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Wild-type CantonS flies of Drosophila melanogaster were treated with ellagic acid at 100 μM and 200 μM concentrations. Longevity assay showed male flies fed with 200 μM ellagic acid displayed longer mean lifespan and maximum lifespan than control flies. Female flies fed with 200 μM ellagic acid laid less number of eggs than control. The eclosion time was less in female flies fed with 200 μM ellagic acid. Ellagic acid fed female flies performed better than male flies and control flies for heat shock tolerance and starvation stress. Male flies treated with 100 μM ellagic acid recovered faster from cold shock compared with control flies. Male and female flies treated with ellagic acid displayed increased survival following exposure to 5% hydrogen peroxide. Gene expression studies displayed upregulated expressions of CAT, dFOXO, ATG1, and SOD2 in ellagic acid-treated male flies, and upregulated expressions of dFOXO, CAT, and SOD2 in ellagic acidtreated female flies. Results from these studies show the pro-longevity effect of ellagic acid on Drosophila melanogaster.

Alveolar soft-part sarcoma (ASPS) is an extremely rare disease arising from connective tissues with a propensity for recurrence and metastasis. Clinically, it can be confused with hemangioma or arterio-venous malformations. Thus, a high index of suspicion and histopathological examination are required to make a definitive diagnosis. We report a case of recurrent ASPS in a young female with multiple sites involvement without any features of metastasis who has been treated with excision of the symptomatic lesions followed by chemotherapy.

Checkpoint activation and gene expression modulation represent key determinants of cellular survival in adverse conditions. The former is regulated by cyclin-dependent kinases (CDKs) while the latter can be controlled by mitogen-activated protein kinases (MAPKs). Association between cell-cycle progression and MAPK-dependent gene expression exists in cells growing in optimal environments. While MAPK-mediated regulation of the cell cycle is well characterised, the reciprocal influence of mitotic CDK on stress response is not well studied. We present evidence that CDK activity can regulate the extent of MAPK activation in Schizosaccharomyces pombe cells. We show that increasing or decreasing mitotic CDK (Cdc2) activity in S. pombe cells can affect the activation of stress responsive MAPK (Spc1) even in the absence of stress stimuli. Our results indicate that the strong correlation between Cdc2 activity and Spc1 MAPK-activity in S. pombe is important in regulating mitotic timing. This article has an associated First Person interview with the first author of the paper.

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