By Dan Cossins | July 1, 2013
Excerpt: Researchers discover that unlike brown fat cells, white fat cells can directly sense cooling temperatures to switch on genes that control heat production.
My comment: The study reports findings consistent with what is currently known about Nutrient-dependent / Pheromone-controlled thermodynamics and thermoregulation (prepublication), which is exemplified in model organisms that now include a human population. Kamberov et al and Grossman et al detailed the adaptive evolution of a population in what is now central China.
A single nutrient-dependent amino acid substitution incorporates what is currently known about the thermodynamics of intracellular signaling, internuclear interactions, and stochastic gene expression of de novo genes via alternative splicings that result in organism-level thermoregulation (in species from microbes to man). Cause and effect is established through the conserved molecular mechanisms for adaptive evolution (i.e., via ecological, social, neurogenic, and socio-cognitive niche construction). See for example: Nutrient–dependent / pheromone–controlled adaptive evolution: a model (published 6/14/13).
I suspect it will not be long until nutrient-dependent thermodynamic control of antibiotic resistence in E. Coli — and perhaps in other gram negative or gram positive organisms — will be linked to cause of death by sepsis in cases where the organism more effectively thermoregulates than the invidual it kills. Unfortunately, however, I don’t know of anyone not associated with Bonnie Bassler who is examining aspects of quorum-sensing in bacteria, which will lead to incorporating nutrient-dependent pheromone-controlled reproduction of microbes in the treatment of human bacterial diseases and possibly in obesity-linked cancer et al.