-A rare case.Indian jounal of Mednodent and alled sciences2014;2:3.  Bargotya M, Agarwal K, Bhusan R, Rautela  A. Extraskeletal Ewing’s sarcoma presenting as nasopharyngeal mass- rare tumor and rarest presentation. World journal of pathology2014;4.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcarePREVALENCE AND CHARACTERISTICS OF PERIPHERAL RETINAL DEGENERATION IN MYOPIC INDIAN ADULTS English1719Nutan BediEnglish Sharda PunjabiEnglishObjective: To evaluate the relationship between peripheral retinal lesions and axial length of the myopic patients. Material and Methods: A sample of 360 eyes from 224 myopic patients was examined at eye out patient department of tertiary care hospital from July 2008 to March 2010. Sonography was used for measurement of axial length of Eye ball and peripheral retina was studied by indirect ophthalmoscope examination and slit lamp microscopy. Chi square test for these qualitative variables with 5% significance was used for statistical analysis. Results: The average age was 45.32±11.34 years and the myopia was between 0.5 and 20 dioptres. The peripheral retina showed benign changes including pigment clumps in 128 eyes (35.55%), paving stone degeneration in 102 eyes (28.33%). Snowflakes degenerations were present in 40 eyes (11.11%) and white without pressure degeneration was found in 18 eyes (5%) of patients While 36 eyes (10%) of patients had lattice degeneration, and only 36(10%) patients had normal peripheral retina. Conclusions: Myopia is a pathological condition associated with peripheral retinal lesions and it can also predispose to various retinal disorders, so it important to diagnose early and treat these patients so that future complications can be minimize. EnglishPeripheral Retinal lesions, Paving stone degeneration, Snowflakes degenerations, Lattice degeneration Introduction Elongation/ increased axial length of globe are associated with refractive error, usually more than 6 diopteric myopia. (1, 2, 3) In Asian population prevalence of myopia is quite high. (1, 2) Due to elongation of globe in myopic patients choroid and retina tends to stretch continually which leads to thinning of these layers which ultimately results in retinal degenerative changes.(4) Peripheral retinal degenerations, retinal tears, retinal detachment, posterior staphyloma, chorioretinal atrophy, retinal pigment epithelial atrophy, lacquercracks, choroidal andmacular haemorrhage are certain common complications to which myopes are usually susceptible. (4, 5, 6) Some of these retinal lesions may be associated with severe irreversible visual loss andtherefore it is important for clinicians to be aware of the retinal pathologies in high myopia. Material and Methods This was a cross sectional, observational, descriptive analytic study conducted in department of Ophthalmology at tertiary health care medical institute. The study included 360 myopic eyes of 224 patients. Immersion technique of sonography was used for measurement of axial length of eye ball and peripheral retina was studied by indirect ophthalmoscope examination and slit lamp bio microscopy. Inclusion Criteria Age above 10 years Ability to cooperate in retinal examination no symptoms of light flashes and floaters no history of retinal disease, uveitis, vascular retinopathy, glaucoma no history of ocular surgery, antiglucoma treatment Exclusion Criteria Patients of age less than ten years Patients who rejects to participate in study. Procedure Institutional Ethics Committee permission and approval was taken before starting the study. OPD - Patient of ophthalmology department were r contacted personally and study was explained to them in brief in their own a language. Informed Consent of participants was taken. Appropriate statistical tests were used  for analysis of  results Results The 360 eyes from 224 patients included in this study ranged in age from 20-70 years (mean age 45.32±11.34 years for females and 38.22±12.3 years for males). 192 patients were females while 168 patients were males (Table 1). Table 1: Age and sex distribution of patients   Male Female years No. of eyes % No  of eyes % 20-30 16 9.5 28 14.5 31-40 58 34.5 38 19.79 41 -50 44 26.2 61 31.77 51- 60 26 15.5 43 22.39 61-70 24 14.3 30 15.6 Total 168 100 192 100 The myopic refractive error ranged from -0.5 diopter to – 20 diopter (mean refractive error is 10.21±5.43 D (Table2). Table 2: Degree of refractive error in examined patients Refractive error No  of eyes % -0.5D  to -5.0D 52 14.44 -5.0D to -10D 126 35 -10D to -15D 116 32.22 -15D to -20D 66 18.33   360 100   Examination of the peripheral retina revealed the following retinal changes: The peripheral retina showed benign changes including pigment clumps in 128 eyes (35.55%), paving stone degeneration in 102 eyes (28.33%). Snow-flakes degenerations were present in 40 eyes (11.11%) and white without pressure degeneration was found in 18 eyes (5%) of patients. While 36 eyes (10%) of patients had lattice degeneration, and only 36 (10%) patients had normal peripheral retina. Table 3: Type of retinal lesions in patients Retinal lesions Number %  Pigment clumps 128 35.55 Paving stone degeneration 102 28.33 Snow-flakes degeneration 40 11.11 White without pressure 18 5 Lattice degeneration 36 10 normal 36 10 Total 360 100 Englishhttp://ijcrr.com/abstract.php?article_id=180http://ijcrr.com/article_html.php?did=180  Sperduto RD, Seigel D, Roberts J, Rowland M. Prevalence of myopia in theUnited States.Arch Ophthalmol.1983; 101:405-7. Wu HM, Seet B, Yap EP, Does education explain ethnic differences inmyopia prevalence? A population-based study of young adult male’s in Singapore. Optom Vis Sci. 2001; 78:234-9. Grossniklaus HE, Green WR. Pathological Findings in Pathologic Myopia.Retina.1992; 12:127-33. Pierro L, Camesasca FI, Mischi M, Brancato R. Peripheral retinal changesand axial myopia.Retina.1992;12:12-7. Celorio JM, Pruett RC. Prevalence of Lattice Degeneration and Its Relationto Axial Length in Severe Myopia.Am J Ophthalmol.1991; 111:20-3. Hyams SW, Neumann E. Peripheral retinal in myopia. With particularreference to retina breaks.Br J Ophthalmol1969; 53,300-6. Lai TYY, Fan DSP, Lai WWK, Lam DSC. Peripheral and posterior poleretinal lesions in association with high myopia: a cross-sectionalcommunity-based study in Hong Kong.Eye2006 Sep 1. Hikichi T, Trempe CL. Relationship between floaters, light flashes or both andcomplications of posterior vitreous detachment. Am J Ophthalmol. 1994; 117(5):593-598. Rasheed AM, Shehab SY Types of peripheral retinal degenerations in highly myopic Iraqi Patients MJBU,2012;30:10-13 O Malley PF, Allen RA, Straatsma BR. Pavingstone degeneration of the retina. Arch Ophthalmol 1965; 73:169-170. Straatsma BR, Zeegen P, Foos RY, Lattice degeneration of the retina. Trans Am Acad Ophthalmol Otolaryngol 1974; 78:87-89. Lam DS, Fan DS, Chan WM, Tam BS, Kwok AK, Leung AT, et al. Prevalence and characteristics of peripheral retinal degeneration in Chinese adults with high myopia: A cross sectional prevalence survey. Optomvis sci. 2005; 82(4):235-238.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareA STUDY TO EVALUATE DEPRESSION, ANXIETY AND STRESS AMONG UNDERGRADUATE PHYSIOTHERAPY STUDENTS - AN INSTITUTION BASED PILOT STUDY English2024Tarpan ShahEnglish Megha D. PatelEnglish Hiral ShahEnglishIntroduction: At colleges nationwide, large percentage of college students are feeling overwhelmed, sad, hopelessness and so depressed that they are unable to function well. It is seen that Anxiety disorders affect a lot to adults every year, and its levels among college students have been rising since long. The objective of the present study was to explore the severity of depression, anxiety and stress among undergraduate physiotherapy students. Methodology: 246 undergraduate physiotherapy students from one institute have been selected for the study purpose .Questionnaire based survey study was done. A DASS 21 questionnaire was given to the students and the aim of the study was explain to them. Duly completed forms were taken away for research study purpose. Result: Among all of total 246 students; Depression-145 were reported under normal category, 52 of them in mild, 35 in moderate level, 10 in severe category and 4 had fallen in the extremely severe category. The Anxiety scale reported 125 in normal, 34 in mild, 49 in moderate level, 20 in severe and 18 of them have been under extremely severe category. The study reported 159 normal cases for Stress scale, 35 were in mild, 31 in moderate, 20 in severe and 1 case in extremely severe score. Conclusion: Present study revealed maximum number of students in the normal category and some student’s in raised level of anxiety and stress among undergraduate Physiotherapy students. Discussion: Consequently it is advised that the institute should take appropriate steps for reducing the level of depression and stress by undertaking counseling of the students and help them to cope up with their difficulties up to the institutional limit. EnglishDASS-Depression Anxiety Stress Scale, DASS21-Depression anxiety stress scale 21INTRODUCTION AND BACKGROUND Physiotherapy College in Surat, Shree Swaminarayan Physiotherapy College has an intake capacity of 50 undergraduates Physiotherapy students per year. Physiotherapy course has four years of curriculum and 6 months of compulsory internship to get the best practical experience in this duration. These four years may be stressful for students to successfully realize their dreams. We have explored their level of depression, anxiety and stress through the Depression Anxiety Stress Scale (DASS21). Depression has afflicted mankind ever since its inception. It has attracted public interest rather recently 1. WHO rates depression to be the world’s fourth most disabling health problems 2. WHO has projected that depressive disorder will be ranked as second most disabling disorders, unless appropriate measures are taken for early diagnosis, prompt and effective treatment and prevention of depression. According to the National Depressive and Manic Depressive Association (NDMDA), depression is an undergraduate and undertreated disorder.3 Untreated depression results in high morbidity and mortality. Proper diagnosis and treatment cannot be overemphasized.4 Anxiety is experienced as an emotion by everybody in day to day life and it is defined as a state of fearful expectation or apprehension as a result of real external danger or intrapsychic conflict such as anxiety in the face of examination and before delivering a lecture. So this is called normal, physiological, adaptive or realistic anxiety. Contrary to that, anxiety as an abnormal state is pathological, maladaptive and unrealistic. Anxiety is often differentiated from fear, as fear is an apprehension in response to an external danger while in anxiety the danger is largely unknown (internal). Roughly about 5% of population suffers from anxiety disorder. Anxiety is a response to threatening experience, while depression is a reaction to a loss. They usually occur together because danger and loss are usually there in many cases.5 As Seyle noted, stress occurs as a response to a range of circumstances. Biologically, stress reactions evolved as an emergency response intended to prepare an individual for fight or flight-that is, either to defend oneself or try to run away from a threat. In psychological terms, stress is a response to the body to whatever is perceived as an emergency situation6. Depression slows thinking, making it difficult to concentrate and remember. Depressed people frequently become dependent, passive, and helpless, at times covertly using their symptoms to manipulate others into meeting their needs. Even some medications may cause depression like adrenal steroids, Crabamazepine, L-dopa, reserpine, oral contraceptives, and etc. Depression may be associated with several psychiatric disorders that significantly affect its course, prognosis, and treatment. Suicide occurs most frequently in patients who are depressed and alcoholic. Suicide is a complication of up to 15% of cases of depression. Many demographic data (e.g.: being older, being male, experiencing social isolation, or having chronic or terminal illness.) have said to increase the risk.7 Anxiety is like fear in that it involves mental and physical mobilization to meet a perceived danger. Excessive levels of anxiety however paralyze mental resources in amorras of continuous and futile mobilization of mind and body. Anxiety is manifested by mental, depletion, and in ability to rise to a challenge. Physical complaints, which usually represent heightened awareness of arousal of the sympathetic nervous system and motor tension, are common in anxious patients. Typical symptoms include insomnia, nausea, diarrhea, abdominal pain, difficulty swallowing, dry mouth, hot flashes, tremor, muscle tension and soreness, difficulty swallowing, urinary frequency, sexual dysfunction, faintness, tremor, fatigue, headaches, diaphoresis, cold, clammy hands, headaches. Hyperventilation produce by anxiety causes shortness of breath, dizziness, light-headedness, numbness and paraesthesias. Non-prescription drugs that may cause anxiety include caffeine, withdrawal from CNS depressants (e.g.: alcohol, tranquillizers), any drug that clouds sensorium in hyper vigilant patients.7 Stress and excitement commonly cause insomnia by stimulating the arousal system, which easily becomes predominant over the sleep-inducing system7. Physiological signs and symptoms occur mostly as result of sympathetic nervous system and adrenal activity like dilated pupils, increased heart rate, increased rate and depth of respirations, skin pallor, decreased urinary output, dry mouth, and increased muscle tension, increased blood sugar. Psychological signs and symptoms include anxiety, fear, anger, depression, denial, etc.6 There is increasing concern about the stress in health, education and training especially in medical, dental, nursing and to certain extent physiotherapy education. Stress during Physiotherapy Education is inevitable. Although stress is not necessarily a symptom of more formal anxiety or depressive disorders it can be precursor to these problems. High level of depression, anxiety and stress may have a detrimental effect on the academic curriculum8. However there is deficit of the information regarding the depression, anxiety and stress among undergraduate physiotherapy students. So in present study would aim to evaluate depression, anxiety and stress in undergraduate physiotherapy students in SSPTC, Surat. MATERIALS AND METHODOLOGY Study Design: In this questionnaire based survey study the samples were selected from Shree Swaminarayan Physiotherapy College students and were performed in the same institution only. Duration for this study was 6 months and this study comprises of 246 undergraduate female physiotherapy students. The students who were registered as undergraduate physiotherapy student in Shree Swaminarayan Physiotherapy College, in the age group of 18-23 years were only recruited. Students who are not in the field of under graduation Physiotherapy and who are undergoing post graduation in Physiotherapy, Students who were not conversant in English were excluded from this study. For collecting the data questionnaire method was used. Method: This study was conducted in the Shree Swaminarayan Physiotherapy College, Kadodara, Surat, which is the one and only women’s residential teaching institute for Physiotherapy in India. The data were collected from all four years and interns of B.P.T. of this college during 2015-16 academic years. Participation in the study was voluntary and an informed consent was obtained. The participating students were briefed about the aim of study and informed that their data would be safe and was guaranteed confidentiality. The DASS questionnaire was distributed among the students and was collected back for analysis once they were duly filled by the participants. DASS baseline scores were collected during relaxed state when there were no exams. The scale has been tested and found to possess excellent reliability, good validity and simple in language and required less time. Severity Depression Anxiety Stress Normal 0-9 0-7 0-14 Mild 10-13 8-9 15-18 Moderate 14-20 10-14 19-25 Severe 21-27 15-19 26-33 Extremely severe 28+ 20+ 34+ RESULTS  Out of the 246 physiotherapy students: 198 were going through their academic performance while the rest 48 of them were rummaging through getting their new experiences according to the internship schedule. When we analyzed, the depression score, among all of total 246 students; 145 were reported under normal category, 52 of them in mild, 35 were in moderate level, 10 in severe category and 4 had fallen in the extremely severe category. The anxiety scale reported 125 in normal, 34 in mild, 49 have been in moderate level, 20 in severe and 18 of them have been under extremely severe category. The study reported 159 normal cases for stress scale, 35 were in mild, 31 in moderate, 20 in severe and one case in extremely severe score. DISCUSSION This study in Shree Swaminarayan Physiotherapy College has revealed that the students who had actively participated in this research, a total of 246 students, 4 were in extremely severe depression score, 18 were in extremely severe anxiety score and only 1 in extremely severe stress category. High amount of depression, anxiety and stress can be because of multiple reasons. It could be their personal reasons, environmental reasons and academic reasons. Different contributing factors to lead to abnormal depression, anxiety and stress among the students can be due to various factors like, physical factors, academic factors, social factors, emotional factors, personality factors, etc. Medical and Paramedical students are expected to learn and master a huge amount of knowledge, attitudes and skills for which they have to work hard which in turn put them under lots of stress. Studies done by Balkishan Sharma, Rajshekhar Wavare on academic stress due to depression among medical and Para-medical students in an Indian medical college identified that there was no difference between Mean Depression Score in the students of MBBS  and physiotherapy course during their academic examination. It was also observed that academic examination for medical and Para-medical students are stressful and produces changes in vital parameters which affected their academic performance. Academics and examination are the most powerful stressors in medical and Para-medical students.9 First and Second year students have not been found in extreme depression or stress. This may be due to new arrival in the Para-medical field, they would find this as a new experience and they may seem it’s easy. Alternatively third year, final year and internship student were found to be more severe in depression, anxiety and stress. This could be due to their increased self study hours, increased level of study from previous years, aspiration of scoring more in academics, increasing concern about their profession as a carrier and lots more. In interns it could be due to their worry of getting job placement, treating the patients with complete and proper handling with full confidence and independently, new responsibilities they need to take now and so on. Consequently it is advised that the institute should take appropriate steps for reducing the level of depression and stress by undertaking counseling of the students and help them to cope up with their difficulties up to the institutional limit. Introducing some of such strategies to the college can help to achieve a normal level of depression, anxiety and stress among students. So the further same research again will show no severity of depression, anxiety and stress.  CONCLUSION After analyzing the DASS data which were collected from undergraduate physiotherapy students from Shree Swaminarayan Physiotherapy College, Kadodara, Surat, has revealed that maximum number of students are in the normal category of Depression, Anxiety and Stress and very few of  them are in the extremely severe category. ETHICAL CLEARANCE Ethical clearance for the present study was obtained from ethical committee of Shree Swaminarayan Physiotherapy College. ACKNOWLEDGEMENT The author acknowledges the immense help received from the Scholars whose article 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 are extremely grateful to IJCRR editorial board members and IJCRR team of reviewers who have helped to bring quality to this manuscript. Source of Funding There was no source of funding. Conflict of Interest There was no conflict of interest. Englishhttp://ijcrr.com/abstract.php?article_id=181http://ijcrr.com/article_html.php?did=181 Akiskal, H.S. (2000): Mood disorders: Introduction and overview. In: Comprehensive Textbook of Psychiatry, Vol.1, Edn.7, (Eds) Sadock,  B.J. and Sadock, V.A., pp 1284-1297, Phialdelphia: Williams and Wilkins. Fava, M. et al (June 2003): Background and rationale for the sequenced treatment of alternatives to relieve depression. Psychiatric Clinics of North America, (Eds) Rosenbaum, J. F., Dunner, D. L., Philadelphia: W. B. Saunders. Hirschfeld, R. M., Keller, M.B., Panico, S. et al (1997): The national depressive and manic-depressive association consensus statement on the undertreatment of depression. Journal of American Medical Association, 277, 333-340. Alan De Sousa, Dhanalakshmi De Sousa, Avinash De Sousa. Psychiatry in Asia. Vikas    Medical Publishers, Mumbai. First edition-2005, page no: 231. Dr. P. D. Garg Concise Psychiatry for undergraduates. Arya Publishers. First edition-2006, page no: 103. Amanpreet Kaur. A textbook of Psychology. S. Vikas and CO. Edition-2011, page no: 172, 176. Steven L, Dubovsky, M.D. Clinical Psychiatry. First Indian edition 1992, page no: 3, 8, 10, 22, 50, 51, 63, 88, Jaypee Brothers. Subhash M. Khatri. “Stress in undergraduate physiotherapy students at KIPT” Indian Journal of Physiotherapy and Occupational Therapy. July-September 2009, Vol. 3, No.3, page no: 85-89. Balkishan Sharma, Rajshekhar Wavare “Academic stress due to depression among medical and Para-medical students in an Indian medical college: Health initiative cross sectional study”. Journal of Health Sciences (J of H Sc) 2013; 3(5):29-38.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareA STUDY OF NEONATAL HYPERBILIRUBINEMIA IN A TERTIARY CARE HOSPITAL IN THE NORTH EASTERN REGION OF INDIA English2529Sungdirenla JamirEnglish Arunkumar Singh NgangomEnglish Davina HijamEnglish Chubalemla LongkumerEnglish Abhishek DubeyEnglish M. Amuba SinghEnglish Kh. Ibochouba SinghEnglishNeonatal jaundice is yellow colouration of the skin and the sclera of newborn babies due to accumulation of bilirubin. This is associated with hyperbilirubinaemia, a condition where bilirubin level is raised in the circulation. Objectives: To assess the etiological factors of neonatal hyperbilirubinemia and therapeutic interventions in a tertiary care hospital in the north eastern region of India. Methods: A prospective cohort study was carried out in the Department of Biochemistry, Regional Institute of Medical Sciences (RIMS), Imphal, Manipur for a period of two years. One hundred fifty newborns with jaundice aged up to 28 days, both term and preterm were included in this study. Careful clinical assessments were done to assess the possible etiologies. Serum bilirubin was determined by colorimetric method as described by Jendrassik and Grof [12]. Monitoring of serum bilirubin was done by serial measurements once a day in the morning. Results: Significant hyperbilirubinemia (TSB>15mg %) was seen in 58 (38.7%) neonates while 92 (61.3%) had TSBEnglishNeonatal hyperbilirubinemia, Phototherapy, Exchange transfusionvvvvINTRODUCTION: Hyperbilirubinemia is a common and in most cases, benign problem in neonates. Jaundice is observed during the 1st week of life in approximately 60% of term infants and 80% of preterm infants.[1] The serum bilirubin level varies with birth weight, gestational age, chronological age and internal milieu of the body. When total serum bilirubin (TSB) level exceeds a critical limit, it crosses the blood brain barrier. [2] Neonatal hyperbilirubinemia (NNH), defined as a TSB level above 5 mg per dL (86 μmol per L), is a frequently encountered problem. Chemical hyperbilirubinemia is defined as TSB levels >2mg/dl, is universal in newborns during first week. Although up to 60 percent of term newborns have clinical jaundice in the first week of life, few have significant underlying disease. [3]  Neonatal hyperbilirubinemia is termed as significant when it needs close supervision, further evaluation and sometimes intervention.[4,5]  In case of preterm newborn significant hyperbilirubinemia varies according to gestational age and birth weight.[6,7] Neonatal hyperbilirubinemia results from a predisposition to the production of bilirubin in newborn infants and their limited ability to excrete it. The infants, especially preterm infants, have higher rates of bilirubin production than adults, because they have red cells with a higher turnover and a shorter life span. [8]   Neonatal jaundice refers to the yellow colouration of the sclera and skin of newborn babies that result from hyperbilirubinemia. It is the most common condition requiring medical attention in newborn babies. It is also a common cause of readmission to hospital after early discharge of the newborn babies. [9] Some of the most common causes of neonatal jaundice include physiological jaundice, breast feeding or non-feeding jaundice, breast milk jaundice, prematurity leading to jaundice and various pathological causes like hemolytic disease, liver dysfunction, neonatal sepsis, deficiency of glucose-6-phosphatase (G6PD) enzyme, Rh-incompatibility, hypothyroidism and rare conditions such as Gilbert’s syndrome, Crigler-Najjar syndrome etc.[10] The early diagnosis and treatment of neonatal hyperbilirubinemia is of utmost importance as bilirubin is toxic to CNS and elevated serum bilirubin can cause neurological complication. Further, the incidence, etiological and contributory factors to neonatal jaundice differ in ethnicity and geographical distribution. Thus the present study is undertaken to assess the etiological factors of neonatal hyperbilirubinemia and therapeutic interventions in a tertiary care hospital in the north eastern region of India. MATERIAL AND METHODS: A prospective cohort study was carried out in the Department of Biochemistry, Regional Institute of Medical Sciences (RIMS), Imphal in collaboration with the Department of Pediatrics, RIMS, Imphal, Manipur for a period of two years (November 2012 – October 2014). One hundred fifty newborns with Jaundice aged up to 28 days, both term and preterm were included in this study while those with age more than 28 days or with major malformations were excluded from this study. A detailed history of both mother and baby and meticulous physical examination of the baby were carried out. Gestational age was calculated from the 1st day of the last menstrual period of the mother. Those babies born between 37-41 weeks of gestation were classified as term babies. Those born before 37 weeks were classified as preterm babies. Babies weighing less than 2500g were defined as low birth weight babies and those weighing 0.05).  Table VI shows that among neonates with physiological HB, the mean ± SD total serum bilirubin (TSB) at the time of initial assessment was 12.72 ± 4.10 mg/dL. The mean ± SD peak level (TSB peak) was 14.28 ± 2.54 mg/dL while mean ± SD at the time of discharge (TSB last) was 10.35 ± 2.27 mg/dL. In this study, peak level of serum bilirubin was reached by the mean age of 5 days falling rapidly thereafter over the next few days. These findings were consistent with the findings of Shartsho JT. [21] In this study, the incidence of hyperbilirubinemic neonates receiving either PT or ET or both was found to be 54.7% (Table IV). 65(43.3%) were given phototherapy and 19(12%) received blood exchange transfusion. Out of these, 2 neonates received both PT and ET. So 45.3% were not treated by either PT or ET or both. These findings are similar with the findings of Rasul CH et al[22] who reported that the most common treatment in their study was phototherapy(62.6%) while ET was used only in 5.2% cases. 61% patients required only phototherapy in a study by Khaton S et al[23]. It is evident from Table V that Neonates with higher mean serum bilirubin (23.8 ± 3.95mg/dL) received both phototherapy and exchange transfusion (pEnglishhttp://ijcrr.com/abstract.php?article_id=182http://ijcrr.com/article_html.php?did=182 Kliegman RM, Behrman RE, Jensen HB, Stranton B: Nelson Textbook of Pediatrics. Jaundice and hyperbilirbinemia in the newborn. 19th ed. Philadelphia: Saunders; 2012.p. 603-12. Brown AK, Damus K, Kim MH et al. Factors relating to readmission of term and near-term neonates in the first-two weeks of life. Early discharge survey group of the Health Professional advisory board of the Greater NY Chapter of the March of Dimes. J Perinat. Med 1999; 27(4): 263-75. IAP- NNF National Task Force 2006 on guidelines for level II neonatal care. IAP-NNF guidelines 2006 on level II neonatal care. Jaundice in newborn; 2006.p. 187-210. Bhutani VK, Johnson L,Sivieri EM. Predictive ability of a predischarge hour serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and nearterm newborns. Pediatrics 1999; 103:6-14. Newman TB, Maisels MJ. Evaluation and treatment of jaundice in the term newborn. A kinder, gentle approach. Pediatrics1992; 89:809-18. Bhat YR, Rao A. Transcutaneous bilirubin in predicting hyperbilirubinemia in term neonates. Indian J Pediatr 2008; 75:119-23. Linn S, Schoenbaum SC, Monson RR Rosner B, Stubblefield PG, Ryan KJ.  Epidemiology of neonatal hyperbilirubinemia. Pediatrics1988; 75:770-74. Brouillard R. Measurement of red blood cell life-span. JAMA 1974; 230:1304-5. Akobeng AK: Neonatal jaundice, Clinical evidence. Am Fam Physician 2005; 71(5):947-48. Madan A, James RM, Stevenson DK. Neonatal Hyperbilirubinemia. In: Taeusch HW, Ballard RA, Gleason CA. Avery’s diseases of the new born. 8th ed. Philadelphia: Elsevier Saunders; 2004.p. 1226-56. Tooley WH. Intensive care nursery house staff manual. Very low and extremely low birth weight Infants. UCSF hospital. University of California. 8th ed. 2003; 65-8. Jendrassik L. and Grof P; Biochem. Z. 1938; 81:297. Paediatrics Vol. 114 (1) July 2014 Nepal D, Banstola D, Dhakal AK, Mishra U and Mahaseth C. Neonatal hyperbilirubinemia and its early outcome. JIOM 2009; 31(3): 17-20. Dhanjal GS, Jain G and Singh M. Clinico-etiological study of neonatal jaundice in a tertiary carecentre in Ambala (Haryana) India. JBPR 2014; 3(1): 64-67. Dholakia A, Darad D and Chauhan C. Neonatal hyperbilirubinemia and its correlation with G6PD enzyme deficiency in a tertiary care hospital in Gujarat. National J of Medical Research 2012; 2(1): 59-62. Dhanjal GS, Jain G and Singh M. Clinico-etiological study of neonatal jaundice in a tertiary carecentre in Ambala (Haryana) India. JBPR 2014; 3(1): 64-67. Bahl L, Sharma R, Sharma J. Etiology of neonatal jaundice at Shimla. Indian J Pediatr 1994; 31: 1275-8. Mallick PK, Alam B. Aetiological study of neonatal hyperbilirubinaemia-A hospital based prospective study. Medicine Today 2012; 24(2): 73-4. Kuruvilla KA. Atanu ST, Jana K. Glucose-6-Phosphate dehydrogenase deficiency in neonatal hyperbilirubinemia in a South Indian Referral Hospital. Indian J Pediatr 1998; 35: 52-4. Shartsho JT (2007). A study on neonatal jaundice (0-14). Unpublished doctoral dissertation, Manipur University, Canchipur, Manipur. Rasul CH, Hasan MA, Yasmin F. Outcome of neonatal   hyperbilirubinemia in a tertiary care hospital in Bangladesh. Malaysian J Med Sci. 2010; 17 (2):40-4. Khaton S, Islam MN. Neonatal jaundice-clinical profile of 140 cases. Bang J Child Health. 1993; 17:158-63.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareORAL LICHEN PLANUS: AN UPDATE English3033Md. Asad IqubalEnglish Mobeen KhanEnglish Umesh Chandra ChaudharyEnglish SwetarchiEnglish Bushra FarhatEnglish Nazish AkhtarEnglishLichen planus is a mucocutaneous disease affecting approximately 1.5 to 2% of the world population. Oral lichen planus (OLP) is a chronic mucosal condition. It has various oral manifestations, the reticular form being the most common. The course of the disease is usually unpredictable with bouts of remission and exacerbation being common. The most widely accepted treatment for lesions of OLP involves topical or systemic corticosteroids to modulate the patient’s immune response. EnglishLichen planus, Mucocutaneous disease, Oral lichen planus, Lichenoid reaction, CorticosteroidsINTRODUCTION It is a chronic, inflammatory disease that affects mucosal and cutaneous tissues. Oral lichen planus (OLP)occurs more frequently than the cutaneous form and tends to be more persistent and more resistant to treatment.1 lichen planus is a relatively common disorder, estimated to affect 0.5% to 2.0% of the general population.2Thereis a strong preference for the female sex3 Sousa and Rosa (2005) surveyed 79 oral lichen planus cases diagnosed between 1974 and 2003, and found that women are nearly four times more affected by this condition than men, and that white individuals are five and a half times more likely to develop this disease compared to other races.4 Clinically, oral lichen planus has specific and clearly identifiable features,5 usually presenting in one of two main forms - the reticular and the erosive forms – although other forms are not rare.6 In fact, according to Mollaoglu (2000), four other forms were originally described: the papular, “plate-like”, bullous and atrophic forms.7 The management of OLP should begin by taking the proper history and clinical examination. Elimination of any form of irritants-like maloccluded teeth, ill-fitting dentures, amalgam fillings should be removed. Incisional biopsy should be done to confirm the diagnosis. The patients with erosive or atrophic forms particularly should be observed periodically as it has malignant transformation potential varying between 0.3% and 3%. For the effective management of OLP, one has a wide range of drugs to choose from. When a patient with OLP presents with a burning sensation, usually as a first line of treatment one can prescribe a topical preparation of steroid and retinoids. As a second line of treatment in cases of steroids resistant, we may prescribe immunomodulatory drugs such as levamisole and dapsone. In resistant cases, where it is not responding to topical preparations or in a severe form of OLP tacrolimus, and systemic corticosteroids in conjunction with immunosuppressive like azathioprine can be given. So, it is essential to choose appropriate drug, mode of administration and dosage regimens individually and equal importance should be given for stress management.8 ETIOLOGY The cause of OLP is unknown. It is said some certain factors mention below may trigger an inflammatory disorder.  Hepatitis C infection and other types of liver disease.  Allergy-causing agents (allergens), such as foods, dental materials or other substances.  Genetic background.  Immunodeficiency disorder.  Some bacterial and viral diseases.  Certain medications for heart disease.  High blood pressure or arthritis.  Certain drugs like ibuprofen and naproxen.  Stress.  Graft versus host disease.9,10 CLINICAL FEATURES Lichen planus affects primarily middle-aged adults, and the prevalence is greater among women.11 Children are only rarely affected.12 The classic skin lesions of the cutaneous form of lichen planus can be described as purplish, polygonal, planar, pruritic papules and plaques. These skin lesions commonly involve the flexor surfaces of the legs and arms, especially the wrists. The nail beds may also be affected, with resultant ridging, thinning and subungual hyperkeratosis.13 Scalp involvement, if untreated, can lead to scarring and permanent hair loss. Since 30% to 50% of patients with oral lesions also have cutaneous lesions, the presence of these characteristic cutaneous lesions can aid in the diagnosis of OLP. Several types of OLP have been described, the 2 main types being reticular and erosive OLP.1 It is not uncommon for the same patient to present with multiple forms of OLP. HISTOLOGY Lichen planus has a unique microscopic appearance that is similar between cutaneous, mucosal and oral. A Periodic acid-Schiff stain of the biopsy may be used to visualise the specimen. Histological features seeninclude: 14 Thickening of the stratum corneum both with nuclei present (parakeratosis) and without (orthokeratosis). Parakeratosis is more common in oral variants of lichen planus. Thickening of the stratum granulosum Thickening of the stratum spinosum (acanthosis) with formation of colloid bodies (also known as Civatte bodies, Sabouraud bodies) that may stretch down to the lamina propria. Liquefactive degeneration of the stratum basale, with separation from the underlying lamina propria, asa result of desmosome loss, creating small spaces(Max Joseph spaces). Infiltration of T cells in a band-like pattern into theDermis12 “hugging” the basal layer. Development of a “saw-tooth” appearance of therete pegs, which is much more common in non-oral forms of lichen planus. CLINICAL SIGNIFICANCE OF ORAL LICHEN PLANUS OLP is one of the most common mucosal conditions affecting the oral cavity.15Therefore; dentists in clinical practice will regularly encounter patients with this condition. Because patients with the atrophic and erosive forms of OLP typically experience significant discomfort, knowledge of the treatment protocols available is important. The similarity of OLP to several other vesiculoulcerative conditions, some of which can lead to significant morbidity, makes accurate diagnosis essential. TREATMENT Topical steroids are the mainstay of palliative treatment of OLP but alternative therapeutic approaches are highly regarded given the lack of strong evidence on any available treatment modality.16,17 Various new agents have been recently suggested to treat OLP. Corticosteroids Corticosteroids are the first line of treatment for OLP because of their activity in dampening cell mediated immune activity there by modulating the immune function. The drugs are administered either topically, intralesionally or systemically. The mild to moderate symptomatic lesions are treated using topical corticosteroids. Eg. Triamcinolone acetonide 0.1%, 0.05% flucinonide, 0.025% clobetasol propionate etc.18 Patients are instructed to apply a thin layer of the prescribed topical corticosteroid upto 3 times a day for 2 weeks. The advantage of topical steroid application is that side effects are fewer than with systemic administration. Adverse effects like secondary candidiasis, thinning of the oral mucosa and discomfort on application are seen with the use of these drugs. Prolonged use of potent topical corticosteroids with occlusal dressing can cause adrenal suppression. Intra lesional steroid therapy Local injection of up to 0.2 to 0.4 ml of triamcinolone acetonide containing 10 mg/ml is used to treat persistent localized lesions. Systemic steroid therapy Prednisolone is the most commonly prescribed systemic steroid to manage OLP. The approach to therapy is to prescribe a high-dose, short-course regimen to maximize therapeutic effect while minimizing side effects. A single daily morning dose of 40 to 80 mg of prednisone is prescribed for no more than 10 days. The risk of the Hypothalamic-pituitary-adrenal axis (HPA-axis) suppression is negligible with such short-term bursts, thus tapering is not necessary. However, other possible adverse side effects may occur and include insomnia, diarrhea, mood swings, nervousness, fluid retention, muscle weakness, hypertension, and decreased resistance to infection. Another approach to reduce the amount of total prednisolone necessary is to concurrently prescribe a steroid-sparing agent such as the immunosuppressant drug azathioprine (50 to 100 mg/day) or levamisole (150 mg/day). Azathioprine appears to act synergistically with prednisone to reduce inflammation and allow for a lowering of the therapeutic prednisone dose. Possible side effects include nausea, vomiting, diarrhea, pancreatitis, bone marrow suppression, hepatotoxicity, arthralgias, and retinopathy. Levamisole in a dose of 150 mg/day and prednisolone25 mg/day for 3 consecutive days each week for 4-6weeks, showed improved results in the management of erosive OLP. Minor rashes, insomnia and head ache are few of the noted side effects.19 Prolonged use of any of the above modalities without supervision will result in undesirable systemic effects and adverse local effects including candidiasis and atrophy. Immunosuppressant - Cyclosporine Cyclosporine is an immunosuppressant and reduces the production of lymphokins. This drug may be used topically or in the form of mouth rinse. Cyclosporin can be used as an alternative therapy to conventional treatments for initial control of oral Lichen planus. The most common side effects of this drug are Hypertension and nephrotoxicity which limits its use in the treatment of oral lichen planus.20 Immunosuppressant - Tacrolimus Tacrolimus is a macrolide immunosuppressant with a mechanism of action similar to cyclosporine, but is 10 to100 times more potent and with better mucosal penetrating properties. Topical use of tacrolimus is a safe, well tolerated, and effective therapy for oral lichen planus lesions recalcitrant to traditional therapies.21 Retinoids Retenoids have also been tried for the treatment of OLP. Previous studies revealed that side effects were common and troublesome with marginal improvement. Topical application of Fenretinide(4-HPR), a newer retinoid showed to have a positive result with minimal side-effects in the treatment of OLP.22 UV radiation UV irradiation, especially in combination with psoaralens modulates the function of cells of the immune system. A study showed that PUVA with methoxypsoaralen which produced a marked improvement in 9 out of 18 patients, with common side effects such as nausea, dizziness and sun sensitivity.23 Griseofulvin Griseofulvin has been advocated for the treatment of erosive-ulcerative lesions when steroid treatment is contraindicated or when the lesions are resistant to steroids. Anti-malarials Hydroxy-chloroquine sulphate showed positive results in management of OLP. 9 out of 10 patients showed excellent response to hydroxychloroquine when given in dosage of200 to 400 mg daily as a monotherapy for 6 months.24 Dapsone Use of dapsone in the management of OLP has revealed some benefit, but disappointing results have been seen in gingival lesions. Generally the use of dapsone is precluded because of significant adverse effects like hemolysis, nausea and headache.25 Phenytoin It is an anti-epileptic drug with immunomodulatory and wound healing properties. Photodynamic therapy Photodynamic therapy (PDT) uses a photo sensitizing compound like methylene blue which is activated at a specific wavelength of laser light PDT have immunomodulatory properties which may induce apoptosis in the hyperproliferating inflammatory cells present in diseases like psoriasis and lichen planus, there by reversing the hyperproliferation and inflammation of lichen planus.26 Surgical management Surgical treatment is more applicable to the plaque-like lesions, because the affected surface epithelium can be removed easily. Surgical management is not suitable for the erosive and atrophic types because the surface epithelium is eroded. Cryosurgery and carbon dioxide laser therapies have been tried in management of OLP lesions. NATURAL ALTERNATIVES Lycopene is a potent antioxidant. Supplementing with 8 mg/day of lycopene for 8 weeks showed favourable results in OLP patients. Burning sensation was reduced by84% and lowered oxidative stress in a placebo-controlled trial.27Higher dosages of curcumin (up to 6,000 mg/day) helped a significant number of OLP patients control their symptoms. Minimal side effects like diarrhea and gastrointestinal discomfort may occur, which are usually dose related.28 Green tea (epigallocatechin-3-gallate) is known to have possessing anti-inflammatory and chemopreventive properties. Green tea is known to inhibit T-cell activation, migration, proliferation, antigen presentation and control other inflammatorymediators.29 DISCUSSION Oral lichen planus (OLP) is a common chronic inflammatory disorder. Identification of the causative agent is essential for the treatment of the oral lichen planus. Relief form symptoms of oral lichen planus can be achieved by the topical application of corticosteroids alone or in combination with other immunomodulatory topical agents. Systemic corticosteroids are used to control the disease. CONCLUSION Oral lichen planus (OLP) is a chronic mucosal condition commonly encountered in clinical dental practice. Proper history and clinical examination is very important for diagnosis. Incisional biopsy should be done to confirm the diagnosis. For the effective management of OLP, one has a wide range of drugs to choose from. Continuous development in management protocol for OLP is required due to recent increase in the incidence of malignant transformation rate even in the non-risk population group. ACKNOWLEDGEMENT Authors acknowledge the immense help received from the scholars whose articles are cited and included in reference of this manuscript. The authors are 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=183http://ijcrr.com/article_html.php?did=183 Scully C, Carrozzo M. Oral mucosal disease: Lichen planus. Br J Oral Maxillofac Surg 2008; 46:15-21. McCreary CE, Mc Cartan BE. Clinical management of lichen planus. Brit J Oral Maxillofacial Surg 1999; 37(5):338-43. Gorsky M, Epstein JB, Hasson-Kanfi H, Kaufman E. Smoking habits among patients diagnosed with oral lichen planus. Tobacco Induced Diseases 2004; 2(2):103-8. Sousa FACG, Rosa LEB. Perfil epidemiológico dos casos de líquen plano oral pertencentes aos arquivos da Disciplina de Patologia Bucal da Faculdade de Odontologia de São José dos Campos - UNESP. Cienc Odontol Bras 2005; 8(4):96-100. Eisen D, Carrozzo M, Sebastian J-VB, Thongprasom K. Oral lichen planus:clinical features and management. Number V. Oral Dis 2005; 11(6):338-49. Edwards PC, Kelsch R. Oral lichen planus: Clinical presentation and management. J Can Dent Assoc 2002; 68(8):494-9. Mollaoglu N. Oral lichen planus:a review. Br J Oral Maxillofac Surg 2000; 38(4):370-7. Gujjar P, Zingade J, Patil S, Hallur J. Recent Update on Treatment Modalities of Oral Lichen Planus- A Review. IJSS Case Reports and Reviews 2015; 2(4):40-44. Ismail SB, Kumar SKS, Zain RB. Oral lichen planus and Lichenoid reactions; etiopathogenesis, diagnosis, management and malignant transformation. J Oral Sci 2007; 49:89–106. Sumairi B. Ismail, Satish K. S. Kumar and Rosnah B. Zain. Oral lichen planus and lichenoid reactions: etiopathogenesis diagnosis, management and malignant transformation. Journal of Oral Science, 2007; 49(2):89-106. Brown RS, Bottomley WK, Puente E, Lavigne GL. A retrospective evaluation of 193 patients with oral lichen planus. J Oral Pathol Med 1993; 22(5):69-72. Jungell P. Oral lichen planus: a review. Int J Oral Maxillofac Surg 1991; 20(3):129-35.  Katta R. Lichen planus. Am Fam Physician 2000; 61(11):3319-28. Thongprasom, K; Carrozzo, M; Furness, S; Lodi, G (Jul 6, 2011). “Interventions for treating oral lichen planus.”The Cochrane database of systematic reviews (7): CD001168. doi:10.1002/14651858.CD001168.pub2. PMID 21735381. Pynn BR, Burgess KL, Wade PS, Mc Comb RJ. A retrospective survey of 2021 patients referred to the Toronto Hospital Mouth Clinic. Ont Dent 1995; 72(1):21-4. Sahebjamee M, Arbabi-Kalati F. Management of oral lichen planus. Arch Iran Med 2005; 8:252-6. Cheng S, Kirtschig G, Cooper S, Thornhill M, Leonardi-Bee J, Murphy R. Interventions for erosive lichen planus affecting mucosal sites. Cochrane Database Syst Rev 2012; 2: CD008092. Plemons J, Ree T, Zachariah N. Absorption of topical steroid and eva­luation of adrenal suppression in patients with erosive lichen planus. Oral Surg Oral Med Oral Pathol. 1990; 69:42-44. Lu SY, Chen WJ, Eng HL. Response to levamisole and low-dose prednisolone in 41 patients with chronic oral ulcers: a 3-year open clinical trial and follow-up study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998; 86:438-45. Harpenau LA, Plemons JM, Rees TD. Effectiveness of a low dose of cyclosporine in the management of patients with oral erosive lichen planus. Oral Surg Oral Med Oral Pathol Oral Radiol En­dod. 1995; 80:161-67. Stoopler ET, Sollecito TP, DeRossi SS. Oral lichen planus. Upda­te for the general practitioner. N Y State Dent J. 2003; 69:26-28. PMID: 13677863 Tradati N, Chiesa F, Rossi N, Grigolato R, Formelli F, Costa A, et al. Successful topical treatment of oral lichen planus and leukoplakias with fenretinide (4- HPR). Cancer Lett. 1994:76:109-11. PMID: 8149338 Lundquist G, Forsgren H, Gajecki M, Emtestam L. Photochemothera­py of oral lichen planus: A cotrolled study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995; 79:554-58. Eisen D. Hydroxychloroquine sulfate (Plaquenil) improves oral lichen planus: An open trial. J Am Acad Dermatol. 1993; 28:609-612. Falk DK, Latour DL, King LE Jr. Dapsone in the treatment of erosive lichen planus. J Am Acad Dermatol. 1985; 12:567-70. PMID: 3989015 Aghahosseini F, Arbabi-Kalati F, Fashtami LA, Fateh M, Djavid GE. Treatment of oral lichen planus with photodynamic therapy media­ted methylene blue: A case report. Med Oral Patol Oral Cir Bucal. 2006; 11:E126-9. Saawarn N, Shashikanth MC, Saawarn S, Jirge V, Chaitanya NC, Pinakapani R. Lycopene in the management of oral lichen planus: A placebo-controlled study. Indian J Dent Res. 2011; 22:639-643. Chainani-Wu N, Collins K, Silverman S Jr. Use of curcuminoids in a cohort of patients with oral lichen planus, an autoimmune di­sease. Phytomedicine. 2012; 19(5):418-423. Zhang J, Zhou G. Green tea consumption: an alternative approa­ch to managing oral lichen planus. Inflamm Res. 2012; 61:535-9.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareCHANGES IN BIOCHEMICAL COMPOSITION IN THE HAEMOLYMPH OF FIFTH INSTAR LARVAE OF PHILOSAMIA RICINI DURING THERMAL STRESS English3437Shuchita ChandorkarEnglish Shobha ShoucheEnglish JPN PathakEnglishHaemolymph of Philosamia ricini is a water reservoir which maintains homeostasis. When the insect is exposed to stresses naturally then it passes through various changes in biochemical composition. Fifth instar larvae of eri silk worm Philosamia ricini were kept under thermal stress of low and high temperature to observe the changes in carbohydrates, proteins and free amino acids. At high temperature carbohydrates showed a significant increase and a significant decrease at low temperature. Proteins and amino acids showed a significant decrease at high temperature and increase at low temperature. EnglishHomeostasis, Stress, Haemolymph, TemperatureIntroduction It is evident that amino acids, carbohydrates and proteins play an important role to maintain the internal environment of haemolymph in different stages of insect life. They largely affect various metabolic pathways as well as physiological conditions of insect (Edwards, 1982) Three different reviews of Chen (1962, 1966, 1971) provide comprehensive information on the concentration of free amino acids, in the haemolymph of insects. The studies related to the occurrence of proteins and amino acids during the unusual conditions i.e. during the high temperature, desiccation, and low temperature are still very scanty. Recently Malik and Malik (2009) studied the fluctuations in the biochemical composition of silk worm Bombyx mori under the thermal stress. In 2010, Singh et. al. also reported the changes in the certain biochemical composition of fifth instar larvae of Philosamia ricini  when they were exposed to low temperature.      In general pattern the haemolymph is the water reservoir, when water is removed from haemolymph, then the osmotic conditions are disturbed to replace cellular water. The osmotic steady state is maintained by removal of solutes. The various stresses such as deficiency of food, temperature and desiccation may decrease the hemolymph volume,    Albers and Bradley (2004) proposed that in the dehydrated Drosophila melanogaster, osmotic concentration was maintained by reducing the haemolymph volume up to 60% when the dehydration was prolonged. The osmoregulation continued during the period of rehydration and recovery from desiccation. On this basis they concluded that this insect does not require any external source of osmolytes or energy to regulate the osmotic concentration of haemolymph. According to Denlinger and Lee (2010) low temperature affects insects differently based on the severity of cold and duration of exposure. In insects, ions, sugars, proteins, amino acids and other dissolved solutes in haemolymph colligatively depress the melting point by 1.86?C per osmol of solute and protect the insect. Cohen and Patana (1982) reported that in cold stressed larvae of Spoddoptera exigua, haemolymph osmotic pressure is highest as compared to the normal control larvae. There is little change in sodium ion concentration at low temperature but potassium concentration increased significantly. There was a decrease in calcium and magnesium ion concentration in comparison to the control. Delinger and Lee (2010) mentioned that magnitude of chilling injury is closely associated with the loss of ions homeostasis, particularly increase in potassium concentration and decrease in sodium and magnesium concentration in the haemolymph. Similar conclusions were made by Kostal et al (2007) in a bug Pyrrochorus. Wyatt et al. (1955) studied the concentration of sugar, proteins and free amino acids in the silk worm Bombyx mori and other species of insects. The effect of high temperature on haemolymph sugar levels in the three selected races of silk worm was reported by Malik and Reddy (2008). They reared the fifth instar larvae and pupae at two selected temperatures i.e. 31?C and 36?C. At higher temperatures, an increase in blood sugar level and trehalase acitivity was observed in the spinning larvae (Malik and Malik, 2009).They exposed the larvae and pupae to selected temperatures i e. 31?C and 36?C the glucose and trehalose levels increased significantly, and increase was higher at 36?C than 31?C. The protein level of haemolymph was found to be significantly lower in pupal stage as compared to the larval stage. At high temperatures the protein level decreased significantly in larvae as well as in pupae, which was more at 36?C than 31?C. Free amino acids in pupae were higher as compared to the larval haemolymph. At high temperatures it increased significantly, and this increase was higher at 36?C than 31?C.  Thus to maintain osmotic balance during stresses, the insect passes through many changes in solute composition. In the present study we have observed the changes in three important components of haemolymph i.e. carbohydrates, proteins and free amino acids.     Material and Methods 2.1 Control               The worms of Philosamia ricini, were reared under normal conditions i. e. at 29?C ±2?C, R.H. 90%±5% (Pant and Agarwal, 1965). The larvae of Philosamia ricini are voracious feeder, specially fifth instar larvae, and were provided full diet as per recommendation of Sericulture Department. 2.2 Thermal stresses Fifth instar larvae were kept at 36ºC±2ºC, and relative humidity was 90%±5% for three days. Haemolymph was withdrawn on the fifth day for analysis (i.e. they were exposed to high temperature stress for three days). Worms for low temperature stress were kept at 10ºC±2ºC, R.H. 90%±5%, for three days. Thus in both cases, haemolymph was withdrawn on the fifth day for analysis.     Estimation of total carbohydrates                The estimation of carbohydrates was performed by the method of Dubois et al. (1956). Estimation of total Proteins               The total proteins were estimated by the method of Lowry et al. (1951). Estimation of total free amino acids               The free amino acids were analyzed by colorimetric method (Lee and Takahashi; 1966). Results As shown in graph and table (1) the concentration of carbohydrates increased in the fifth instar worms which were reared at high temperature and decreased at low temperature (graph and table 2). The variation was significant. The concentration of proteins decreased at high temperature The decrease in concentration was statistically significant. The worms which were reared at low temperature showed an increase in the concentration of proteins significantly. The free amino acids in the haemolymph of fifth instar larvae decreased at high temperature and increased significantly at low temperature. Discussion Many workers have performed experiments on different insects to observe the effect of temperature. Cohen and Patana (1982) observed the stress related changes in the beet army worm Spodoptera exigua. They were of the opinion that the concentration of carbohydrates decreased due to stress of heat. Malik and Reddy (2009) studied the impact of high temperature in the Bombyx mori and concluded a significant increase in the concentration of glucose and trehalose in the worms reared at high temperature and the increase was higher at 36? C as compared to 31?C. Pant and Gupta (1979) studied the impact of cold stress in the larvae of Philosamia ricini and concluded that the total soluble carbohydrates decrease in the worms when exposed to low temperature. Singh et al. (2010) investigated the impact of low temperature on the fifth instar larvae of Philosamia ricini and concluded that the concentration of total carbohydrates decrease in the haemolymph of worms exposed to low temperature. Thus our observations in Philosamia ricini under the stress of high and low temperature, supports the view of above mentioned workers.  Malik and Malik (2009) studied the impact of high temperature on the concentration of proteins in the haemolymph of fifth instar larvae of Bombyx mori. They kept the worms at two different temperatures i.e. 31?C and 36?C. In their studies, they found a significant decrease in protein concentration of haemolymph. They further reported that the order of decrease was found to be more at 36?C then at 31?C. The concentration of proteins in the haemolymph of fourth instar larvae Spodoptera exigua was higher when exposed to low temperature (Cohen and Patana, 1982). Pant and Gupta (1979) also studied the impact of cold stress in Philosamia ricini and suggested that the increase in concentration of proteins takes place at low temperature. Singh et al. (2010) reported that in Philosamia ricini the concentration of proteins increased when fifth instar larvae were exposed to low temperature.  When worms were reared at high temperature (36?C±2?C), the total protein concentration decreased significantly while at low temperature the protein concentration increased significantly. Therefore, we conclude that due to high temperature the quantity of storage protein decreases while in the worms which were reared at low temperature, the concentration of storage proteins increases.                                             In present study, when the fifth instar worms were reared at high temperature, there was a significant decrease in the amino acid concentration, while the worms which were exposed to low temperature showed a significant increase in concentration amino acids.                      Cohen and Patana (1982) suggested that there was a dramatic increase in the concentration of the total free amino acids in the haemolymph of fourth instar larvae of Spodoptera exigua when exposed to high temperature (40?C) for 20 hours. They also suggested that at low temperature the concentration of total free amino acids decreased significantly when larvae were exposed to 10?C for 20 hours. Pant and Gupta (1979) reported that the concentration of free amino acids increased at low temperature in fifth instar larvae of Philosamia ricini when these larvae were exposed to 2?C. Malik and Malik (2009) reported that the concentration of total free amino acids increased at high temperature which was higher at 36?C than that of 31?C. Singh et al. (2010) suggested that at low temperature the concentration of free amino acids increased significantly when the fifth instar worms of Philosamia ricini were reared at low temperature i e. 10?C. The increase in concentration of total amino acid was about 11 to 29% as compared to the control. Our observations of amino acids in the Philosamia ricini at low temperature were same as reported by Singh et al. (2010). The increase may be due to less consumption of proteins at low temperature. Conclusion The change in concentration of carbohydrate, protein and amino acid was observed at high and low temperature. The concentration of carbohydrate increased at high temperature and decreased at low temperature which may be due to the more and less activity of insect. The protein concentration decreased at high temperature and increased at low temperature due to decrease in storage protein and breakdown of proteins to fight against stresses. Total free amino acids increased at low temperature may be due to less consumption of proteins and decrease at high temperature is due to more excretion through malpighian tubules.  Acknowledgemet We are thankful to the principal of Govt. M.V.M. Ujjain (M.P.) and Sericulture Department, Ujjain (M.P.). We are also thankful to the authors, editors and publishers of articles and journals from where the literature has been taken. Englishhttp://ijcrr.com/abstract.php?article_id=184http://ijcrr.com/article_html.php?did=184 Albers M. A. and  Bradley T. J.  (2004)  Osmotic regulation in adult Drosophila melaogaster  during dehydration and rehydration. J. Exp.  Biol.  207, 2313-2321. Chen, P. S. (1962). Free amino acids in insects. In Amino Acid Pools. Edited by J. T. Holden, 115-138. Chen, P. S. (1966). Amino acid and protein metabolism in insect development. Adv. Insect. Physiol. 3, 53-132.    Chen, P. S. (1971). Biochemical aspects of insects of insect`s development. S. Karger, Basel., pp. 55-56. Cohen, A. C. and Patana, R. (1982). Ontogenetic and stress related changes in the haemolymph chemistry of beet armyworms. Comp. Biochem. Physiol. 71A, 193. 66)   Denlinger, D. L. and R. E. Lee. 2010. Low Temperature Biology of Insects. Cambridge: Cambridge University Press.390pp. Dubois, M., Gilles, K. A., Hamilton, J. K., Rebers, P.A., Smith, F., (1956).  Colorimetric method of determination of sugars and related substances. Analytical chemistry, 28, pp. 350-356. Edwards, H. A. (1982). Free amino acids as regualtors of  osmotic pressure in aquatic insect larvae. J. exp. Biol.       101, 153-160. Kostal V. et al. (2007). Insect cold tolerance and repair of chill injury at fluctuating thermal regimes: role of ion homeostasis. Comp. Biochem. Physilo. A Mol Integer Physiol. 147 (1): 231-242. Lee, Y. and Takahashi, T. (1966). An improved colorimetric determination of amino acids with the use of ninhydrin. Analy. Boichem, vol. 14, pp 71-77. Lowry, O. H. Rosenberg, N.J., Favor A.I. and Remdall, R. J.(1951). Protein measurement with the Folin phenol     reagent. J Biol. Chem. 193: 265-275. Malik, A. and Malik, F.A. (2009). Ontogenic changes in haemolymph biochemical composition in the silkworm, Bombyx mori L under thermal stress.Acad. J. Entomol 2 (1) 16-21: 2009. Malik F. A. and Reddy Y. S. (2008). Effect of high temperature on haemolymph sugar levels in three selected silkworm races. Acta Entomol. Sin. 51(11):  1113-1120. Okasha, A. Y. K. (1967). Effect of sub-letahl temperature on an insect, Rhodnius prolixus. J. Exp. Biol. 48, 475 Pant R, and Agarwal,H. C., (1965). Biochem. J., 96, 824 Pant R., and Gupta, D. K. (1979). The effect of exposure to low temperature on the metabolism of carbohydrates, lipids and protein in the larvae of Philosamia ricini. J. Biosci., Vol.1, 4, pp. 441-446. Singh, A., Sharma, R. K., and Sharma, B.(2010). Low temperature induced alterations in certain biochemical constituents of 5th instar larvae of Philosamia ricini. Insect Physiol. 2: 11-16. Wyatt, G. R., Loughheed, T. C. and  Wyatt, S. S. (1955). The chemistry of insect haemolymph.  J. Gen. Physiol. 39, 853-68. 

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareEFFECT OF GENDER ON THE ANTHROPOMETRIC PARAMETERS OF NEWBORNS OF UDAIPUR DISTRICT English3842Neha VijayEnglish Ghanshyam GuptaEnglishIntroduction: The health and growth of fetus is entirely depending upon the mental and physical health of a mother. Apart from maternal factor one more important infantile factor affects the anthropometric parameters of newborn i.e. the gender of babies. Aim: the aim of study was to know the effect of gender on anthropometric parameters of newborns of Udaipur district of Rajasthan. Method: A Cross sectional study was conducted in the Department of Anatomy, RNT Medical College and Hospitals, Udaipur, Rajasthan, India. All the anthropometric parameters of 1422 newborns were taken from; newborns delivered at Government health institutes of Udaipur district, at Pannadhay Ward of Maharana Bhopal Government Hospital of RNT Medical College and Hospitals. Results: Mean values of Birth weight, Crown Heel Length, Head Circumference, Chest Circumference, Foot Length and Skin Fold Thickness were significantly higher in male. Mean values for Abdominal Circumference, Thigh Circumference, Mid arm Circumference and Calf Circumference was also higher in male; however it was not statistically significant. Conclusion: The anthropometric parameters of newborns revealed a significant difference between male and female newborns. EnglishNewborn, Anthropometric Parameter, GenderIntroduction: The health and growth of fetus is entirely depending upon the mental and physical health of a mother as she is both “Seed as well as the Soil - in which Fetus grows.” Healthy and well nourished mother deliver to a disease free and normal weighed baby. As such infant’s anthropometry is certainly subjected to Psychology and Physical fitness of a mother. Apart from maternal factor one more important infantile factor affects the anthropometric parameters of newborn i.e. the gender of babies. These factors were investigated by many scholars in their studies in different countries. Various studies like Taksande A M et al (2015)1, Ahmed M et al (2014)2, Anupama MP et al (2012)3, Muhammad N et al (2001)4 etc have reached to conclusion that the identification of nutritional status of newborn by the birth weight alone is insufficient for the detection of neonatal risk because weight only gives an assessment of all the tissue together and greater weight does not necessary signifies good growth. It may achieve at the cost of liquid retention or fat deposition. Apart from this demerit of birth weight, it is necessary to determine the additional or alternative anthropometric parameter to assess the nutritional status of both in males and females newborns. That’s why other Anthropometric measurements e.g. Crown Heel Length, Head Circumference, Chest Circumference, Calf Circumference, Thigh Circumference, Abdominal Circumference, Foot Length, Mid Arm Circumference and Skin Fold Thickness measurements of newborns are an important part of Infant Health Surveillance. It can help to detect over weight and underweight, short stature and faltering growth potentially due to underlying medical problems. Therefore, this study introduces the role of anthropometry in Infant’s health conditions and its assessment. Anthropometry is an easy and cost effective technique having following advantages:- Methods are precise and accurate while providing standardized techniques. Procedures are simple, safe, and non-invasive. Equipments required are inexpensive, portable, and durable and can be purchased or arranged locally. Relatively unskilled persons, trained accordingly, can also follow measurement procedures. The method is also suitable representative samples. Material and Methods: Cross sectional study was conducted in the Department of Anatomy, RNT Medical College and Hospitals, Udaipur, Rajasthan, India. 1422 newborns were included in this study delivered at Government health institutes of Udaipur district, at Pannadhay Ward of Maharana Bhopal Government Hospital of RNT Medical College and Hospitals.              Inclusion/ Exclusion Criteria       (A) Inclusion Criteria  : All the singleton pregnancy without any maternal co morbidity affecting newborns anthropometry. Mother should be native resident of Udaipur district willing to participate in this study. Patient who was able to cooperate for the study (B) Exclusion Criteria        All twin babies Intrauterine death and still born babies. Newborns with gross congenital anomalies. Newborns born to mother with conditions affect fetal growth i.e. hypertensive disorder of pregnancy, gestational diabetes mellitus, chronic infections and illness. Newborns whose gestational age would not be accurately assessed greater than 2 weeks difference between obstetrical and clinical assessed Gestational Age. Mother taking treatment which is likely to affect fetal growth Anthropometric measurements of new born, except birth weight were measured by using standard instruments and techniques by investigator personally. Birth weight was taken from hospital record / admission ticket.  Instruments and Methods  Anthropometric measurements of new born, except birth weight were measured by using standard instruments and techniques by investigator personally. Birth weight was taken from hospital record/ admission ticket.  Following instruments and methods were used for measurement of various anthropometric parameters of newborns:-  Crown Heel Length (CHL) : The baby was placed supine on an infantometer. The head is held firmly in position against a fixed upright headboard, while keeping legs of the baby straight and footboard brought into firm contact with the baby’s heels with toes pointing upwards. Length of the baby is measured from a scale, which is set on the board.          Head Circumference (HC): To get the head circumference measured, a flexible non-stretchable fiber glass measuring tape was used. Being the head circumference, the largest dimension around the head (the occipito-frontal circumference) was obtained with tape placed snugly above the ears. The measurement was taken to the nearest 1 mm.  Chest Circumference(CC) : To measure Chest Circumference, a flexible non-stretchable fiber glass measuring tape  was used, which is most suitable to fit the chest more snugly to ensure accuracy,  while placing the same at the level of the nipples during quite respiration The CC was measured to the nearest of 1 mm. Thigh Circumference (TC): At first, Newborn was placed in supine position to take accurate measurement. Flexible non-stretchable fiber glass measuring tape was placed at the level of the lowest gluteal furrow of the left thigh by extending the tape circumferentially. Measurement was recorded to the nearest of 1 mm.  Calf Circumference (CFC): Flexible non-stretchable fiber glass measuring tape was placed at the level of most prominent point in semi flexed position of the left leg by extending the tape circumferentially. Measurement was recorded to the nearest of 1 mm. Abdominal Circumference (AC): Flexible non-stretchable fiber glass measuring tape was placed at the level of umbilicus by extending the tape circumferentially. Measurement was recorded to the nearest of 1 mm.  Foot Length (FL): A Wooden Scale or Flexible Non-stretchable Fiber glass measuring tape, having division of 1mm, was used for the measurement. Wooden Scale or the Tape was fixed against the foot and the length from the heel to the tip of great toe of the left foot was measured to the nearest of 1 mm, after straightening the foot.  Mid arm circumference (MAC): Flexible non-stretchable fiber glass measuring tape was placed at the level of a point halfway down to the left arm between tip of acromion and olecranon process by extending the tape circumferentially. Measurement is recorded to the nearest of 1 mm. Skin Fold Thickness (SFT): Double skin thickness was measured by Thickness Measuring Caliper in the midline of the posterior aspect of the arm over the triceps muscle, at a point halfway down the left arm between tip of acromion and olecranon process. Calipers used were two pronged type with screw adjustment. Slight pressure was applied on a double fold of skin and distance between prongs measured on a millimetre rule with screw adjustment. .Results In present study out of 1422 newborn babies of Udaipur district 785 were males and 637 were females. Mean values of Birth weight, Crown Heel Length, Head Circumference, Chest Circumference, Foot Length and Skin Fold Thickness were significantly higher in male. Mean values of Abdominal Circumference, Thigh Circumference, Mid Arm Circumference and Calf Circumference was also higher in male; however it was not statistically significant. Table: 1: shows the mean values of all the anthropometric parameters taken into consideration showed a high values in male newborns when compared to female newborns. Also show t-test and their p-values. Table: 2: Shows the percentiles (3rd, 50th and 95th) of all the study measurements   Discussion: In present study out of 1422 newborn babies of Udaipur district 785 were males and 637 were females. Gender is one of the important factors which affect the anthropometric parameters of newborns. Various studies led down to conclusion that male newborns are larger than the female newborns so anthropometric parameters of male are greater than the female newborns. Similar findings were observed in present study. Birth weight of male and female newborns in present study was 2750±430 grams and 2630±400 gram respectively. Birth weight of male newborns was found significantly higher in present study similar to study of Ahmed M et al (2014)2. Taksande AM et al (2015)1 and Anupama MP et al (2012)3 also found higher birth weight of male newborns however, it was not found statistically significant. The crown heel length of male and female was 45.14 ±2.06 and 44.62 ±1.92 cm respectively. Crown heel length of male newborns was found significantly higher in present study. Taksande AM et al (2015)1, Ahmed M et al (2014)2, Anupama MP et al (2012)3, Muhammad N et al (2001)4 also found higher crown heel length of male newborns however, it was not found statistically significant. The head circumference of male and female newborns was 33.42 ±1.38 and 33.02 ±1.41 cm respectively. The head circumference of male newborns found significantly higher in present study. Ahmed M et al (2014)2, Anupama MP et al (2012)3 and Muhammad N et al (2001)4 also obtained higher head circumference of male newborns, however, it was not found statistically significant. The chest circumference of male and female newborns was 31.10 ±1.66 and 30.74 ±1.88 cm respectively.  The chest circumference of male newborns found significantly higher in present study. Taksande AM et al (2015)1, Ahmed M (2014)2, Anupama MP et al (2012)3 and Muhammad N et al (2001)4 also obtained higher chest circumference of male newborns, however, it was not found statistically significant. The abdominal circumference of male and female newborns was 28.38.14 ±1.56 and 28.20 ±1.93 cm. respectively.  The abdominal circumference of male newborns found higher in present study, however it was not statistically significant, similar to studies of Anupama MP et al (2012)3 and Muhammad N et al (2001)4. The mid arm circumference of male and female newborns was 10.04 ±1.00 and 09.97± 0.97 cm. respectively.  Mid arm circumference of male newborns was not found significantly higher in present study similar to study of Ahmed M et al (2014)2, Anupama MP et al (2012)3 and Muhammad N et al (2001)4. Taksande AM (2015)1 found mean ±SD 10.1±1.21 and 10.28± 1.38 for male and female newborns respectively which was not matched to our study because of mean values of male newborns were lower. The calf circumference of male and female was 9.99 ±1.13 and 9.93± 1.11 cm respectively. Mid calf circumference of male newborns was not found significantly higher in present study similar to study of Anupama MP et al (2012)3 and Muhammad N et al (2001)4. Taksande AM et al (2015)1 obtained the mid calf circumference 10.55 ±1.27 and 10.61± 1.11 in male and female newborns respectively. It was not similar to our study. Because of higher mean values in females. The foot length of male and female newborns was 7.45 ±.67 and 7.36± .64 cm respectively.  The foot length of male newborns found significantly higher in present study. Ahmed M et al (2014)2 and Muhammad N et al (2001)4 also obtained higher foot length of male newborns; however, it was not found statistically significant. The thigh circumference of male and female newborns was 13.49 ±1.20 and 13.40± 1.22 cm respectively.  Mid thigh circumference of male newborns was not found significantly higher in present study similar to study of Ahmed M et al (2014)2 and Anupama MP et al (2012)3. Taksande AM et al (2015)1 found mean ±SD 14.23±1.90 and 14.44± 1.54 for male and female newborns respectively which was not matched to our study because of mean values of male newborns were lower. Skin fold thickness of male and female newborns was found 4.42±0.65 and 4.26±0.64 respectively. These values were lower than the values of Kaur H et al (2012)5. Alvear J et al (1978)6 found mean values of skin fold thickness 6.1±1.1, 4.3±.9, 4.9±1.1 in Negroes, Europeans and Indian Asians respectively. Values were matched with the values of J. Alvear (1978) in Europeans and Indian Asians population. They did not specify mean values in male and female newborns. Conclusion: The present study was undertaken with the aim to determine the effect of gender on anthropometric parameters among male and female newborns of Udaipur district, showed statistically significant higher mean values of birth weight; crown heel length, head circumference, chest circumference and skin fold thickness in male newborns which is in conformity with the previous studies. Except for the mean values of abdominal circumference, mid arm circumference, thigh circumference and calf circumference were not statistically significant however, it was higher in males. ACKNOWLEDGEMENT This work was undertaken independently and there were no funding sources. 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=185http://ijcrr.com/article_html.php?did=185 Taksande A M, Lakhkar B, Gadekar A. Anthropometric measurements of term neonates in tertiary care hospital of Wardha district. Al Ameen J Med Sci. 2015; 8(2):140-143. Ahmed M, Colaco S M, Ashraf Ali M, Ahmad Z. Birth Weight Status of Newborn and Its Relationship with other Anthropometric Parameters. Int J Med Health Sci. 2014Jan; 3(1). Anupama M.P, Dakshayani K.R. The Study of Distribution of Anthropometric Measurements in South Indian Male and Female Newborns. Anatomica Karnataka2012;6(3):18-23. Muhammad N, Azis N, Guslihan D, Dachrul Aldy T. Correlation between several anthropometric measurements to birth weight. Paediatrica Indonesiana 2001; 41(11-12):288-291. Kaur H, Bansal R. Anthropometric determinants of low birth weight in newborns of Hoshiarpur district (Punjab) - A hospital based study Human Biology Review 2012; 1( 4) :2012 :376-386. Alveor J, Brooke O. Fetal growth in different racial groups.  Arch. Dis. Child. 1978; 53: 27-32 Narendra K S, Madhu G N, Adarsha E. “Relationship of Anthropometric Parameters of Newborn with Varying Period of Gestational Age”. Journal of Evolution of Medical and Dental Sciences 2014 May 19; 3(20): 5484-5490

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241820EnglishN-0001November30HealthcareHISTOPATHOLOGICAL STUDY OF SOFT TISSUE TUMORS (A STUDY OF 140 CASES) IN TERTIARY CARE CENTER English4348Jobanputra G.P.English Parikh U.R.English Goswami H.M.EnglishBackground: Soft tissue tumors are defined as mesenchymal proliferations which occur in the extraskeletal nonepithelial tissues of the body, excluding the viscera, coverings of brain and lymphoreticular system. Soft tissue tumours are a highly heterogeneous group of tumours that are classified on a histogenetic basis according to the adult tissue they resemble Objective: To study the incidence of Soft tissue tumors at Tertiary Care Teaching Hospital and to study the morphological incidence of various Soft tissue tumors among different age groups and sex. Methods: In the Present Study, all operated cases; excised biopsies and resected specimens are taken into consideration. After processing detail microscopic examination was carried out. Results: The peak age of incidence of soft tissue tumors was between 3rd to 4th decades of age, with the male: female ratio 1.37:1. Benign tumors (89.3%) are more common than malignant tumors (10%). Most common soft tissue tumor is Lipomatous tumors. Conclusion: The study can contribute to epidemiologic knowledge of soft tissue tumors. EnglishSoft tissue tumor, Sarcomas, Mesenchymal tumorsINTRODUCTION Soft tissue can be defined as non-epithelial, extra skeletal tissues of the body exclusive of reticulo-endothelial system, glia and supporting tissues of various parenchymal organs. It is represented by voluntary muscles, fat and fibrous tissue, along with the vessels serving these tissues. By convention it also includes the peripheral nervous system because tumors arising from nerves present as soft tissue masses. Embryologically, soft tissue is derived principally from mesoderm, with some contribution from neuroectoderm. Soft tissue tumors are a highly heterogeneous group of tumors that are classified on a histogenetic basis according to the adult tissue they resemble. Lipomas and liposarcomas, are tumors that recapitulate to a varying degree normal fatty tissue; and hemangiomas and angiosarcomas contain cells resembling vascular endothelium.Within the various histogenetic categories, soft tissue tumors are usually divided into benign, intermediate and malignant forms. Benign tumors, which more closely resemble normal tissue, have a limited capacity for autonomous growth. They exhibit little tendency to invade locally and are attended by a low rate of local recurrence following conservative therapy. Malignant tumors, or sarcomas, are locally aggressive and are capable of invasive or destructive growth, recurrence, and distant metastasis. Radical surgery is required to ensure total removal of these tumors. Some sarcomas, such as dermatofibrosarcoma protuberans, rarely metastasize. It is important to qualify the term sarcoma with a statement concerning the degree of differentiation or the histologic grade. Usually, well-differentiated sarcomas are low-grade lesions, whereas poorly differentiated sarcomas are high-grade neoplasms. There are also borderline lesions for which it is difficult to determine the malignant potential. The annual incidence of soft tissue tumor is 1.4 per 100000 population5. Soft tissue sarcomas account for 15% of all childhood cancers5, which is the fourth most common malignancy in children, after hematopoietic neoplasm, neural tumor and wilms tumor4. Benign tumors outnumber malignant ones by margin of 100:11.Soft tissue sarcomas occur more commonly in males, but gender and age-related incidences vary among the histologic types. There is also no proven racial variation. The use of ancillary techniques like immunohistochemistry, electron microscopy flow cytometry and cytogenetics, has increased insight into the tumor biology and has provided tools for greater diagnostic accuracy. Yet the foundation of these newer techniques rests upon the histologic diagnosis made on light microscopic evaluation of hematoxylin and eosin stained sections and use of special stains. AIMS AND OBJECTIVES The study is undertaken with the following aims and objectives: To study the occurrence of soft tissue tumors in relation to age, sex and anatomical site. To study frequency of occurrence of benign and malignant soft tissue tumors. To analyze the various types and subtypes of soft tissue tumors. To find out the incidence of benign and malignant soft tissue tumors. To assess the relative frequency of soft tissue tumors. MATERIALS AND METHODS The operated specimens or biopsy material of soft tissue tumors received from September 2014, to July, 2015 in the Department of Histopathology of our hospital, were studied in detail. Total 140 cases were collected. In this study we have included only mesenchymal lesions originating in soft tissue. Intraabdominal and retroperitoneal lesions were also included when the lesions were not thought to originate in bowel or abdominal viscera. Thorough gross examination of each specimen was performed. From received surgical specimens representative areas of tissue were taken and submitted to routine tissue processing and paraffin embedding. Hematoxylin and Eosin staining was performed in all cases. After staining thorough microscopic examination was performed to made diagnosis. Detail analysis of results is carried out. Special stain are also used in diagnosis of histological types and subtypes like Phosphotungstic acid haematoxylin  (PTAH), Trichrome stains, Reticulin stain, Alcian blue, Periodic acid Schiff reaction (PAS) etc. OBSERVATIONS AND RESULTS The present study is done by examining surgically removed soft tissue tumor specimens submitted in the Department of Pathology at tertiary Care teaching Hospital. Total 140 cases were included in this study. The results of this study are as follows:  Majority (90%) of the soft tissue tumors were benign in nature, whereas 9% were malignant and 2% were intermediate in nature. Out of total 140 cases in this study, 42% were Male and 58% were female patients. Most common soft tissue tumors were Lipomatous in nature in either sex. There is no sex wise major difference in majority of soft tissue tumors. Second most common tumor are smooth muscle tumor (leiomyoma) most commonly found in female in present study. In this study, age of study subjects were ranging from 0 to 70 years. Peak incidence of the tumors were in the age group of 31 to 40 years (36 cases, 25%), followed by 21 to 30 years (24 Cases, 17.1%). Incidence of tumors were found decreased in both the extreme of age group which are in the 0 to 10 years (11 Cases, 7.9%) and 61 to 70 years (11 Cases, 7.9%). This is 3 dimensional column diagram showing age wise distribution of nature of tumors. The results of this study are : In the age group of 21 to 30 years  ( 24 Cases), all the tumors were found benign, where as in the other age group also around three fourth tumors among each age group were found benign in nature. However intermediate nature of tumors were also found 2.8% and 5.6% in 31 to 40 years and 51 to 60 years age group respectively. Highest number of malignant nature were found in the 51 to 60 (5 Cases, 27.8%) years of age group. It shows chances of malignancy are more in advancing age group. In this study, around one third of the soft tissue tumors were found in the head and neck region(29.2%), followed by Genital tract(25.7%) and (upper limb (15.8%). Soft tissue tumors were also found in other regions like lower limb, Back, CNS, GIT, Abdomen but in lower incidence . Majority of the soft tissue tumors in this study found lipomatous in nature. So lipomatous tumors were the most common benign soft tissue tumor followed by smooth muscle tumor. In the malignant tumors, stromal tumors and fibrous tumors were the most common variety in this study. Whereas intermediate tumors found rarely (2 cases) in this study as a tumor of blood and lymph vessels. DISCUSSION Soft tissue can be defined as non-epithelial, extra-skeletal tissues of the body exclusive of the reticulo-endothelial system, glia and supporting tissues of various parenchymal organs. In the present study, a total 140 cases of soft tissue tumors received in September 2014, to July, 2015 in the Department of Pathology at tertiary Care teaching Hospital. In the study of Mirza et al (2005)4the incidence rate of Benign tumor was 82 %, as in compare to present study 89 %, whereas the incidence rate of malignant tumors is found decreased which is 10.7% in present study as compared to 18% in the study of Mirza et al (2005)4. In the study of Mirza et al (2005)4 the ratio of Benign : Malignant is 4.70 : 1, where as in present study the ratio found 8.3 : 1,which is higher as compared to previous study. The difference found in the result is might be due to recent newer advance technique of diagnosis, tumor can be detected at very early stage.          Average age of occurrence of benign tumor in the study of Mirza et al (2005)4 is 29.2 years, which is in present study 32.1 years, found similar. Whereas the average age of incidence of malignant tumor found highly increased in present study which is 55.6 years as compared to previous study of Mirza et al (2005)4 it was 37.8 years.  The ratio of M: F found of benign and malignant is similar in the study of Mirza et al (2005)4 and in the present study. In the present study, fibrous tumors comprised fifth most common tumor among all soft tissue tumors. Fibrous tumors accounted for 11 cases that comprised 7.9% of all soft tissue tumors. The sex and site of fibrous tumors in the present study are comparable with those studies of the Mirza et al (2005) 4and of Kransdorf’s study8,9,(1995).       In the present study adipose tissue tumors constituted, the commonest soft tissue tumor accounting for 50 % of all soft tissue tumors. The  male to female ratio of 1.34: 1 showing a male predominance.       These findings are in good correlation with most of the study reported in literature of Mirza et al (2005)4, Kransdorf et al 8,9,1995 and Enzinger and Weiss 16,17.   In present study, 22 cases (17.6%) were benign in nature and 2 cases (13.3%) were malignant. Total 24 cases comprised 17.14 % of all soft tissue tumors in this study. These finding are similar to the study of Mirza et al (2005)4 in which Hemangiomas were second most common among benign tumors constituting 20 cases accounting for 17.69% of all benign soft tissue tumors. These findings are also very similar with the studies reported by Kransdorf (1995)8, 9.  In the present study benign-malignant ratio is 8.3: 1 while in the study of Mirza et al (2005)4, benign-malignant ratio of 4.70:1. This is due to the fact that many benign tumors such as lipoma and hemangioma do not undergo biopsy as compared to sarcoma, which come to medical attention quite early11.  However, in Kransdorf (1995)8, 9 study there were increased numbers of malignant tumors, because of the difficult cases being referred to the speciality Centre.  In the present study benign tumors comprised 89% and malignant tumor comprised 10.7% among all tumors. Where as in the study of Mirza et al (2005)4, soft tissue sarcomas accounted for 2.8% of all malignant neoplasms.   In the present study benign soft tissue tumors occurred in second and third decade of life, which is similar to the study conducted by Mirza et al(2005)4,where majority of benign soft tissue tumors occurred in second, third, fourth and fifth decade of life, which were also similar with the literature of Enzinger and Weiss 11 In the present study majority of malignant soft tissue tumors occurred in fifth decade of life where is in the study of Mirza et al4, majority of malignant soft tissue tumors occurred in third, fourth and sixth decade of life. CONCLUSION A good clinical acumen, through description and grossing of specimen, and microscopic evaluation of hematoxylin and eosin stained sections are fundamental aspects in diagnosis of soft tissue tumors. Majority of tumors diagnosed by hematoxylin and eosin stained sections. Painless mass was the most common presenting symptom in our study. Benign soft tissue tumors (89.3%) outnumbered malignant tumors (10%) by a ratio of 8.3:1. In our study Male: Female ratio-1.37:1. In benign soft tissue tumor Male: Female ratio -1.4:1 and in malignant soft tissue tumor Male: Female -1.14:1 in our study. First most common soft tissue tumor are Lipomatous tumors among the all soft tissue tumor. Benign lipomatous tumor is the most common tumors in present study. Most common site soft tissue tumor found in Head neck region in present study. Most common age of soft tissue tumor in 3rd to 4th decade of life. Malignant tumors are 10% reported, most common tumors are stromal tumor (GIST) 75% and most common site in GIT (Stomach) in present study. Second most common tumor are leiomyomas (30 cases) of gynecological origin were tumor to be reported. Leiomyoma most commonly reported in age (4th and 5th decade of life) after menopause. In these study 2 cases of intermediate type of soft tissue tumor - epithelioid hemangioendothelioma are found which are rare. ACKNOWLEDGEMENT The author acknowledges the help received from Professor and Head, Department of Pathology for teaching me the scientific approach of the subject and its subtle aspects, I am also thankful to my PhD Guide for motivating me for doing the work meticulously and her kind co-operation. I would like to give my special thanks to all the technicians of Histopathology Section, for helping me while conducting the present study. Last but not least 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. NOTE : The present study was undertaken at Tertiary Care Teaching Hospital, Gujarat to know the occurrence of different types of soft tissue tumors. In the Present Study, all operated cases; excised biopsies and resected specimens are taken into consideration. Biopsies and whole tumors specimens were taken from admitted patients in different wards of our institute, which are with prior consent of the patients. Ethical committee clearance has not been required as confidentiality of patient’s details has not been published. Englishhttp://ijcrr.com/abstract.php?article_id=186http://ijcrr.com/article_html.php?did=186 Arch Patho Lab Med .2006; 130:2006; Histopathology. 2006; 48:42. Brooks JJ, Perosio PM: Adipose tissue.  Histology for pathologists, 2ndedn. Philadelphia: Lippincott-Raven; 1997:167. Fletcher CDM, Unni K, Mertens K, eds. WHO Classification of Tumours. Pathology and Genetics. Tumors of Soft Tissue and Bone. Lyon: IARC Press; 2002. Mirzaasif Baig et al, Histological study of soft tissue tumor,  2005: 1039-1049Enzinger  and Weiss’s Soft Tissue Tumors; 5th Edi. Rosai J. Soft tissues. Chaper-25 In: Rosai and Ackerman’s Surgical Pathology, Vol. 2, 9th Edition, Mosby. 2004: 2237-2372. Rosenberg AE. Bones, Joints and Soft Tissue Tumors. Chapter-26 In: Robbins and Cotran Pathologic Basis of Disease by Kumar, Abbas and Fausto, 7th Edition, Saunders: Elsevier, 2004; 1273-1324. Nnodim JO: Development of adipose tissues.  Anat Rec 1987; 219:331. Kransdorf MJ. Malignant soft tissue tumors in a large referral population: Distribution of diagnosis by age, sex and location. Am J Roentgenol. 1995; 164: 129.  Kransdorf MJ. Benign soft tissue tumors in a large referral population: Distribution of specific diagnosis by age, sex and location. Am J Roentgenol. 1995; 164: 395 Sternberg’s Diagnostic Surgical Pathology, Mills et.al, Lippinccot Williams and Wikkins, 4th Ed. 2004 Weiss SW, Goldblum JR. General Considerations. Chapter-1 In: Enzinger and Weiss’s Soft Tissue Tumors. 4th Edition, St. Louis: Mosby, 2001: 1-19. Weiss SW, Goldblum JR. Approach to diagnosis of soft tissue tumors. Chapter-7 In: Enzinger and Weiss’s Soft Tissue Tumors, 4th Edition, St. Louis: Mosby, 2001: 189-198 Weiss SW, Goldblum JR. Benign fibrohistiocytic tumors. Chapter-13 In: Enzinger and Weiss’s Soft Tissue Tumors, 4th Edition, St. Louis: Mosby, 2001: 441-490. Weiss SW, Goldblum JR. Malignant fibrohistiocytic tumors. Chapter-15 In: Enzinger and Weiss’s Soft Tissue Tumors. 4th Edition, St. Louis: Mosby, 2001: 535-569. Weiss SW, Enzinger FM. Myxoid variant of MFH. Cancer. 1977; 39: 1672. Weiss SW, Goldblum JR. Benign lipomatous tumors. Chapter-16 In: Enzinger and Weiss’s Soft Tissue Tumors. 4th Edition, St. Louis: Mosby, 2001: 571-639. Weiss SW, Goldblum JR. Liposarcoma. Ch Weiss SW, Goldblum JR. Liposarcoma. Chapter-17 In: Enzinger and Weiss’s Soft Tissue Tumors. 4th Edition, St. Louis: Mosby, 2001: 641-693.