42 research outputs found
THEORY OF SUPERFLUIDITY IN HELIUM- A REVIEW
In nature the inert gas helium exists in two forms, isotopes, with fundamentally different properties. The study of superfluidity and its effect on the property of helium liquid is considered to be principle interest of the researcher from the last century. In this paper a brief account of the property of helium isotopes and the physics involve in the superfluidity of 3He and 4He are being discussed. Also listed in this paper are different methods suggested and work done by various research groups to explain superfluidity and its related property in liquid helium
SURFACE PROPERTIES OF LIQUID 3He AT ZERO PRESSURE
Surface properties of quantum liquids have constituted a field for numerous interesting investigations, both experimental and theoretical. In this paper we study contribution of various nearest neighbours in simple cubic arrangement of the liquid helium toward the surface tension (σ) of liquid 3He. To this effect we use standard inter-atomic potential (Lennard Jones potential). We note that the major part of the contribution comes from its first four nearest neighbours. The agreement between our theoretical results with experimental values is satisfactory
Doctor of Philosophy
dissertationObesity is an independent risk factor for several cardiac pathologies. Sustained exposure to nutrient overload in obesity overwhelms cellular homeostatic apparatus, leading to metabolic disorders and organelle dysfunction. The integrity of homeostatic machinery is crucial for the heart to meet its energy need and for cardiomyocytes to survive. Recently, autophagy has emerged as a major catabolic process in maintaining energy and organelle homeostasis. Growing evidence suggest a role for autophagy in obesity related cardiac pathologies. Yet, the regulation of cardiac autophagy in obesity is unclear. In this study, we explored mechanisms regulating cardiac autophagy in an invivo mouse model of diet-induced obesity and an invitro cell culture model of lipid overload. 12 weeks of high-fat diet (HFD) (45% kcal fat) significantly increased the autophagy marker protein LC3-II and autophagosome number in the murine heart independently of canonical upstream signaling through mTORC1 and AMPK. Interestingly, high-fat fed mice displayed a defective autophagosome turnover that may have led to autophagosome accumulation. Alteration in Beclin1 expression had no effect on HFD-induced autophagy, ruling out a major contribution of autophagy initiation pathways in this process. In vitro, cultured H9C2 cardiomyocytes displayed a biphasic autophagic response to palmitate. To explore the mechanism of early autophagic response to lipid overload, we performed most experiments after 4 h of treatment when features of ER stress and cell death were absent. Similar to HFD, palmitate increased autophagosome accumulation primarily via an impairment in autophagosome turnover. Oleate alone had no effect on autophagy but cotreatment normalized the palmitate-induced autophagosome accumulation. Moreover, palmitate treatment led to a massive accumulation of superoxide which correlated with impaired lysosomal acidification and pH-dependent lysosomal enzyme activity. Using specific inhibitors and siRNA mediated gene silencing, we identified Nox2 as the major source of superoxide production. The activation of Nox2 was dependent on the palmitate-induced activation of classical PKCs. Together, our study has identified a novel mechanism wherein palmitate-induced activation of PKC-Nox2 pathway led to impaired lysosomal enzyme activity and diminished autophagic turnover in cardiomyocytes. The Nox2-mediated inhibition of autophagic flux might contribute to other known pathological roles of Nox2-mediated oxidative stress in obesity
Lipotoxicity: Many Roads to Cell Dysfunction and Cell Death: Introduction to a Thematic Review Series
Characterization of Methyltransferase AlmCII in Chalcomycin Biosynthesis: The First TylF Family O-Methyltransferase Works on a 4′-Deoxysugar
Genetic engineering approach for the production of rhamnosyl and allosyl flavonoids from Escherichia coli
Skeletal muscle autophagy remains responsive to hyperinsulinemia and hyperglycemia at higher plasma insulin concentrations in insulin-resistant mice
A Single Gene Cluster for Chalcomycins and Aldgamycins: Genetic Basis for Bifurcation of Their Biosynthesis
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Insulin receptor substrates differentially exacerbate insulin-mediated left ventricular remodeling
Pressure overload (PO) cardiac hypertrophy and heart failure are associated with generalized insulin resistance and hyperinsulinemia, which may exacerbate left ventricular (LV) remodeling. While PO activates insulin receptor tyrosine kinase activity that is transduced by insulin receptor substrate 1 (IRS1), the present study tested the hypothesis that IRS1 and IRS2 have divergent effects on PO-induced LV remodeling. We therefore subjected mice with cardiomyocyte-restricted deficiency of IRS1 (CIRS1KO) or IRS2 (CIRS2KO) to PO induced by transverse aortic constriction (TAC). In WT mice, TAC-induced LV hypertrophy was associated with hyperactivation of IRS1 and Akt1, but not IRS2 and Akt2. CIRS1KO hearts were resistant to cardiac hypertrophy and heart failure in concert with attenuated Akt1 activation. In contrast, CIRS2KO hearts following TAC developed more severe LV dysfunction than WT controls, and this was prevented by haploinsufficiency of Akt1. Failing human hearts exhibited isoform-specific IRS1 and Akt1 activation, while IRS2 and Akt2 activation were unchanged. Kinomic profiling identified IRS1 as a potential regulator of cardioprotective protein kinase G-mediated signaling. In addition, gene expression profiling revealed that IRS1 signaling may promote a proinflammatory response following PO. Together, these data identify IRS1 and Akt1 as critical signaling nodes that mediate LV remodeling in both mice and humans