Archives details

Accessory parotid glands are an occasional islet of parotid tissue separate from the main parotid gland, lying anteriorly just above the commencement of the parotid duct. They are found in 20% of general population. Though accessory parotid gland draining by a ductule in to the main parotid duct is a common finding, accessory parotid gland draining by a separate duct is a rare occurrence. We present the imaging findings in a case of left accessory parotid gland with a prominent duct of its own which was communicating with main parotid duct with a calculus at their junction

1. Frommer J. The human accessory parotid gland: its incidence, nature, and significance. Oral Surg. Oral Med. Oral Pathol. 1977;43 (5): 671-6. Pubmed citation 2. Ramachar SM, Huliyappa HA. Accessory parotid gland tumors. Ann Maxillofac Surg. 2012; 2 (1): 90-3. doi:10.4103/2231-0746.95334 - Free text at pubmed -Pubmed citation 3. Skandalakis LJ. Surgical Anatomy. P.M.P. ISBN: 9603990744. Read it at Google Books - Find it at Amazon 4. Standring S. Gray's anatomy. 39th edn. Edinburgh: Elsevier Churchill Livingstone; 2005. Neck and upper aerodigestive tract-Development of the face and neck; p. 613. 5. Currarino G, Votteler TP. Lesions of the accessory parotid gland in children. Pediatr Radiol. 2006;36:1–7.[PubMed] 6. Afify SE, Maynard JD. Tumours of the accessory lobe of the parotid gland. Postgrad Med J. 1992; 68 (800): 461-2. Free text at pubmed - Pubmed citation 7. Toh H, Kodama J, Fukuda J et-al. Incidence and histology of human accessory parotid glands. Anat. Rec. 1993; 236 (3): 586-90. doi:10.1002/ar.1092360319 -Pubmed citation 8. Witt RL. Salivary Gland Diseases. Thieme. (2011) ISBN: 1604065370. Read it at Google Books - Find it at Amazon

Introduction: Leprosy (Hansen’s disease, hanseniasis) is a chronic infectious disease caused by Mycobacterium leprae, affecting the peripheral nervous system, the skin, mucous membranes and occasionally other tissues. In leprosy patients, disabilities involving hands, feet, eyes, face are seen. Deformities of hands include ulcers, cracks, scars, blisters, claw hand, wrist drop, dactylitis, contractures of fingers, resorption of fingers, stiff joints. Defomities of feet include ulcers, cracks, scars, blisters, foot drop, claw toes, resorption of toes, contracture of tendo achilles, equinovarus deformity. Aims and Objectives: To study the various factors associated disabilities of hands and feet among leprosy patients reported in a tertiary care center. Material and Method: The present study was conducted in the Post Graduate Department of Dermatology, Venereology and Leprology, Government Medical College, Jammu from November 2012 to October 2013. All patients clinically diagnosed as cases of leprosy both old and new registered in the hospital were included in the study. A detailed history was taken regarding the age, sex, occupation, education, duration of disease, reactional states, treatment status, past history and family history. Complete clinical examination of each patient was performed with respect to skin lesions, nerve involvement and distribution, site, symmetry, type and grading of disability of hands and feet. Results: It was observed that out of total 150 patients, 93 (62%) were diagnosed to be with disability. Among the newly diagnosed patients, 57.97% were disabled whereas among the on treatment patients 64% were disabled. Mean age was 40.22±13.15 years. The male to female ratio for disability was 4.2:1. Maximum number of disabled patients was seen among manual labourers (farmers and labourers) and housewives. Disability was more common among illiterates (73.33%) as compared to literate patients (45%). It was observed that as the duration of disease increases and registration was delayed, the proportion of disabled was increased. Disability rate was increased with increasing number of nerves involved. All the patients with histoid and polyneuritic leprosy were disabled. Disability among lepromatous leprosy and borderline lepromatous leprosy was seen in 89.29% and 75.61% respectively. Conclusion: Thus from the above results we conclude that increasing age, male sex, manual labourers and illiterates were common demographic factors associated with disabilities of hands and feet among leprosy patients. It was also seen that delay in registration, increase in duration of disease and increasing number of nerves involved were common reason for disability. Disability is common in lepromatous leprosy and borderline lepromatous leprosy.

1. Jopling WH and Mac Dougall AC. Defination, epidemiology and world distribution. In:Jopling WH, Mac Dougall AC, ed. Handbook of Leprosy, New Delhi (India).CBC publishers and distributors,5th edition,1995,p.1-8. 2. Thorat DM, Sharma P. Epidemiology. In: Hemanta Kumar Kar and Bhushan Kumar, ed. IAL textbook of Leprosy, Ist edition, New Delhi, Jaypee Brothers Medical Publishers 2010, p.24-31. 3. Rahman F, Murtaza G, Abbasi P, et al. Deformity and Disability index in patients of leprosy in Larkana region. Journal of Pakistan Association of Dermatologists 2008;18:29-32 4. Singhi MK, Ghiya BC, Gupta D, et al. Disability rates in leprosy. Indian J of Dermatol Venereol Leprol 2004; 70(5):314-316. 5. Palit A, Ragunatha S, Inamadar AC. History taking and clinical examination. In: Hemanta Kumar Kar and Bhushan Kumar, ed. IAL textbook of Leprosy, Ist edition, New Delhi, Jaypee Brothers Medical Publishers 2010, p.137-138. 6. Malaviya GN. Deformity/Disability Prevention. In:Hemanta Kumar Kar and Bhushan Kumar, ed. IAL textbook of Leprosy, Ist edition, New Delhi, Jaypee Brothers Publishers 2010,p.449-450. 7. Brandsma and Brakel V. WHO disability grading: operational definations. Lepr Rev(2003)74,366-373 8. Selvaraj G, Prabhakar N, Muliyil J, et al. Incidence of disabilities among multibacillary cases after initiation of multidrug therapy and factors associated with the risk of developing disabilities. Indian J Lepr 1998; 70 suppl: 11s-16s. 9. Saha SP and Das KK. Disability pattern amongst leprosy cases in an urban area (Calcutta). Indian J Lepr 1993 Jul-Sep 65(3) 305-314. 10. Noor SM, Paracha MM, Ali Z, et al. Frequency of disabilities in newly diagnosed patients of leprosy presenting to Lady Reading Hospital, Peshawar. Ann Pak Inst Med Sci 2010; 6(4):210-213. 11. Van Brakel, Sihombing B, Djarir H et al. Disability in people affected by leprosy: the role of impairment, activity, social participation, stigma, discrimination. Glob Health Action 2012, vol.5. 12. Thappa DM, Kaur S, Sharma VK. Disability index of hands and feet in patients attending an urban leprosy clinic. Indian J Lepr 1990 Jul- Sep; 62 (3):328-337. 13. Girdhar M, Arora SK, Lal M, et al. Pattern of disabilities in Gorakhpur (UP). Indian J Lepr 1989 Oct; 61(4)503-513. 14. Htoon MT and Win Z. Disabilities among rural leprosy patients in Myanmar. Int J Lepr Other Mycobact Dis 1994, 62(1); 567-9. 15. Schreuder PA. The occurrence of reactions and impairments in leprosy: experience in the leprosy control program of three provinces in northeastern Thailand, 1987-1995. Neural and other impairments. Int J Lepr Other Mycobact Dis 1998; 66:170-81. 16. Sow SO, Tiendrebeogo A, Lienhardt C, et al. Leprosy as a cause of physical disability in rural and urban areas of Mali. Sante. 1998 Jul-Aug: 8(4):297-302. 17. Solomon S, Kurian N, Ramads P. Incidence of nerve damage in leprosy patients treated with MDT. Int J Lepr 1998; 66(4):451-6. 18. Srinivasan H. The problem and challenge of disability and rehabilitation in leprosy. Asia Pacific Disability Rehabilitation Journal 1998; 9(1). 19. Sarkar J, Dasgupta A, Dutt D. Disability among new leprosy patients, an issue of concern: Indian J Dermatol Venereol Leprol 2012(78):3; 328- 334. 20. Kumar R, Singhasivanon P, Sherchand JB et al. Gender difference in socio-epidemiological factors for leprosy in the most hyper-endemic district of Nepal. Nepal Med Coll J; 2004 Dec, 6(2):98-105. 21. Norman G, Bhushanam JDRS and Samuel P. Trends in Leprosy over fifty years in Gudiyatham Taluk, Vellore, Tamilnadu. Indian J Lepr. 2006; 78: 167-185. 22. Arora M, Katoch K, Natrajan M, et al. Changing profile of disability in leprosy patients diagnosed in a tertiary care centre during years 1995- 2000. Indian J Lepr (2008) 80;257-265 23. Bhat RM and Chaitra P. Profile of New Leprosy Cases Attending a South Indian Referral Hospital in 2011-2012. ISRN Tropical Medicine 2013, 4 pages. 24. Richardus JH, Meima A, Croft RP et al. Case detection, gender and disability in leprosy in Bangladesh: a trend analysis. Lepr Rev 1999; 70: 160-173. 25. Patel P and Chavan LB. Epidemiology of disability in incident leprosy patients at supervisory urban leprosy unit of Nagpur city. National Journal of Community Medicine 2011;2(1):119-122 26. Saha SP and Das KK. Disability pattern amongst leprosy cases in an urban area (Calcutta). Indian J Lepr 1993 Jul-Sep 65(3) 305-314. 27. Jain PK, Tripathi D, Singh CM, et al. A study of high disability rate among leprosy affected persons in Gwalior district. Indian Journal of Community Health 2011, Jul-Dec; 23(2). 28. Nicholls PG, Croft RP, Richardus JH, et al. Delay in presentation, an indicator for nerve function status at registration and for treatment outcome- the experience of Bangladesh acute nerve damage study cohort. Lep Rev (2003) 74, 349-356. 29. Sehgal VN and Sharma PK. Patterns of deformities/disabilities in urban leprosy. Indian J. Lepr. 57(1985) 183-197. 30. Kalla G, Kachchawa D, Salodkar A. Disabilities in leprosy. Int J Lepr 2000; 68(2):182-4. 31. Kumar A, Girdhar A, Girdhar BK. Nerve thickening in leprosy patients and risk of paralytic deformities: A field based study in Agra,India. Lepr Rev(2004)75,135-142. 32. Moschioni C, Antunes C, Grossi M, et al. Risk factors for physical disability at diagnosis of 19,283 new cases of leprosy. Rev Soc Bras Med Trop vol.43 no.1 Uberaba Jan/Feb, 2010. 33. Tiwari VD, Mehta RP. Deformities in leprosy patients of Indian Armed Forces treated/reviewed at Military Hospital Agra (a retrospective study). Lepr India 1981, Jul;53(3):369-78. 34. Kaur P and Singh G. Deformities in leprosy patients attending urban leprosy clinic at Varanasi. Indian J Lepr, 1985 Jan-Mar; 57(1):178-182. 35. Reddy BN and Bansal RD. An epidemiological study of leprosy disability in a leprosy endemic rural population of Pondicherry (South India). Indian J Lepr 1984 Apr- Jun; 56(2):191-198. 36. Hasan S. A survey of leprosy deformities among the patients of Hyderabad city. Lepr India 1977, Jul (49):3; 393-399. 37. Zhang G, Li W, Yan L, et al. an epidemiological survey of deformities and disabilities among 14257 cases of leprosy in 11 countries. Leprosy Review (1993)vol 64,143-149.

150 patients of either sex scheduled for elective surgery were included in the study. All patients were aged more than sixteen years and belonging to ASA PS- 1/ 2. All the patients were assessed preoperatively by modified mallampati test and upper lip bite test. Difficult tracheal intubation was graded on Cormack Lehane scale. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy were calculated. Conclusion: Modified Mallampati test is a better test at predicting difficult endotracheal intubation when compared to upper lip bite test.

1. Zahid Hussain et al. a comparison of the upper lip bite test with modified mallampati classification in predicting difficulty in endotracheal intubation. Anaesthesia and Analgesia 2003; 96:595-599. 2. William H Rosenblatt. Clinical Anaesthesia. IVth Ed; 614-615. 3. S. R. Mallampati. A clinical sign to predict difficult tracheal intubation: A prospective study. Canadian anaesthetic Society Journal 1985; 32: 429-434. 4. H. E. Wilson. Predicting difficult intubation. Br J Anaesth 1988; 61: 211-216. 5. Jimson C Tse. Predicting difficult endotracheal intubation in surgical patients scheduled for general anaesthesia. A prospective blind study. Anaesthesia and Analgesia 1995; 81: 254-258. 6. C. M. Frek. Predicting difficult intubation. Anaesthesia 1991; 46: 1005-1008. 7. R. S. Cormack, J Lehane. Difficult endotracheal intubation in obstetrics. Anaesthesia 1984; 39: 1105-1111. 8. Lloyd F, Redick. The temperomandibular joint and tracheal intubation. Anaesthesia and Analgesia 1987; 66: 675-676 9. Abdel Raouf et al. preoperative airway assessment. Predictive value of a multivariate risk index. Anaesthesia and Analgesia 1996; 82: 1197-1204 10. Keyvan Karkouti et al. Interobserver reliability of the tests used for predicting difficult intubation. Can Jof Anaesth 1996; 43: 554-559 11. Al Ramadhani. Sternomental distance as the sole predictor of difficult laryngoscopy in obstetric anaesthesia . Br J Anaesth 1996; 77: 312-316 12. Oates J D. comparison of two methods for predicting difficult intubation. Br J Anaesth 1991; 66: 305-309 13. Yamamoto, Tsubokawa. Predicting difficult intubation with indirect laryngoscopy. Anaesthesiology 1997; 86: 316-321 14. Arne J, Descoins. Preoperative assessment for difficult intubation in general and ENT surgery: predictive value of a clinical multivariate risk index. Br J Anaesth 1998; 80: 140-146 15. Savva D. Prediction of difficult intubation. Br J Anaesth 1994; 73: 149-153 16. Bilgin H. screening testd for predicting difficult intubation: a clinical assessment in Turkish patients. Anaesth Intensive Care 1998; 26: 382-386 17. R Bhat, S Mishra, A Badhe. R Bhat. Comparison of upper lip bite test and modified mallampati classification in predicting difficult intubation. The Internet Journal of Anaesthesiology 2013; Vol 19: Number 1

Background: There are very few recent studies regarding the diagnostic categories in prisoners with psychiatric disorders in the Indian setting. Methodology: The study was conducted on 50 prisoners admitted to a closed prisoner’s ward. The patient’s history was recorded and their mental status examination was done. The Kuppuswamy’s socio-economic scale and the MINI Plus were administered to the patient. The diagnostic categorization of the prisoners was done according to ICD-10 research criteria. Results: There were 46 males and 4 female prisoners. Out of the 46 male prisoners, 14 were convicted and 32 were under-trial and all the four females were under-trial. 46 males and 4 female prisoners were evaluated and most were from the lower socioeconomic class and rural areas. Schizophrenia, bipolar affective disorder-mania, major depressive disorder, and psychotic disorder NOS, psychotic disorder due to general medical condition and psychosis with mental retardation were the main diagnostic categories observed. The most common diagnostic category was schizophrenia in both males and females prisoners. Murder, attempt to murder, rape, kidnapping, grievous injury and theft were the crimes committed by the prisoners. Murder was the most common crime committed by both male and female prisoners. Most prisoners with violent crimes (murder) had a diagnosis of schizophrenia. Conclusion: This has implications for mental health services, training of mental health professional research and policy in forensic psychiatry in the Indian setting.

1. Brenda Wright, Dearbhla Duffy, Katheriene Curtin, Sally Linehan Stephen Monk, Harry and Kennedy. Psychiatric Morbidity among women prisoners newly committed and amongst remanded sentenced women in the Irish prison system. Ir J Psych med 2006; 23(2):47-53. 2. Ruzanna Zamzam, S. Mohamed Hatta. Specific Psychiatric disorders among, convicted female offenders in Malaysian prison. Malaysian Jr. of Psychiatry, March 2000, Vol. 8 No.1:34-42. 3. Brooke D, Taylor L, Gunn J, Maden A. Point Prevalence of Mental disorder in unconvicted male prisoners in England and Wales. Comment in: BMJ 1996 Dec.14; 313(7071):1497-8, BMJ 1999 Sep.25; 319(7213); 853. BMJ 1996 Dec.14; 313(7071); 1524-7. 4. Fazel S, Danesh J. Serious mental disorder in 23000 prisoners: a systematic review of 62 surveys. Lancet. 2002 Feb16; 359(9306):545-50. Comment in Lancet. 2002 Aug 17; 360(9332):572-3; author reply 573. 5. The ICD-10 Classification of Mental and Behavioural Disorders; Diagnostic criteria for research. World Health Organization, Geneva. 6. Kuppuswamy’s socioeconomic status scale. Revised version 2011. 7. Sheehan D.V and Lecrubier Y. MINI International Neuropsychiatric Interview. English version 5.0.0 (January 1, 2004). 8. Somsundaram O. Crimes of person with affective disorders. Indian J. Psychiat. 1977; 19, 60-62. 9. Somsundaram O. Guilty but Insane. Some aspects of Psychotics crime. Indian J. Psychiat. 1960; 2:81. 10. Bearcroft. J. Psychiatric referrals from courts and prisons. Brit. Med. J. 1965; 2:1519. 11. Taylor P J, Parrott J M. Elderly offenders. A study of age related factors among custodially remanded prisoners. Br. J. Psycriatry 1988 Mar; 152: 340-6. 12. Fazel S. Grann M. Older criminals: a descriptive study of psychiatrically examined offenders in Sweden. Int J Geriatr Psychiatry 2002 Oct; 17(10):907-13. 13. Driessen M, Schroeder T, Widmann B, Von Schonfeld LE, Schneider F. Childhood trauma, Psychiatric Disorders and criminal behavior in Prisoners in Germany ; a comparative study in incarcerated women and men. J Clin Psychiatry 2006 Oct; 67(10):1486-92. 14. Coid J W. Personality disorders in prisoners and their motivation for dangerous and disruptive behavior. Crim Behav Ment Health. 2002; 12(3); 209-26. 15. Jha B. K. A study of the Nature of the Criminal Offences of Mental Patients. Indian J. Psychiat. 1971; 10:166-76. 16. John Lanzkron, MD. Murder and insanity: A Survey. Am. Jr. Psychiatry 1963; 119:754-58. 17. Eric. B. Elbogen, PhD; Sally C. Johnson, MD. The Intricate Link Between Violence and Mental Disorder. Arch Gen Psychiatry. 2009; 66(2):152-61. 18. Louise Arseneault, Terrie E. Moffitt, Avshalom Caspi, Pamela J. Taylor, Phil A. Silvia. Mental disorder and violence in a total birth cohort. Arch Gen Psychiatry.2000;57:979-86 19. Gottfredson, Michael R and Travis Hirschi. A General Theory of Crime. Stanford, CA: Stanford University Press. 20. Sutherland E and Cressey D. Principles of Criminology, Bombay, The times of India press.

Background: Pulmonary function tests are of significance in assessing the functional status of lungs in different individuals exposed to varied conditions and to predict the clinical outcome. Aims: The study has been conducted to evaluate and explain the effects of different lifestyle conditions including the sedentary life style, smoking and yoga exercises on the functioning of the lungs and to signify the importance of regular exercise and to quit smoking to improve the health. Settings and Design: This study was conducted in clinical lab of physiology department on 30 healthy male sedentary non-smoker subjects, 30 healthy male sedentary smoker subjects and30 healthy male ex-smoker Yogis in the age range of 21 to 30 years. Materials and Methods: Five spirometricparameters were used to evaluate the pulmonary function and differences between groups. Lung Function Test was performed using– computerized spirometer“Medspiror”. All the values were recorded and comparison tables were derived after statistical analysis using SPSS statistical software version 20.0 and the results were analyzed. Results and Conclusion: The Pulmonary Function values derived were compared between the study groups. In the present study the ex-smoker Yogis group was having higher mean value of FVC, FEV1, FEV1/FVC, PEFR, and MVV as compared to sedentary smoker and sedentary non-smoker group. Smoker group has significantly less mean values for the lung function variables compared to other two groups. The ex-smoker yogis has higher mean values than sedentary groups suggesting that regular Yoga exercises has improved lung function after cessation of smoking.

1. A report of the Surgeon General. 43. Preventing tobacco use among young peopleUS Department of Health and Human Services. Public Health Service, Center for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office of Smoking and Health. 1994 2. Aaron DJ, Dearwater SR, Anderson R, Olsen T, Kriska AM, Laporte RE. Physical activity and the initiation of high-risk health behaviors in adolescents. Med Sci Sports Exerc 1995; 27: 1639–1645. 3. Anthonisen NR, Skeans MA, Wise RA, Manfreda J, Kanner RE, Connett JE: The effects of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial. Ann Intern Med 2005, 142:233-239. 4. Biersteker MW, Biersteker PA. Vital capacity in trained and untrained healthy young adults in the Netherlands. Eur J ApplPhysiol 1985; 54: 46–53. 5. Doherty M, Dimitriou L. Comparison of lung volume in Greek swimmers, land based athletes, and sedentary controls using allometric scaling. Br J Sports Med 1997; 31: 337–341. 6. Fletcher C, Peto R, Tinker C. The natural history of chronic bronchitis and emphysema. Oxford: Oxford University Press, 1976. 7. Hanavirut R, Khaidjapho K, Jarce P, Pongnaratorn P. Yoga exercise increases chest wall expansion and lung volumes in young healthy Thais. Thai J PhysiolSci 2006;19:1-7. 8. Joshi LN, Joshi VD, Gokhale LV (1992). Effect of short term 'Pranayam 'practice on breathing rate and Ventilatory functions of lung, Indian J.Physiol. Pharmacol. 36(2): 105-108. 9. Mauch AD, Dr. Day. The Effects of a Two week Yoga Program on Pulmonary Functions. BIO 493 2008; 1-9. 10. Mehrotra PK, Varma N, Tiwari S, Kumar P. Pulmonary functions in Indian sportsmen playing different sports. Indian J PhysiolPharmacol 1998; 42: 412–416. 11. Miller MR, Hankinson J, Brusasco V, Burgos F, Casaburi R, Coates A et al.. Standardization of spirometry series and#8220;ATS/ERS Task Forceand#8221;: Standardization of Lung Function Testing. European Respiratory Journal; 26 (2): 321 / 326 12. Murthy K J R , Sahay B K ,Sunita M P :.Effect of yoga on Ventilatory functions in healthy volunteers lung India (aug);1(5)189-192 . 13. Peto R, Darby S, Deo H, Silcocks P, Whitley E, Doll R: Smoking, smoking cessation, and lung cancer in the UK since 1950: combination of national statistics with two case-control studies. Bmj 2000, 321:323-329. 14. Soni R, Munish K, Singh K, Singh S. Study of the effect of yoga training on diffusion capacity in chronic obstructive pulmonary disease patients: A controlled trial. Int J Yoga 2012;5:123-7. 15. Singh S, Soni R, Singh KP, Tandon OP- Effect of yoga practices on pulmonary function tests including transfer factor of lung for carbon monoxide (TLCO) in asthma patients. Indian J PhysiolPharmacol. 2012 Jan-Mar;56(1):63-8 16. Twisk JW, Staal BJ, Brinkman MN, Kemper HC, Van Mechelen W. Tracking of lung function parameters and the longitudinal relationship with lifestyle. EurRespir J 1998; 12: 627–634. 17. Upadhyay Dhunqel K, Malhotra V, Sarkar D, Prajapati R (2008). Effectof alternate nostril breathing exercise on cardio respiratory functions:Nepal Med. Coll. J. 10(1): 25-27. 18. Yang X, Telama R, Leino M, Viikari J. Factors explaining the physical activity of young adults: the importance of early socialization. Scand J Med Sci Sports 1999; 9: 120–127. 19. World Health Organization. Guidelines for controlling and monitoring the tobacco epidemic. WHO, Geneva, 1998; 76-101.

Introduction: In leprosy patients, disabilities involving hands, feet, eyes, face are seen. Deformities of hands include ulcers, cracks, scars, blisters, claw hand, wrist drop, dactylitis, contractures of fingers, resorption of fingers, stiff joints. Defomities of feet include ulcers, cracks, scars, blisters, foot drop, claw toes, resorption of toes, contracture of tendo achilles, equinovarus deformity. Aims and Objectives: To study the pattern of disabilities of hands and feet among leprosy patients reported at tertiary care centre. Material and Method: The present study was conducted in the Post Graduate Department of Dermatology, Venereology and Leprology, Government Medical College, Jammu from November 2012 to October 2013. All patients clinically diagnosed as cases of leprosy both old and new registered in the hospital were included in the study. A detailed history was taken regarding the age, sex, occupation, education, duration of disease, reactional states, treatment status, past history and family history. Complete clinical examination of each patient was performed with respect to skin lesions, nerve involvement and distribution, site, symmetry, type and grading of disability of hands and feet. Results: It was observed that out of total 150 patients, 93 (62%) were diagnosed to be with disability. Disability among lepromatous leprosy and borderline lepromatous leprosy was seen in 89.29% and 75.61% respectively. Both hands and feet were involved in 70.97% of disabled patients. Bilateral involvement of hands and feet was seen in 83.87% of disabled patients. Grade II disability was seen in 62.37% of disabled patients whereas grade I disability was diagnosed in 37.63% of disabled patients. In hands, 62.07% of patients had wasting in form of flattening of thenar or hypothenar eminence or guttering as the commonest deformity followed by clawing in 51.72% and ulceration in 18.97%. In feet, 24.14% of patients had ulceration as the commonest deformity followed by wasting. Disability increased with increasing number of nerves involved. This finding is statistically significant (χ²=61.28; p=0.0005). Conclusion: Thus we conclude that wasting and clawing was most common disability in hand whereas ulceration and wasting was common disability in feet. The most common pattern of disability was bilateral involvement of both hands and feet with grade II class of disability. Increasing age, male sex, lepromatous and borderline lepromatous leprosy was the common factors associated with disability.

1. Shah A and Shah N. Deformities of face, hand, feet and their management. In:Hemanta Kumar Kar and Bhushan Kumar, eds. IAL textbook of Leprosy, Ist edition, New Delhi, Jaypee Brothers Medical Publishers 2010,p.449-450. 2. Singhi MK, Ghiya BC, Gupta D, et al. Disability rates in leprosy. Indian J of Dermatol Venereol Leprol 2004; 70(5):314-316. 3. Palit A, Ragunatha S, Inamadar AC. History taking and clinical examination. In: Hemanta Kumar Kar and Bhushan Kumar, ed. IAL textbook of Leprosy, Ist edition, New Delhi, Jaypee Brothers Medical Publishers 2010, p.137-138. 4. Brandsma and Brakel V. WHO disability grading: operational definations. Lepr Rev(2003)74,366-373 5. Jain PK, Tripathi D, Singh CM, et al. A study of high disability rate among leprosy affected persons in Gwalior district. Indian Journal of Community Health 2011, Jul-Dec; 23(2). 6. Selvaraj G, Prabhakar N, Muliyil J, et al. Incidence of disabilities among multibacillary cases after initiation of multidrug therapy and factors associated with the risk of developing disabilities. Indian J Lepr 1998; 70 suppl: 11s-16s. 7. Saha SP and Das KK. Disability pattern amongst leprosy cases in an urban area(Calcutta). Indian J Lepr 1993 Jul-Sep 65(3) 305-314. 8. Noor SM, Paracha MM, Ali Z, et al. Frequency of disabilities in newly diagnosed patients of leprosy presenting to Lady Reading Hospital, Peshawar. Ann Pak Inst Med Sci 2010; 6(4):210-213. 9. Van Brakel, Sihombing B, Djarir H et al. Disability in people affected by leprosy: the role of impairment, activity, social participation, stigma, discrimination. Glob Health Action 2012, vol.5. 10. Girdhar M, Arora SK, Lal M, et al. Pattern of disabilities in Gorakhpur (UP). Indian J Lepr 1989 Oct; 61(4)503-513. 11. Htoon MT and Win Z. Disabilities among rural leprosy patients in Myanmar. Int J Lepr Other Mycobact Dis 1994, 62(1); 567-9. 12. Schreuder PA. The occurrence of reactions and impairments in leprosy: experience in the leprosy control program of three provinces in northeastern Thailand, 1987-1995. Neural and other impairments. Int J Lepr Other Mycobact Dis 1998; 66:170-81. 13. Sow SO, Tiendrebeogo A, Lienhardt C, et al. Leprosy as a cause of physical disability in rural and urban areas of Mali. Sante. 1998 Jul-Aug: 8(4):297-302. 14. Solomon S, Kurian N, Ramads P. Incidence of nerve damage in leprosy patients treated with MDT. Int J Lepr 1998; 66(4):451-6. 15. Srinivasan H. The problem and challenge of disability and rehabilitation in leprosy. Asia Pacific Disability Rehabilitation Journal 1998; 9(1). 16. Sarkar J, Dasgupta A, Dutt D. Disability among new leprosy patients, an issue of concern: Indian J Dermatol Venereol Leprol 2012(78):3; 328- 334. 17. Kumar R, Singhasivanon P, Sherchand JB et al. Gender difference in socio-epidemiological factors for leprosy in the most hyper-endemic district of Nepal. Nepal Med Coll J; 2004 Dec,6(2):98-105. 18. Norman G, Bhushanam JDRS and Samuel P. Trends in Leprosy over fifty years in Gudiyatham Taluk, Vellore, Tamilnadu. Indian J Lepr. 2006; 78: 167-185. 19. Arora M, Katoch K, Natrajan M, et al. Changing profile of disability in leprosy patients diagnosed in a tertiary care centre during years 1995- 2000. Indian J Lepr (2008) 80;257-265 20. Bhat RM and Chaitra P. Profile of New Leprosy Cases Attending a South Indian Referral Hospital in 2011-2012. ISRN Tropical Medicine 2013, 4 pages. 21. Thappa DM, Kaur S, Sharma VK. Disability index of hands and feet in patients attending an urban leprosy clinic. Indian J Lepr 1990 Jul- Sep; 62 (3):328-337. 22. Tiwari VD, Mehta RP. Deformities in leprosy patients of Indian Armed Forces treated/reviewed at Military Hospital Agra (a retrospective study). Lepr India 1981, Jul; 53(3):369-78. 23. Kaur P and Singh G. Deformities in leprosy patients attending urban leprosy clinic at Varanasi. Indian J Lepr, 1985 Jan-Mar; 57(1):178-182. 24. Hasan S. A survey of leprosy deformities among the patients of Hyderabad city.Lepr India 1977, Jul (49):3; 393-399. 25. Saha SP and Das KK. Disability pattern amongst leprosy cases in an urban area (Calcutta). Indian J Lepr 1993 Jul-Sep 65(3) 305-314. 26. Singhi MK, Ghiya BC, Gupta D, et al. Disability rates in leprosy. Indian J of Dermatol Venereol Leprol 2004; 70(5):314-316. 27. Ramos JM, Reyes F, Lemma D, et al. Disability profile in leprosy patients’ diagnoses in a rural reference leprosy centre in Ethopia during 1999-2009. Trop Doct (2011) Jan; 41(1)51-53. 28. Nagabhushanam P. Gross deformities in leprosy- a group survey. Indian J dermatol venereol leprol 1967; 33(2):70-72. 29. Iyere BB. Leprosy deformities: experience in Molai Leprosy Hospital, Maiduguri, Nigeria. Lepr Rev 1990 Jun; 61(2):171-9. 30. Schipper A, Lubbers WJ, Hogeweg M, et al. Disabilities of hands, feet and eyes in newly diagnosed leprosy patients in eastern Nepal. Lepr Rev.1994 Sep; 65(3):239-247. 31. Kumar A, Girdhar A, Girdhar BK. Nerve thickening in leprosy patients and risk of paralytic deformities: A field based study in Agra,India. Lepr Rev (2004)75,135-142. 32. Brunel W, Schecter WP, Schecter G. Hand deformity and sensory loss due to Hansen’s disease in American Samoa. J Han Surg Am. 1988 Mar; 13(2):279-83. 33. Moschioni C, Antunes C, Grossi M, et al. Risk factors for physical disability at diagnosis of 19,283 new cases of leprosy. Rev Soc Bras Med Trop vol.43 no.1 Uberaba Jan/Feb, 2010.

Numerous diseases mimic appendicitis, and it is often difficult to rule it out on the basis of clinical presentation. Based on the clinical, laboratory and radiological findings can help in the diagnosis of acute appendicitis. A prospective, single centre based observational study carried out at our Rural Medical College. 100 patients were admitted with preliminary complains of pain Right iliac fossa. Clinical examination along with the laboratory and radiological findings was able to differentiate patients who came with pain Right iliac fossa but were having normal appendix from the patients who were actual cases of acute appendicitis. In patients with histologically confirmed acute appendicitis taking as the standard. The WBC count ,Ultrasonography and CT Scan when combined with reliable clinical signs and symptoms is an excellent diagnostic marker of the disease is so that proper handling of the patient can be done and we can prevent unnecessary appendectomies in pain Right iliac fossa.

1. Blomqvist PG, Andersson RE, Granath F et al (2001) Mortality after appendectomy in Sweden, 1987–1996. Ann Surg 233:455– 460 2. Schwarz A, Bolke E, Peiper M et al (2007) Inflammatory peritoneal reaction after perforated appendicitis: continuous peritoneal lavage versus nonlavage. Eur J Med Res 12:200–205 3. Carrol ED, Thomson AP, Hart CA (2002) Procalcitonin as a marker of sepsis. Int J Antimicrob Agents 20:1–9 4. Kouame DB, Garrigue MA, Lardy H et al (2005) Is procalcitonin able to help in paediatric appendicitis diagnosis? Ann Chir 130 (3) :169–174 5. Alvarado A. A practical score for the early diagnosis of acute appendicitis. Ann Emerg Med 1986; 15(5):557-64. 6. Soomro AG, Siddiqui FG, Abro AH, Abro S, Shaikh NA, Memon AS. Diagnostic accuracy of Alvarado scoring system in acute appendicitis. J Liaquat Univ Med Health Sci 2008;7:93-6. 7. Memon ZA, Irfan S, Fatima K, Iqbal MS, Sami W. Acute appendicitis: Diagnostic accuracy of Alvarado scoring system. Asian J Surg2013; 36(4):144-9. 8. Pinto F, Pinto A, Russo A, Coppolino F, Bracale R, Fonio P, et al. Accuracy of ultrasonography in the diagnosis of acute appendicitis in adult patients: review of the literature. Crit Ultrasound J 2013; 5 Suppl 1:S2. 9. Birnbaum BA, Jeffrey RB Jr. CT and sonographic evaluation of acute right lower quadrant abdominal pain. AJR Am J Roentgenol1998; 170(2):361-71. 10. Jahn H, Mathiesen FK, Neckelmann K, Hovendal CP, Bellstrøm T, Gottrup F. Comparison of clinical judgment and diagnostic ultrasonography in the diagnosis of acute appendicitis: experience with a score-aided diagnosis. Eur J Surg 1997; 163(6):433-43. 11. Birnbaum BA, Wilson SR. Appendicitis at the millennium. Radiology 2000; 215(2):337-48. 12. Paulson EK, Kalady MF, Pappas TN. Clinical practice. Suspected appendicitis. N Engl J Med 2003; 348(3):236-42.

Pregnancy induced hypertension is one of the threatening problem among pregnancy related health problems. Complications arising from it are also common which leads to several maternal and foetal deaths. During pregnancy, examination of mother and foetus done properly but what is overlooked is placenta, as it cannot be measured directly until after birth. Foetal distress, intrauterine foetal death and placental abnormalities are common in pregnancy induced hypertension. Rate of preterm birth ranges from 5 to10 percent of deliveries in developing countries (Hsleh TʼSang- TʼSang 2005). About two third of preterm deliveries are due to spontaneous onset of preterm labour or preterm premature rupture of membranes. Approximately one third follow induction of labours or caesarean section performed for maternal or foetal indication such as preeclampsia, haemorrhage, non-reassuring foetal heart rate or intrauterine growth retardation. Thus, pathologists are frequently called on to evaluate preterm placenta, to determine the cause of the spontaneous preterm birth and/or correlate placental finding with the clinical history (O. M. Faye-Petersen 2008). The risk is increased if placental function has been impaired by pre-eclampsia, post maturity and threatened abortion. The margin may be narrow and hazard may be greater if the placenta is unusually small. Weight of placenta is “functionally significant” because it is related to villous surface area and to total foetal metabolism (Udainia A, Bhagwat S). Pregnancy complicated by hypertension is commonly associated with placental insufficiency, there by resulting in foetal growth retardation. Again reduced utero-placental blood flow has been recognized in cases of severe preeclampsia with hypertension. As stated above, foetal growth is retarded in preeclampsia and that a small infant has usually a small sized placenta. In previous studies it has been revealed that there is clear relationship between pregnancy induced hypertension and morphometric changes in placenta and which ultimately reflects foeto-maternal status. Placental weight is one of placental measure by which placental growth can be characterised. So the present study is carried out on placentae from mothers with pregnancy induced hypertension and placentae from mothers without any materno-foetal complication (normal placentae). Two hundred and one placentae, 101 from normal pregnancies and 100 from pregnancy induced hypertension pregnancies, were examined. Weight of placenta was taken in gram by using standard weighing machine after removing membranes and cutting cord leaving 2.5 cm attachment. Weight of new born baby was taken on standard weighing machine immediately after cord tying and cutting. In present study the mean placental weight in normal group is 469.50gm. And in pregnancy induced hypertension group is 420.98gm., from this finding it is concluded that the placental weight in pregnancy induced hypertension cases is significantly less than the placental weight in normal group. The mean birth weight in normal group is 2556.9gm. and in pregnancy induced hypertension it is 2192.50gm. So the birth weight in pregnancy induced hypertension is significantly low as compared to normal group. The ratio between birth weight and placental weight in pregnancy induced hypertension group is significantly lower than normal. It is concluded that correlation between birth weight and placental weight in normal group is moderately correlated (r=0.484), where as in pregnancy induced hypertension is strongly correlated(r=0.836).

1. HSIeh T’Sang-T’Sang, M.D (2005): perinatal transport: status in developing countries: J. of Neonatology: 19(4). 2. O M Faye – Petersen (2008): The placenta in preterm birth. J. of clinical pathology. 61(12):1261-75. (Dec2008). 3. Udainia A, Bhagwat SS, Mehta CD (2004): Relation between Placental Surface Area, Infarction and Foetal Distress in Pregnancy Induced Hypertension with Clinical Relevance. J. of the Anatomical society of India. 53(1):27-30.2004. 4. Udainia, A; Jain,M.L (2001): Morphological study of placenta in pregnancy induced hypertension with its clinical relevance. J. Anatomical society of India 50 (1) 24-27 (2001). 5. Thomson A. M., Billewicz W. Z., Hytten F. E. (1969): The weight of the placenta in relation to birth weight. J.of Obstet. Gynec. Brit. Comm. wealth. 76(10):865-872. 6. Majumdar S, Dasgupta H, Bhattacharya K, Bhattacharya A (2005): A study of placenta in normal and hypertensive pregnancies. J. Anat. Soc. India 54 (2) 1-9. 7. Luis A. Cibils, M.D (1974): The placenta and newborn infant in hypertensive conditions. J. Obstetrics and Gynecology. 118(2):256-267. 8. Samuel Lurie, Michael Feinstein, Yaakov Mamet (1999): Human Fetal-Placental Weight Ratio in Normal Singleton Near-Term Pregnancies. Gynecol Obstet Invest 1999; 48:155-157. 9. Rath G, Garg K, Sood M (2000): Insertion of umbilical cord on the placenta in hypertensive mother. J. Anat. Soc. India 49(2) 149-152. 10. Janthanaphan M, Kor-Anantakul O, Geater A (2006): Placental weight and its ratio to birth weight in normal pregnancy at Songkhlanagarind hospital. J.med Assoc Thai. 89(2): 1

Objective: We attempted to determine the immunisation status of children as per national immunisation schedule admitted in paediatric ward. Design: Hospital based Descriptive, Cross-sectional study conducted from January 2014 to June 2014. Setting: Tertiary referral teaching hospital. Patients: All patients admitted in paediatric ward satisfying inclusion criteria were included in the study. Information regarding immunisation status was taken from the primary care giver preferably mother and available medical records of immunisation status were verified. Children were classified as completely immunised as per age and national immunisation schedule or partially immunised or unimmunised. Results: Out of total 840 children 520 (61. 91%) were completely immunised, 312 (37.14%) were partially immunised and 8 (0.95%) were unimmunised. Fully immunised percentage of male was 61.40% and that of female was 62.69%. The ratio of fully immunized children was 38.2%, 52.63%, 70.72% and 100% in illiterate, primary educated, HSC educated and graduate mother respectively. Conclusion: The observed percentage of fully immunized children 1-5 years of age was 61.91%. Dropping out trend in immunization increases as the age advances. Among the routine vaccines under 1 year of age, OPV/DPT 3rd dose and Measles vaccine were the least to be received. Mother's education significantly influences the immunization coverage among the under-fives. Sex of a child had not significant association with immunization coverage in 1-5 year.

1. National Family Health Survey. (NFHS-3) 2005–06 India Volume I September. 2. Wadgave HV, Pore PD, Missed opportunities of immunization in under-fives in adopted area of Urban Health Centre Centre. Ann Trop Med Public Health 2012; 5:436-40. 3. Yadhav RJ, Singh P. Immunization status of children and mothers in the state of Madhya Pradesh, Indian J Community Med 2004;29:147-8. 4. Prabhakaran Nair TN, Varughese E. Immunization coverage of infants-Rural-Urban difference in Kerala. Indian Pediatr 1994; 31:139-43. 5. Nath B, Singh JV, Awasthi S, Bhushan V, Kumar V, Singh SK. A study on determinants of immunization coverage among 12-23 months old children in urban slums of Lucknow district, India. Indian J Med Sci, 2007; 61:598-606. 6. Mathew JL, Babbar H, Yadav S. Reasons for non-immunization of children in an urban, low income group in North India. Trop Doct 2002; 32:135-8. 7. Kumar D, Aggarwal A, Gomber S. Immunization status of children admitted to a tertiary-care hospital of north India: Reasons for partial immunization or non-immunization. J Health Popul Nutr 2010; 28:300-4. 8. Manjunath U, Pareek RP. Maternal knowledge and perceptions about the routine immunization programme -a study in a semiurban area in Rajasthan. Indian J Med Sci 2003; 57:158-63. 9. Bhandari B, Mandowasa SL, Gupta GK. Evaluation of vaccination Coverage. Indian J Pediatr 1990; 57:197-201. 10. Nirupam S, Chandra R, Srivastava VK. Sex bias in immunization coverage in the urban area of U.P. Indian Pediatr 1990; 27:338-41.

Acute pancreatitis has wide spectrum of clinical illness that ranges from mild self-limited symptoms to early severe acute pancreatitis (ESAP), rapid deterioration and death. Prior assessment of severity allows the managing physician to identify those patients who are most likely to have a severe episode early administration of therapies to reduce severity. The present study was intended to compare the predictive accuracy of 04 different severity scoring systems for acute pancreatitis- Ranson’s score, Acute Physiology and Chronic Health Evaluation [APACHE] II, Balthazar CT Severity Index (CTSI) and Goris Multi Organ Failure(MOF) scale for prediction of severe pancreatitis. This prospective study has been conducted by selecting 30 consecutive CECT confirmed patients of acute pancreatitis admitted during the period October 2012 to June 2014 in MGM Medical College, Kishanganj, Bihar. Patients have been evaluated, examined and investigated as per the study proforma. Severity assessment was done for every patient on admission and at 48 hrs using clinical, hematological, biochemical and radiological parameters by calculating severity scoring points in respect to Ranson’s, APACHE II on admission, APACHEII after 48 hrs, Balthazar CT severity index score, Goris MOF score (at cut off>0), (at cut off ≥2) on admission and after 48 hrs .All cases were followed up for a period of next 06 months. In this study, out of 30 patients 24 (80%) cases were in the age group of 20-59 yrs. However only 6 (20%) cases were in the age group >60 yrs. Sex ratio was Male: female = 27:3. Alcohol and Gall stone disease was aetiology of pancreatitis in 17 (56.67%) patients and 7 (23.33%) patients. There was one case of hyperlipidemia and the remaining 5 cases were of idiopathic pancreatitis. 80% of the cases presented with upper abdominal pain and repeated vomiting. Classical presentation of radiation of pain to back and relief on leaning forward was present only in 09 (30%) and 6 (20 %) cases respectively. 20 (50%) patients presented with history of obstipation and about 44% patients presented with abdominal distension misleading the diagnosis initially towards intestinal obstruction on admission. In 8 patients amylase was not elevated and basis for a diagnosis of pancreatitis was characteristic pain, strong clinical suspicion and evident pancreatitis in CECT abdomen. In this study out of total 30 patient 11(37%) developed severe pancreatitis whereas 19(63%) developed mild pancreatitis. Out of 11 severe pancreatitis cases one patient died due to sepsis and multi organ failure during 5th week of hospital admission .Incidence of organ failure and MODS in this study was 83.33% and 10%. Hepatic dysfunction was present in all patients who developed organ failure. The sensitivity, specificity, Positive predictive value, Positive Likelihood Ratio and negative likelihood ratio of Ranson’s score was found to be 73%, 63%, 53%, 1.97 and 0.43 respectively. There is no significant difference in median APACHE II score on admission and after 48 hrs in our study. CTSI score had almost equal AUC under ROC curve (0.653), NPV (79%) and equal specificity (73%) as of Ranson’s score. However about 50% cases who had necrosis in CECT did not develop clinical severe pancreatitis This demonstrate a very low PPV (50%) for CTSI score. Goris MOF score (at cut off >0) on admission and after 48 hrs had the highest sensitivity (82%) of all scores. In this study, all patients who were predicted to develop severe pancreatitis due to persistence or progression of organ failure during first week actually developed severe pancreatitis later on. Also, all the patients who did not develop severe pancreatitis were correctly predicted as mild pancreatitis by the absence of persistent/progressive organ failure during first week. Thus a specificity and PPV of 100% were obtained by persistent organ failure criterion. Persistence or progression of organ failure during the first week of admission was also found to have the greatest area under the curve (AUC=0.727) under the receiver operating characteristic (ROC) curve and specificity (100%) denoting its highest predictive accuracy in comparison to other scores. However, the drawback of this score was that it takes one week observation of the patient prior to prediction of severity. Whereas APACHEII or Goris MOF score can be obtained as early as on admission making them more useful.

1. John H.C. Ranson. “Maingot’s Abdominal operations”.10th Ed. Vol II 2. Michael Trede, Sir David c. Carter, “Surgery of the Pancreas” 2nd Ed. 3. Bradley EL III. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, GA, September11- 13, 1992. Archives of Surgery 1993; 128:586–590. 4. Zhu AJ, Shi JS, Sun XJ. Organ failure associated with severe acute pancreatitis. World J Gastroenterol 2003; 9: 2570- 2573 5. Mann DV, Hershman MJ, et al. Multicentre audit of death from acute pancreatitis. Br J Surgery 1994; 81: 890–893. 6. McKay CJ, Evans S, et al. High early mortality rate from acute pancreatitis in Scotland, 1984-1995. Br J Surgery 1999; 86: 1302–1305. 7. Talamini G, Bassi C, Falconi M, Sartori N, Frulloni L, Di Francesco V, et al. Risk of death from acute pancreatitis. Role of early, simple “routine” data. Int J Pancreatology 1996; 19: 15–24. 8. Carnovale A, Rabitti PG, Manes G, Esposito P, Pacelli L, Uomo G. Mortality in acute pancreatitis: is it an early or a late event? JOP 2005; 6: 438-444) 9. Gotzinger P, Sautner T, Kriwanek S, Beckerhinn P, Barlan M, Armbruster C,Warmser P, Fugger R. Surgical treatment for severe acute pancreatitis: extent and surgical control of necrosis determine outcome. World J Surg 2002; 26:474 – 478 10. Ting-Kai Leung, Chi-Ming Lee et al.Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II scoring system in predicting acute pancreatitis outcome. World J Gastroenterol 2005;11(38):6049-6052 11. Chatzicostas, Constantinos, Roussomoustakaki, Maria et al. Balthazar Computed Tomography Severity Index is superior to ranson criteria and apache ii and iii scoring systems in predicting acute pancreatitis outcome. journal of clinical gastroenterology: march 2003;36:253-260 12. Lankish PG, Pflichthofer D, Lehnick D. No strict correlation between necrosis and organ failure in acute pancreatitis. Pancreas 2000;20:319 -322 13. Wiesner W, Studler U, Kocher T, Degen L, Buitrago-Tellez CH, Steinbrich W. Colonic involvement in non-necrotizing acute pancreatitis: correlation of CT findings with the clinical course of affected patients. Eur Radio l2003; 13: 897-902 14. Inoue K, Hirota M, Beppu T, et al. Angiographic features in acute pancreatitis: the severity of abdominal vessel ischemic change reflects the severity of acute pancreatitis. J Pancreas 2003; 4:207 -213 15. Mortele KJ, Mergo P et al. Renal and perirenal space involvement in acute pancreatitis: state-of-the-art spiral CT findings. Abdom Imaging 2000; 25:272 -278 16. Lecesne R, Tourel P, et al. Acute pancreatitis: interobserver agreement and correlation of CT and MRCP with outcome. Radiology1999; 211:727 -735 17. Buchler MW, Gloor B, Muller CA, et al. Acute necrotizing pancreatitis: Treatment strategy according to the status of infection. Ann Surg2000;232:619-626

During routine dissection, in one of the female cadaver, the accessory spleen was found in the lieno-renal ligament. This variation is important for the radiologists and surgeons.

1. Moore P. the developing human- clinically oriented embryology, 2003 2. Grays anatomy thirty-eighth ed. Churchill livingstone, 2000 3. Gayer G, Zissin R, Apter S, Atar E, Portnoy O, Itzchak Y. CT findings in congenital anomalies of the spleen. Br J Radiol. 2001; 74:767–772 4. Hollinshead WH. Anatomy for surgeons: The kidneys, ureter and suprarenal glands. 2nd ed Harper and Row publishers, New York, Vol. 2, 1971; 518-573 5. Settle EB. The surgical importance of accessory spleens: with report of two cases. Am J Surg 1940; 50:22 6. Halpert B and Eaton WL. Accessory spleens: A pilot study of 600 necropsies. Anat Rec 1951; 109:371 7. Weiand G and Mangold G. Accessory spleen in the pancreatic tail - a neglected entity? A contribution to embryology, topography and pathology of ectopic splenic tissue. Chirurg. 2003; 74(12):1170-7 8. Mund R. Accessory spleen as a normal variation. PedRad [serial online] vol 2, no. 8.URL: www.PedRad.info/?search=20020827150244 9. Abu-Hijleh MF. Multiple accessory spleens: Case report and literature review. Clinical Anatomy 1993 Volume 6 Issue 4, Pages 232 - 239 10. Rudowski WJ. Accessory spleens: Clinical significance with particular reference to the recurrence of idiopathic thrombocytopenic purpura. World Journal of Surgery 1985; 9(3): 422-430 11. Velanovich V, Shurafa M. Laparoscopic excision of accessory spleen. Am J Surg 2000; 180:62–64 12. Gayer G, Zissin R, Apter S, Atar E, Portnoy O, Itzchak Y. CT findings in congenital anomalies of the spleen. Br J Radiol. 2001; 74:767–772

Atropa belladonna is a topical agent used in the treatment of skin wounds in Slovak folk medicine. The aim of this study was to assess the effect of A. belladonna extract on wound tensile strength and collagen maturation in wistar rats. Wistar rats of either sex were divided into 2 groups. Group I: Animals served as wounded control, treated with normal saline. Group II: Animals were daily administered Atropa belladonna extract (0.3ml /100gm /rat) orally once daily from day 0 to 9 via intragastric tube. Dead space wound model was used for this study and granulation tissue was used to analyze the biochemical parameters of wound healing such as hydroxyproline, hexosamine and hexuronic acid. Significant increase in hydroxyproline and glycosaminoglycans content in granulation tissue were observed in rats treated with the extracts of Atropa Belladonna. The mean tensile strength of both A. belladonna extract treated groups was significantly higher than the untreated group. Present result shows that Atropa extract has significant wound healing promoting activity indicating collagen maturation as indicated by increase in hydroxyproline, hexosamine and hexuronic acid levels in the granulation tissue. The wound breaking strength also increased significantly.

1. Toporcer T, Grendel T, Vidinský B, Gál P, Sabo J, Hudák R. Mechanical properties of skin wounds after Atropa belladonna application in rats. Journal of Metals, Materials and Minerals. 2006; 16(1):25-9. 2. Gillitzer R, Goebeler M. Chemokines in cutaneous wound healing. Journal of leukocyte biology. 2001; 69(4):513-21. 3. Stadler I, Lanzafame RJ, Evans R, Narayan V, Dailey B, Buehner N, et al. 830‐nm irradiation increases the wound tensile strength in a diabetic murine model*. Lasers in surgery and medicine. 2001; 28(3):220-6. 4. Midwood KS, Williams LV, Schwarzbauer JE. Tissue repair and the dynamics of the extracellular matrix. The international journal of biochemistry and cell biology. 2004; 36(6):1031-7. 5. Cytokines in Dermal Regenerative Medicine (Part 1 of a Series) 2012 [cited 2015 18/4/2015]. Available from: http://barefacedtruth.com/2012/06/29/cytokines-in-dermal-regenerative-medicine-part-1/. 6. Enoch S, Price P. Cellular, molecular and biochemical differences in the pathophysiology of healing between acute wounds, chronic wounds and wounds in the aged. World Wide Wounds. 2004:1-16. 7. Gál P, Vasilenko T, Kováč I, Kostelníková M, Jakubčo J, Szabo P, et al. Atropa belladonna L. water extract: modulator of extracellular matrix formation in vitro and in vivo. Physiological Research. 2012; 61(3):241-50. 8. Biswas TK, Mukherjee B. Plant medicines of Indian origin for wound healing activity: a review. The international journal of lower extremity wounds. 2003; 2(1):25-39. 9. Kumarasamyraja D, Jeganathan N, Manavalan R. A review on medicinal plants with potential wound healing activity. International Journal of Pharmaceutical Sciences. 2012; 2:105-11. 10. Jimenez PA, Rampy MA. Keratinocyte growth factor-2 accelerates wound healing in incisional wounds. Journal of Surgical Research. 1999; 81(2):238-42. 11. Witte MB, Thornton FJ, Kiyama T, Efron DT, Schulz GS, Moldawer LL, et al. Metalloproteinase inhibitors and wound healing: a novel enhancer of wound strength. Surgery. 1998; 124(2):464-70. 12. Rashed A, Afifi F, Disi A. Simple evaluation of the wound healing activity of a crude extract of Portulaca oleracea L.(growing in Jordan) in Mus musculus JVI-1. Journal of Ethnopharmacology. 2003; 88(2):131-6. 13. Agarwal P, Singh A, Gaurav K, Goel S, Khanna H, Goel R. Evaluation of wound healing activity of extracts of plantain banana (Musa sapientum var. paradisiaca) in rats. 2009.

Atropa belladonna is a topical agent used in the treatment of skin wounds in Slovak folk medicine. The aim of this study was to assess the effect of A. belladonna extract on wound tensile strength and collagen maturation in wistar rats. Wistar rats of either sex were divided into 2 groups. Group I: Animals served as wounded control, treated with normal saline. Group II: Animals were daily administered Atropa belladonna extract (0.3ml /100gm /rat) orally once daily from day 0 to 9 via intragastric tube. Dead space wound model was used for this study and granulation tissue was used to analyze the biochemical parameters of wound healing such as hydroxyproline, hexosamine and hexuronic acid. Significant increase in hydroxyproline and glycosaminoglycans content in granulation tissue were observed in rats treated with the extracts of Atropa Belladonna. The mean tensile strength of both A. belladonna extract treated groups was significantly higher than the untreated group. Present result shows that Atropa extract has significant wound healing promoting activity indicating collagen maturation as indicated by increase in hydroxyproline, hexosamine and hexuronic acid levels in the granulation tissue. The wound breaking strength also increased significantly.

1. Toporcer T, Grendel T, Vidinský B, Gál P, Sabo J, Hudák R. Mechanical properties of skin wounds after Atropa belladonna application in rats. Journal of Metals, Materials and Minerals. 2006; 16(1):25-9. 2. Gillitzer R, Goebeler M. Chemokines in cutaneous wound healing. Journal of leukocyte biology. 2001; 69(4):513-21. 3. Stadler I, Lanzafame RJ, Evans R, Narayan V, Dailey B, Buehner N, et al. 830‐nm irradiation increases the wound tensile strength in a diabetic murine model*. Lasers in surgery and medicine. 2001; 28(3):220-6. 4. Midwood KS, Williams LV, Schwarzbauer JE. Tissue repair and the dynamics of the extracellular matrix. The international journal of biochemistry and cell biology. 2004; 36(6):1031-7. 5. Cytokines in Dermal Regenerative Medicine (Part 1 of a Series) 2012 [cited 2015 18/4/2015]. Available from: http://barefacedtruth.com/2012/06/29/cytokines-in-dermal-regenerative-medicine-part-1/. 6. Enoch S, Price P. Cellular, molecular and biochemical differences in the pathophysiology of healing between acute wounds, chronic wounds and wounds in the aged. World Wide Wounds. 2004:1-16. 7. Gál P, Vasilenko T, Kováč I, Kostelníková M, Jakubčo J, Szabo P, et al. Atropa belladonna L. water extract: modulator of extracellular matrix formation in vitro and in vivo. Physiological Research. 2012; 61(3):241-50. 8. Biswas TK, Mukherjee B. Plant medicines of Indian origin for wound healing activity: a review. The international journal of lower extremity wounds. 2003; 2(1):25-39. 9. Kumarasamyraja D, Jeganathan N, Manavalan R. A review on medicinal plants with potential wound healing activity. International Journal of Pharmaceutical Sciences. 2012; 2:105-11. 10. Jimenez PA, Rampy MA. Keratinocyte growth factor-2 accelerates wound healing in incisional wounds. Journal of Surgical Research. 1999; 81(2):238-42. 11. Witte MB, Thornton FJ, Kiyama T, Efron DT, Schulz GS, Moldawer LL, et al. Metalloproteinase inhibitors and wound healing: a novel enhancer of wound strength. Surgery. 1998; 124(2):464-70. 12. Rashed A, Afifi F, Disi A. Simple evaluation of the wound healing activity of a crude extract of Portulaca oleracea L.(growing in Jordan) in Mus musculus JVI-1. Journal of Ethnopharmacology. 2003; 88(2):131-6. 13. Agarwal P, Singh A, Gaurav K, Goel S, Khanna H, Goel R. Evaluation of wound healing activity of extracts of plantain banana (Musa sapientum var. paradisiaca) in rats. 2009.

Neurosurgical patients are operated in supine, prone, lateral and sitting positions, which cause physiological changes in cardiorespiratory parameters. Various monitors, both non invasive and invasive are used to monitor these changes. NICO monitor developed by Novametrix Medical System Inc is a non-invasive cardiac output monitor, which also measures and displays various other parameters like stroke volume, cardiac index, pulmonary capillary blood flow, alveolar and dead space ventilation, peak flow rates, airway pressures and respiratory volumes. We felt that a study using the NICO monitor in anaesthetised patients being operated in different positions would provide a complete characterization of cardiopulmonary function, help in defining risk factors and improve intraoperative management. Hence, forty consecutive patients undergoing neurosurgical procedures- twenty in prone, sixteen in lateral and four in sitting position were studied. The haemodynamic and cardiorespiratory parameters were noted in supine position about 15 minutes after induction of general anaesthesia using standard protocol and 15 minutes after giving surgical position using NICO monitor. We concluded that under anaesthesia, while the respiratory parameters are not significantly affected, the prone and sitting position negatively affect derived cardiac parameters like cardiac output, cardiac index and stroke volume and lateral position tends to improve these parameters.

1. Nakao S, Come P C, Miller M J et al. Effects of supine and lateral positions on cardiac output and intracardiac pressures: An experimental study. Circulation 1986; 73: 579-585. 2. Wadsworth R, Anderton J M, Vohra A. The effect of four different surgical prone positions on cardiovascular parameters in healthy volunteers. Anaesthesia 1996; 51(9): 819-22. 3. Kamenik M. The influence of left lateral position on cardiac output changes after Head-up Tilt measured by impendence cardiography. Journal of Clinical Monitoring and Computing 1999; 15(7-8): 519-523. 4. Backofen J E, Schauble J F. Hemodynamic changes with prone positioning during general anesthesia. Anesthesia and Analgesia 1985; 64: 194. 5. Jaffe MB. Partial CO2 rebreathing cardiac output - operating principles of the NICO system. J Clin Monit 1999; 15: 387-401 6. Haryadi D G, Orr J A, Kuck K et al. Partial CO2 Rebreathing Indirect Fick Technique for Non-Invasive Measurement of Cardiac Output. Journal of Clinical Monitoring and Computing 2000; 16(5-6) : 361-374 7. Haryadi D G, Orr J A, Kuck K et al. Evaluation of a partial carbon dioxide rebreathing Fick technique for measurement of cardiac output. Anesthesiology 1998; 89(3): A534. 8. Bailey P L, Haryadi D G, Orr J A, Westenskow D R. Partial carbon dioxide rebreathing Fick technique for non-invasive measurement of cardiac output. Anesthesia and Analgesia 1998; 86: SCA53. 9. Loeb R G, Brown E A, DiNardo J A, Orr J A, Watt R C. Clinical accuracy of a new non-invasive cardiac output monitor. Anesthesiology 1999; 91(3A): A474. 10. Kothari N, Amaria T, Hegde A, Mandke A, Mandke NV. Measurement of cardiac output: Comparison of four different methods. Indian Journal of Thoracic Cardiovascular Surgery 2003; 19: 163-168. 11. Botero M, Hess P, Kirby D., Briesacher K et al Measurement of cardiac output during coronary artery bypass grafting (CABG): comparison of pulmonary artery catheter, Noninvasive partial CO2 rebreathing, and direct aortic flow. Anesthesia and Analgesia, April 2000; V90(4S); SCA87 12. Sudheer P S, Logan S W, Ateleanu and Hall J E. Haemodynamic effects of the prone position: A comparison of propofol total intravenous and inhalational anaesthesia. Anaesthesia 2006; 61(2): 138-141. 13. Srivastava S, Pandey CK. Anesthesia in prone lithotomy position. Canadian Journal of Anesthesia 2001; 48: 827. 14. Alexianu D, Skolnick E, Pinto C et al. Severe hypotension in the prone position in a child with neurofibromatosis, scoliosis and pectus excavatum presented for posterior spinal fusion. Anesthesia and Analgesia 2004; 98. 334-335. 15. Buhre W, Weyland A, Buhre K et al. Effect of the sitting position on the distribution of blood volume in patients undergoing neurosurgical procedures. British Journal of Anaesthesia 2000; 84(3): 354-7. 16. Palmon S C, Kirsch J R, Deeper J A, Toung T J K. The effect of prone position on pulmonary mechanics is frame-dependent. Anesthesia and Analgesia 1998; 87(5): 1175-80. 17. Soro M, Gareia-Perez M L, Belda F J et al. Effects of prone position on alveolar dead space and gas exchange during general anaesthesia in surgery of long duration. Eur J Anaesthesiol.2007; 24(5) :431-7 18. Pelosi P, Croci M, Calappi E, Cerisara M et al. The prone positioning during general anesthesia minimally affects respiratory mechanics while improving functional residual capacity and increasing oxygen tension. Anesthesia and Analgesia 1995; 80(5): 955-60.

The casualty department is backbone of every Hospital because almost all cases of Medical emergencies reported first to Casualty Department of Hospital, and apart from these Medical emergencies, Casualty Department also deals with the Medico legal cases more frequently than any other department of Hospital The study was conducted in a retrospective manner and all the Medico-legal cases which came to the emergency department of the hospital between Jan 2014 to Dec 2014 were studied. The males were the dominant group (67.6%). The most of the victims were of the age group 21-30 years (45.1%). The Road traffic accident cases had the highest incidence in relation to the cause of admission (36.9%), followed by poisoning. Most of the patients (53.2%) reported in the hospital within one hour of sustaining the injury/other causes. In simple language it is a medical case with legal implications for the attending doctor where the attending doctor, after eliciting history and examining the patient, thinks that some investigation by law enforcement agencies is essential.

1. White, Brenda M., "Duncan, Andrew (1773–1832)", Oxford Dictionary of National Biography (online ed.), 2004 2. Kumar A. Evidentiary value of medical evidence in Indian courts. JIAFM ;4:136 3. Garg Vishal, Verma S K- profile of medico legal cases at Adesh institute of medical sciences and research, Bhatinda Punjab. Journal of Indian academy of forensic medicine volume 32 (2) 150- 152. 4. Malik Yogendra, Chawla Rahul et al- profile of medico legal cases in causality of a rural medical college of Hariyana. Journal of Indian Academy of Forensic Medicine vol. 35 (4) 367-368. 5. S. Malhotra and R.S. Gupta A STUDY OF THE WORKLOAD OF THE CASUALTY DEPARTMENT OF A LARGE CITY HOSPITAL, Health and Population-Perspectives and Issues 15(land2):68-76, 1992 6. Jitesh Dhingra, Girish Arora, Paschal D’souza – A study of pattern of medico-legal cases in a premier hospital in New Delhi 7. M. Z. Marri, U. Baloch, “Frequency and Pattern of Medico Legal Cases Reported at Sandeman Civil Hospital, Quetta Balochistan- One Year Study”, 2012 8. Vol 22, Number 2 Journal of Forensic Medicine, Science and Law (Jul-Dec 2013) A Journal of Medicolegal Association of Maharashtra 9. Harish KN, Srinivasa RP. Analysis of Medico-Legal Cases at Harsha Hospital Nelamangala, Bangalore Rural. Indian Journal of Forensic Medicine andToxicology 2013; 7(1): 254-287

Thalassemia major is cause of severe anemia. Anemia is treated with repeated blood transfusion. All this leads to ineffective erythropoiesis and hemochromatosis. The present study was conducted to assess the severity of anemia and iron overload due to repeated blood transfusion leading to oxidative stress.

1. Draper and Hadley: Method in enzymology 1990; 186: 421-431. 2. Watanabe: Urinary protein as measured with a pyrogallol red molybdate complex, manually and in Hitachi 726 automated analyzer. Clin Chem 1986; 32:1551-54. 3. Teitz NW: Text Book of Clinical chemistry. W.B.Saunders Co 1986; 602-613. 4. Mc Donagh KT, Neinhuis AW, Nathan DI, Oski FA (eds): Hematology of infancy and childhood, 4th edn Saunder, Philadelphia 1993; 783-879. 5. Lamb E, Newman DJ, Prince CP: Kidney function tests: In Tietz textbook of clinical chemistry and mol Ehlers KH, Giardina PJ, Lessor ML et al: Improved survival in patients with thalassemia major on desferoxamine, J Pediatr 1991; 118: 540. 6. Logothetis J, Constantenlakis M, Economidose J et al: Thalassemia major (homozygous, beta thalassemia): a study of 138 cases. Neurology 1972; 22: 294. 7. Ecular diagnostics. Burtis CA, Ashwood ER, Bruns DE (ed): WB Saunders 4th edition 2006: 808-811. Livrea MA, Tesoriere L, Pintaudi AM, Calabrese A, Maggio A, Freisleben HJ, D’Arpa D, D’Anna R, Bongiorno A: Oxidative stress and antioxidant status in beta thalassemia major: iron overload and depletion of lipid soluble antioxidants. The Amercian Society of Hematology. 1996; Vol 88(9):3608-3614. 8. Livrea MA, Tesoriere L, Pintaudi AM, Calabrese A, Maggio A, Freisleben HJ, D’Arpa D, D’Anna R, Bongiorno A: Oxidative stress and antioxidant status in beta thalassemia major: iron overload and depletion of lipid soluble antioxidants. The Amercian Society of Hematology. 1996; Vol 88(9):3608-3614. 9. Lapatsanis P, Sbyrakis S, Vertos C, Karaklis BA, Dosiadir S: Phosphaturia in thalassemia. Pediatrics 1976 Dec; 58(61), 885-92. 10. Koren G, Bentur Y, Strong D, Harvey E, Klein J, Baumal R, Spielberg SP, Freedman MH. A J Dis Child 1989 Sep; 143(9): 1077-80. 11. Cighetti G, Duca L, Bortone L, Sala S, Nava I, Fiorelli G, Cappellini MD: Oxidative status and Malondialdehyde in beta thalassemia patients. Eur J Clin Invest 2002 March; 32 Suppl 1: 55-60.

Tinospora cordifolia (Willd.) Miersis an important medicinal plant belongs to family Amaranthaceae found in India. The plant has medicinal properties like treat convalescence from severe illness, arthritis (or joint diseases), liver disease, eye diseases, urinary problems, anemia, cancer, diarrhea, and diabetes. It also helps to remove toxins from the body. The successful protocol for in vitro propagation has been achieved for the medicinal important plant T. cordifolia by using nodal and apical shoot tip segments as explants. In vitro plantlets raised on Murashige and Skoog (MS) medium containing 0.5–3.00 mg/l BAP in combination with 0.2-1.00 mg/l IAA, 3% sucrose, and 0.3% clerigar. After 21 days maximum percentage of shoot organogenesis was obtained on medium containing 2.0 mg/l BAP and 0.2 mg/l IAA. The regeneration protocol developed in this study provides an important method of micropropagation of this plant. Furthermore, this protocol may be used for a large scale production of its medicinally active compounds and genetic transformations for further improvement.

1. Sinha, K., N. P. Mishra, J. Singh and S. P. S. Khanuja (2004). Tinospora cordifolia (Guduchi), a reservoir plant for therapeutic applications: A review. Indian Journal of Traditional Knowledge, 3(3): 257-270. 2. Mishra P., P. Jamdar, S. Desai, D. Patel and D. Meshram (2014). Phytochemical analysis and assessment of in vitro antibacterial activity of Tinospora cordifolia.Int. J. Curr. Microbiol.App.Sci., 3(3): 224-234. 3. Kirtikar K. R. and B. D. Basu (1987). Indian Medicinal Plants. International Book Distributors, Dehradun, India, (1): pp.77-80. 4. Aditi, S., K. Saroj, P. Aunji, R. Sabari and M. Niran (2009). In vitro study of Tinospora cordifolia (Willd.)Miers (Menispermaceae), BotanicaOrientalis: Journal of Plant Science, 6: 103–105. 5. Murashige, T. and F. Skoog (1962). A revised medium for rapid growth and bioassay for tobacco tissue cultures.Physiol. Plant, 15: 473-497. 6. Kumari, M. (2012). Evaluation of methanolic extracts of in vitro grown Tinospora cordifolia (Willd) for antibacterial activities. Asian J. Pharm Clin. Res., 5(3): 172-175. 7. Sivakumar, V., M. Dhana Rajan, A. M. Sadiq and A. Jayanthi (2012). In vitro micropropagation of Tinospora cordifolia (Willd.)Miers ex Hook. F. andThoms - An important medicinal plant, 3(2): 5-10. 8. Neeraja, P. V. and M. Elizabeth (2013). AmruthvalliJournal of Pharmacognosy andPhytochemistry(Tinospora cordifolia) multipurpose rejuvinator, International Journal of Pharmacuetical, Chemical and Biological Sciences, 3(2): 233-241. 9. Singh, S.S, S. C Pandey, S. Srivastava, V. S. Gupta and A. C. Ghosh (2003). Chemistry and medicinal properties of Tinospora cordifolia (Guduchi).Indian Journal of Pharmacology, 35: 83-91.

Diabetes mellitus is a common complication of chronic pancreatitis, can disturb the metabolism of zinc, copper, magnesium and selenium1. The serum magnesium and copper levels were estimated in sixty patients admitted in medicine department in GMC, Nagpur and in non diabetic healthy subjects. The result of study showed that serum copper were increased and magnesium level were decreased significantly in diabetic group compared to non-diabetic group. Thus it is concluded that these changes play an important role in the pathogenesis of type 2 DM by the involvement of these elements in the oxidative stress and may have a contributory role in the progression of DM and later development of complications.

1. Quilliot D, Dousset B., Guerci B, Dubois F, Drouin P, Ziegler O. Evidence that diabetes mellitus favors impaired metabolism of zinc, copper, and selenium in chronic pancreatitis. Pancreas 2001; 22: 299-306 2. Sarkar A, Dash S, Barik BK, Muttigi MS, Kedage V, Shetty JK. et al. Copper and Ceruloplasmin levels in relation to total thiols and GST in type 2 diabetes mellitus patients. Ind J Clin Biochem 2010; 25:74-76. 3. Viktorínová A, Toserová E, Krizko M, Durackova Z. Altered metabolism of copper, zinc, and magnesium is associated with increased levels of glycated hemoglobin in patients with diabetes mellitus. Metabolism 2009; 58:1477-1482 4. Zargar AH, Shah NA, Masoodi SR, Laway BA, Dar FA, Khan AR. et al. Copper, zinc, and magnesium levels in non-insulin dependent diabetes mellitus. Postgrad Med J 1998; 74:665-668. 5. Ankush RD, Suryakar AN, Ankush NR. Hypomagnesaemia in type-2 diabetes mellitus patients: a study on the status of oxidative and nitrosative stress. Ind J Clin Biochem 2009; 24:184-189. 6. Evliyaoglu O, Kebapcilar L, Uzuncan N, Kılıçaslan N, Karaca B,Kocaçelebi R. et al. Correlations of serum Cu+2, Zn+2, Mg+2 and HbA1c in Type 1 and Type 2 Diabetes Mellitus. Turkish Journal of Endocrinology and Metabolism 2004; 2: 75-79. 7. F Hussain, Maan MA, Sheikh MA, Nawaz H, Jamil A. Trace elements status in type 2 diabetes. Bangladesh Journal of Medical Science 2009; 8:44-45. 8. Pham T PC, Pham T PM, Pham SV, Miller JM, Pham PT. Hypomagnesemia in Patients with Type 2 Diabetes. Clin J Am Soc Nephrol 2007; 2: 366–373. 9. Trinder P. Determination of Glucose in blood using glucose-oxidase with an alternative oxygen acceptor. Annals Clinical Biochemistry 1969; 6: 24-27 10. Abernathy M.H, Fowler RT. "Micellar Improvement of the Calmagite Compleximetric measurement of magnesium in plasma". Clin Chem 1982; 28: 3. 11. Abe A, Yamashita S, Nona A . Sensitive and direct colorimetric assay for copper in serum clin chem. 1989; 35 (4):552-54. 12. Garber AJ. The importance of early insulin secretion and its impact on glycaemic regulation. Int J Obes Relat Metab Disord 2000; 24: Supp l: 32−37 13. Mishra S, Padmanaban P, Deepti GN, Sarkar G, Sumathi S, Toora BD. Serum Magnesium and Dyslipidemia in Type-2 Diabetes Mellitus. Biomedical Research 2012; 23: 295-306. 14. Paolisso G, Scheen A, D‘Onofrio F, Lefebvre P. Magnesium and glucose homeostasis. Diabetologia 1990; 33: 511-514. 15. Nadler JL, Buchanan T, Natarajan R, Antonipillai I, Bergman R, Rude R. Magnesium deficiency produces insulin resistance and increased thromboxane synthesis. Hypertension 1993; 21: 1024-1029 16. Kareem I, Jaweed SA, Bardapurkar JS, Patil VP. Study of magnesium, glycosylated haemoglobin and lipid profile in kdiabetic retinopathy. Ind J Clin Biochem 2004; 19: 124-127 17. unningham J, Leffell M, Mearkle P, Harmatz P. Elevated plasma ceruloplasmin in insulin-dependent diabetes mellitus: evidence for increased oxidative stress as a variable complication. Metabolism 1995; 44: 996-999. 18. Evans JL, Goldfine ID, Maddux BA, Grodsky GM. Oxidative stress and stress-activated signaling pathways: A unifying hypothesis of type 2 diabetes. Endo Rev 2002; 23: 599-622 19. Schlienger JL, Grunenberger F, Maier EA, Simon C, Chabrier G, Leroy MI. Disorders of plasma trace elements in diabetes, relation to blood glucose equilibrium. Presse Med 1988; 17:1076-1079.

Background and objective: Autism spectrum disorders are behaviourally defined disorder affecting 1 in 88 individuals. It is a complex neurodevelopmental disorder. The reaction time is an indirect index of processing capability of central nervous system and also a simple means for sensory and motor performance. Material and methods: The present study was conducted in Dept. of Physiology, MGM’S Medical College and Aurangabad. The study included 20 autistic children from “Arambh” autistic school and 20 normal children in the age group 10 to 15 years were taken for the control match. Auditory reaction time was determined by using an instrument reaction time apparatus designed by Anand agency, Pune. The data was statistically analyzed by using students paired “t” test. Result: Auditory reaction time was significantly increased in ASD children as compared with control. Conclusion: There is significant increase in auditory reaction time. Also delay in MSI in autism.

1. American Psychiatric Association 1994 Diagnostic and Statistical Manual of Mental Disorders: DSM-IV. 4th ed. American Psychiatric Association, Washington, D.C 2. Center for Disease Control. (2009). Autism and Developmental Disabilities Monitoringnetwork. Retrieve from: http://www.cdc.gov/ncbddd/autism/addm.html 3. Lindsay M. Oberman, Joseph P. McCleery, Edward M. Hubbard, etal Developmental changes in mu suppression to observed and executed actions in autism spectrum disorders Social Cognitive and Affective Neuroscience Advance Access published February 1, 2012 4. Kanner L 1943 Autistic disturbances of affective contact. Nervous Child 2:217–250 5. Elysa J. Marco, Leighton B.N ,etal Sensory processing in autism: Review of Neurophysiological findings. Pediatric Research 69: 48R- 54R,2011. 6. Weels: Robert J.Kosinsi, A Literature review on reaction time ,Clemson University, http://biology.clemson.edu/bp/lab/110/reaction.htm 7. R.D. Oades I, M.K. Walker 2, L.B. Geffen’ and L.M. Stern 3 Event-related potentials in autistic and healthy children on an auditory choice reaction time task International Journal of Psychophysiology, 6 (1988) 25-31 8. Dunn MA, Gomes H, Gravel J 2008 Mismatch negativity in children with autism and typical development. J Autism DevDisord 38:52–71 9. Courchesne E, Courchesne RY, Hicks G, Lincoln AJ 1985 Functioning of the brain-stem auditory pathway in non-retarded autistic individuals. Electroencephalogram ClinNeurophysiol 61:491–501 10. Rosenhall U, Nordin V, Brantberg K, Gillberg C 2003 Autism and auditory brainstem responses. Ear Hear 24:206–214 11. Kwon S, Kim J, Choe BH, Ko C, Park S 2007 Electrophysiologic assessment ofcentral auditory processing by auditory brainstem responses in children with autismspectrum disorders. J Korean Med Sci 22:656–659 12. Russo N, Nicol T, Trommer B, Zecker S, Kraus N 2009 Brainstem transcription ofspeech is disrupted in children with autism spectrum disorders. DevSci 12:557–567 13. Russo NM, Skoe E, Trommer B, Nicol T, Zecker S, Bradlow A, Kraus N 2008Deficient brainstem encoding of pitch in children with Autism Spectrum Disorders. Clin Neurophysiol 119:1720–1731 14. Whitehouse AJ, Bishop DV 2008 Do children with autism ‘switch off’ to speechsounds? An investigation using event-related potentials. DevSci 11:516–524 15. O’Neill M, Jones RS 1997 Sensory-perceptual abnormalities in autism: a case formore research? J Autism DevDisord 27:283–293 16. Courchesne E, Lincoln AJ, Kilman BA, Galambos R 1985 Event-related brainpotential correlates of the processing of novel visual and auditory information inautism. J Autism DevDisord 15:55–76 17. Courchesne E, Lincoln AJ, Yeung-Courchesne R, Elmasian R, Grillon C 1989Pathophysiologic findings in nonretarded autism and receptive developmental languagedisorder. J Autism DevDisord 19:1–17 18. Russo N, Foxe JJ, Brandwein AB, Altschuler T, Gomes H, Molholm S 2010Multisensory processing in children with autism: high-density electrical mapping ofauditory-somatosensory integration. Autism Res 3:253–267 19. Belmonte MK, Yurgelun-Todd DA 2003 Functional anatomy of impaired selectiveattention and compensatory processing in autism. Brain Res Cogn Brain Res17:651–664

Mesentric fibromatosis a predominantly histological diagnosis has been linked to the mesentry because of its anatomic location. Giant abdominal masses from the mesentry are uncommon. A case of mesenteric fibromatosis presenting as giant intra abdominal tumor is being reported here.

1. Mohammed Khalid Mirza Ghari, Salman Yousuf Guraya, Amir Mounir Hussein, Moustafa Mahmoud nafady Hego. Giant Mesentric Fibromatosis: Report of a case and review of the literature. World j Gastrointest Surg 2012 march 27; 4(3): 79-82. 2. Angela D. Levy, LTC, MC, USA. Fordi Rimola, MD. Anupamjit K. Mehrotra, MD. Leslie H. Sobin, MD. From the Archives of the AFIP, Benigh Fibrous Tumors and Tumorlike Lesions of the Mesentry: Radiologic Pathologic Correlation. Radiographics 2006; 26:245 – 264. 3. J. Janinis, m. Patriki, l. Vini, G. Arqavantinos and J.S Whelan. The pharmacological treatment of aggressive fibromatosis: a systematic review. Anals of Oncology 14: 181-190, 2003. 4. Jaime A. Rodriguez, MD, Luis a. Guarda, MD, and Juan Rosai, MD. Mesenteric Fibromatosis with Involvement of the Gastrointestinal Tract. Am J Clin Pathol 2004; 121: 93-98. 5. Olgu sunumu. Mesenteric fibromatosis: A case report. 6. Christos n Stoidis, Basileios G Spyropoulos, Evangelos P misiakos, Christos K Fountzilas, Panorea P Paraskeva, Constantine i Fotiadis. Surgical treatment of giant mesenteric fibromatosis presenting as a gastrointestinal stromal tumor: a case report. Stoidis et al, journal of medical case reports 2010, 4:314. 7. Rohan Shetty, Shubha Bhat, Rajesh Ballal, pramod Makannavar and Anil kumar K. N. Aggressive Mesentric Fibromatosis: a rare case report and review of literature.NUJHS Vol.3, no.1, March 2013, ISSN 2249-7110. 8. Geeta karbeet Radhakrishna, P. R. Bhat, Rajgopal K. Shenoy, Srinivas Pai, Harpreet Singh. Primary Mesenteric fibromatosis: A Case Report with Brief Review of Literature. Indian j Surg DOI 10.1007/s12262-012-0515-7. 9. I.A.Jan, S. Asim, S. Ahmad, T. Barqi, A. A. Chugtai, Infantile fibromatosis presenting as a neck mass. JPMA, February 2001. 10. Debner Louis P. Soft tissue, peritoneum, Retroperitoneum in pediatric surgical pathology, 2nd edition, Baltimore, USA. Williams and Wilkins 1987. PP885-90. 11. Enzinger FM, Weiss SW, Fibromatosis In: Enzinger FM, Weiss SW, editor soft tissue tumor St. Louis, MO; CV mosby CO; 1995. PP 201-229.

Background: Adverse health outcomes like maternal mortality and morbidity due to abortion could be drastically brought down if the women have access to safe abortion services. Abortion is one of the most fundamental health care needs of women. Aims: To assess care seeking behavior of currently married women in case of unwanted pregnancy and its social correlates. Settings: 12 Villages and 4 wards of Paschim Midnapur District of West Bengal. Participants: 2000 currently married women of reproductive age groups (15-49 yrs). Methods and Materials: Community based cross-sectional study was carried out among 2000 currently married women (15-49 yrs) in Paschim Midnapur district of West Bengal during May to October 2009 by stratified multistage random sampling and interviewed eligible women through pre-designed and pre-tested proforma by house to house survey. Statistical analysis: Proportions, Chi-square test. Results: Out of total study population, majority were in the age group of 24-29 yrs (31.5%). Most of the respondents belonged to illiterate and just literate group (46.9%), 87% were Hindu by religion. Regarding providers choice , majority (43.3%) were in favour of government hospital followed by nursing home (32.7%). 11.3%, 10.5% and 2.2% were in favour of Quacks, others group of providers and unaware respectively. 14.7 % of the educated women (secondary andabove) still preferred quacks. Preference of others group of providers was more (15.7%) among Low socio-economic group (BPL) than APL group (3.8%). So 24% of the study subjects having proper lack of knowledge either wrong perception (21.8%) or unawareness (2.2%) for safe abortion procedure. Preference of quacks was more among Muslims than Hindus as well as the women belonged to nuclear families and rural community. Conclusion: Awareness generation about safe abortion practice to be enhanced through mass media advocacy and interpersonal communication. Utilization of safe abortion services through more effective behavior change strategy.

Background: Adverse health outcomes like maternal mortality and morbidity due to abortion could be drastically brought down if the women have access to safe abortion services. Abortion is one of the most fundamental health care needs of women. Aims: To assess care seeking behavior of currently married women in case of unwanted pregnancy and its social correlates. Settings: 12 Villages and 4 wards of Paschim Midnapur District of West Bengal. Participants: 2000 currently married women of reproductive age groups (15-49 yrs). Methods and Materials: Community based cross-sectional study was carried out among 2000 currently married women (15-49 yrs) in Paschim Midnapur district of West Bengal during May to October 2009 by stratified multistage random sampling and interviewed eligible women through pre-designed and pre-tested proforma by house to house survey. Statistical analysis: Proportions, Chi-square test. Results: Out of total study population, majority were in the age group of 24-29 yrs (31.5%). Most of the respondents belonged to illiterate and just literate group (46.9%), 87% were Hindu by religion. Regarding providers choice , majority (43.3%) were in favour of government hospital followed by nursing home (32.7%). 11.3%, 10.5% and 2.2% were in favour of Quacks, others group of providers and unaware respectively. 14.7 % of the educated women (secondary andabove) still preferred quacks. Preference of others group of providers was more (15.7%) among Low socio-economic group (BPL) than APL group (3.8%). So 24% of the study subjects having proper lack of knowledge either wrong perception (21.8%) or unawareness (2.2%) for safe abortion procedure. Preference of quacks was more among Muslims than Hindus as well as the women belonged to nuclear families and rural community. Conclusion: Awareness generation about safe abortion practice to be enhanced through mass media advocacy and interpersonal communication. Utilization of safe abortion services through more effective behavior change strategy.

Any drug with potential to cause toxic reactions to structures of the inner ear, including the cochlea, vestibuler, semicircular canals, is considered ototoxic. The evidence for the ototoxicity of aminoglycoside antibiotics is overwhelming. Drug induced damage to the structures of the auditory and balance system can result in hearing loss, tinnitus and disequibrium. Fetal ototoxicity have been described after maternal exposure to aminoglycoside toxicity, are evaluated. There is susceptibility and genetic predisposition for Aminoglycoside ototoxicity. Relative oxygen species (ROS) participate in the cellular events leading to aminoglycoside induced hearing loss. Monitoring and challenges to hearing loss discussed. Prevention and future prospects explored.

1. ROBERT E. BRUMMETTl* AND KAYE E. FOX2 Aminoglycoside-Induced Hearing Loss in Humans ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, June 1989, p. 797-800 Vol. 33, No. 6 2. Rakesh Shrivastav, Ototoxicity. An illustrated Textbook of Ear,Nose and Throat and Head and Neck Surgery, Jaypee Brothers Edition2014 3. Pamela A Mudd, MD; Chief Editor: Arlen D Meyers, MD Ototoxicity http://emedicine.medscape.com/article/857679-overview#a30 4. M. E. Huth, A. J. Ricciand A. G. Cheng Mechanisms of Aminoglycoside Ototoxicity and Targets of Hair Cell Protection Mechanisms of Aminoglycoside Ototoxicity and Targets of Hair Cell Protection International Journal of Otolaryngology Volume 2011 (2011), Article ID 937861, 19 pages 5. Mohan Bansal, Sensoryneural Hearing Loss Diseases of Ear,Nose and Throat JAPEE Brothers 2013 Edition. 156-165 6. Dr Alka B. Patil Emerging Role of oxidative stress in female reproduction Indian Journal of obstetrics and Gynaecology Vol 1 No 2 July -December 2013 page 7-16 7. Damian G. Deavall, Elizabeth A. Martin, Judith M. Horner, and Ruth Roberts Drug-Induced Oxidative Stress and Toxicity Journal of Toxicology Volume 2012 (2012), Article ID 645460, 13 pages 8. Audiol Neurootol 2002;7:171–174 (DOI:10.1159/000058305) 9. Wu W.-J. • Sha S.-H. • Schacht J. Recent Advances in Understanding Aminoglycoside Ototoxicity and Its Prevention Audiol Neurootol 2002;7:171–174 http://emedicine.medscape.com/article/260725-overview#aw2aab6b8 Aminoglycosides 10. Ryan W, Sachin D (2014) Drug Induced Ototoxicity. Clin Exp Pharmacol 4:e132. doi: 10.4172/2161-1459.1000e132

Objective: The purpose of the present study was to determine the expression of cyclooxygenase-2 (COX-2) in patients with carcinoma of prostate and its clinical significance in relation to clinical pathological parameters. Materials and Methods: A total of 100 cases of prostatic tissue specimens consisting of 88 adenocarcinoma prostate and 12 Benign Prostatic Hyperplasia (BPH) were included in the study. Formalin-fixed paraffin-embedded tissue samples were initially stained using Hematoxylin and Eosin stains and graded according to Gleason scoring system. Immunohistochemistry for COX-2 were performed on these blocks. The expression pattern was determined and correlated with clinicopathological parameters. Results: A majority of well differentiated prostate carcinoma and BPH cases showed strong COX-2 expression. In contrast poorly differentiated and most of the moderately differentiated cases showed weak positivity. COX-2 expression pattern for different grades were found to be statistically significant (p=0.03). Clinically proven metastatic samples showed negative COX-2 expression. Correlation between serum PSA level with COX-2 expression did not show any significant relationship. Conclusion: COX-2 expression was found to be strong in well differentiated carcinoma of prostate irrespective of the PSA levels. Inhibitors of COX-2 may prove useful as a alternative therapeutic adjunct for the treatment of low grade prostatic carcinoma.

Objective: The purpose of the present study was to determine the expression of cyclooxygenase-2 (COX-2) in patients with carcinoma of prostate and its clinical significance in relation to clinical pathological parameters. Materials and Methods: A total of 100 cases of prostatic tissue specimens consisting of 88 adenocarcinoma prostate and 12 Benign Prostatic Hyperplasia (BPH) were included in the study. Formalin-fixed paraffin-embedded tissue samples were initially stained using Hematoxylin and Eosin stains and graded according to Gleason scoring system. Immunohistochemistry for COX-2 were performed on these blocks. The expression pattern was determined and correlated with clinicopathological parameters. Results: A majority of well differentiated prostate carcinoma and BPH cases showed strong COX-2 expression. In contrast poorly differentiated and most of the moderately differentiated cases showed weak positivity. COX-2 expression pattern for different grades were found to be statistically significant (p=0.03). Clinically proven metastatic samples showed negative COX-2 expression. Correlation between serum PSA level with COX-2 expression did not show any significant relationship. Conclusion: COX-2 expression was found to be strong in well differentiated carcinoma of prostate irrespective of the PSA levels. Inhibitors of COX-2 may prove useful as a alternative therapeutic adjunct for the treatment of low grade prostatic carcinoma.

During routine cadaveric dissection of lower abdomen and groin region for first M.B.B.S students in department of anatomy, Shri Bhausaheb Hire Government Medical College, Dhule, a case of bilateral undesended testes was found in formalin fixed male cadaver. Cryptorchidism is a condition in which testes fail to move down to scrotum. In some children testes reach to scrotum but later on rise above, these are known as acquired undescended testes. Although exact cause of undescended testis is not known but failure of formation of androgens is important cause. If both testes are undescended, they may remain immature and results in infertility. Uncorrected cases may develop germ cell tumor.

1. KL Moore, TVS Persaud, The developing human, clinically oriented embryology, 8th edition, south Asia edition,2008, Saunders Elsevier publication: 279-281 2. T.W Saddler, Langman’s medical embryology, 10th edition,Urogenital system, Lippincott William and wilkins, new Delhi, 2006: page 24. 3. S. B. Pillai and G. E. Besner, “Pediatric testicular problems,” Pediatric Clinics of North America, vol. 45, no. 4, pp. 813–830, 1998. 4. Arai Y, Mori T, Suzuki Y, Bern HA, Long term effects of perinatal exposure to sex steroids and Diethystilbesterol on the reproductive system of male mammals. Int Rev Cytol 84:235-268 5. Greco Tl, Duello TM, Gorski J, 1993, Estrogen receptors, estradiol and Diethystilbesterol in early development: the mouse as a model for study of estrogen receptors andestrogen sensitivity in embryonic development of male and female reproductive tracts, Endoer Rev 14: 59-71 6. Sharpe RM, Skakkebaek NE, 1993, Are estrogen involves in falling sperm counts and disorders in male reproductive tract? Lancet 341:1392-1395 7. Whitehead ED, Leiter E, 1981, Genital abnormalities and abnormal semen analysis in male patients exposed to Diethystilbesterol in utero, J Urol 125:47-50 8. Stillman R, 1982, In utero exposure to Diethystilbesterol: adverse effectson thereproductive tract and reproductive performance in male and female offspring. Am J Obst Gynecol 142:909-921 9. Adlercreutz H, 1990 Dietr, breasr cancer and sex hormones metabolism. Ann NY Acad Sci. 595: 281-290 10. SharpeRM, 1994, Regulation of spermatogenesis in: Knobil E, NeillJD (edi) The physio;ogy of reproduction, 2nd edition, Raven press, New York. 11. Williams, P.L., Bannister, L.H., Berry, M.M., Collins, P.,Dyson, M., Dussek, J.E. and Ferguson, M.W.J.: Gray’s Anatomy In: Nervous system. 38th Edn; Churchill Livingston. Edinburgh: 211-212(1995). 12. Werdelin, L., and Nilsonne, A. (1999). The evolution of the scrotum and testicular descent: A phylogenetic view. Journal of Theoretical Biology, 196, 61-72. 13. Moore, C. R. (1926). The biology of the mammalian testis and scrotum. Quarterly Review of Biology, 1, 4-50. 14. Bedford, J. M. (1978). Anatomical evidence for the epididymis as the prime mover in the evolution of the scrotum. American Journal of Anatomy, 152, 483-508. 15. Short, R. V. (1997). The testis: The witness of the mating system, the site of mutation and the engine of desire. Acta Paediatric Supplement, 422, 3-7. 16. Freeman, S. (1990). The evolution of the scrotum: A new hypothesis. Journal of Theoretical Biology, 145, 429-445. 17. Portman, A. (1952). Animal forms and patterns. New York: Schocken. 18. Setchell, B. P. (1998). The Parkes Lecture: Heat and the testis. Journal of Reproduction and Fertility, 114, 179-194. 19. Appell, R. A., Evans, P. R., and Blandy, J. P. (1977). The effect of temperature on the motility and viability of sperm. British Journal of Urology, 49, 751-756. 20. Makler, A., Deutch, M., Vilensky, A., and Palti, Y. (1981). Factors affecting sperm motility. VIII. Velocity and survival of human spermatozoa as related to temperatures above zero. International Journal of Andrology, 5, 559-569. 21. Valeri, A., Mianne, D. Merouze, F., Bujan, L., Altobelli, A., and Masson, J. (1993). Etude de la temperature scrotale chez 258 hommes sains, selectionnes par triage au sort dans une population d’hommes de l8 a 23 ans. Analyse statistique, observations epidemiologiques et mesure des diameters testiculaires. Progres en Urologie, 3, 444-452. 22. Evolutionary Psychology www.epjournal.net – 2009. 7(4): 517-526 23. Marin-Briggiler, C. I., Tezon, J. G., Miranda, P. V., and Vazquez-Levin, M. H. ((2002). Effect of incubating human sperm at room temperature on capacitation-related events. Fertility and Sterility, 77, 252-259. 24. Makler, A., Deutch, M., Vilensky, A., and Palti, Y. (1981). Factors affecting sperm motility. VIII. Velocity and survival of human spermatozoa as related to temperatures above zero. International Journal of Andrology, 5, 559-569. 25. Shrishailesh.D.M, Perinatal Torsion of Undescended Testis: Case Report, International journal of scientific research, 3(4), April 2014: 347

Aim: This study is aimed to find out the incidence of thrombocytopenia in leptospirosis patients and to correlate thrombocytopenia with other parameters like hepatorenal failure, lung involvement and bleeding manifestations. Material and Methods: This study was conducted at Department of Microbiology, JSS Medical College and Hospital, Mysore, India from September 2014 to February 2015. Ethical approval was obtained from the Institutional Ethics Committee. The medical records of all serologically confirmed leptospirosis patients were retrospectively reviewed. Thrombocytopenia was then categorized as mild, moderate and severe and then correlated with renal dysfunction, hepatic dysfunction and haemorrhagic manifestations along with the course of infection. Results: A total of 60 patients were serologically positive for leptospirosis during this study period. Thrombocytopenia was observed in 52/60 cases, bleeding manifestations were seen in11, 43 had hepatic failure, 22 had renal failure. Conclusion: Thrombocytopenia in patients with Pyrexia of Unknown Origin (PUO) should alert physicians to the differential diagnosis of leptospiral infection and prompt the institution of appropriate therapy. It is important to recognize thrombocytopenia early in the course of leptospirosis so that appropriate steps can be taken to prevent further complications associated with thrombocytopenia in such patients.

1. Vinetz JM. Leptospirosis. CurrOpin Infect Dis.2001; 14(5): 527-38. 2. Nicodemo AC, Del Negro G, Amato NV, Thrombocytopenia and leptospirosis. Rev Inst Med Trop Sao Paulo. 1989; 31:71-79. 3. Turgut M, Sunbul M, Bayirli D, Bilge A, LeblebicigluH, Thrombocytopenia Complicating the clinical course of leptospiral infection, The Journal of International Medical Research.2002;30:535-540. 4. Sumana MN, Linda RJ, Tabasum BM, Seroprevalence of Dengue and Leptospira co-infection in Mysore, Karnataka: A study in children at a tertiary care hospital Int.J.Inv.Pharm.Sci.2014;2(3):774-778. 5. Parimal P, Alka N, Grishma T, Serological correlation of clinically suspected cases of Leptospirosis in Valsad, South Gujarat, NJIRM. 2014; 5(4):22-24. 6. Jayashree S, Moushumi S, Thrombocytopenia in leptospirosis and role of platelet transfusion. Asian J Transfus Science. 2007; 1(2):52-55. 7. Dahler E F, Brunetta DM, de Silva Junior GB, Puster RA, Patrocinio RM, Pancreatic involvement in fatal human leptospirosis. Clinical and Histopathological features, Rev Inst Med Trop Sao Paulo. 2003; 45:307-13. 8. Nicodemo AC, Del Negro G, Amato Neto V, Thrombocytopenia and leptospirosis, Rev Ins Med Trop Sao Paulo.1990;32:252-9. 9. Kirchner GI, Krug N, Bleck JS, Fliser D, Manns MP, Wagner S, Fulminant course of leptospirosis complicated by multiple organ failure. Z Gastroenterol.2001; 39:587-592. 10. Higgin R, Coustneau G, The pathogenesis of leptospirosis Hemorrhages in experimental leptospirosis in guinea pigs.Can J Comp Med. 1977;41:174-181. 11. Edwards CN, Nicholson GD, Everard CO, Thrombocytopenia in leptospirosis. Am J Trop Med Hyg. 1982; 31(4):827-829. 12. Yang HY, Hsu PY, Pam MJ, Wu MS, Lee CH, Yu CC et al. Clinical distinction and evaluation of leptospirosis in Taiwan: A case control study, J Mephrology. 2005; 18:45-53. 13. Tantitanawat S, TanjathamS, Prognosticfactors associated with leptospirosis, J Med Assoc Thai.2003; 86(10):925-931.

Background: It is caused by Mycobacterium Tuberculosis (MTB), the causative organism of TB is spread almost exclusively by the respiratory route. Tuberculosis is the leading cause of death among HIV infected people; Rates of HIV-related tuberculosis have risen in countries in Europe, United States and South America, and the rates have increased so rapidly in India. Aim: find out treatment outcome in both HIV positive and HIV negative tuberculosis patients Objective: 1) find out treatment outcome in HIV positive TB patients 2) Find out treatment outcome in HIV negative TB patients. 3) Compare both result and give the summary. Method: A community based longitudinal study was conducted. All the participant who visit to hospitals Tb & chest department and register for the tuberculosis treatment. We are conducting three visits to collect the result of TB treatment. Result: Out of 206 Tb patient 42 patients was HIV patient & 164 HIV negative patient. In HIV positive patients we are found 50% cure rate, 11.9% of failure & 0% defaulter. About HIV negative cure rate was 82.9%Failure rate 7.9% and defaulter 2.4%. Conclusion: Cure rate was not up to RNTCP data because we contain both HIV positive patient and HIV negative patient. We are work for decrease the deflators in HIV negative group.

1. Murray, Christopher J.L., Lopez, Alan D.: The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries and risk factors in 1990 and projected to 2020: summary – WHO Geneva, Switzerland, 1996; W 74 96GL-1/1996. 2. TBC INDIA ,Ministry of Health and Family Welfare INDIA 3. History of TB Control TBC INDIA Director General of Health Services 4. Joint United Nations Programme on HIV/AIDS (2006). "Overview of the global AIDS epidemic" (PDF). 2006 Report on the global AIDS epidemic 5. The HIV- TB Co-infection Program Coordination Guidelines for Clinicians & Standard Operating Procedures National AIDS Control Organization & Central TB Division Ministry of Health and Family Welfare Nirman Bhawan, New Delhi-110011 6. Lucélia Henn+, Fabiano Nagel Comparison between Human Immunodeficiency Virus Positive and Negative Patients with Tuberculosis in Southern Brazil, Mem Inst Oswaldo Cruz, Rio de Janeiro. May/Jun. 1999 94(3): 377-381 7. H. T. Quy,* F. G. J. Cobelens Treatment outcomes by drug resistance and HIV status among tuberculosis patients in Ho Chi Minh City, Vietnam The International Journal of Tuberculosis and Lung Disease 2003 10(1):45–51 8. Jill Murray, Pamela Sonnenberg, Stuart C. Shearer, and Peter Godfrey-Faussett Human Immunodeficiency Virus and the Outcome of Treatment for New and Recurrent Pulmonary Tuberculosis in African Patients Am. J. Respir. Crit. Care Med., Volume 159, Number 3, March 1999, 733-740 9. Ackah AN, Coulibaly D, et al. Response to treatment, mortality, and CD4 lymphocyte counts in HIV-infected persons with tuberculosis in Abidjan, Côte d'Ivoire , Lancet. 1995 34 :607-10.

The present study is six years retrospective analysis (2008-2013) to find out the seroprevalence of HIV in pregnant women in a tertiary care hospital in rural area of Latur, Maharashtra. A total of 9763 pregnant women were screened for HIV as per the NACO (National AIDS Control Organization) guidelines out of which 22 (0.22%) were found positive for HIV. Highest number of HIV positive cases (nine) was found in the year 2008 and only one case was found positive in the year 2013. A significant decline from 0.38% in 2008 to 0.09% in 2013 was observed in last 6 years. These results indicate that there is an overall decline in HIV prevalence rate in ANC attendees.

1. R. Anantnarayan and C. K. Paniker. Human immunodeficiency Virus: AIDS. Textbook of Microbiology.9thedition.2013; 570-85. 2. Indian J Med. Micro 2009,July ;27;(3) 276-81 3. MSACS 4. NACO Annual report 2002-2004 5. HIV/AIDS in India.htt//en.wipedia.org/wiki/HIV/AIDS in India 6. Current epidemiological situation of HIV/AIDS chapter 2 Annual Report 2009-;2010; 1-6 7. Das HK, Goswami A, Sonowal R, Das MK. Assessment of HIV/AIDS sero-positivity Rate in the state of Nagaland, North-East India. Int Res. J. Med Sci 2014; (2); 17-23.

Introduction: The identification of sex in human skeleton is important for many anthropologists, anatomists and forensic experts. Pelvis remains the most reliable region for assessing sex. Sacrum, as a part of pelvis also demonstrates differences. The most useful aspect of such studies is to determine appropriate standards of parameters for sexual dimorphism in different populations. Hence this study was undertaken to evaluate the role of different parameters of sacrum in sex determination. Materials and Methods: Study was carried out in Department of Anatomy, BVDU Medical College, Pune. Adult, dry sacra were collected randomly from Anatomy department of different Medical colleges of Maharashtra, with the kind permission of the concerned authorities.141 sacra were classified in to male and female bones by observing parameters like length of sacrum, width of sacrum, transverse diameter of body of S1, anteroposterior diameter of S1, length of ala of sacrum. Results: As a part of univariate analysis, demarcating point (D.P.) was obtained for each of the parameter. The % of bones identified beyond D.P. was found for each of them. The accuracy of this method varied from parameter to parameter. Ventral straight length of sacrum, mid-ventral curved length, anteroposterior and transverse diameter of body of S1 were more in male than female sacra with statistically significant difference in them. Whereas values for the parameters like sacral width (breadth) and length of ala of sacrum were more in female than male sacra with statistically significant difference. Conclusion: For different populations based on geographic areas different anthropometric criteria should be applied which could be specific to that particular population. It can be concluded that to identify the sex of sacrum with 100 % accuracy, single parameter was not sufficient instead it requires multiple parameters and indices to reach at the most accurate result.

1. Stewart T.D.: Evaluation of the evidence from the skeleton. In the Legal Medicine era, 1954;407-450 2. Pearsons K.: On problem of sexing osteometric material. Biometrica 10, 479- 81 3. Flander L.: Univariate and Multivariate methods of sexing the sacrum. Am. J Phys. Anthropology, 1978; 49: 103-110. 4. Fisher R. A.: The use of multiple measurements in taxonomic problems.1936 Ann ---Egenetics, 179-88, cited by Giles. (1970) 5. Krogman W. M.: The human skeleton in legal medicine. Medical aspects. In Symposium of Medical problems Series II Levingson S. A. Editor Lippincott Philadelphia.1949 6. Fawcett F.: The sexing of the human sacrum. Journal of anatomy. 1938; 72:633 7. Davinvongs V.: The pelvic girdle of the Australian Aborigine, sex differences and sex determination. Am. Phys. Anthropology, 1963; 21(4): 443-455 8. Williams and Warwick.: Gray, s Anatomy (1995); 38th Edn : 528- 531 9. Raju P. B, Singh S. P.: Identification of sex from hip bone Demarcating Points. Journal of Anatomical society of India, 1977; 26: 111-117. 10. Siddiqui.: Dissertation for M.S. Anatomy, 2000. 11. Mishra S. R, Singh J. et al.: Identification of sex of sacrum of Agra region. Journal of Anatomical society of India, 2003; 52 (2): 132-136 12. Renuka: Sacrum: A Tool for Sex Identification M.S. (Anatomy) Dissertation, 2007.

During routine dissection of 50 year old male cadaver in the department of anatomy for undergraduate students we found variation of common facial vein, in which it was draining into external jugular vein of same side instead of internal jugular vein. This is rare isolated anomaly of common facial vein. Many other investigators also reported similar findings in previous studies.We are reporting here, the rare occurrence of the common facial vein draining into the external jugular vein unilaterally.Variation in the venous drainage of veins of the neck is having clinical importance for surgeon for the success of procedures in the neck also to avoid the complication during the procedures. This variation is also having embryological basis that will be discussed in this paper.

1. Standring S: Gray’s Anatomy: The Anatomical Basis of Clinical Practice, 39 edition. Edinburgh, Elsevier Churchill Livingstone, 2006, pp 273-4. 2. Choudhry R, Tuli A, Choudhry S: Facial vein terminating in the external jugular vein. An embryologic interpretation.SurgRadiol Anat. 1997; 19: 73-77. 3. Siddaraju KS:UnusaualDrinage of Common Facial Vein.Int. J. Chem. and Life Sciences, 2013, 02 (07), 1193-1194. 4. Pikkieff, Ellen: Subcutaneous veins of the neck. Journal of Anatomy, 1937, 72-119. 5. Peuker ET, Fischer G, Filler TJ (2001) Facial vein terminatingin the superficial temporal vein: a case report. JAnat, 198: 509-510. 6. Bertha A, et al. Anatomical Variations in Termination of Common Facial Vein. Journal of Clinical andDiagnostic Research [serial online] 2011 February [cited: 2011 Sep 30], 5, 24-27. 7. Abeysekara AM, Siriwardana HP, Prabaharan B, Tiwari A, adipolagedara N, Jacob S: Common facial vein: an alternative patch material in carotid angioplasty. ANZ.J.Surg. 2008; 78: 185-8. 8. Sabharwal P, Mukherjee D: Autogenous common facial vein or external jugular vein patch for carotid endarterectomy. Cardiovasc.Surg. 1998; 6: 594-7. 9. Hamilton, Boyd and Mossman: Human embryology 4th edition 1972, 261. 10. SuhaniSumalathaD’Silva et al Termination of thefacial vein into the external jugular vein: ananatomical variation, J Vasc Bras 2008, 7,174-175. 11. Kopuz et al. An unusual coursing of the facialvein.KaibogakuZasshi, 1995, 70, 20-2. 12. Hollinshead WH. Anatomy for surgeons; 2nd Edition1956, 1, 530-531. 13. ShilpaBathla, RituSingroha, S.K. Srivastava:(2012) Eur J Anat, 16 (3): 212-215)

patient was a post natal day 5 case with severe anemia(Hb 5 gm%) after home delivery who presented with grade 3 dyspneoa. Examination showed subinvolution of uterus. Ultrasound revealed POC of 5*4 cm .She was chosen for conservative management after informed consent in view of her high risk status due to severe anemia. She received 2 packed cell transfusions followed by parenteral Iron therapy in view of her iron deficiency picture as per investigations report.

1. Morgan M, Atalla R: Mifepristone and Misoprostol for the management of placenta accreta – a new alternative approach. BJOG2009;116:1002–1003. 2. Pandey D, Majumdar A:MIFEPRISTONE: a Promising Adjunct toConservative Management of Placenta Accreta.South Pacific Journal of Pharma and BioScience;2014,2(1):123-125. 3. Chen Y ,Wang Y ,Zhuang Y, Zhou F ,Huang L, Mifepristone increases the cytotoxicity of uterine natural killer cells by acting as a Glucocorticoid Antagonist via ERK Activation,2012, PLoS ONE 7(5) :e36413. doi:10.1371/journal.pone.0036413.

Radial artery has been used in coronary artery bypass grafting, in forearm flap surgeries and in renal dialysis by making an autogenous fistula. In present study, ninety upper limbs from 45 formalin-fixed cadavers were dissected meticulously to expose the radial artery from its origin to its termination. The morphometric parameters like distance between interepicondylar line and bifurcation of brachial artery, length of radial artery and internal diameter of radial artery at various levels were measured. In cases of usual bifurcation of brachial artery, mean distance between interepicondylar line (IEL) and bifurcation of brachial artery on right side was 3.56 cm and on left side it was 3.49 cm and the mean length of radial artery on the right side was 26.73 cm and on left side it was 26.58 cm. Average distance of high bifurcation of brachial artery above the interepicondylar line was found to be 5.1 cm on the right side and 4.9 cm on the left side. The length of radial artery from its origin to the first dorsal interosseous space in the cases of high bifurcation of brachial artery was found to be in the range of 27.0 - 46.5 cm on the right side and 28.0 – 47.0 cm on the left side. The length of radial artery from its origin to the first dorsal interosseous space in the cases of high origin of radial artery was found to be in the range of 40.0 - 45.0 cm. The mean diameter of radial artery on right side was 2.35 mm and on left side it was 2.30 mm.

1. Williams PL, Bannister LH, Berry MM el al. Grey’s Anatomy. In: Cardiovascular System. 38th ed. London Churchill Livingstone, 1999; 299. 2. A.Y. Nasr. The radial artery and its variation: anatomical study and clinical implication. Folia morphol.2012; 71(4): 252-62. 3. Drizenko A, Maynou C, Mestdagh H, Bailleul JP. Variations of radial artery in man. Surg Radiol Anat. 2000; 22(5-6): 299-303. 4. Patnaik, VVG, Kalsey G, Singla, R K. Bifurcation of Axillary artery In Its 3rd Part -A case report. J. Anat. Soc. India.2001; 50(2): 166-169. 5. Mullan, Geoffrey, Naeem PJ, Ellis H. Variation in the bifurcation of brachial artery in 30 Caucasian cadavers. Clin. Anat. 2003; 16(5): 461-465. 6. Mc Cormack LJ, Cauldwell EW, Anson BJ. Brachial and antebrachial arterial patterns; a study of 750 extremities. Surg Gynecol Obstet.1953; 96: 43–54. 7. Acar C, Jebara VA, Portognese M, Fontaliran F, Devaniam P, Chchques JC, Meinger V, Carpenter A : Comparative anatomy and histology of the radial artery and the internal thoracic artery :implication for coronary artery bypass. Surg. Radiol Diagnosis 1991; 13: 283-288. 8. Barry MM, Foulon P, Touati G, Ledoux B, Sevestre H, Carmi M. Comparative histological and biometric study of the coronary, radial and left internal thoracic arteries. Surg. Radiol Anat. 2003; 25: 284-289.

Aim and Objectives: 1) To compare learning gain between traditional demonstration and modified demonstration. 2) To implement better method throughout the year. 3) Application of knowledge of anatomy for the better patient care. Methodology: Ist MBBS (100) students 2014-15 batch pretest on bones of upper extremity was taken and evaluated. Students are divided into two groups Group-A and Group-B50 students each. For the one Group-A demonstration is done by routine demonstrations and for the Group –B teaching was started with modified method that is with bones and showing the video clips of respective bones. After the completion of demonstration of bones of upper extremity posttest was taken and evaluated. Statistical analysis was done with the help of excel program. Results: For the bones of upper extremity demonstration, mean score of the Group- B is more as compared to Group A. The calculated Z-value is three times greater than standard error value. Hence the observed difference in mean score of two groups is real in 99% students and is due to the intervention given to the students. Conclusions: The learning gain for the group-B is more than Group-A. More learning gain for this group is because of intervention that is video clip.

1. Forrest S. Learning and teaching: the reciprocal link. J ContinEducNurs2004; 35:74-9. 2. Falk-Nilsson E, Walmsley D, Brennan M, Fournier DM, Junfin Glass B, Haden K. Cognition and learning. Eur J Dent Educ 2002; 6:27-32. 3. Ormrod JE, editor. Human learning. 3rd ed. Sydney: Prentice Hall; 1999. 4. Chadwick SM, Bearn DR. Teaching and learning: an update for the orthodontist. J Orthodont2002; 29:162-7. 5. Chadwick SM, Bearn DR, Jack AC, O'Brien KD. Orthodontic undergraduate education: developments in a modern curriculum. Eur JDent Educ2002; 6:57-63. 6. Stewart AM. Centre for Medical Education. Principles of teaching and learning. Scotland: Univer Dundee; 2005. 7. Nickerson RS, Perkinns DN, Smith EE, editors. The teaching of thinking. New Jersey: Lawrence Erlbaum Associates Publishers; 1985. 8. Fotheringham MJ, Owies D, Leslie E, Owen N. Interactive healthcommunication in preventive medicine: internet-based strategiesin teaching and research. Am J Prev Med 2000; 19:113-20. 9. Alkin MC, editor. Encyclopedia of educational research. 6th ed. New York: McMillan Publishing; 1992. 10. Steckner K, Borkowski R. On-line resources for the pain medicine physician. RegAnesth Pain Med 2002; 25:291-5. 11. Geuna S, Giacobini-Robecchi MG. 2002. The use of brainstorming for teaching human anatomy.Anat Rec 269:214–216. 12. Carmichael SW, Pawlina W. 2000. Animated Power Point as a tool to teach anatomy.Anat Rec 261:83–88. 13. Galva´n SM, Visciglio S, Andreotti C, et al. 1999. The effects of the use of image technologies in the learning of facticsubjects upon students of veterinary anatomy. Rev ChilAnat 17:1–15 14. Schwartz EL. 1980. Computational anatomy and functional architecture of striate cortex: A spatial mapping approach to perceptual coding. Vision Res 20:198– 216. 15. Trelease RB. 2002. Anatomical informatics: Millennial perspectives on a newer frontier. Anat Rec 269:224–235. 16. VanSint Jan S, Crudele M, Gashegu J, et al. 2003. Development of multimedia learning modules for teaching human anatomy: Application to osteology and functional anatomy. Anat Rec (New Anat) 272B:98–106. 17. Bukowski EL. 2002. Assessment outcomes: Computerized instruction in a human gross anatomy course. J Allied Health 31; 153-158. 18. Brown G, Manogue M. AMEE Medical Education Guide No.22: Refreshing lecturing: a guide for lecturer, Medical Teacher. 2001; 23(3):231-44. 19. Brill J.M, Galloway C. Perils and Promises: University Instructors Integration of Technology in Classroom- Based Practices, British Journal of Educational Technology, 2007; 38:95-105.