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Impaired insulin secretion due to pancreatic β-cell injury is an important cause of type 2 diabetes (T2D). Regulators of guanine nucleotide binding protein (G protein) signaling proteins played a key role in regulating insulin sensitivity in vivo. To explore the role of RGS7 on palmitic acid-induced pancreatic β-cell injury, pancreatic β-cells Beta-TC-6 and Min6 were treated with palmitic acid (PA) to similar type 2 diabetes (T2D) injury in vitro. The 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT), 5-ethynyl-2′-deoxyuridine (EdU), and flow cytometry were used to analyze cell viability, proliferation, and apoptosis, respectively. Enzyme-linked immunosorbent assay (ELISA) kits were used to analyze the changes of inflammation-related cytokines. The expression of gene and protein was measured by quantitative real-time PCR (qRT-PCR) and western blot. PA modeling induced apoptosis, increased levels of inflammation-related cytokines, and suppressed cell viability and proliferation of pancreatic β-cells. RGS7 silence markedly alleviated the cell injury induced by PA. RGS7 overexpression further aggravated apoptosis and inflammatory response in PA-induced pancreatic β-cells and inhibited cell viability and proliferation. It is worth noting that RGS7 activated the chemokine signaling pathway. Silence of the key gene of the chemokine signaling pathway could eliminate the negative effect of RGS7 on PA-induced pancreatic β-cells. RGS7 silence protects pancreatic β-cells from PA-induced injury by inactivating the chemokine signaling pathway.

Background/Aims: Long non-coding RNAs (lncRNAs) have emerged as key players in several biological processes and complex diseases. The risk of type 2 diabetes (T2D) is determined by a combination of environmental factors and genetic susceptibility. The purpose of this study was to identify aberrant lncRNAs involved in T2D pathogenesis. Methods: Microarray analysis was performed using whole blood samples from patients newly diagnosed with T2D and healthy controls. Pathway and Gene Ontology (GO) analyses were utilized to annotate the target genes. Coding non-coding co-expression (CNC) analysis was performed to construct a co-expression network. Results: We found 55 lncRNAs and 202 mRNAs were differentially expressed in the T2D group compared to the healthy control group. Pathway and GO analyses demonstrated that dysregulated mRNAs were mainly associated with immune regulation, inflammation, and insulin resistance, whereas CNC analysis identified 10 pairs of co-expressed lncRNA-mRNAs in our patient cohort (R > 0.99). Furthermore, expression of the top three upregulated lncRNAs in the T2D group was correlated with measures of glycometabolism (P < 0.05). Conclusion: This study identified aberrantly expressed lncRNAs and mRNAs in Han Chinese patients with T2D, and demonstrated that dysregulated lncRNAs may have roles in T2D pathogenesis through regulation of inflammation and insulin resistance.

BACKGROUND: A number of studies evaluated the association of intracellular adhesion molecule-1 (ICAM-1) K469E (rs5498, A/G) gene polymorphism with diabetic microvascular complications (DMI) including diabetic nephropathy (DN) and diabetic retinopathy (DR) in different populations. However, the results of individual studies remain conflicting. METHODS: A comprehensive search was conducted to identify all eligible studies of the above-mentioned associations. The pooled odds ratios (ORs) and 95% confidence intervals (CIs) were assessed using the fixed or random effect model. RESULTS: Seven studies involving 3411 subjects were included. Overall, the meta-analysis showed a significant association of the A allele with increased risk of DMI susceptibility in a recessive model (OR = 1.37, 95% CI 1.04-1.80, P = 0.02). In the subgroup analysis stratified by ethnicity, significant association was found in Asians but not in Caucasians (OR = 1.78, 95% CI 1.13-2.81, P = 0.01; OR = 1.10, 95% CI 0.79-1.54, P = 0.58, respectively). Moreover, it showed a significant association between the A allele and risk of DN in a recessive model (OR = 1.25, 95% CI 1.02-1.55, P = 0.04). CONCLUSIONS: This meta-analysis suggested that the K469E polymorphism in ICAM-1 gene might affect individual susceptibility to DMI and showed a discrepancy in different ethnicities. Further investigations are needed to validate the association.

We discuss our investigation of electron trapping in a diamond amplifier (DA). Our previous work demonstrated that some electrons reaching the DA’s hydrogenated surface are not emitted. The state and the removal of these electrons is important for DA applications. We found that these stopped electrons are trapped, and cannot be removed by a strong reversed-polarity electric field; to neutralize this surface charge, holes must be sent to the hydrogenated surface to recombine with the trapped electrons through the Shockley-Read-Hall surface-recombination mechanism. We measured the time taken for such recombination on the hydrogenated surface, viz. the recombination time, as less than 5 ns, limited by the resolution of our test system. With this measurement, we demonstrated that DA could be operated in an rf cavity with frequency of a few hundred megahertz.

A hydrogen-terminated diamond is a proven efficient electron emitter that can support emission of high average current. Several factors dictate the amplifier’s gain: the number of secondary electrons created at their point of entry into the diamond, the fraction of created electrons transmitted to the emitting face, and the fraction of transmitted electrons emitted. In this paper, we present a model detailing the impact of charge trapping at the surface on the instantaneous electric field inside the diamond, and its effect on the transmission gain. The ratio of instantaneous emitted electrons to the transmitted electrons depends on the electron’s energy distribution and the surface barrier. We calculated the latter by evaluating the magnitude of the negative-electron affinity that is modified by the Schottky effect due to the presence of the external applied field. The instantaneous values then were time integrated to yield the time-averaged ratio of the number of emitted electrons to the transmitted ones. The findings from the model agree very well with our experimental measurements. As an application of the model, we estimate the energy spread of the electrons inside the diamond from the measured secondary-electron emission.

We recently developed a reliable hydrogenation procedure for the diamond amplifier that assures the generation of a high-current, high-brightness beam. In this paper, we compare room-temperature hydrogenation with that at high temperatures. We identified the factors leading to the decay of quantum efficiency. The optimum temperature for heat treatment ranged from 400–450°C; its superiority was proven in the gain test. Hydrogenated diamond amplifiers exposed to N_{2} and air exhibited a good emission after being heated to 350°C; the highest gain we registered in emission scanning was 178. Our systematic study of hydrogenation resulted in the reproducible fabrication of diamond amplifiers.

We discuss the mechanics of emittance compensation for a compact superconducting rf gun with a solenoid, a drift space, and a linac system, and give general rules for designing such a system. It is preferable to ensure that the cathode is recessed and that the solenoid is close to it. The drift length, the solenoid’s strength, the size of the waist spot, and the linac’s accelerating gradient can be determined from the size of the beam’s spot at the gun exit, all of which are easily obtained from simulations. Chromaticity effects generally start at the solenoid but can be ignored in the gun. The energy spread extends the spread of the slices’ waist positions, and therefore degrades the emittance compensation. The gun cavity should be designed to minimize energy spread at the gun’s exit; this can be achieved by shortening the effective length of the cavity cell. The linac gradient required to minimize chromaticity by focusing at the linac entrance is larger than the gradient required for matching the linac’s invariant envelope. The applied solution must be a compromise between these two parameters. For a beam with limited energy spread, its waist must be in front of the linac’s entrance.

This paper examines the impact of the Chinese recycling subsidy policy (CRS-policy) on the recycling and reuse industry across the whole product life cycle. We propose a closed-loop dynamic system to illustrate the production flow and interactions among various industry and market factors. A simulation analysis is conducted using data on gas auto engines in China to evaluate the effectiveness of the CRS-policy in encouraging product recycling and reuse. Specifically, we analyze the preventative and regenerative effects of the CRS-policy, and its impact on environmental pollution and social welfare. We further investigate how market factors, including the manufacturer's innovation environment, consumer environmental awareness and sensitivity to the subsidy, and recycling and reuse industry profit, affect the effectiveness of the CRS-policy. The study provides strong evidence of the important role of the subsidy policy in the recycling and reuse industry and offers insightful recommendations for enhancing the effectiveness of the subsidy policy. [ABSTRACT FROM AUTHOR]

In the present study, the expression levels and DNA methylation status of microRNA (miRNA)-375 in patients with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) were analyzed and the role of DNA methylation of miRNA-375 in the pathogenesis of T2DM was investigated. Compared with the miR-375 levels in patients with normal glucose tolerance (NGT; n=53), the samples from patients with IGT (n=44) exhibited downregulation of miR-375, while those from patients with T2DM (n=54) exhibited upregulation of miR-375 in the plasma. Additionally, the samples from patients with IGT were observed to be hypermethylated compared with those from patients with T2DM and NGT (P=0.042). Analysis of three CpG units (CpG1.2, CpG20 and CpG25.26.27) from 17 CpG sites (between -990 and -1,258 bp, relative to the transcription start site) revealed higher methylation levels in patients with IGT compared with those in patients with NGT (P<0.05). The methylation of two CpG units (CpG1.2 and CpG25.26.27) was higher in patients with IGT than in the patients with T2DM (P<0.05). Thus, the present study demonstrated that the miR-375 promoter was hypermethylated and the levels of miR-375 in the plasma were downregulated in the patients with IGT. DNA hypomethylation may have an important role in the regulation of miR-375 expression and may contribute to the pathogenesis of T2DM. [ABSTRACT FROM AUTHOR]

Recent studies have shown that DNA methylation in the promoter of microRNA-375 (miR-375) downregulates its expression during tumorigenesis. However, it is not known if CpG methylation of the miR-375 promoter also has a role in the pathogenesis of type 2 diabetes mellitus (T2DM). In this study, the expression level and CpG methylation status of miR-375 in patients with T2DM were analyzed. Plasma samples from 100 patients with T2DM and 100 healthy controls with normal glucose tolerance (NGT) were collected. The plasma levels of miR-375 were examined using quantitative polymerase chain reaction (qPCR) and the methylation status of 17 CpG sites in the promoter of the miR-375 were determined using Mass ARRAY spectrometry. The plasma levels of miR-375 were found to be upregulated in patients with T2DM compared with controls with NGT (P<0.05). Overall, the methylation levels of the miR-375 promoter in patients with T2DM were not significantly different compared with controls with NGT; however, further studies revealed that four of the eight analyzed individual CpG units within the amplicon were significantly hypomethylated in T2DM samples compared with the NGT samples. This study demonstrated for the first time, to the best of our knowledge, that miR-375 is over expressed in plasma in patients with T2DM, and this may be used as a novel biomarker to distinguish between patients with T2DM and healthy individuals. It was also demonstrated in this study that the miR-375 promoter is hypomethylated, in patients with T2DM, which may regulate the expression of miR-375 and contribute to the pathogenesis of T2DM. [ABSTRACT FROM AUTHOR]