Broken Th17/Treg balance has been reported contributing to several inflammatory autoimmune diseases. The objective of the study was to investigate whether the Th17/Treg balance was impaired in the peripheral blood of patients with rheumatoid arthritis (RA). The frequencies of Treg cells and Th17 cells and mRNA expression of transcription factor RORγt and FoxP3 in peripheral blood of RA patients (n = 37) and healthy controls (n = 30) were determined by flow cytometry and real-time PCR, respectively. Eleven serum cytokines were analyzed by using cytometeric bead array (CBA). The results demonstrated that active RA patients exhibited increased peripheral Th17 cells, Th1- and Th17-related cytokines and RORγt expression while decreased Treg cells and FoxP3 expression. In addition, Th17/Treg ratios were positively correlated with serum concentrations of Th1- and Th17-related cytokines. In conclusion, our results indicated that Th17/Treg balance was broken in peripheral blood, which may play an important role in the development of RA.

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Aims:  To investigate the antibiofilm effect of cinnamaldehyde on methicillin‐resistant Staphylococcus aureus (MRSA) and analyse the effect of subminimum inhibitory concentrations (MICs) of cinnamaldehyde on the expression of the biofilm‐related gene sarA. Methods and Results:  The MICs and minimum bactericidal concentrations (MBCs) were determined using a microtitre broth dilution method. Biofilm susceptibility was determined using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) staining and colony forming unit (CFU) counting assays. Antibiofilm effects were studied with scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM). SarA expression was assessed by real‐time PCR. MICs and MBCs were in the range 0·0625–0·5% (v/v). The killing effects were concentration dependent. At a concentration of 5× MIC, all strains in biofilm were decreased to lower than 20% of the control groups. SEM and CLSM images indicated that a 5× MIC concentration of cinnamaldehyde was able to detach and kill existing biofilms. Apart from strain JB‐06, real‐time PCR showed that the expression of sarA of all other strains was decreased upon exposure to sub‐MICs of cinnamaldehyde. Conclusions:  These data showed the strong killing effect of cinnamaldehyde against MRSA within biofilms. Significance and Impact of the Study:  This study indicated the potential of cinnamaldehyde as an inhibitory agent for use in MRSA biofilm‐related infections.

Phenotypic flexibility of various morphological and physiological characters is widespread in animals. Resident endothermic animals of temperate climates provide a natural experiment in phenotypic flexibility. In this study, we took an integrative approach to assess seasonal and geographic influences on metabolism in Eurasian tree sparrows (Passer montanus). We measured resting metabolic rate (RMR), masses of internal organs, mitochondrial respiration capacities in liver and muscle, cytochrome C oxidase (COX) activities in liver and muscle, and circulating levels of plasma triiodothyronine (T3) and thyroxine (T4) in summer and winter sparrows at two sites from southeastern (Wenzhou) and northeastern (Qiqihar) China that differ in climate. Body masses of tree sparrows were significantly higher in winter than in summer at both sites but did not differ with latitude. RMRs of tree sparrows varied significantly with both latitude and season, with RMRs of Qiqihar birds being higher than those of Wenzhou birds and with RMRs being higher in winter than in summer. Consistently, dry masses of brain, lung, liver, gizzard, small intestine, rectum, and total digestive tract varied significantly with either latitude or season. State 4 respiration and COX activity in liver and muscle were remarkably higher in Qiqihar and increased significantly in winter. Circulating levels of plasma T3 also showed significant seasonal and latitudinal variation and was higher in Qiqihar in winter than in other groups. These data suggest that tree sparrows mainly coped with cold by enhancing thermogenic capacities through heightened activity of respiratory enzymes and higher levels of plasma thyroid hormones (T3). These results are consistent with a pronounced seasonal and latitudinal phenotypic flexibility mediated through physiological and biochemical adjustments in Eurasian tree sparrows.

Keratin8 (KRT8) is the major component of the intermediate filament cytoskeleton and predominantly expressed in simple epithelial tissues. Aberrant expression of KRT8 is associated with multiple tumor progression and metastasis. However, the role of KRT8 in gastric cancer (GC) remains unclear. In this study, KRT8 expression was investigated and it was found to be upregulated along with human GC progression and metastasis at both mRNA and protein levels in human gastric cancer tissues. In addition, KRT8 overexpression enhanced the proliferation and migration of human gastric cancer cells, whereas the knock‐down of KRT8 by siRNA only inhibited migration of human gastric cancer cells. Integrinβ1‐FAK‐induced epithelial‐mesenchymal‐transition (EMT) only existed in the high KRT8 cells. Furthermore, KRT8 overexpression led to increase in p‐smad2/3 levels and TGFβ dependent signaling events. KRT8 expression in GC was related to tumor clinical stage and worse survival. Kaplan–Meier analysis proved that KRT8 was associated with overall survival of patients with GC that patients with high KRT8 expression tend to have unfavorable outcome. Moreover, Cox's proportional hazards analysis showed that high KRT8 expression was a prognostic marker of poor outcome. These results provided that KRT8 expression may therefore be a biomarker or potential therapeutic target to identify patients with worse survival.

We studied 47 hepatitis E virus (HEV) isolates from hospitalized patients in Nanjing and Taizhou, eastern China. Genotypes 1, 3, and 4 were prevalent; genotype 3 and subgenotype 4b showed a close relationship with the swine strains in eastern China, thus indicating that HEV genotype 3 had infected humans in China.

BackgroundAlthough Helicobacter pylori (H.pylori) is the dominant gastrointestinal pathogen, the genetic and molecular mechanisms underlying H.pylori-related diseases have not been fully elucidated. Long non-coding RNAs (lncRNAs) have been identified in eukaryotic cells, many of which play important roles in regulating biological processes and pathogenesis. However, the expression changes of lncRNAs in human infected by H.pylori have been rarely reported. This study aimed to identify the dysregulated lncRNAs in human gastric epithelial cells and tissues infected with H.pylori.MethodsThe aberrant expression profiles of lncRNAs and mRNAs in GES-1 cells with or without H.pylori infection were explored by microarray analysis. LncRNA-mRNA co-expression network was constructed based on Pearson correlation analysis. Gene Ontology (GO) and KEGG Pathway analyses of aberrantly expressed mRNAs were performed to identify the related biological functions and pathologic pathways. The expression changes of target lncRNAs were validated by qRT-PCR to confirm the microarray data in both cells and clinical specimens.ResultsThree hundred three lncRNAs and 565 mRNAs were identified as aberrantly expressed transcripts (≥2 or ≤0.5-fold change, P < 0.05) in cells with H.pylori infection compared to controls. LncRNA-mRNA co-expression network showed the core lncRNAs/mRNAs which might play important roles in H.pylori-related pathogenesis. GO and KEGG analyses have indicated that the functions of aberrantly expressed mRNAs in H.pylori infection were related closely with inflammation and carcinogenesis. QRT-PCR data confirmed the expression pattern of 8 (n345630, XLOC_004787, n378726, LINC00473, XLOC_005517, LINC00152, XLOC_13370, and n408024) lncRNAs in infected cells. Additionally, four down-regulated (n345630, XLOC_004787, n378726, and LINC00473) lncRNAs were verified in H.pylori-positive gastric samples.ConclusionOur study provided a preliminary exploration of lncRNAs expression profiles in H.pylori-infected cells by microarray. These dysregulated lncRNAs might contribute to the pathological processes during H.pylori infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s12920-015-0159-0) contains supplementary material, which is available to authorized users.

Recombination of Hepatitis E Virus (HEV) has rarely been reported. In the present study, phylogenetic and recombination analyses were performed on 134 complete HEV genomes. Three potentially significant recombination events, including both intra-genotype and one inter-genotype, were identified by recombination detection analysis. Recombination events I and II occurred intra-genotype and inter-genotype, respectively, among three isolates, including the lineage represented by CHN-XJ-SW13 (GU119961, swine isolate), E067-SIJ05C (AB369690, human isolate), and JJT-Kan (AB091394, human isolate), and lead to the recombinant swine isolate swCH31 (DQ450072). Recombination event III occurred between the lineage represented by the NA1 (M73218) and K52-87 (L25595), which resulted in the recombinant Xingjiang-1 (D11092). Our analyses proved that that recombination could occur between human and swine HEV strains, double recombination events existed in HEV, and recombination event could happen within ORF2 region of HEV. These results will provide valuable hints for future research on HEV diversity.