94 research outputs found
\u3cem\u3eIn situ\u3c/em\u3e pressure study of Rb\u3csub\u3e4\u3c/sub\u3eC\u3csub\u3e60\u3c/sub\u3e insulator to metal transition by Compton scattering
Compton scattering has been shown to be a powerful tool for studying the ground state electronic density in real materials. Using synchrotron radiation, we have studied pressure effects on Rb4C60 by measuring the Compton profiles below and above the insulator to metal transition at 0.8 GPa. The experimental results are compared with the corresponding calculated results, obtained from new ab initio energy band structure calculations. These results allow us to quantitatively evaluate contributions to the Compton profiles resulting from the contraction of the unit cell as well as from the contraction of the C60 molecule itself. In this paper, we point out an unexpected contraction of the volume of the C60 molecule, leading to a major effect on the electronic density of the Rb4C60 compound
Evidence for distinct polymer chain orientations in KC60 and RbC60
The KC60 and RbC60 polymer phases exhibit contrasting electronic properties
while powder diffraction studies have revealed no definite structural
difference. We have performed single crystal X-ray diffraction and diffuse
scattering studies of these compounds. It is found that KC60 and RbC60 possess
different chain orientations about their axes, which are described by distinct
space groups Pmnn and I2/m, respectively. Such a structural difference will be
of great importance to a complete understanding of the physical properties.Comment: To be published in Phys. Rev. Let
Homocysteine metabolism pathway is involved in the control of glucose homeostasis: a cystathionine beta synthase deficiency study in mouse
Cystathionine beta synthase (CBS) catalyzes the first step of the transsulfuration pathway from homocysteine to cystathionine, and its deficiency leads to hyperhomocysteinemia (HHcy) in humans and rodents. To date, scarce information is available about the HHcy effect on insulin secretion, and the link between CBS activity and the setting of type 2 diabetes is still unknown. We aimed to decipher the consequences of an inborn defect in CBS on glucose homeostasis in mice. We used a mouse model heterozygous for CBS (CBS+/-) that presented a mild HHcy. Other groups were supplemented with methionine in drinking water to increase the mild to intermediate HHcy, and were submitted to a high-fat diet (HFD). We measured the food intake, body weight gain, body composition, glucose homeostasis, plasma homocysteine level, and CBS activity. We evidenced a defect in the stimulated insulin secretion in CBS+/- mice with mild and intermediate HHcy, while mice with intermediate HHcy under HFD presented an improvement in insulin sensitivity that compensated for the decreased insulin secretion and permitted them to maintain a glucose tolerance similar to the CBS+/+ mice. Islets isolated from CBS+/- mice maintained their ability to respond to the elevated glucose levels, and we showed that a lower parasympathetic tone could, at least in part, be responsible for the insulin secretion defect. Our results emphasize the important role of Hcy metabolic enzymes in insulin secretion and overall glucose homeostasis
Small-molecule inhibitors of the cystic fibrosis transmembrane conductance regulator increase pancreatic endocrine cell development in rat and mouse
Glucose Amplifies Fatty Acid-Induced Endoplasmic Reticulum Stress in Pancreatic β-Cells via Activation of mTORC1
BACKGROUND: Palmitate is a potent inducer of endoplasmic reticulum (ER) stress in beta-cells. In type 2 diabetes, glucose amplifies fatty-acid toxicity for pancreatic beta-cells, leading to beta-cell dysfunction and death. Why glucose exacerbates beta-cell lipotoxicity is largely unknown. Glucose stimulates mTORC1, an important nutrient sensor involved in the regulation of cellular stress. Our study tested the hypothesis that glucose augments lipotoxicity by stimulating mTORC1 leading to increased beta-cell ER stress. PRINCIPAL FINDINGS: We found that glucose amplifies palmitate-induced ER stress by increasing IRE1alpha protein levels and activating the JNK pathway, leading to increased beta-cell apoptosis. Moreover, glucose increased mTORC1 activity and its inhibition by rapamycin decreased beta-cell apoptosis under conditions of glucolipotoxicity. Inhibition of mTORC1 by rapamycin did not affect proinsulin and total protein synthesis in beta-cells incubated at high glucose with palmitate. However, it decreased IRE1alpha expression and signaling and inhibited JNK pathway activation. In TSC2-deficient mouse embryonic fibroblasts, in which mTORC1 is constitutively active, mTORC1 regulated the stimulation of JNK by ER stressors, but not in response to anisomycin, which activates JNK independent of ER stress. Finally, we found that JNK inhibition decreased beta-cell apoptosis under conditions of glucolipotoxicity. CONCLUSIONS/SIGNIFICANCE: Collectively, our findings suggest that mTORC1 mediates glucose amplification of lipotoxicity, acting through activation of ER stress and JNK. Thus, mTORC1 is an important transducer of ER stress in beta-cell glucolipotoxicity. Moreover, in stressed beta-cells mTORC1 inhibition decreases IRE1alpha protein expression and JNK activity without affecting ER protein load, suggesting that mTORC1 regulates the beta-cell stress response to glucose and fatty acids by modulating the synthesis and activity of specific proteins involved in the execution of the ER stress response. This novel paradigm may have important implications for understanding beta-cell failure in type 2 diabetes
Genomic copy number variation in Mus musculus.
BACKGROUND: Copy number variation is an important dimension of genetic diversity and has implications in development and disease. As an important model organism, the mouse is a prime candidate for copy number variant (CNV) characterization, but this has yet to be completed for a large sample size. Here we report CNV analysis of publicly available, high-density microarray data files for 351 mouse tail samples, including 290 mice that had not been characterized for CNVs previously.
RESULTS: We found 9634 putative autosomal CNVs across the samples affecting 6.87% of the mouse reference genome. We find significant differences in the degree of CNV uniqueness (single sample occurrence) and the nature of CNV-gene overlap between wild-caught mice and classical laboratory strains. CNV-gene overlap was associated with lipid metabolism, pheromone response and olfaction compared to immunity, carbohydrate metabolism and amino-acid metabolism for wild-caught mice and classical laboratory strains, respectively. Using two subspecies of wild-caught Mus musculus, we identified putative CNVs unique to those subspecies and show this diversity is better captured by wild-derived laboratory strains than by the classical laboratory strains. A total of 9 genic copy number variable regions (CNVRs) were selected for experimental confirmation by droplet digital PCR (ddPCR).
CONCLUSION: The analysis we present is a comprehensive, genome-wide analysis of CNVs in Mus musculus, which increases the number of known variants in the species and will accelerate the identification of novel variants in future studies
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We report on 23Na and 13C NMR measurements on Na2C60 and Na6C60 compounds. The 23Na NMR spectrum of A2C60 shows one line at 73 ppm and the one of A6C60 presents two lines at 73 and 147 ppm. The intensity ratio of the latter lines is about 2:1. According topreviously reported x-ray data we attribute the line at 147 ppm to the Na tetramers in the octahedral sites and the line at 73 ppm to the Na cations in the tetrahedral ones which are singly occupied. The room-temperature 13C NMR spectra of Na2C60 and Na6C60 samples present a narrow isotropic line at 172 and 176 ppm, respectively. The Na6C60 resonance is shifted 20 ppm more down field than the resonances of A6C60 compounds with heavier alkalis, indicating a partial charge transfer to the threefold degenerate t1u level which is totally filled in the latter compounds
NMR; 129Xe; alkali metals; Metal clusters; bimetallic; AlPO4-5; NaY
International audienceDehydrated NaY zeolite and AlPO4-5 molecular sieves have been reacted with sodium, rubidium and cesium metal vapor and sodium metal vapor, respectively. Using 129Xe, 23Na, 87Rb and 133Cs solid state NMR technique, we were able to characterize the sodium nanoparticles and Na-M bimetallic alloys (M=Rb, Cs) formed in the cavities of NaY zeolite and in the channels of AlPO4-5 molecular sieves
E.S.R. STUDY DURING THE ELECTROCHEMICAL N-TYPE DOPING OF (CH)x
Nous présentons et discutons les résultats préliminaires d'une étude par RPE du dopage avec Li+ par voie électrochimique de films de cis (CH)x. Pour les taux de dopage faibles (< 10-3 molaire), on observe une diminution progressive du nombre d'électrons non appariés alors que la largeur de raie du signal RPE ne change pas. Nous interprétons ces résultats en termes de dopage sélectif des parties trans du polymère.We present and discuss some preliminary results concerning the EPR study during the electrochemical Li+ doping of cis rich (CH)x films. With low doping levels (< 10-3 molar) we observe a continuous decrease of the unpaired electrons number While the EPR linewidth does not change. These results are interpreted in term of preferential doping of the trans parts of the polymer
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