Abstract
Severe heat stress is becoming a more frequent problem for both humans and animals as climate change progresses. Heat stress intolerance (HSI) is likely to have poorly understood genetic susceptibility factors. Expressed mutations in RYR1 confers intolerance is one of the best known monogenic causes of HSI that may be mediated by uncontrolled loss of Ca2+ from SR/ER stores in muscle fibers and possibly neurons. Dehydropiandrosterone (DHEA), an endogenous steroid hormone precursor, is one of the most abundant circulating steroids in humans.
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