Indian Journal of Medical Sciences
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Item 0.5 percent silver nitrate in treatment of burns.(1981-06-01) Agrawal, B R; Yemul, V L; Khairatkar, S NItem 17-Ketosteroid excretion in urine in duodenal ulcer patients.(1981-02-01) Shah, M A; Akhtar, M A; Shah, S N; Shah, M Y; Togoo, M SItem 2009H1N1 Infection in a 1-day-old neonate.(2010-12) Valvi, Chhaya; Kulkarni, Rajesh; Kinikar, Aarti; Khadse, SandhyaA full-term female neonate was delivered with meconium stained amniotic fluid by cesarean section by a 2009H1N1 positive 22-year-old second gravida mother, who developed symptoms 8 days prior to delivery. The neonate was completely and immediately isolated from the mother after delivery. Oseltamivir was started at birth to the neonate who had a potential possibility of 2009H1N1 infection. At 5 hours of life, the neonate developed respiratory distress. The neonate's throat swab sent for 2009H1N1 by real-time polymerase chain reaction (RT-PCR) assay was positive. The neonate required oxygen by hood for 3 days and made an uneventful recovery. The mother developed acute respiratory distress syndrome after delivery, requiring ventilatory care for 14 days and was discharged after 25 days stay in hospital. 2009H1N1 infection, although rare, needs a high index of suspicion and prompt therapy in neonates. Clinicians should be alert about the possibility of perinatal transmission of 2009H1N1.Item A 24 year-old male with yellow nail syndrome having bronchiactasis without pleural effusion as a pulmonary manifestation.(2013-07) Saeed, Rebeen R; Mustafa, Hemn MYellow nail syndrome is a rare entity of unknown etiology. Classically, it consists of a triad of slow-growing yellow nails of fingers and toes, lymphedema, and pulmonary manifestations mainly pleural effusion. Other pulmonary manifestations also have been described in the literature such as bronchiectasis, recurrent pneumonias, bronchitis, and sinusitis. This paper describes a case of yellow nail syndrome which did not have the classic triad of the condition; he presented with progressive yellow hand and toe nails, intermittent lymphedema, bronchiactasis, and sinusitis without pleural effusion.Item 298 alleged anti-fertility plants of India.(1960-07-01) CASEY, R CItem 400 million children deprived of safe water.(2006-03-21)Item Abdominal tubectomy--as a safe OPD procedure in rural area.(1989-10-01) Verma, DItem The aberrant replacing arteries.(1975-06-01) Murthy, C KItem Ablation of the pituitary.(1971-03-01) Deodhar, S DItem Abnormal radial artery in down syndrome: A rare but clinically important association.(2008-04-01) Karande, Sunil; Jagtap, Sujit; Garg, AshwinItem ABO agglutinins in the saliva of Indians form Bombay.(1972-08-01) Badaktere, S S; Bhatia, H MItem ABO and AB blood groups in Punjab.(1958-11-01) TALWAR, C L; SAWHNEY, C PItem ABO blood group genes in schizophrenia and manic depressive psychosis.(1972-08-01) Gaekwad, R S; Niyogi, A K; Jagtiani, RItem ABO blood groups and pulmonary tuberculosis.(1962-06-01) SHENOY, M A; DAFTARY, V GItem ABO blood groups in active cases of smallpox.(1966-02-01) Sukumaran, P K; Master, H R; Undevia, J V; Balakrishnan, V; Sanghvi, L DItem ABO blood groups in relation to cancer cervix.(1967-09-01) Tyagi, S P; Tiagi, G K; Pradhan, SItem Absence of factor V Leiden (G1691A) mutation, FII G20210A allele in coronary artery disease in North India.(2003-12-01) Gupta, N; Khan, F; Tripathi, M; Singh, V P; Tewari, S; Ramesh, V; Sinha, N; Agrawal, SBACKGROUND: Interaction between various genetic and environmental factors is associated with coronary artery diseases (CADs). Factor V Leiden mutation (FVL) and FII G20210A polymorphism are two recently described genetic factors with a propensity towards venous thrombosis, however, with a doubtful role in coronary artery disease and myocardial infarction. AIM: Present study was conducted to assess the relationship of both these factors in coronary artery disease in population from North India. SETTING AND DESIGN: Case control study. MATERIAL AND METHODS: Two hundred angiographically proven coronary artery disease patients were studied to examine the association of Factor V Leiden mutation and FII G20210A mutation with coronary artery disease and myocardial infarction. Out of 200 patients, 51 had myocardial infarction. Two hundred controls were selected who were from north India and were also age and sex matched. RESULTS AND CONCLUSIONS: Our results indicate that both these polymorphisms were totally absent in our population, therefore, these variants cannot be considered as independent risk factors or as a predictor for CAD. However, there is a need to confirm the above findings on patients from different populations from different parts of the country as there are reports which show that the incidence of Factor V Leiden varies from 1.3 % to 10%.