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Objective: To explore the associations between partner-seeking activities through internet and HIV/AIDS related risk behaviours among men who have sex with men (MSM)., Methods: Target sampling, anonymous questionnaires were adopted and analyzed with SPSS 11.0., Results: Data from 45.6% of the 2178 valid questionnaires showed that most partner-seeking activities was through internet. 73.1% of them landed on gay website, in which 83.0% looked for sexual partners and 91.7% of them had intercourse with other men met through internet when compared with MSM who did not seek sex activities through internet. The internet group obviously had fewer numbers of partners (5.73 vs. 10.3), oral sex partners (5.13 vs. 8.71), passive anus sex partners (4.67 vs. 8.26) and active anus sex partners (3.51 vs. 6.06) in the past 6 months (P < 0.01 respectively) and obviously had fewer group sex (16.7% vs. 20.5%) activities in the past one year but had more activities on oral sex (94.7% vs. 89.6%), anus sex (95.1% vs. 86.5%), regular sexual partner (52.6% vs. 46.7%) in the past 6 months (83.4% vs. 75.5%) (P < 0.01 respectively) and more likely to have finger intercourse (52.2% vs. 38.5%), hemorrhage sexual intercourse (36.4% vs. 21.9%, OR = 2.04), non-local sexual intercourse (28.1% vs. 22.7%) (P < 0.01 respectively)., Conclusion: Seeking sexual partners through internet had positive and double effects on MSM's risk behaviours, suggesting that it is of urgent need to take the advance of internet and gay website to disseminate HIV/AIDS prevention message.

Background: The balance between vasodilation and vasoconstriction plays a major role in maintaining vascular homeostasis. However, the underlying mechanisms are unclear. More and more evidence suggested that there was an interaction in the regulation of vasorelaxation between nitric oxide (NO) and hydrogen sulfide (H(2)S). We explored the interaction between and effects of NO and H(2)S on the relaxation of pulmonary arteries in rats., Methods: Seven male Sprague-Dawley rats were anaesthetized with chloral hydrate and the pulmonary arteries of each rat separated for the study of vascular activities. The vasorelaxing activities of pulmonary artery rings in response to different doses of a NO donor, sodium nitroprusside (SNP), or a H(2)S donor, sodium hydrogen sulfide (NaHS), were measured in vitro. When pulmonary artery rings were treated with a cystathionine-gamma-lyase inhibitor, DL-propargylglycine, in the presence of SNP or a nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester, in the presence of NaHS, the changes in relaxing activities were analyzed., Results: The relaxation of pulmonary artery rings was in a dose dependent manner in response to either SNP or NaHS. The relaxation rates of pulmonary artery rings increased from (30.90+/-4.62)% to (60.50+/-8.08)% when the concentration of SNP increased from 1 micromol/L to 3 micromol/L and from (26.13+/-4.12)% to (53.09+/-14.01)% when the concentration of NaHS increased from 25 micromol/L to 100 micromol/L. However, when appropriate inhibitor was added, the relaxation responses to SNP and NaHS decreased., Conclusions: The results suggested that similarly to NO, H(2)S acted as a vasorelaxant either independently of, or synergistically with NO in the regulation of vasorelaxation. The interaction between NO and H(2)S played an important role in regulating relaxing activities of pulmonary arteries.

Aim: To investigate the interaction between hydrogen sulfide (H2S)/cystathionine gamma-lyase (CSE) and carbon monoxide (CO)/heme oxygenase (HO) pathways in aortic smooth muscle cells (ASMC)., Methods: The ASMCs were divided into the following groups: (1) the control group; (2) the zinc protoporphyrin (ZnPP) 20 micromol/L group; (3) the propargylglycine (PPG) 2 mmol/L, 4 mmol/L and 10 mmol/L groups; and (4) the sodium hydrosulfide (NaHS) 1 x 10(-5) mol/L, 1 x 10(-4) mol/L and 1 x 10(-3) mol/L groups. Each of the groups was further divided into 6 h, 12 h, 18 h and 24 h subgroups. The CO level, represented by carboxyhemoglobin (HbCO) content was measured using a spectrophotometric method and H2S content was detected by a sensitive electrode method. CSE and HO-1 expressions were detected by Western blotting., Results: The H2S content in the medium and CSE expression by ASMC were markedly increased by ZnPP compared with the control group. HbCO content in the medium and HO-1 expression by the ASMC started strengthening following 24 h treatment with PPG at 2 mmol/L, but were further strengthened following 18 h and 24 h treatment with PPG at 4 mmol/L compared with the controls (P < 0.01). PPG at 10 mmol/L increased the HbCO level in the medium following 18 h treatment and increased HO-1 expression by the ASMC following 12 h treatment. Moreover, NaHS at 1 x 10(-5) mol/L and 1 x 10(-4) mol/L decreased the HbCO level in the medium and HO-1 expression by the ASMC after 6 h and 12 h treatment, while NaHS at 1 x 10(-3) mol/L decreased them at all time points of the treatments., Conclusion: The results suggested that endogenous CO/HO and H2S/CSE pathways inhibited each other in ASMC under physiological conditions.

Pulmonary hypertension is a complicated and important pathological process in the development of a variety of cardiovascular and pulmonary diseases, and directly affects the development of the diseases and their prognosis. but its mechanisms are still not fully understood. Therefore, to clarify the mechanisms is an important task in this field. Nitric oxide (NO) and carbon monoxide (CO) have special significance in pulmonary circulation as compared with other organs for their special biological properties including continuous production, fast transmission and extensive action, etc, which attracts great attention in the life science research and initiates the new research field of gasotransmitters. Hydrogen sulfide (H2S), which has been recognized as a toxic gas, can be endogenously produced in the body. We considered it to be a new cardiovascular regulatory gasotransmitter based on the studies of its synthesis and distribution in cardiovascular system and cardiovascular effects under physiologic and pathophysiologic conditions. We found it exerted a general regulatory significance in cardiovascular diseases. Based on the research of the three gasotransmitters in hypoxic and high pulmonary blood flow-induced pulmonary hypertension, it was found that the dysfunction of the gasotransmitter pathways was involved in the pathogenesis of pulmonary hypertension and the supplement of gasotransmitters could alleviate pulmonary hypertension and pulmonary vascular remodeling. The mechanisms included that they could regulate vessel dilation, correct the imbalance between smooth muscle cell proliferation and apoptosis, inhibit the excess synthesis and stimulate the degradation of collagen, therefore inhibiting abnormal accumulation of collagen, etc. All these results indicated the significant regulatory effects of gasotransmitters in the pathogenesis of pulmonary hypertension.

Aim: To investigate the effect of epigallocatechingallate (EGCG) on acute lung injury induced by oleic acid in mice and the possible mechanism., Methods: Acute lung injury was induced by oleic acid in mice. Light microscopy and electron microscopy were used to examine histological changes and lung index as well as wet to dry weight ratio was calculated. Serum TNF-a level was measured by enzyme linked immunosorbent assay (ELISA) and the phosphorylation of p38 MAPK was determined by Western blotting., Results: Pretreatment of EGCG significantly alleviated oleic acid induced lung injury accompanied by reduction of lung index and wet to dry weight ratio, decreased of TNF-a level in serum and inhibition of phosphorylation of p38 MAPK., Conclusion: EGCG showed beneficial effect on acute lung injury induced by oleic acid in mice. The ultimate reduction of TNF-alpha in serum caused by inhibition of phosphorylated p38 MAPK is involved in the mechanism of action of EGCG.

Transcarboxylase from Propionibacterium shermanii is a 1.2 MDa multienzyme complex that couples two carboxylation reactions, transferring CO(2)(-) from methylmalonyl-CoA to pyruvate, yielding propionyl-CoA and oxaloacetate. The 1.9 A resolution crystal structure of the central 12S hexameric core, which catalyzes the first carboxylation reaction, has been solved bound to its substrate methylmalonyl-CoA. Overall, the structure reveals two stacked trimers related by 2-fold symmetry, and a domain duplication in the monomer. In the active site, the labile carboxylate group of methylmalonyl-CoA is stabilized by interaction with the N-termini of two alpha-helices. The 12S domains are structurally similar to the crotonase/isomerase superfamily, although only domain 1 of each 12S monomer binds ligand. The 12S reaction is similar to that of human propionyl-CoA carboxylase, whose beta-subunit has 50% sequence identity with 12S. A homology model of the propionyl-CoA carboxylase beta-subunit, based on this 12S crystal structure, provides new insight into the propionyl-CoA carboxylase mechanism, its oligomeric structure and the molecular basis of mutations responsible for enzyme deficiency in propionic acidemia.