Clearly water replacement and vitrification are indispensable for successful induction of anhydrobiosis. Nevertheless, our present data suggest that such protective mechanisms are insufficient for the maintenance of structural integrity of DNA in dry cells. Concerning this point, genetic adaptations to anhydrobiosis in the sleeping chironomid show some functional analogies with those of the radiotolerant bacteria Deinococcus radiodurans, in which both desiccation and irradiation cause severe DNA damage, Reversine 656820-32-5 followed by prolonged DNA recovery period associated with delay in cell cycle. At the same time there are clear differences in these two phenomena, i.e., DNA reparation machinery and oxidative stress-response are different in eukaryotes and prokaryotes, genome organization in insects is much more complex and there is cell and tissue specification. In addition, recent studies have suggested that DNA breaks take place in other anhydrobionts such as bdelloid rotifers. Therefore, this convergent characteristics, as well as molecular protection by glasses, must be taken into account for future development of biotechnology, i.e., dried cell preservation. The anhydrobiotic chironomid larvae presumably experience nuclear DNA fragmentation with each cycle of desiccation and rehydration, and must have overcome this threat efficiently to survive the drought season. It is likely that an initial increase in the expression of genes coding for antioxidants and DNA repair enzymes as well as the increase in antioxidant activity are rather typical reactions of common insects to desiccation stress. During the course of evolution, P. vanderplanki might have intensified this response, concomitantly with the acquisition of an ability to preserve the viability of cells beyond the dehydration threshold at which other insects would die. This anhydrobiosisrelated evolution of augmented antioxidant protective mechanisms and DNA repair machinery is also most likely responsible for the remarkable cross-resistance of P. vanderplanki larvae in both dry and hydrated forms to the different types of ionizing radiation. Adipose tissue dysfunction belongs to the primary defects in obesity and may link obesity to several health problems including increased risk of type 2 diabetes, fatty liver, and cardiovascular disease. Altered adipokine serum concentrations are an early symptom of impaired adipose tissue function and may contribute to the development of obesity-associated disorders. In patients with type 2 diabetes, elevated tumor necrosis factor a, C-reactive protein, interleukin plasminogen activator inhibitor-1, retinol binding protein 4, chemerin, fetuin-A, visfatin/Nampt, resistin and reduced adiponectin and IL-10 serum concentrations have been reported.