Analyses of frequency profiles of markers on disease or drug-response related genes in diverse populations are important for the dissection of common diseases. We report the results of analyses of data on 405 SNPs from 75 such genes and a 5.2 Mb chromosome, 22 genomic region in 1871 individuals from diverse 55 endogamous Indian populations. These include 32 large (>10 million individuals) and 23 isolated populations, representing a large fraction of the people of India. We observe high levels of genetic divergence between groups of populations that cluster largely on the basis of ethnicity and language. Indian populations not only overlap with the diversity of HapMap populations, but also contain population groups that are genetically distinct. These data and results are useful for addressing stratification and study design issues in complex traits especially for heterogeneous populations.

Results suggest significant improvements in grading of fatty liver, liver span, measures of insulin resistance, and lipids with use of canola and olive oil compared with control oils in Asian Indians with NAFLD.

Epidemiological data in COVID-19 mortality indicate that men are more prone to die of SARS-CoV2 infection than women, but biologic causes for this sexual dimorphism are unknown. We discuss the prospective behavioral and biological differences between the sexes that could be attributed to this gender-based differentiation. The female sex hormones and the immune stimulatory genes including toll-like receptors, interleukins, micro-RNAs present on X-chromosome may impart lesser infectivity and mortality of the SARS-CoV-2 in females over males. The sex hormone estrogen interacts with the Renin-Angiotensin-Aldosterone System, one of the most critical pathways in COVID-19 infectivity, and modulate the vasomotor homeostasis. Testosterone on the contrary enhances the levels of the two most critical molecules angiotensin converting enzyme 2 (ACE2) and the transmembrane protease, serine-type 2 (TMPRSS2), transcriptionally and post-translationally, thereby increasing viral load and delaying viral clearance in men as compared to women. We propose that modulating sex hormones, either by increasing estrogen or anti-androgen, may be a therapeutic option to reduce mortality from SARS-CoV-2.

High-altitude illnesses (HAIs) result from acute exposure to high altitude/hypoxia. Numerous molecular mechanisms affect appropriate acclimatization to hypobaric and/or normobaric hypoxia and curtail the development of HAIs. The understanding of these mechanisms is essential to optimize hypoxic acclimatization for efficient prophylaxis and treatment of HAIs. This review aims to link outcomes of molecular mechanisms to either adverse effects of acute high-altitude/hypoxia exposure or the developing tolerance with acclimatization. After summarizing systemic physiological responses to acute high-altitude exposure, the associated acclimatization, and the epidemiology and pathophysiology of various HAIs, the article focuses on molecular adjustments and maladjustments during acute exposure and acclimatization to high altitude/hypoxia. Pivotal modifying mechanisms include molecular responses orchestrated by transcription factors, most notably hypoxia inducible factors, and reciprocal effects on mitochondrial functions and REDOX homeostasis. In addition, discussed are genetic factors and the resultant proteomic profiles determining these hypoxia-modifying mechanisms culminating in successful high-altitude acclimatization. Lastly, the article discusses practical considerations related to the molecular aspects of acclimatization and altitude training strategies.

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