OBJECTIVE:The objectives were to study the relationships of insulin resistance with generalized and abdominal obesity, and body fat patterning in urban postpubertal Asian Indian children. DESIGN: Cross-sectional, population-based epidemiological study. SUBJECTS: In all, 250 (155 males and 95 females) healthy urban postpubertal children. MEASUREMENTS: Anthropometric profile, percentage of body fat (%BF), fasting serum insulin, and lipoprotein profile. RESULTS: Fasting insulin correlated significantly with body mass index (BMI), %BF, waist circumference (WC), central and peripheral skinfold thicknesses and sum of four skinfold thicknesses ( P 4SF) in both sexes, and with systolic blood pressure and waist-to hip circumference ratio (W-HR) in males only. Consistent increase in fasting insulin was noted with increasing values of central skinfold thickness at each tertile of peripheral skinfold thickness, WC, and %BF. Central skinfold thickness correlated with fasting insulin even after adjusting for WC, W-HR, and %BF. The odds ratios (OR) (95% CI) of hyperinsulinemia (fasting insulin concentrations in the highest quartile) were 4.7 (2.4-9.4) in overweight subjects, 8 (4.1-15.5) with high %BF, 6.4 (3.2-12.9) with high WC, 3.7 (1.9-7.3) with high W-HR, 6.8 (3.3-13.9) with high triceps skinfold thickness, 8 (4.1-15.7) with high subscapular skinfold thickness, and 10.1 (5-20.5) with high P 4SF. In step-wise multiple logistic regression analysis, %BF [OR (95% CI): 3.2 (1.4-7.8)] and ?4SF [OR (95% CI): 4.5 (1.8-11.3)] were independent predictors of hyperinsulinemia, similar to insulin resistance assessed by HOMA (homeostatic model of assessment) in the study. CONCLUSION: A high prevalence of insulin resistance in postpubertal urban Asian Indian children was associated with excess body fat, abdominal adiposity, and excess truncal subcutaneous fat. Primary prevention strategies for coronary heart disease and diabetes mellitus in Asian Indians should focus on the abnormal body composition profile in childhood.

Direct massively parallel sequencing of SARS-CoV-2 genome was undertaken from nasopharyngeal and oropharyngeal swab samples of infected individuals in Eastern India. Seven of the isolates belonged to the A2a clade, while one belonged to the B4 clade. Specific mutations, characteristic of the A2a clade, were also detected, which included the P323L in RNA-dependent RNA polymerase and D614G in the Spike glycoprotein. Further, our data revealed emergence of novel subclones harbouring nonsynonymous mutations, viz. G1124V in Spike (S) protein, R203K, and G204R in the nucleocapsid (N) protein. The N protein mutations reside in the SR-rich region involved in viral capsid formation and the S protein mutation is in the S 2 domain, which is involved in triggering viral fusion with the host cell membrane. Interesting correlation was observed between these mutations and travel or contact history of COVID-19 positive cases. Consequent alterations of miRNA binding and structure were also predicted for these mutations. More importantly, the possible implications of mutation D614G (in S D domain) and G1124V (in S 2 subunit) on the structural stability of S protein have also been discussed. Results report for the first time a bird's eye view on the accumulation of mutations in SARS-CoV-2 genome in Eastern India.

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The mechanism of indomethacin-induced gastric ulcer healing by ellagic acid (EA) in experimental mice model is described in our study. Ulcer index (UI) and myeloperoxidase (MPO) activity of the stomach tissues showed maximum ulceration on the third day after indomethacin (18 mg/kg, single dose) administration. Preliminary observation of UI and MPO activity suggests that EA possesses ulcer-healing activity. Other anti-ulcer parameters such as the levels of prostaglandin E(2), cyclooxygenase (COX) 1 and 2 enzymes, anti-inflammatory cytokines [interleukin (IL)-4 and -5], pro-angiogenic factors, e.g. vascular endothelial growth factor, hepatocyte growth factor (HGF), and endothelial growth factor (EGF) were down-regulated by indomethacin. EA (7 mg/kg/day) treatment for 3 days shifted the indomethacin-induced pro-inflammatory biochemical parameters to the healing side. These activities were correlated with the ability of EA to alter the COX-2-dependent healing pathways. The ulcer-healing activity of EA was, however, compromised by pre-administration of the specific COX-2 inhibitor, celecoxib, and NS-398. Taken together, these results suggested that the EA treatment accelerates ulcer healing by inducing IL-4, EGF/HGF levels and enhances COX-2 expression.