The complement cascade, as a part of innate immune system, plays a major role in phagocytosis, clearance of apoptotic cells, immune response and inflammation.As an initiator of the classical pathway, C1q not only facilitates apoptotic debris removal but also gets involved in the maintenance of vascular endothelial integrity.As a result, deficiency, excessive consumption or dysfunction of C1q leads to the imbalance of such mechanisms and increases the susceptibility of nephropathy, atherosclerosis and central nervous system diseases.Recenlty, C1q was identified as a new biomarker of aging.C1q could be a useful indicator for early diagnosis, therapy and prognosis.

Lipoprotein (a) [Lp (a)] is an LDL-like molecule consisting of an apolipoprotein (B) [Apo (B)] particle attached by a disulphide bridge to apolipoprotein (a) [Apo (a)].Because of the LPA gene polymorphisms,there exists Lp (a) molecular heterogeneity in the human population.Recently,several observations have pointed out that elevated serum Lp (a) levels may be an independent risk factor of cardiovascular disease and an predictive indicator of cardiovascular disease.Recent findings suggest that Lp (a)-lowering therapy might be beneficial in patients with high Lp(a) levels.Currently,there are some problems in Lp(a) assay,including clinically diverse methods,the Lp (a) molecular heterogeneity between reference materials and test samples.Standardization of the Lp (a) reference reagents and measurement methods may be helpful for the wide application of Lp(a) in clinical medicine and be helpful for assuring the role of Lp(a) as an independent risk factor and predictive indicator of cardiovascular diseases.

While several lines of evidence prove that elevated concentrations of low-density lipoproteins (LDL) usually contribute to the development of atherosclerosis and its clinical consequences, high-density lipoproteins (HDL) are widely believed to exert atheroprotective effects. Hence, HDL cholesterol (HDL-C) is in general still considered as good cholesterol. Recent researches, however, suggest that this might not always be the case and that a fundamental reassessment of the clinical significance of HDL-C is warranted. The main function of HDL is to transfer the cholesterol outside the liver into the liver for catabolism.The liver′s cholesterol metabolism and other biological effects are dependent on the number of HDL particles and its proteins and lipid contents. These functions are difficult to be described simply with the HDL-C concentration. If the components of HDL particles change, they may have adverse effects on the blood vessels. Thus, high concentrations of HDL-C in plasma are not always protective factors, and some clinical trials improving HDL-C concentrations have failed to confirm a protective effect. To explore the complex relationship and pathological mechanism between HDL and atherosclerotic diseases, it is instructive for clinical application of the HDL measurement.

Objective To investigate the clinical application value of serum lipoprotein associated phospholipase A2(Lp‐PLA2) in coronary atherosclerotic heart diseases(CAD) .Methods Using the case‐control study ,790 patients with coronary computed tomography angiography (CTA) in our hospital from October 2013 to June 2015 were selected and divided into the CAD group (352 cases) and control group (438 cases) according to the results of coronary artery CTA .According to the number of coronary artery lesion vessels the CAD group was re‐divided into three subgroups :single branch coronary artery lesion (118 cases) ,double branch coronary arterial lesions(n=107) and multiple branch coronary arterial lesions(132 cases) .The levels of Lp‐PLA2 ,hs‐CRP , TG ,TC ,HDL‐C ,LDL‐C ,glucose ,HbA1c and other indexes were measured and comprehensively analyzed .The t test or variance a‐nalysis was used to compare the means between or among groups .The correlation of different indicators was analyzed with the Pearson linear correlation analysis .Results Compared with the control group ,the CAD group was significantly higher than the con‐trols in the levels of Lp‐PLA2 ,hs‐CRP ,age ,GLU ,HbA1c and ApoB ,the differences were statistically significant(P<0 .05) .The Lp‐PLA2 level had statistical difference among different branch coronary artery lesions in the CAD group(F=4 .941 ,P<0 .05) ,the level of Lp‐PLA2 in the CAD group with multiple branch coronary artery disease was higher than that in single branch coronary ar‐tery disease(P<0 .05) .No statistically significant difference between multiple branch coronary artery disease and double branch coronary arteries disease was observed .No statistically significant difference between double branch coronary arteries disease and single branch coronary artery disease was observed .The Pearson linear correlation analysis showed that Lp‐PLA2 and hs‐CRP had no correlation (r=0 .042 ,P>0 .05) .Conclusion Serum Lp‐PLA2 level increase is a risk factor of CAD and could be used to assess coronary arterial atherosclerosis and number of coronary arterial lesions .

Objective To express the immunodominant epitopes of the branched chain 2 oxo acid dehydrogenase complex (BCOADC), the pyruvate dehydrogenase complex (PDC), the 2 oxo glutarate dehydrogenase complex (OGDC) and a triple hybrid clone (designated as BPO), and use BPO as a tool for the detection of M2 specific for primary biliary cirrhosis (PBC). Methods The cDNA fragments encoding the M2 reactive epitopes of BCOADC, PDC and OGDC were amplified using PCR with total RNA extracted from human peripheral mononuclear blood cell. The fragments were cloned into pQE 30 and then transformed into plasmid E.coli M15. Its products were induced by isopropylthio ? D galactoside and confirmed with SDS PAGE and Western blot. Results Four specific proteins induced from the transformants containing the fused plasmid were shown to have antigenic reactivity with PBC sera, but not with normal control sera. Conclusions We succeeded in expressing three immunodominant epitopes and a hybrid clone which can be used as a powerful and specific method for the diagnosis of PBC.

Objective To study the effects of citrullinated vimentin (cVim) on the maturation and immunologic function of dendritic cells (DCs) from rheumatoid arthritis (RA) peripheral blood.Methods In the present study,mononuclear cells were isolated from the peripheral blood of patients with RA and cultivated in media containing GM-CSF and IL-4 to generate immature DCs (imDCs).The imDCs generated were stimulated with citrullinated vimentin and vimentin.LPS was used as the positive control and PBS was used as the negative control.The expression of surface molecules on the DCs,such as CD14,CD80,CD83,CD86,MHC Ⅰ and MHC Ⅱ were analyzed with FACS.The capability of the stimulatory activity of the DCs on allogeneic T cells in mixed reaction was tested by MTS.t-test was used for statistical analysis.Results Compared to untreated DCs,DCs treated with LPS increased the expression levels of MHC Ⅱ,CD80,CD83 and CD86 (1.07±0.14,1.25±0.13,1.90±1.08,2.44±0.65,P＜0.05),while cVim increased the expression levels of MHC Ⅱ ( 1.18±0.09,P＜0.05) and CD83 ( 1.97±0.99,P＜0.01 ),and Vim decreased the expression levels of CD80 (0.82±0.18,P＜0.01 ).It was demonstrated that the expression levels of MHC Ⅱ on DCs pulsed with cVim were significantly higher than that of the DCs with LPS,but the expression levels of CD80 and CD86 were not significantly different.The expression levels of MHC Ⅱ and CD83 on DCs pulsed with cVim were significantly higher than that of the DCs with Vim.The mixed lymphocyte reaction showed that the DCs induced by LPS and cVim trigerred the proli-feration of allogenic T cells obviously.Conclusion This result suggests that cVim could promote the phenotypic maturation of DCs and increase the expression of costimulatory molecules.

Objective To explore the detection value of peripheral blood human cartilage glycoprotein‐39 in the patients with pri‐mary Sjogren′s syndrome(pSS) .Methods 50 patients with newly diagnosed pSS in our hospital from July 2011 to July 2014 were selected as the pSS group and contemporaneous 50 individuals undergoing physical examination were selected as the normal control group .Venous blood was sampled in all subjects and the erythrocyte sedimentation rate (ESR) ,C‐reactive protein (CRP) ,human cartilage glycoprotein‐39 levels were measured and compared .The lesion number of oral gland lymphocytes and saliva flow rate were checked and compared .Results The pSS group had significantly higher peripheral blood human cartilage glycoprotein‐39 than the normal control group (t=25 .207 ,P<0 .001) .The peripheral blood human cartilage glycoprotein‐39 level in the patients with pSS was positively correlated with the lesion number of oral gland lymphocytes (r=0 .46 ,P=0 .001) ,ESR(r=0 .48 ,P=0 .001) , CRP(r=0 .70 ,P<0 .001) ,RF(r=0 .41 ,P=0 .004) and IgG (r=0 .50 ,P<0 .001) ,and negatively correlated with the saliva flow rate (r= -0 .42 ,P=0 .003) .The eripheral blood human cartilage glycoprotein‐39 level in the patients with pSS and complications was (252 .4 ± 23 .5)μg/L ,which was significantly higher than (174 .6 ± 21 .7) μg/L in the patients without complications (t=11 .678 ,P<0 .001) .Conclusion Human cartilage glycoprotein‐39 can serve as the disease activity index of pSS and its significant increase can prompt that the patient may have complications .Human cartilage glycoprotein‐39 is also an index reflecting the disease condition of pSS objectively and comprehensively and can be widely used in clinic .

Objective This study was performed to investigate the effect of hypoxia on glucose-6-phosphate isomerase (G6PI) expression and cell cycle of fibroblast-like synoviocytes from synovium of rheumatoid arthritis (RA) and osteoarthritis (OA) under hypoxia or normoxia.Methods Fibroblast-like synoviocytes were cultured with either of hypoxia (3％ oxygen) or normoxia (21％ oxygen) for 24 hours.The mRNA expression of G6PI and HIF-1α was tested by PCR quantification,while the protein levels of G6PI and HIF-1α were measured by western blot.Cell cycle was performed by FACS.T-test and Mann-Whitney U were used for statistical analysis.Results The expression levels of G6PI mRNA under hypoxia in RA were higher than those of OA (2.6±0.4 vs 1.5±0.4,P＜0.05).The protein levels of G6PI in RA were higher than those of OA (P＜0.05).The expression levels of HIF-1α mRNA under hypoxia in RA were higher than those of OA (2.9±0.8vs 1.4 ±0.4,P＜0.05).The protein levels of HIF-1α in RA were higher than those of OA (P＜0.05).The G1 phase ratio of cell cycle was decreased significantly under hypoxia than those of normoxia in RA ELs (t=1 1.31,P＜0.05).The S and G2 phase ratio of cell cycle were increased.Conclusion Hypoxia upregulates G6PI and HIF-1α expression and improves proliferation in fibroblast-like synoviocytes.

Objective To investigate the influence of classically activated macrophage (M1) on the proliferation of rheumatoid arthritis (RA) fibroblast-like synovial (FLS) and osteoarthritis (OA) FLS proliferation.Methods Human monocytes leukemia cells (THP)-1 were induced into M1 by lipopolysaccharides (LPS) and interferon gamma (IFN-γ),M1 specific surface molecular markers human leukocyte antigen (HLA)-DR and CD197 were detected by flow cytometry (FCM).RA-FLS and OA-FLS were co-cultured with M1 by transwell chambers,the proliferation of RA-FLS and OA-FLS were observed by crystal violet staining assay.MTS was used to detect cytokines secreted from M1 on the multiplication of RA-FLS and OA-FLS.TNF-α and IL-12 were detected by enzyme linked immunosorbent assay (ELISA).Paried student t test was used for statistical analysis.Results THP-1 were induced into M1 by LPS and IFN-γ,the expression rates of M1 surface specific molecular markers HLA-DR and CD197 were 78.25％ and 87.96％.Crystal violet staining showed that RA-FLS and OA-FLS proliferation were significantly inhibited after co-cultured with M1 48 h,RA-FLS and OA-FLS of each vision under microscope in co-culture groups were (64 ±30) and (85 ±23) respectively,while the RA-FLS and OA-FLS in separate culture groups were (467±87) and (263±78) respectively,the difference was statistically significant (t=7.459,3.791;P＜0.05).MTS assay indirectly reflected that the cytokines from M1 suppressed RA-FLS and OA-FLS proliferation (t=-7.155,-8.111;P＜0.05).The concentration of TNF-α in cell culture supernatants secreted from RA-FLS group and RA-FLS/M1 co-culture group respectively were (0.024±0.01 1) ng/ml and (0.832±0.241) ng/ml respectively,the concentration of IL-12 from the two groups were (0.033±0.015) ng/ml and (0.372±0.122) ng/ml respectively.TNF-α from OA-FLS and OA-FLS/M1 co-culture group respectively were (0.031±0.017) ng/ml and (0.852±0.323) ng/ml,IL-12 were (0.012±0.009) ng/ml,(0.373±0.144) ng/ml.Compared with FLS separate culture group,the concentration of TNF-α and IL-12 were obviously elevated (t=-4.997,-4.777,-4.407,-4.334;P were all ＜0.05).Conclusion M1 can significantly inhibite RA-FLS and OA-FLS proliferation,this may be related to the increased concentration of TNF-α and IL-1 β in from cell culture supernatant.

Humans ; Liver Cirrhosis, Biliary ; etiology