Metabolic Effects of CCN5/WISP2 Gene Deficiency and Transgenic Overexpression in Mice

CCN5/WISP2 is a matricellular protein, the expression of which is under the regulation of Wnt signaling and IGF-1. Our initial characterization supports the notion that CCN5 might promote the proliferation and survival of pancreatic β-cells and thus improve the metabolic profile of the animals. More recently, the roles of endogenous expression of CCN5 and its ectopic, transgenic overexpression on metabolic regulation have been revealed through two reports. Here, we attempt to compare the experimental findings from those studies, side-by-side, in order to further establish its roles in metabolic regulation. Prominent among the discoveries was that a systemic deficiency of CCN5 gene expression caused adipocyte hypertrophy, increased adipogenesis, and lipid accumulation, resulting in insulin resistance and glucose intolerance, which were further exacerbated upon high-fat diet feeding. On the other hand, the adipocyte-specific and systemic overexpression of CCN5 caused an increase in lean body mass, improved insulin sensitivity, hyperplasia of cardiomyocytes, and increased heart mass, but decreased fasting glucose levels. CCN5 is clearly a regulator of adipocyte proliferation and maturation, affecting lean/fat mass ratio and insulin sensitivity. Not all results from these models are consistent; moreover, several important aspects of CCN5 physiology are yet to be explored.     

Importance of Both Imprinted Genes and Functional Heterogeneity in Pancreatic Beta Cells: Is There a Link?

Diabetes mellitus now affects more than 400 million individuals worldwide, with significant impacts on the lives of those affected and associated socio-economic costs. Although defects in insulin secretion underlie all forms of the disease, the molecular mechanisms which drive them are still poorly understood. Subsets of specialised beta cells have, in recent years, been suggested to play critical roles in “pacing” overall islet activity. The molecular nature of these cells, the means through which their identity is established and the changes which may contribute to their functional demise and “loss of influence” in both type 1 and type 2 diabetes are largely unknown. Genomic imprinting involves the selective silencing of one of the two parental alleles through DNA methylation and modified imprinted gene expression is involved in a number of diseases. Loss of expression, or loss of imprinting, can be shown in mouse models to lead to defects in beta cell function and abnormal insulin secretion. In the present review we survey the evidence that altered expression of imprinted genes contribute to loss of beta cell function, the importance of beta cell heterogeneity in normal and disease states, and hypothesise whether there is a direct link between the two.     

微胶囊材料在涂料中的应用

简介了微胶囊材料的性能特点及制备方法,分析了微胶囊材料在涂料行业特别是特种功能型涂料领域内的应用,指出了微胶囊材料在涂料行业中广泛的应用前景。     

The thermal stability investigation of microencapsulated ammonium polyphosphate/siloxane‐modified epoxy resin composites

In this investigation, epoxy resin composites containing phosphate and silicone were prepared from microencapsulated ammonium polyphosphate (MFAPP) and poly(methylphenyl siloxane) (PMPS). Silicone‐containing epoxy (E‐S) copolymers were gained by the grafting reaction between ? OCH₃ of PMPS and ? OH of E51. And, a fixed weight of MFAPP was introduced to epoxy systems via the physical blending method. The chemical structure of the E‐S copolymer was determined by Fourier transform infrared spectroscopy (FTIR) and ¹H‐NMR. The impact testing results revealed that the impact toughness was improved slightly. The thermogravimetric analysis (TGA) results demonstrated that the thermal degradation property in high temperature region and solid residue yield at 800 °C were enhanced remarkably with increasing PMPS content, whether the testing atmosphere was in nitrogen or oxygen. Moreover, an obvious synergistic effect of silicon and phosphorus on promoting the thermo‐oxidative degradation stability and solid residue at 800 °C was proved. Furthermore, the scanning electron microscope micrographs and FTIR result of residual charred crusts of EA‐S systems after the TGA testing in air manifested that the bubbled charred layer and silicon‐ and phosphorus‐containing residue took chief responsibility for thermo‐oxidative degradation property and solid residue yield. So the MFAPP/siloxane‐modified epoxy resin composites have a significant development prospect in high‐temperature resistant organic adhesives and coatings. © 2017 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2017 , 134 , 45272.     

Multifunctional silicone rubber/paraffin@PbWO4 phase-change composites for thermoregulation and gamma radiation shielding

A new type of silicone rubber (SR)-based gamma radiation shielding and thermal regulation composite was developed with paraffin (Pn) @lead tungstate (PWO) phase-change microcapsules as functional fillers. These SR/Pn@PWO composites have a PWO component that not only exhibits excellent photon attenuation but also can provide a barrier to the molten phase-change material core. The thermal and mechanical properties of the composites were characterized by differential scanning calorimetry, thermal regulation experiment and mechanical tests. Thermal analysis indicated that the SR/Pn@PWO composites not only reveal reliable energy storage performance which can reach to 52.72 J g⁻¹ enthalpy values but also exhibit good thermal durability. In addition, SR/Pn@PWO composites have enhanced mechanical properties and excellent thermoregulation performance. And the more microcapsules content, the more significant enhancement effect is. A high-purity germanium gamma spectrometer to measure the attenuation coefficient of the composites for gamma radiation showed that the SR/Pn@PWO composites have good γ-ray-shielding property, which increased with the increase of the microcapsules content.     

复合纳米铝和羧基化碳纳米管相变微胶囊的制备及特性

采用原位聚合法制备了以石蜡为芯材、三聚氰胺-甲醛-尿素树脂为壁材、复合纳米铝(Al)及羧基化碳纳米管(C-CNT)的相变微胶囊(MPCM)。测试分析了无添加剂、只复合单一物质以及同时复合Al和C-CNT的MPCM的外观、粒径、导热系数、过冷度以及悬浮液物理稳定性。结果表明:制备的MPCM成型良好;添加剂提高了微胶囊的导热系数,降低了过冷度,与Al相比,C-CNT的改善效果较为明显;添加质量分数为2%CCNT和4.5%Al调节微胶囊密度接近基液密度,实现了悬浮液48 h不分层。     

In-vivo analysis of angiogenesis and revascularization of transplanted pancreatic islets using confocal microscopy

A technique to measure angiogenesis and revascularization in pancreatic islets transplanted at the renal subcapsular site in the rat has been developed. In-vivo imaging of the microcirculation of transplanted pancreatic islets was conducted using a confocal scanning laser microscope (CSLM) to achieve optical sectioning through the graft in order to perform a computer reconstruction of the three-dimensional neovascular morphology. Individual islets were harvested by enzymatic digestion of excised pancreas from Fischer 344 rats. Isolated islets were cultured for 24 h, and approximately 300–350 islets were transplanted at the renal subcapsular site of the left kidney in an anaesthetized rat. Six to 14 days post-transplantation, the animal was anaesthetized and prepared for in-vivo imaging of the microvasculature on a Zeiss LSM-10. Optical contrast of the microvasculature was enhanced by the administration of fluorescein-labelled dextran into the circulating blood. The transplant site was identified and serial sections were obtained through the vascular bed at varying z-intervals. Complementary fluorescence video images were also obtained via a silicon intensifier tube camera mounted on the CSLM. At completion of the imaging procedure, the kidney was returned into the body cavity, the area was sutured and the animal was allowed to recuperate for subsequent examinations. Image processing algorithms, such as grey-level thresholding, median filtering, skeletonization and template matching, were applied to compute the vessel density and diameters and extrapolated to measure 3-D vessel lengths and the tortousity index of the neovasculature.     

Mercuric Compounds Induce Pancreatic Islets Dysfunction and Apoptosis in Vivo

Mercury is a toxic heavy metal that is an environmental and industrial pollutant throughout the world. Mercury exposure leads to many physiopathological injuries in mammals. However, the precise toxicological effects of mercury on pancreatic islets in vivo are still unclear. Here, we investigated whether mercuric compounds can induce dysfunction and damage in the pancreatic islets of mice, as well as the possible mechanisms involved in this process. Mice were treated with methyl mercuric chloride (MeHgCl, 2 mg/kg) and mercuric chloride (HgCl₂, 5 mg/kg) for more than 2 consecutive weeks. Our results showed that the blood glucose levels increased and plasma insulin secretions decreased in the mice as a consequence of their exposure. A significant number of TUNEL-positive cells were revealed in the islets of mice that were treated with mercury for 2 consecutive weeks, which was accompanied by changes in the expression of the mRNA of anti-apoptotic (Bcl-2, Mcl-1, and Mdm-2) and apoptotic (p53, caspase-3, and caspase-7) genes. Moreover, plasma malondialdehyde (MDA) levels increased significantly in the mice after treatment with mercuric compounds for 2 consecutive weeks, and the generation of reactive oxygen species (ROS) in the pancreatic islets also markedly increased. In addition, the mRNA expression of genes related to antioxidation, including Nrf2, GPx, and NQO1, were also significantly reduced in these islets. These results indicate that oxidative stress injuries that are induced by mercuric compounds can cause pancreatic islets dysfunction and apoptosis in vivo.