Raman Spectra of Cis and Trans Decalines

This paper deals with the Raman Spectra of Cis and Trans Decalines@IAC

Raman Speatra Of Quinoline, Quinaldine, isoquinoline and alpha & beta Picolines

This paper dials with the Raman Speatra Of Quinone, Quinaldine, Isoquinoline and alpha & beta Picolines@IAC

Dipole Moments of Polyatomic Molecules

IN calculating the dipole moments of polyatomic molecules, it is assumed that the observed moment is vectorially composed of the moments of the various links or bonds. The bond moments so deduced have no simple relationship to the values calculated from the internuclear distances and the electronic charge. The valency angles calculated from them vary and do not agree with theoretical values or even those found by other methods; interactions of the bond moments have been postulated in order to produce agreement between the calculated and the observed values. There is no vector between the bonds connected by single links due tofree rotation or uncoupling

Relationship between Dielectric Constant of Liquids and Solids and Dipole Moments

IT has been found that the molecular electric susceptibility of liquids, $P = (\epsilon-1) \times M|d = 4\pi N (\alpha + \mu^2/kT)$, where \epsilon is the dielectric constant of the pure liquid and \mu the moment

The Raman Spectra of Isomeric Alcohols

This paper describes the Raman spectra of isomeric alcohols@IAC

Targeting hepatic glutaminase activity to ameliorate hyperglycemia

Glucagon levels increase under homeostatic, fasting conditions, promoting the release of glucose from the liver by accelerating the breakdown of glycogen (also known as glycogenolysis). Glucagon also enhances gluconeogenic flux, including from an increase in the hepatic consumption of amino acids(1). In type 2 diabetes, dysregulated glucagon signaling contributes to the elevated hepatic glucose output and fasting hyperglycemia that occur in this condition. Yet, the mechanism by which glucagon stimulates gluconeogenesis remains incompletely understood. Contrary to the prevailing belief that glucagon acts primarily on cytoplasmic and nuclear targets, we find glucagon-dependent stimulation of mitochondrial anaplerotic flux from glutamine that increases the contribution of this amino acid to the carbons of glucose generated during gluconeogenesis. This enhanced glucose production is dependent on protein kinase A (PKA) and is associated with glucagon-stimulated calcium release from the endoplasmic reticulum, activation of mitochondrial alpha-ketoglutarate dehydrogenase, and increased glutaminolysis. Mice with reduced levels of hepatic glutaminase 2 (GLS2), the enzyme that catalyzes the first step in glutamine metabolism, show lower glucagon-stimulated glutamine-to-glucose flux in vivo, and GLS2 knockout results in higher fasting plasma glucagon and glutamine levels with lower fasting blood glucose levels in insulin-resistant conditions. As found in genome-wide association studies (GWAS), human genetic variation in the region of GLS2 is associated with higher fasting plasma glucose(2,3); here we show in human cryopreserved primary hepatocytes in vitro that these natural gain-of-function missense mutations in GLS2 result in higher glutaminolysis and glucose production. These data emphasize the importance of gluconeogenesis from glutamine, particularly in pathological states of increased glucagon signaling, while suggesting a possible new therapeutic avenue to treat hyperglycemia.US NIH CA211437 FONDECYT 1160332 CONICYT/FONDAP 1515001