Objective:To study the correlation between the degree of rh eumatoid arthritis(RA) and periodontal bone loss. Methods:70 cas es of RA were included. Periodontal bone loss was examined by clinical attachmen t loss(CAL) test and radiography. The degree of RA was determined by the measure ments of morning stiffness time (MST),erythrocyte sedimentation rate(ESR)and C -reactive protein(CRP).Results:MST,ESR and CRP were positivel y related to the levels of bone loss(P

BACKGROUND:Nuclear transcription factor(NTF) ?B is a transcription factor,which exists universally in eukaryocyte.It has been identified that its overacting is correlated to the ongoing and development of many diseases.Among the pathomechanism of rheumatoid arthritis,the abnormal activation of NTF ?B has a lot to do with the inflammatory hyperplasia of synovium and the erosion of tissue around articulation.OBJECTIVE:To review the recent progress of NTF ?B,pathogenesis and treatment of rheumatoid arthritis.RETRIEVAL STRATEGY:A computer-based online search of PubMed database was undertaken to identify the articles published in English from January 2000 to July 2007,with the Key words of "nuclear transcription factor ?B,rheumatoid arthritis,pathogenesis,treatment".Meanwhile,Wanfang database was searched for the related Chinese articles published between January 2000 and July 2007,with the same key words in Chinese.A total of 72 articles were finally selected for the first trial.Inclusive criteria:the articles focus on the NTF ?B,the pathogenesis and treatment of rheumatoid arthritis.Exclusive criteria:repeated experiments.LITERATURE EVALUATION:Among the 30 inclusive literatures,7 were related to reviews while the others were clinical or basic researches.DATA SYNTHESIS:①NTF ?B is a significant transcription factor,which participates in regulating many genes related to immune function and inflammation reaction.The promoters of many genes have the binding sites of NTF ?B.②It is indicated that the abnormal activation of NTF ?B plays an important role in the pathogenesis of rheumatoid arthritis.In recent years,many researches inhibiting its activation through different components of signaling pathways have been doing,which become very hot in anti-inflammatory and anti-rheumatism treatment.③In recent years,people have been making great progress in the therapy of rheumatoid arthritis aiming at cytokine and its receptor,however,interfering NTF ?B to treat rheumatoid arthritis is still in study stage.CONCLUSION:NTF ?B target therapy provides a new therapeutic strategy for the treatment of rheumatoid arthritis,which is a very exciting prospect indeed.

Objective To study the roles of apoptosis and expression of the related genes in minor labial salivary gland of patients with primary Sjogren′s syndrome (pSS). Methods Biopsies of minor submucosal labial salivary gland (SG) were obtained from 30 patients with pSS and 10 control individuals. The in situ end labeling and immunohistochemical staining were used to detect the apoptotic cells and the expression of Fas, FasL and Bcl-2. Results The percentage of apoptotic acinar and ductal epithelial cells (AEC and DEC) in labial salivary glands of patients with pSS was significantly higher than that of control respectively, but the percentage of apoptotic infiltrating mononuclear cells (IMC) showed no significant difference compared with that of control, pSS AEC and DEC showed increased expression of Fas/FasL and decreased expression of Bcl-2, whereas pSS IMC showed increased expression of Fas, Fas/FasL and Bcl-2. There was significant positive correlation between the percentage of apoptotic cells and the cells expressing Fas and FasL in pSS AEC DEC and IMC, respectively, and there was significant negative correlation between the percentage of the apoptotic cells and that of cells expressing Bcl-2 in pSS DEC and IMC, but there wasn′t correlation between the percentage of the apoptotic cells and that of cells expressing Bcl-2 in pSS AEC. Conclusions The apoptotic cells increased in the epithelial cells and decreased in IMC of the labial salivary glands may be one of the mechanisms leading to the glandular destruction found in pSS. In pSS labial salivary glands, the expression of Fas and FasL may promote apoptosis, while the expression of Bcl-2 may inhibit apoptosis. The increased expression of Bcl-2 in pSS IMC indicates that IMC may be able to escape apoptosis, resulting in inflammatory cell foci.

The abdominal CT findings of cirrhosis of advanced schistosomiasis in 262 cases were analyzed.All the cases had the calcification in liver in varying degrees,hypodense structure in junction areas and blood vessel in centre,calcification in portal vein system,calcification of colon and so on.The characteristics of CT performance can provide the evidence for defferential diagnosis.

Objective To examine the expression of CD8+CD28- T cells in the peripheral blood and explore their roles in the pathogenesis of AS. Methods The expression of CD8+CD28- T cells obtained from 50 AS patients and 21 healthy controls were assayed by flow cytometry. CRP was also measured. Results The percentage of peripheral blood CD8+CD28- T cells in patients with AS was significantly increased compared to normal individuals [(18±6)% vs (14±5)%, P=0.020], while the percentage of peripheral blood CD3+,CD8+ CD28+ T cells in patients with AS was significantly decreased[ (65±9)% vs (69±8)%, P=0.039]; [ (15±5)% vs(18±4)%, P=0.038]. No difference was found in CD8+ T cells between patients with AS and normal individuals(P＞0.05). Conclusion The percentage of peripheral blood CD8+CD28- T cells in patients with AS is significantly increased comparing to normal individuals. This suggests that CD8+CD28- T cells may play an important role in the pathogenesis of AS.

BACKGROUND:The etiological factor for rheumatoid arthritis remains unclear, but the effects of nuclear factor-κB on the onset of rheumatoid arthritis have been gradual y paid great attention by rheumatologists.
OBJECTIVE:By using the RNA interference (RNAi) technique to block the signal pathway of nuclear factor-κB
mRNA of human rheumatoid arthritis synovial cells, this study explored its application prospect in the treatment of rheumatoid arthritis.
METHODS:The synovial cells were isolated, digested, and cultured for further use. In accordance with the
design principle of smal interfering RNA (siRNA), target sequences of siRNA of nuclear factor-κB were identified, and siRNA expression vector of nuclear factor-κB was synthesized and constructed. The four pGenesil-1/nuclear factor-κB siRNA expression vectors were transfected into the first passage of synovial cells that wel grew. Blank and negative control groups were set. cells at 12, 24, 48, 72 hours, 5 and 7 days after transfection were col ected, and RNA was extracted. Intracellular nuclear factor-κB mRNA expression levels were measured, and siRNA plasmid vector that could effectively inhibit nuclear factor-κB mRNA expression was screened out.
RESULTS AND CONCLUSION:Nuclear factor-κB highly expressed in synovial cells after human rheumatoid arthritis. 3#pGenesil-1/nuclear factor-κB apparently suppressed nuclear factor-κB mRNA expression in synovial cells with human rheumatoid arthritis. RNAi technique blocked nuclear factor-κB mRNA expression. Therefore, the block of nuclear factor-κB signal pathway might be a good target for rheumatoid arthritis gene therapy.

Objective Rapamycin can improve characteristic pathology of AD by improving the level of autophagy.But, its internal mechanism still needs further study.This study was aimed to observe the protective effect of Rapamycin (RAPA) on the injury of rat pheochromocytoma (PC12) cells induced by β-amyloid protein25-35 (Aβ25-35).Methods PC12 cells in the logarithmic phase were randomly divided into 5 groups: control group(similar free-serum DMEM), model group, 10μmol/L RAPA treated group, 40μmol/L RAPA treated group and 160μmol/L RAPA treated group(add 10μmol/L, 40μmol/L RAPA, 160μmol/L respectively).Except the control group, each group was cultured with 20μmol/L Aβ25-35 to established the cell injury model.Results ①Compared with the survival rate of cells[(51.47±2.59)%] and the apoptosis rate of cells[(52.22±2.33)%] of the model group,the survival rate of cells in 10、40、160μmol/L RAPA treated groups and control group[(54.64±2.42)%, (64.79±2.91)% ,(56.50±2.55)% and (99.98±0.73)%] significantly increased, but the apoptosis rate of cells [(45.33±2.83)%, (36.89±2.85)%, (48.00±2.83)% and (3.33±2.45)%] significantly decreased(All P<0.05).②In model group,the expressions of p-PKB is 0.33±0.01, p-mTOR is 1.97±0.05, p-tau is 2.09±0.19.Compared with model group, in 10、40、160μmol/L RAPA treated groups and control group,these expressions of p-PKB (0.37±0.01, 0.42±0.01, 0.40±0.01 and 0.44±0.02) were significantly increased, however p-mTOR (1.64±0.05, 0.66±0.04, 0.35±0.01 and 0.62±0.01) and p-tau (2.02±0.15, 1.79±0.05, 1.86±0.06 and1.53±0.04) were decreased(All, P<0.05).ConclusionRAPA can increase Aβ25-35-induced PC12 cells viability, decrease cells apoptosis rates, and have a protective effect on Aβ25-35-induced PC12 cells death.The mechanism of its protective effect may be related to the inhibition of mTOR regulating PI3K/PKB/mTOR signal transduction pathway by negative feedback and the reduction of tau protein hyperphosphorylation.

Objective To study the protective effect of chlorogenic acid(CGA)on the apoptosis of PC12 cells induced byβ-amyloid protein23-35(Aβ25-35)and its mechanism. Methods The cells model of death was estab-lished by Aβ25-35 (20 μmol/L)-induced PC12 cells. The cells were interfered with 5 different concentrations of CGA. CCK-8 assay was used to detect cells viability to determine the 3 concentrations of CGA in future experi-ments. The cells were divided randomly into control group ,model group and interference groups with 3 different concentrations of CGA. Cells apoptosis rates were detected by flow cytometry;colorimetry method was used to detect MDA,SOD and GSH-Px. The mitochondrial membrane potential(MMP)was detected by fluorescent staining and the expression of caspase-3 by western blot. Results Compared with model group,the cells viability of CGA groups were increased but the apoptosis rates were reduced;the activity of SOD and GSH-Px were increased but the level of MDA,MMP and caspase-3 were decreased(P<0.05). Conclusions CGA has a protective effect on Aβ25-35-induced PC12 cells apoptosis and it may be related to the improvement of cellular antioxidation capacity and mitochondrial damage.

ObjectiveTo investigate the possible pathogenesis of EB virus (EBV) latent membrane protein 1 in inducing systemic lupus erythematosus (SLE).MethodsThe mRNA expression levels of LMP1 and apoptosis-related genes bcl-2,bax in SLE patients and healthy controls were detected by real-time fluorescence quantitative polymerase chain reaction (PCR).The serum BAFF levels of SLE patients and normal healthy controls were detected by ELISA.2 test was used for positive rate analysis,2-△△Ct method was used for comparing the gene expression level,and Student-Newman-Kqeuls method was used for pair-wise comparison between the means.Results① The positive rate of LMP1 expression in 67 SLE cases was 25％,which was significantly higher than the 11％ in 65 healthy controls (P＜0.05).② The 2-△Ct value of bcl-2 mRNA expression level of SLE patients was 0.0257,1.41 times to that (0.0183) of healthy controls and the difference was statistically significant.③ The 2-△Ct value of bcl-2 mRNA expression level of LMP1 positive SLE patients was 0.0427,1.98 times to that of LMP1 negative SLE patients (0.0217),the difference was statistically significant.④ The serum BAFF levels of LMP1 positive SLE patients,LMP1 negative SLE patients,LMP1 positive healthy controls and LMP 1 negative healthy controls were ( 106± 15 ),(82± 19),( 68±19),(64±17) μg/L,respectively.There were significant differences between serum BAFF levels of LMPl-positive SLE patients and other groups(P＜0.0l ).There were significant difference between serum BAFF levels of LMP1-negative SLE patients and the control groups (P＜0.01).ConclusionEBV may induce and/or promote SLE by LMP1 through apoptosis-related genes bcl-2 expression and induction of B lymphocytes that produce BAFF,all these mechanisms can prolong the infected auto-reactive B lymphocytes survival.

Objective To construct an efficient eukaryotic expression recombinant vector of human interleukin-1O(hIL-lO),and observe its expression in rabbit synoviocytes(RSCs).Methods Total RNA was extracted from peripheral blood mononuclear cells(PBMCs)of a patient with drug allergy.Specific Drimers for full-length open reading frames(ORFs)of hIL-10 were designed according to GeneBank(NM 000572).Withtotal RNA as the template,full-length ORFs of hIL-10 were amplified by reverse transcription Dolymerase chain reaction(RT-PCR).RT-PCR products were digested by restrictive endonucleotidase.then inserted into plasmid pcDNA4/HisMaxA.Both restrictive endonucleotidase analysis and DNA sequencing Were carried out for inserts verification.RSCs were transfected with recombinant plasmid expression vector PcDNA4 HisMaxA-hiL10 by liposome-mediated gene transfer methods,then cultured in vitro.The supernatants were collected af-ter transfection for 12 hours,24 hours,48 hours,72 hours,7 days,14 days respectively for IL-10 measure-ment by enzyme linked immunosorbent assay(ELISA).Results Full-length ORFs of hIL-1o(0.54 kb)had been successfully cloned from PBMCs through RT-PCR.The inserts and insert location of pcDNA4 HisMaxA were in a fight way verified by enzyme analysis and DNA sequencing.ELISA results showed that exogenous hIL-10 gene had expressed in the transfected RSCs from 12 hours to 7 days after transfection,and hIL-10level of transfection group significantly higher than that of the control group.Conclusion pcDNA4 HisMaxA-hiL10,the hIL-10 efficient eukaryotic expression vectors,has been suecessfully constructed.