It has been demonstrated that connective tissue growth factor(CTGF) may enhance proliferation and differentiation of osteoblasts,inhibit the functions of osteoblasts,increase osteoclastogenesis in patients with Rheumatoid Arthritis,stimulate proliferation and differentiation of chondrocytes,and induce angiogenesis in vivo and vitro.Above all,CTGF plays an important role in sustaining growth of skeleton and cartilage,and thus maintaining bone quantity.

Objective To investigate the relationships between serum concentration of RBP-4 and the parameters of inflammatory, lipid metabolism, insulin resistance in patients with T2DM. Methods 71 patients newly diagnosed with T2DM and 34 subjects with normal glucose tolerance (NGT) were enrolled in this cross-sectional study. Additionally, another subset analysis was performed. Subjects were divided into normal weight (NW) and overweight or obesity (OW/OB) group on the basis of BMI. Serum RBP-4 was measured with ELISA. Serum concentrations of hs-CRP, free fatty acids (FFA), triglyceride (TG), total cholesterol (TC) and insulin were measured in fasting status. Insulin resistance was assessed by HOMA-IR. Results Ln (HOMA-IR) and the concentrations of TG, FFA, In(hs-CRP) in T2DM were significant-ly higher than that of NGR group[1.20±0.38 vs 0.76±0.34,(2.74±2. 20)mmol/L vs (1.88±1.41),(0. 80±0. 29)mmol/L vs (0.61±0.22)retool/L,0.62±1.00 vs -0. 17±1.07] . InRBP-4 showed a positive relationship with In (HOMA-IR) ( r =0. 382, P <0. 05), but no association with TC, TG, FFA and In(hs-CRP). In the group of T2DM, InRBP-4 showed a positive relationship with FFA ( r =0. 242, P <0.05) and In (hs-CRP) ( r =0.346, P <0.01), but no association with TC, TG and In (HOMA-IR). There were no relationships between InRBP-4 and In (HOMA-IR), TC, TG, FFA and In (hs-CRP)in NW, while in OW/OB group, InRBP-4 showed a positive relationship with In (HOMA-IR) ( r =0. 290,P < 0. 05 ) and In (hs-CRP) ( r = 0. 295, P <0.05 ), but no association with TC, TG and FFA. In a mul-tiple linear regression analysis, In( hs-CRP), TC, TG, FFA or In(HOMA-IR) was not the independent de-terminant of InRBP-4 in any group. Conclusion In patients with T2DM, InRBP-4 is positively correlatedwith In (hs-CRP) and FFA, and it may be a new marker of inflammation.

Human osteoblast was treated with recombinant human connective tissue growth factor (rCTGF). This experiment showed that rCTGF increased membrane type-1 matrix metalloproteinase and matrix metalloproteinase-2 protein expression in a dose- and time-depentent manner in human osteoblasts. rCTGF induced activation of p38 MAPK in human osteoblasts. p38 MAPK inhibitor SB23058 abrogated the effect of rCTGF on the expressions of membrane type-1 matrix metalloproteinase and matrix metalloproteinase-2 in human osteoblasts.

Objective To evaluate the relationship between hyperuricemia and nonalcoholic fatty liver disease(NAFLD) by observing the prevalence of NAFLD among healthy individuals with different levels of serum uric acid.Methods The data of 5 230 persons from medical centers for health examination were analyzed,such as height,weight,blood pressure,blood lipids,blood sugar, hepatitis-related markers, and abdominal color Doppler ultrasound examination were conducted in the fasting state.The diagnosis of NAFLD was made according to the diagnostic criteria adopted by China Institute of Liver Disease and Alcoholic Liver Disease Group.Results The incidences of overweight or obesity, hypertension,hyperlipidemia, and metabolic syndrome were raised with serum uric acid greater than 333 μmol/L in male and＞233 μmol/L in female subjects(P＜0.05 or P＜0.01). Excluding the metabolic syndrome in male subjects, the incidence of NAFLD was increased with serum uric acid,＞333 μmol/L in males or ＞233 μmol/L in females(P＜0.05 or P＜0.01). In further studies with subjects without any metabolic syndrome, the detection rate of NAFLD was higher in males than in females at the same serum uric acid level(P＜0.01). Logistic regression analysis showed that sex, body mass index, blood glucose, and triglyceride, low-density lipoprotein cholesterol, uric acid grading were risk factors of NAFLD(OR 1.344, 2.500, 1.292, 1.279, 1.244, 1.256 respectively).Conclusion A high serum uric acid level is associated with an increased risk of NAFLD.

Objective To investigate the advantages, indications and efficiency of video-assited thoraco-scopic sugery in spontaneous pneumothorax. Methods 31 patients with spontaneous pneumothorax underwent video-assited thoracoscopic sugery, performed with endoscopic manual suture without use of endoscopic cutters. Results All patients were cured without recurrence. Conclusions Video-assited thoracoscopic sugery is the first choice in treating spontaneous pneumothorax,with minimal trauma,less bleeding. Endoscopic manual suture can obviously re-duce the treatment cost.

Objective To investigate the effects of recombinant human connective tissue growth factor (rCTGF) on the proliferation, differentiation and apoptosis in human osteoblasts. Methods Human osteoblasts were treated with rCTGF, cell proliferation was measured by [3 H] -thymidine ([3 H] -TdR) incorporation method,the activity of alkaline phosphatase (ALP) was determined using α-nitrophenyl phosphate as a substrate, the expression of type Ⅰ collagen was determined by Western blotting, osteocalcin in conditioned media was measured by radioimmune assay, and cell apoptosis was assayed by flow cytometry. Results rCTGF promoted proliferation and differentiation of human osteoblasts in a dose-depentent manner, rCTGF increased ALP activity, osteocalcin and type I collagen secretion in a dose-depentent manner, rCTGF inhibited human osteoblastic apoptosis induced by serum deprivation. Conclusion rCTGF can promote osteoblastic proliferation, and differentiation and protect osteoblast against apoptosis, suggesting that CTGF plays an essential role in bone metabolism.

Objective To investigate the effects of recombinant human connective tissue growth factor (rCTGF) on the expression of osteoprotegerin (OPG) and RANKL ( receptor activator of NF-κB ligand ) in human osteoblasts, as well as the mechanisms involved. Methods Human osteoblasts were treated with rCTGF. The expressions of OPG and RANKL were assessed by Western blotting. The expressions of focal adhesion kinase ( FAK), mitogen-activated protein kinase (MAPK) were also observed. Results rCTGF inhibited RANKL protein expression in a dose-and time-depentent manner in human osteoblasts, while the expression of OPG kept unchanged. rCTGF induced activation of p38MAPK and dephosphorylation of FAK in human osteoblasts, but had no effect on ERK and JNK phosphorylation. p38MAPK inhibitor SB23058 abrogated the inhibitory effect of rCTGF on RANKL in human osteoblasts. Conclusion rCTGF inhibits the expression of RANKL in human osteoblasts via activation of p38MAPK and dephosphorylation of FAK.

Genotypes of estrogen receptor gene (ER) α and β in 110 patients with non-alcoholic fatty liver disease (NAFLD) and 100 control subjects were examined by polymerase chain reaction-based restriction fragment length polymorphism.The haplotype analysis was conducted by SHEsis on-line computing platform.The results showed that there were no differences in the genotype frequencies and allele frequencies of ERα at Xba Ⅰ and Pvu Ⅱ enzyme cutting sites between two groups (P ＞ 0.05).There existed significant differences in the genotype frequencies and allele frequencies of ERβ at Rsa Ⅰ and Alu Ⅰ enzyme cutting sites between these two groups (P ＜ 0.05 or P ＜0.01).The risk of NAFLD in postmenopausal women with R or a allele was 1.833 (95％ CI1.209-2.779,P＜0.05)or 1.782 (95％ CI 1.037-3.061,P＜0.05) fold of that with allele r or A.The frequency of r-A haplotype in ERβ was significantly lower in NAFLD group than that in control group (OR =0.529,95％ CI 0.348-0.805).Logistic regression analysis showed the relationship of fasting blood glucose,triglyceride,body mass index,diastolic pressure,Alu Ⅰ genotype with NAFLD (all P＜0.01).The risk of NAFLD in postmenopausal women with Aa/aa genotype was 1.345 (95％ CI 1.028-2.505,P＜0.05) folds of that with AA genotype.

Objectives To explore the role of hydrogen sulfide(H_(2)S) in lipopolysaccharide(LPS)-induced acute lung injury(ALI) in rats and the underlying mechanisms.Methods Sixty-four Sprague-Dawley rats were randomly divided into four groups: control,LPS(instilled intratracheally to induce ALI),NaHS(H_(2)S donor)+LPS,propargylglycine [inhibitor of cystathionine-?-lyase(CSE),PPG]+LPS.Animals were sacrificed at(4 h) or 8h after agent administration.Lung weight/body weight ratio(LW/BW) was measured and calculated.Morphological changes of lung tissues were observed,H_(2)S concentration and carbon monoxide(CO) level in plasma were tested.Malondialdehyde(MDA) content,CSE activity and heme oxygenase(HO) activity of the lung were determined.Immunohistochemisty technique was performed to examine the expression and the absorbance value of(HO1) protein in lung tissues.Results Compared with control conditions,severe injuries of lung tissues and a raised LW/BW and MDA content were observed in rats treated with LPS.LPS also lead to a drop in plasma H_(2)S concentration and lung CSE activity.The enzyme activity of HO,the protein expression of(HO-1) and plasma CO level increased after LPS instillation. Administration of NaHS before LPS could atten-uated the changes induced by LPS.Pre-administration of PPG exacerbated the injuries induced by LPS,but there was no prominent variation in CO level,HO activity and(HO-1) protein expression compared with those of LPS group.Conclusions Downregulation of H_(2)S/CSE was involved in the pathogenesis of acute lung injury induced by LPS.Exogenous(H_(2)S) provided protection against the lung injuries to some extent,which may be explained by its anti-oxidative effects and the upregulation of CO/(HO-1) system.

AIM: To investigate the effect of H_2S on pulmonary artery hypertension during acute lung injury induced by LPS and the interaction between the systems of hydrogen sulfide (H_2S)/cystathionine-?-lyase (CSE) and nitric oxide (NO)/nitric oxide synthase (NOS) in this process. METHODS: Seventy-two adult male rats were randomly divided into four groups: control group, LPS group, LPS+L-NAME group and LPS+propargylglycine (PPG) group. Mean pulmonary artery pressure (mPAP) of each rat was examined at 2 h, 4 h, 6 h and 8 h after treatment. H_2S and NO contents in plasma, NO content, iNOS, cNOS and CSE activity in lung were measured at 4 h or 8 h after treatment, respectively. Expression of iNOS in lung tissue was also detected by immunohistochemistry technique, and the injury of lung was evaluated with morphological changes under microscope. RESULTS: LPS could induce severe lung injury, and mPAP, NO content, iNOS activity and its protein expression in LPS group significantly increased, but cNOS activity, H_2S content and CSE activity decreased compared with those of control group. Administration of L-NAME before LPS could attenuate the changes induced by LPS. Pre-administration of PPG, a CSE inhibitor, exacerbated the injury by LPS, but there was no prominent variation in cNOS activity. CONCLUSION: Reduced endogenous H_2S could increase pulmonary artery hypertension during acute lung injury induced by LPS. There is a negative effect between H_2S/CSE system and NO/NOS system in this process.