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Ray, G.

Publications and source records attributed to Ray, G..

2 recordsLinked to original sources

Carboxylic acids that drive mosquito attraction to humans activate ionotropic receptors

The mosquito, Aedes aegypti, is highly anthropophilic and continues to transmit debilitating arboviruses within human populations. Female mosquitoes are attracted to sources of blood by responding to odor plumes that are emitted by their preferred hosts. Acidic volatile compounds, including carboxylic acids, represent particularly salient odors driving this attraction. Importantly, carboxylic acids are major constituents of human sweat and volatiles generated by skin microbes. As such, they are likely to impact human host preference, which is a dominant factor in disease transmission cycles. A more complete understanding of mosquito host attraction will necessitate the elucidation of molecular mechanisms of volatile odor detection that function in peripheral sensory neurons. Recent studies have shown that members of the variant ionotropic glutamate receptor gene family are necessary for physiological and behavioral responses to acidic volatiles in Aedes. In this study, we have identified a subfamily of variant ionotropic receptors that share sequence homology across several important vector species and are likely to be activated by carboxylic acids. Moreover, we demonstrate that selected members of this subfamily are activated by short chain carboxylic acids in a heterologous cell expression system. Our results are consistent with the hypothesis that members of this receptor class underlie acidic volatile sensitivity in vector mosquitoes and provide a frame of reference for future development of novel mosquito attractant and repellent technologies.

molecular biology↗

Rapid eye movement sleep deprivation causes apoptotic cell-death of the hepatocytes in rat

IntroductionThe rapid eye movement sleep deprivation (REMSD) of rats relates with increased inflammations, acute phase response, oxidative damage, neuronal cell loss, and neurodegenerative diseases. Whereas, its role outside brain are not well studied. This study tried to explore the causal effect of REM sleep loss on hepatocytes.\n\nMethodsWe deprived the rats of REM sleep using standard flower pot method. We focused on liver to see the REMSD affects which controls most of the metabolic processes of the body.\n\nResultsWe report here that flower pot induced REMSD causes apoptotic cell death of hepatocytes (~10% by Annexin Assay & ~20% by TUNEL assay). This were further got alleviated up to extent after sleep recovery of 5 days (recovered approximately 8.0% by Annexin Assay & 14% by TUNEL assay). The gene expression and protein level profiling revealed the up-regulation of p53, Bax, Cytochrome c, Caspase 3, and Caspase 9. While, Bcl2 which is an anti-apoptotic protein were down-regulated in response to REMSD. Relentless recovery of 5 days affected the expression pattern of these genes/proteins.\n\nConclusionsOur study offer great pathological and physiological significance for sleep loss, by inferring the apoptotic cell-death in the hepatocytes of rat. This further signifies the functional and preventive role of REM sleep which is unique to mammals and avians with certain exceptions, as its loss can affect the natural well-being and survival of the individuals.\n\nHighlights of the studyO_LIWe observed significant apoptosis in the hepatocytes of REMSD group of rats.\nC_LIO_LIOur expression analysis confirmed altered expression for genes p53, Bcl2, Bax, and Caspase-3 after REMSD.\nC_LIO_LIProtein level analysis supported our gene expression results for p53, Bcl2, Bax, Caspase 3 and Caspase 9 after REMSD.\nC_LIO_LISleep recovery improved the respective genes and protein expression levels towards normalcy, signifying the functional role of REM sleep.\nC_LI

molecular biology↗