水杨酸处理诱导采后甜瓜抗坏血酸-还原型谷胱甘肽循环代谢清除过氧化氢的作用及机制

目的：研究抗坏血酸（ascorbic acid，AsA）-还原型谷胱甘肽（reduced glutathione，GSH）循环代谢在水杨酸处理采后甜瓜诱导的过量H2O2清除过程中的作用。方法：用4 mmol/L水杨酸浸泡‘玉金香’厚皮甜瓜10 min，测定处理后果实常温贮藏过程中丙二醛（malondialdehyde，MDA）含量，分析活性氧的积累水平、超氧化物歧化酶（superoxide dismutase，SOD）和过氧化氢酶（catalase，CAT）活力，以及AsA-GSH循环过程相关酶活力及产物和底物含量。结果：水杨酸处理降低了果实MDA含量，第10天处理组MDA含量较对照组降低14.6%；显著提高了果实O2－·的产生速率和H2O2含量（P＜0.05），其中处理后第2天O2－·的产生速率高出同期对照组的1.9 倍，第6天H2O2含量高出对照组果实29.7%；提高了果实SOD活力，但抑制了CAT活力，说明H2O2的清除可能是依赖于除酶促系统外的其他系统。此外，水杨酸处理提高了果实抗坏血酸过氧化物酶、单脱氢抗坏血酸过氧化物酶、脱氢抗坏血酸还原酶和谷胱甘肽还原酶的活力，增加了AsA和氧化型谷胱甘肽的含量，降低了脱氢抗坏血酸和GSH的含量。结论：水杨酸处理诱导了厚皮甜瓜果实的氧爆，抑制了MDA产生，由水杨酸诱导产生的过量H2O2主要依靠AsA-GSH循环系统清除。     

Simultaneously achieving high energy-storage density and power density under low electric fields in NBT-based ceramics

Aiming at the problem that power density and energy density are difficult to obtain simultaneously under low field, a novel composition (1-x)Na_0·5Bi_0·5TiO₃-xBaZn_1/3Ta_2/3O₃((1-x)NBT-xBZT) was designed and fabricated via solid-state methods. With the addition of BZT, the crystal lattice, structural symmetry, grain size, and dense degree were all increased proved by XRD, Raman, and Archimedes drainage method et al. Because of the enhancement of relaxor behavior, the x=0.10 sample displayed a high permittivity ε_r of 2871±15% and a low dielectric loss tan δ ≤ 0.025 in the wide temperature range of 60–400 ^oC. This ceramic also showed maximum recoverable energy density W_d (2.07 J/cm³) with high efficiency η (71.5%) under a low field of 150 kV/cm. Moreover, pulse discharge testing proved that this ceramic possessed both a significant discharge energy density W_D (0.96 J/cm³) and a record high power density P_D (108.54 MW/cm³). This work provided a promising material for high power and energy applications.     

Phase formation,structure and properties of light-weight aluminosilicate proppants based on clay-diabase and clay-granite binary mixes

One of the drawbacks of fusible clays is the narrow sintering interval due to a sharp increase in the amount of iron-silicate melt at a temperature of 1000–1100 °C, which hardens in the form of a glass phase upon cooling. This leads to a relatively low mechanical strength of the calcined samples and causes the danger of melting the granular material surface from such clays during the firing process. To increase the strength of samples of fusible clays, the influence of diabase and granitoid rocks was considered. It was found that the strengthening effect of diabase and granitoid rock additives in an amount of 20–50% in a mixture with fusible clay is due to an increase of total content of the crystalline phase (mullite, cristobalite and residual quartz) from 18–20% in clays without additives to 22–28 % - in mixtures with diabase and to 28–34% - with granitoid additives) at a temperature of 1050–1100 °C. This increase is due to the activation of synthesis processes of secondary mullite and crystallization from alkali-rich feldspar melt of amorphous silica, released from the structure of clay minerals. The established influence of the igneous rocks used made it possible to develop compositions and propose process flow sheet for producing aluminosilicate proppants based on fusible clays. The use of granitoid and diabase rocks in an amount of 20–70% with fusible clays produces lightweight aluminosilicate proppants with bulk density of 1.40–1.46 g/cm³ at temperature range of 1050–1100 °C, which can endure destructive pressures up to 34.5–52 MPa.     

Metformin Preserves β-Cell Compensation in Insulin Secretion and Mass Expansion in Prediabetic Nile Rats

Prediabetes is a high-risk condition for type 2 diabetes (T2D). Pancreatic β-cells adapt to impaired glucose regulation in prediabetes by increasing insulin secretion and β-cell mass expansion. In people with prediabetes, metformin has been shown to prevent prediabetes conversion to diabetes. However, emerging evidence indicates that metformin has negative effects on β-cell function and survival. Our previous study established the Nile rat (NR) as a model for prediabetes, recapitulating characteristics of human β-cell compensation in function and mass expansion. In this study, we investigated the action of metformin on β-cells in vivo and in vitro. A 7-week metformin treatment improved glucose tolerance by reducing hepatic glucose output and enhancing insulin secretion. Although high-dose metformin inhibited β-cell glucose-stimulated insulin secretion in vitro, stimulation of β-cell insulin secretion was preserved in metformin-treated NRs via an indirect mechanism. Moreover, β-cells in NRs receiving metformin exhibited increased endoplasmic reticulum (ER) chaperones and alleviated apoptotic unfold protein response (UPR) without changes in the expression of cell identity genes. Additionally, metformin did not suppress β-cell mass compensation or proliferation. Taken together, despite the conflicting role indicated by in vitro studies, administration of metformin does not exert a negative effect on β-cell function or cell mass and, instead, early metformin treatment may help protect β-cells from exhaustion and decompensation.     

MicroRNAs,Parkinson’s Disease,and Diabetes Mellitus

Parkinson’s disease (PD) is a neurodegenerative disorder that affects 1% of the population over the age of 60. Diabetes Mellitus (DM) is a metabolic disorder that affects approximately 25% of adults over the age of 60. Recent studies showed that DM increases the risk of developing PD. The link between DM and PD has been discussed in the literature in relation to different mechanisms including mitochondrial dysfunction, oxidative stress, and protein aggregation. In this paper, we review the common microRNA (miRNA) biomarkers of both diseases. miRNAs play an important role in cell differentiation, development, the regulation of the cell cycle, and apoptosis. They are also involved in the pathology of many diseases. miRNAs can mediate the insulin pathway and glucose absorption. miRNAs can also regulate PD-related genes. Therefore, exploring the common miRNA biomarkers of both PD and DM can shed a light on how these two diseases are correlated, and targeting miRNAs is a potential therapeutic opportunity for both diseases.