Objeictivie To investigate the diagnostic value of anti-mutated citrullinated vimentin (anti-MCV) antibody, anti-cyclic citrullinated peptide (anti-CCP) antibodies and glucose-6-phospha-teisomerase (GP1) for rheumatoid arthritis (RA). Methods Anti-MCV antibody, GPI and anti-CCP antibody were detected in serum samples of 109 RA patients, 24 non-RA rheumatic diseases patients and 19 healthy blood donors. The sensitivity and specificity of these parameters for the diagnosis of RA were analyzed. Results Both the positive rate and average cut off concentration of anti-MCV and GPI in RA were higher than those of non-RA rheumatic diseases or healthy controls (P<0.05). A significant difference was found between anti-MCV and GPI in RA patients. The most sensitive and specific parameter in RA was anti-MCV (99.1%) and anti-CCP (90.7%) respectively, but, when anti-MCV combined with anti-CCP, or GPI or anti-CCP and GPI, the specificity could be up to 98.1%. Coniclusions Anti-MCV, anti-CCP and GPI alone or in combination may be valuable parameters for the diagnosis of RA.

BACKGROUND:Distraction osteogenesis is one of the most important tissue engineering technologies. However, the exact signaling pathway controling mesenchymal stem cel-osteoblast lineage (MSC-OB) migration during distraction osteogenesis has not yet been elucidated. More efforts should be paid to make a ful understanding of the mechanism on MSC-OB lineage migration, which can improve the clinical efficacy of distraction osteogenesis.
OBJECTIVE:To evaluate the effects of mechanical stretch on the ability of MSC-OB mobility and expression of mammalian target of rapamycin (mTOR) signaling pathway as wel as matrix metaloproteinases (MMPs) in MSC-OB, and to make clear the mechanism by which controls MSC-OB migration during distraction osteogenesis.
METHODS:Twelve Sprague-Dawley rats were randomized into two groups: experimental group (n=6), anin vivo rat mandibular distraction osteogenesis model was established on the right side of rats; non-stretch group (n=6), only the mandibular resection was done but with no distraction osteogenesis. Immunohistochemical staining was used to detect phosphorylated mTOR expression in new osteotylus at 15 days after operation. In addition, an in vitro cel stretch model was made in the mandibular mesenchymal stem cels from healthy Sprague-Dawley rats under resting tension force (6%, 4 hours); no distraction was done in control group. The ability of MSC-OB mobility, the expression of mTOR, Raptor, p70S6K and MMPs were evaluated using experiment methods including immunohistochemistry staining, real-time PCR and scratch assay.
RESULTS AND CONCLUSION: The expression of phosphorylated mTOR in MSC-OB was upregulated in the mandibular bone calus of the stretch group than the non-stretch group (P < 0.05). In thein vitro experiments, MSC-OB applied with mechanical stretch (6%, 4 hours) showed elevated gene expression levels of mTOR, Raptor, p70S6K, MMP-2, MMP-9 and MMP-13 compared with the control group (0%, 4 hours). Meanwhile, MSC-OB in the experiment group (6%, 4 hours) showed a greater ability of mobility, as demonstrated by a farther distance after 48 hours of observation (P < 0.05). The present study suggests that the enhancement of MSC-OB mobility correlates with increase of the gene expression of MMPs and mTOR signaling pathway. Mechanical stretch may promote MSC-OB migration through activation of mTOR/MMPs signaling pathway.

Objective This research aimed to investigate the expression and mechanism of miR-155 and suppressor of cytokine signaling 1(SOCS1)in rheumatoid arthritis(RA).Methods RT-PCR and flow cytometry were applied to detect the expression differences of miR-155,Th17,and Treg cells in peripheral blood of RA patients(RA group)and control group(HC group).Bioinformatics analysis and dual-luciferase reporter assay were conducted to investigate the regulatory relationship between miR-155 and SOCS1.CD4+T cells were isolated from peripheral blood of RA patients and transfected with miR-155 inhibitor,si-SOCS1,and their respective negative control sequences,and divided into four groups:miR-NC group,miR-155 inhibitor group,miR-155 inhibitor+si-NC group,and miR-155 inhibitor+si-SOCS1 group.The cells were treated with Th17-inducing differentiation medium,and flow cytometry was used to determine the ratio of Th17 cells in each group of CD4+T cells.Western blot was used to determine the ratio of p-STAT3/STAT3 in the cells.Results Compared to the HC group,RA patients showed increased expression of miR-155 and Th17 ratio(P<0.01),and decreased Treg cell ratio(P<0.01).MiR-155 could target and inhibit the expression of SOCS1.Compared to the miR-NC group,the miR-155 inhibitor group,miR-155 inhibitor+si-NC group,and miR-155 inhibitor+si-SOCS1 group showed decreased Th17 ratio and p-STAT3/STAT3 ratio(P<0.01).Compared to the miR-155 inhibitor group,the miR-155 inhibitor+si-SOCS1 group exhibited increased Th17 ratio and p-STAT3/STAT3 ratio in CD4+T cells(P<0.05).Conclusion Elevated expression of miR-155 in RA patients may mediate the differentiation of CD4+T cells into Th17 cells through the SOCS1/STAT3 pathway,contributing to the imbalance of Th17/Treg cells in peripheral blood of RA patients.

In recent 10 years, social neuroscience has developed rapidly, which integrates social psychology, cognitive neuropsychology, and neuroscience, and puts forward the concept of social cognition. Clinical studies have shown that social cognitive impairment is easy to occur after stroke, which seriously affects the neurological rehabilitation and quality of life of patients. This article reviews the concept, mechanism, clinical manifestations, neuropsychological evaluation and intervention measures of social cognitive impairment in stroke patients, hoping to improve neurologists' awareness of the social cognitive impairment in stroke patients, actively prevent the occurrence of social cognitive impairment after stroke, and give corresponding intervention, so as to help patients better adapt to social life.