In-situ probing of the thermal treatment of h-BN towards exfoliation

Two-dimensional (2D) hexagonal boron nitride (h-BN) is becoming increasingly interesting for wider engineering applications. Thermal exfoliation is being suggested as a facile technology to produce large quantities of 2D h-BN. Further optimization of the process requires fundamental understanding of the exfoliation mechanism, which is hardly realized by ex-situ techniques. In this study, time resolved in-situ synchrotron X-ray powder diffraction experiments are conducted while heat treating bulk h-BN up to 1273 K. During the heating process, linear expansion of c-axis is observed and the contraction of a-axis up to around 750 K is consistent with previous research. However, a changing behavior from contraction to expansion in a- axis direction is newly observed when heating over 750 K. With the consideration of previous thermally oxidation studies, a hypothesis of thermal assisted exfoliation with oxygen interstitial and substitution of nitrogen at high temperature is proposed

Peritumoral Lymphovascular Invasion Impacts the Incidence of Sentinel Lymph Node (Sln) Metastasis in Early Breast Cancer Patients (Pts) with Favorable Prognostic Features: a Retrospective Study on 345 Cases

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Energy Expenditure Evaluation in Humans and Non-Human Primates by SenseWear Armband : Validation of Energy Expenditure Evaluation by SenseWear Armband by Direct Comparison with Indirect Calorimetry

Introduction:The purpose of this study was to compare and validate the use of SenseWear Armband (SWA) placed on the arm (SWA ARM) and on the back (SWA BACK) in healthy humans during resting and a cycle-ergometer exercise and to evaluate the SWA to estimate Resting Energy Expenditure (REE) and Total Energy Expenditure (TEE) in healthy baboons.Methods:We studied 26 (15F/11M) human subjects wearing SWA in two different anatomical sites (arm and back) during resting and a cycle-ergometer test and directly compared these results with indirect calorimetry evaluation (IC), performed at the same time. We then inserted the SWA in a metabolic jacket for baboons and evaluated the TEE and REE in free living condition for 6 days in 21 (8F/13M) non-human primates.Results:In humans we found a good correlation between SWA place on the ARM and on the BACK with IC during the resting experiment (1.1\ub10.3 SWAs, 1\ub10.2 IC kcal/min) and a slight underestimation in the SWAs data compared with IC during the cycle-ergometer exercise (5\ub11.9 SWA ARM, 4.5\ub11.5 SWA BACK and 5.4\ub12.1 IC kcal/min). In the non-human primate (baboons) experiment SWA estimated a TEE of 0.54\ub10.009 kcal/min during free living and a REE of 0.82\ub10.06 kcal/min.Conclusion:SWA, an extremely simple and inexpensive apparatus, provides quite accurate measurements of energy expenditure in humans and in baboons. Energy expenditure data obtained with SWA are highly correlated with the data obtained with "gold standard", IC, in humans. \ua9 2013 Casiraghi et al

Exenatide regulates pancreatic islet integrity and insulin sensitivity in the nonhuman primate baboon Papio hamadryas.

The glucagon-like peptide-1 receptor agonist exenatide improves glycemic control by several and not completely understood mechanisms. Herein, we examined the effects of chronic intravenous exenatide infusion on insulin sensitivity, β cell and α cell function and relative volumes, and islet cell apoptosis and replication in nondiabetic nonhuman primates (baboons). At baseline, baboons received a 2-step hyperglycemic clamp followed by an l-arginine bolus (HC/A). After HC/A, baboons underwent a partial pancreatectomy (tail removal) and received a continuous exenatide (n = 12) or saline (n = 12) infusion for 13 weeks. At the end of treatment, HC/A was repeated, and the remnant pancreas (head-body) was harvested. Insulin sensitivity increased dramatically after exenatide treatment and was accompanied by a decrease in insulin and C-peptide secretion, while the insulin secretion/insulin resistance (disposition) index increased by about 2-fold. β, α, and δ cell relative volumes in exenatide-treated baboons were significantly increased compared with saline-treated controls, primarily as the result of increased islet cell replication. Features of cellular stress and secretory dysfunction were present in islets of saline-treated baboons and absent in islets of exenatide-treated baboons. In conclusion, chronic administration of exenatide exerts proliferative and cytoprotective effects on β, α, and δ cells and produces a robust increase in insulin sensitivity in nonhuman primates

Exploring patterns of Alteration in Alzheimer's disease brain networks: A combined structural and functional connectomics analysis

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a severe derangement of cognitive functions, primarily memory, in elderly subjects. As far as the functional impairment is concerned, growing evidence supports the "disconnection syndrome" hypothesis. Recent investigations using fMRI have revealed a generalized alteration of resting state networks (RSNs) in patients affected by AD and mild cognitive impairment (MCI). However, it was unclear whether the changes in functional connectivity were accompanied by corresponding structural network changes. In this work, we have developed a novel structural/functional connectomic approach: resting state fMRI was used to identify the functional cortical network nodes and diffusion MRI to reconstruct the fiber tracts to give a weight to internodal subcortical connections. Then, local and global efficiency were determined for different networks, exploring specific alterations of integration and segregation patterns in AD and MCI patients compared to healthy controls (HC). In the default mode network (DMN), that was the most affected, axonal loss, and reduced axonal integrity appeared to compromise both local and global efficiency along posterior-anterior connections. In the basal ganglia network (BGN), disruption of white matter integrity implied that main alterations occurred in local microstructure. In the anterior insular network (AIN), neuronal loss probably subtended a compromised communication with the insular cortex. Cognitive performance, evaluated by neuropsychological examinations, revealed a dependency on integration and segregation of brain networks. These findings are indicative of the fact that cognitive deficits in AD could be associated not only with cortical alterations (revealed by fMRI) but also with subcortical alterations (revealed by diffusion MRI) that extend beyond the areas primarily damaged by neurodegeneration, toward the support of an emerging concept of AD as a "disconnection syndrome." Since only AD but not MCI patients were characterized by a significant decrease in structural connectivity, integrated structural/functional connectomics could provide a useful tool for assessing disease progression from MCI to A

The Glial Glutamate Transporter 1 (GLT1) is Expressed by Pancreatic beta-Cells and Prevents Glutamate-Induced beta-Cell Death

Glutamate (GLUT) is the major excitatory neurotransmitter of the central nervous system and may induce cytotoxicity through activation of glutamate receptors and oxidative stress. Its extracellular concentration is regulated by high affinity glutamate transporters including the glial glutamate transporter GLT-1. GLUT is co-secreted with glucagon by the alpha-cells in islets , acting as a signalling molecule and hormone secretion modulator. We investigated whether GLUT plays a role on islet cells viability and the role of GLT-1 in this process. We used mouse betaTC3, alphaTC1 cell lines and human islets of Langerhans to test whether the effects of an acute and chronic exposure to GLUT exerts a cytotoxic effect in alpha and beta cells. Cells were grown for 24 h and then exposed to either GLUT, dihydrokainate (DHK) a selective GLT-1 inhibitor, Ceftriaxone (CEF) or GLUT receptor inhibitors (APV and CNQX) for 5 days. Viability was measured by the MTT and apoptosis by TUNEL. GLT1 expression and content in betaTC3 cells and human islets was tested by RT-PCR, Western Blotting and confocal microscopy. 5 days incubation with 0.05, 0.5 and 5 mM GLUT increased betaTC3 apoptosis by in a dose-dependent fashion up to 53% (p<0.01) as compared to only 20% at 5mM in alphaTC1 cells (p<0.05). GLT1 was expressed in betaTC3 cells while no expression was found in alphaTC1. These data were confirmed by Na-dependent [3H]-D-aspartate uptake in betaTC3 cells, that was inhibited by DHK. GLT-1-shRNA induced down-regulation of 35%, also caused a 2-4 fold increase in apoptosis in betaTC3 incubated in 0.5mM GLUT (p<0.001). In contrast, CEF induced 2 fold increased of GLT1 expression and provided dose dependent protection from glutamate-induced toxicity (p<0.05). GLT1 was expressed exclusively in the cell membrane in the beta cells in human pancreas, as demonstrated by double-confocal immunocytochemistry with GLT-1and insulin antibodies. GLT-1 inhibition with DHK inhibited Na-dependent [3H]-D-aspartate uptake by 60% in human islets. 5 mM GLUT caused a 80% increase and 0.1 mM DHK caused a 60% in human islets' apoptosis and 50% reduction in 16.7mM glucose-stimulated insulin release and 70% increase in the proinsulin release (all p<0.05). Quantitation by electron-, immunoelectron and double confocal microscopy of apoptotic/degenerated confirmed that apoptosis occured exclusively in beta-cells. GLT1 is a new player in glutamate homeostasis in the islet of Langerhans, controlling extracellular glutamate levels and beta-cells integrity