Reg2 treatment is protective but the induced Reg2 autoantibody is destructive to the islets in NOD mice.

Regenerating family protein 2 (Reg2) is a trophic factor which stimulates ß-cell replication and resists islet destruction. However, Reg2 also serves as an islet autoantigen, which makes it complicated to judge the effectiveness in treating diabetes. How Reg2 treatment behaves in non-obese diabetic (NOD) mice is to be investigated. NOD mice were treated with recombinant Reg2 protein, Complete Freund's adjuvant (CFA) + PBS and CFA+Reg2 vaccinations, CFA+PBS- and CFA+Reg2-immunized antisera, and single chain variable fragment (scFv)-Reg2 and mIgG2a-Reg2 antibodies. Glycemic level, bodyweight, serum Reg2 antibody titer, glucose tolerance, and insulin secretion were determined. Islet morphological characteristics, insulitis, cell apoptosis, islet cell components, and T cell infiltration were analyzed by histological examinations. The autoantigenicity of constructed Reg2C and Reg2X fragments was determined in healthy BALB/c mice, and the bioactivity in stimulating cell proliferation and survival was assessed in insulinoma MIN6 cells. Reg2 administration alleviated diabetes in NOD mice with improved glucose tolerance and insulin secretion but elevated serum Reg2 autoantibodies. Histomorphometry showed reduced inflammatory area, TUNEL signal and CD8 + T cell infiltration, and increased ß-cell proportion in support of the islet-protective effect of Reg2 treatment. CFA+PBS and CFA+Reg2 immunizations prevented diabetic onset and alleviated insulitis while injections of the antisera offered mild protections. Antibody treatments accelerated diabetic onset without increasing the overall incidence. Reg2C fragment depletes antigenicity, but reserves protective activity in streptozotocin (STZ)-treated MIN6 cells. In conclusion, Reg2 treatment alleviates type 1 diabetes (T1D) by preserving islet ß-cells, but induces Reg2 autoantibody production which poses a potential risk of accelerating diabetic progression.

Anti-inflammatory effects of physalin E from Physalis angulata on lipopolysaccharide-stimulated RAW 264.7 cells through inhibition of NF-κB pathway.

Physalin E is a naturally occurring seco-steroid isolated from the stems and aerial parts of Physalis angulata L. (Solanaceae). This study was aimed to explore the anti-inflammatory effects of physalin E on RAW 264.7 mouse macrophages stimulated by lipopolysaccharide (LPS) and the potential underlying mechanisms. The results showed that physalin E significantly inhibited LPS-induced tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) expression and secretion in a dose-dependent manner. Unlike dexamethasone, these effects could not be blocked by miferstone (RU486). Meanwhile, physalin E reduced the degradation of I-kappa B protein in the cytoplasm and downregulated the nuclear factor-κB (NF-κB) p65 protein in the nuclear, which resulted in the inhibition of the NF-κB nuclear translocation. In conclusion, physalin E exerts its anti-inflammatory activities in LPS-induced macrophages. Physalin E can inhibit the production of inflammatory cytokines by targeting the NF-κB signaling pathway.

Is sham acupuncture as effective as traditional Chinese acupuncture? It's too early to say.

Many clinical trials and experimental studies claim that sham acupuncture is as effective as traditional Chinese acupuncture. However, these studies have no standard sham acupuncture control and many other factors can affect the clinical effect. These factors include needle retention time, treatment frequency, and the total number of treatments needed for satisfactory results, and all can change the clinical effect. The majority of existing acupuncture treatment studies do not consider these factors and lack standard dosage criteria. Therefore, it is still too early to conclude that sham acupuncture is as effective as traditional Chinese acupuncture. This article investigates the factors that influence the curative effect of acupuncture as to help set a standard for acupuncture studies in the future.

[Identification of disease targets for precision medicine by integrative analysis of multi-omics data].

With the development and improvement of high-throughput sequencing technologies, the acquisition and processing approaches of various biological omics data on different levels are becoming more mature. Despite several new disease-associated factors have been discovered based on single omics data analysis, identification of disease targets by integrative analysis of multi-omics data is still growing. Since life is a complex regulatory system in which the regulation of gene mutations, epigenetic alterations, abnormal gene expression as well as anomalous variations in signal pathway are related with the occurrence and development of diseases, it is obvious that finding therapeutic factors using single omics data analysis has its limitation. Systematical studies of clinical and pathological mechanisms and identification of optimal therapeutic targets through integrative analysis of multi-omics data from different levels and resources have become an important research direction of precision medicine, which would provide innovative perspectives on disease study and new theoretical basis for early diagnosis, personalized treatment and medicine guide. In this review, we introduce new technologies and research progresses in screening therapeutic targets using systematic omics such as genomics, transcriptomics and epigenomics, and also discusse new strategies and advantages of integrative analysis among them.

[Genetic variability and phylogenetic analysis of 39 short tandem repeat loci in Beijing Han population].

In this study, we studied the genetic polymorphisms of short tandem repeat (STR) loci from 13 CODIS and 26 non-CODIS system in Beijing Han population for the first time, and established a database of 39 STR loci whose forensic parameters were further evaluated. Our results demonstrated no significant deviation from the Hardy-Weinberg equilibrium of 39 STR loci and no pairwise linkage disequilibrium between them. The power of discriminations, expected heterozygosity, polymorphic information content, and power of exclusion of 39 STR loci ranged from 0.7740-0.9818, 0.6000-0.9350, 0.5317-0.9047 and 0.2909-0.8673. The cumulated discrimination power and cumulative probability of exclusion were 0.999999999999999999999999999999999999999964971 and 0.999999999973878, respectively. Moreover, the genetic distance was calculated based on allele frequency and phylogenetic tree was built using STR loci data from Beijing Han and other 11 Chinese ethnic groups.This study provides important basic data for Chinese forensic DNA database and population genetics database, and has important significance in carrying out forensic individual identification, paternity testing, and population genetic study.

The phase transformation of CuInS2 from chalcopyrite to wurtzite.

In the present work, CuInS2 nanoparticles have been successfully synthesized by water-bath method with deionized water as solvent and thioglycolic acid as complexing agent at 80°C. The phase transition of CuInS2 from chalcopyrite to wurtzite was realized by adjusting the pH value of reaction solution. The emergence of Cu2S in the condition of higher pH value of reaction solution led to the formation of wurtzite CuInS2. This facile method that controls the phase structure by adjusting the solution pH value could open a new way to synthesize other I-III-VI2 ternary semiconductor compounds.

α7 Nicotinic Acetylcholine Receptor is a Novel Mediator of Sinomenine Anti-Inflammation Effect in Macrophages Stimulated by Lipopolysaccharide.

Sinomenine (SIN), an alkaloid derived from the plant Sinomenium acutum, has anti-inflammatory and analgesic effects and has been used for rheumatoid arthritis treatment in China. This study aims to verify the hypothesis that SIN acts on α7 nicotinic acetylcholine receptor (α7nAChR) to inhibit the activation of macrophages stimulated by lipopolysaccharide. The prototypical α7nAChR antagonist α-bungarotoxin and mecamylamine attenuated the effect of SIN on tumor necrosis factor-α and interleukin-6 in RAW264.7 murine macrophage-like cells and primary peritoneal macrophages of mouse induced by lipopolysaccharide. With the knockdown of α7nAChR expression in RAW264.7 cells by small interfering RNA, the inhibitory effect of SIN on tumor necrosis factor-α and interleukin-6 was reversed. Sinomenine decreased p65 expression in nuclear and increased IκBα expression in cytoplasm, and these effects were reversed by the α7nAChR small interfering RNA as well. These results indicate that the anti-inflammatory effects of SIN on macrophages in vitro depend on α7nAChR.