Self-Repairing Function of Ni₃S₂ Layer on Ni Particles in the Na/NiCl₂ Cells with the Addition of Sulfur in the Catholyte

The role of the Ni₃S₂ layer on Ni particles in the electrochemical performance of Na/NiCl₂ cells with the addition of sulfur into the cathode is studied. It was found that the Ni₃S₂ layer could be in situ generated on nickel particles and exhibit a self-repairing function during cycling when sulfur exists in the cathode due to the reaction between the sulfur and nickel particles. The self-repairing function of the Ni₃S₂ layer could enhance the blocking effect and improve the battery cycle performance. The capacity of the cell with the optimum amount of sulfur (with self-repairing function) after 50 cycles is about 12% greater than that of the cell with the optimum level of Ni₃S₂ (without self-repairing function). The effect of the self-repairing function of the Ni₃S₂ layer is determined by the amount of sulfur in the cathode

Additional file 1 of Transcriptome analysis reveals the potential mechanism of the response to scale insects in Camellia sasanqua Thunb

Additional file 1: Fig S1. Correlation analysis. N: normal leaves, SL: the leaves infected by scale insects. Fig S2. qRT-PCR validation of DEGs. Table S1. The sequenced result in normal leaves and leaves infected by scale insects. Table S2 Primer sequence of qPCR

Selective Electrochemical Reduction of CO₂ to Ethylene on Nanopores-Modified Copper Electrodes in Aqueous Solution

Electrochemical reduction of carbon dioxide was carried out on copper foil electrodes modified with nanopores on the surface. Such nanopores modified structure was obtained through an alloying–dealloying process. Scanning electron microscopy, energy dispersive X-ray spectroscopy, X-ray diffraction, and X-ray photoelectron spectroscopy confirmed the formation of alloy layer and the final nanoporous morphology of such copper electrodes. When used in electrolysis process, the as-prepared nanopores-modified electrodes can suppress the Faradaic efficiency toward methane to less than 1%, while keeping that of ethylene in a high level of 35% in aqueous 0.1 M KHCO₃ solution under −1.3 V (vs reversible hydrogen electrode), thus revealing a remarkable selectivity toward ethylene production. The high yield of ethylene can be ascribed to the exposed specific crystalline orientations

Assembly of Multifunctional Ni₂P/NiS_0.66 Heterostructures and Their Superstructure for High Lithium and Sodium Anodic Performance

The combination of structure designs at the microscopic and macroscopic level can efficiently enable electrode materials with greatly enhanced lithium and sodium storage. In this paper, the construction of Ni₂P/NiS_0.66 heterostructures and their assembly into a superstructure at the nanoscale were successfully achieved by a facile and effective strategy. In the obtained superstructure, the Ni₂P/NiS_0.66 heterostructures are homogeneously coated with ultrathin carbon layers (HT-NPS@C) and, at the same time, assembled into a yolk–shell nanosphere. Upon evaluation as the anode materials for Li-ion batteries, the HT-NPS@C delivers a high reversible capacity of 430 mA h g^–1 after 200 cycles at 200 mA g^–1 and ultrastable cyclability with negligible capacity loss over 500 cycles. Furthermore, the coin-type full cell with the LiNi_1/3Co_1/3Mn_1/3O₂ (LNCMO) cathode and HT-NPS@C anode deliver a high specific capacity of 323.5 mA h g^–1 after 50 cycles at 0.3 A g^–1. Apart from an excellent performance as promising anode materials for LIBs (Li-ion batteries), the Na-ion batteries with HT-NPS@C sphere electrodes also manifest a remarkable electrochemical performance

Chronic Exposure to Aroclor 1254 Disrupts Glucose Homeostasis in Male Mice via Inhibition of the Insulin Receptor Signal Pathway

Epidemiological studies demonstrate that polychlorinated biphenyls (PCBs) induce diabetes and insulin resistance. However, the development of diabetes caused by PCBs and its underlying mechanisms are still unclear. In the present study, male C57BL/6 mice were orally administered with Aroclor 1254 (0.5, 5, 50, and 500 μg/kg) once every 3 days for 60 days. The body weight and the fasting blood glucose levels were significantly elevated; the levels of serum insulin, resistin, tumor necrosis factor α (TNFα), and interleukin-6 (IL-6) increased, while glucagon levels decreased in the animals treated with Aroclor 1254. Pancreatic β-cell mass significantly increased, while α-cell mass was reduced. Aroclor 1254 inhibited the expression of the insulin receptor signaling cascade, including insulin receptor, insulin receptor substrate, phosphatidylinositol 3-kinase-Akt, and protein kinase B and glucose transporter 4, both in the skeletal muscle and the liver. The results suggested that chronic exposure to Aroclor 1254 disrupted glucose homeostasis and induced hyperinsulinemia. The significant elevation of serum resistin, TNFα and IL-6 indicated that obesity caused by Aroclor 1254 is associated with insulin resistance. The elevation of blood glucose levels could have been mainly as a result of insulin receptor signals pathway suppression in skeletal muscle and liver, and a decrease in pancreatic α-cells, accompanied by a reduction of serum glucagon levels, may play an important role in the development of type 2 diabetes

Overexpression of ALDH2 protected PC12 cells from 4-HNE-induced injury.

<p>(A) A representative image of an immunoblot showing the overexpression of ALDH2 in PC12 cells. (B) The ROS levels in PC12 cells for each group (n = 8); (C) The MDA levels in PC12 cells for each group (n = 8); (D) The ALDH2 activity for each group (n = 8). All values are expressed as the mean ±SD. Con: Control group; 4-HNE: 4-HNE treated group; +ALDH2(O): 4-HNE+ALDH2 overexpression; +εV1-2: 4-HNE+ALDH2 overexpression+εV1–2; +Vector: 4-HNE+Vector; and +Vehicle: 4-HNE+DMSO. **<i>P</i><0.01, compared with Con, ##<i>P</i><0.01, compared with 4-HNE, ++ <i>P</i><0.01, compared with +ALDH2(O).</p

General characteristics of the IS and PSE patients.

<p>Cr: Creatinine; TG: Triglyceride; TC: Total cholesterol.</p><p>General characteristics of the IS and PSE patients.</p

IS patients and PSE patients with the rs671 A allele showed increased 4-HNE levels.

<p>The descriptive results are expressed as the mean ±SD, n = 120. GG: GG genotype; GA: GA genotype: AA: AA genotype. **<i>P</i><0.01, compared with corresponding GG genotype, #<i>P</i><0.05, compared with corresponding GA genotype.</p

Chronic Exposure to Tributyltin Chloride Induces Pancreatic Islet Cell Apoptosis and Disrupts Glucose Homeostasis in Male Mice

It has been reported that organotin compounds such as triphenyltin or tributyltin (TBT) induce diabetes and insulin resistance. However, histopathological effects of organotin compounds on the Islets of Langerhans and exocrine pancreas are still unclear. In the present study, male KM mice were orally administered with TBT (0.5, 5, and 50 μg/kg) once every 3 days. The fasting plasma glucose levels significantly elevated, and the levels of serum insulin or glucagon decreased in the animals treated with TBT for 60 days. In animals treated for 45 days, the number of apoptotic cells in the islets and exocrine pancreas was elevated in a dose-dependent manner. The percentage of proliferating (PCNA-positive) cells was decreased in the islets, while it was increased in exocrine acinar cells. Immunohistochemistry analysis showed that estrogen receptor (ER) and androgen receptor (AR) were present in vascular endothelium, ductal cells, and islet cells, but absent from pancreatic exocrine cells. TBT exposure decreased the production of estradiol and triiodothyronine and elevated the concentration of testosterone, and resulted in a decrease of ERα expression and an elevation of AR in the pancreas measured by Western boltting. The results suggested that TBT inhibited the proliferation and induced the apoptosis of islet cells via multipathways, causing a decrease of relative islet area in the animals treated for 60 days, which could result in a disruption of glucose homeostasis. The different presence of ERs and AR between the islets and exocrine pancreas might be one of reasons causing different effects on cell proliferation

Frequencies of ALDH2 genotypes and alleles in IS patients and PSE patients.

a<p>Adjusted for age, sex, hypertension, BMI, and drinking.</p>b<p><i>P</i> = 0.00036,</p>c<p><i>P</i> = 0.00010.</p><p>Frequencies of ALDH2 genotypes and alleles in IS patients and PSE patients.</p