ABSTRACT
Objective To estimate the association between high-sensitivity C-reactive protein (hs-CRP) and cardiovascular events as well as all-cause mortality events.Methods During 2009-2010,out of the 11 623 individuals,1 000 participants aged 35-64 years,were recruited and divided into 12 age-groups,to have received a study on CVD risk factors.Information on the risk factors of cardiovascular diseases was also collected.Fasting blood sample was gathered for all the participants,with hs-CRP tested.Participants in 7 out of the 12 sites were followed,with 6.21 years (36 075 personyears) as the median follow-up period.Cardiovascular and all-cause mortality events were collected.A total of 6 177 participants had been followed after excluding participants who had baseline infections,or did not take hs-CRP test/physical examination at the baseline.Finally,5 984 participants were included for analysis.Participants were categorized into three groups based on the hs-CRP (mg/L) values:＜ 1,1-3 and ＞3,respectively.Cox proportional hazards regression model was used to analyze the relationships between hs-CRP with cardiovascular events or all-cause mortality events,after adjusting for confounding factors.Results Mean age of the participants was 50.2 years.The incidence rates of cardiovascular disease events were 3.6/1 000 person-years,7.1/1 000 person-years,and 10.4/1 000 person-years among three groups and 3.0/1 000 person-years,5.7/1 000 person-years,9.1/1 000 person-years for all-cause mortality events,respectively.After adjusting for confounding factors,the hazard risks (HR) for cardiovascular events were 1.33 (95％CI:0.95-1.84) in the hs-CRP 1-3 mg/L group and 1.76 (95％CI:1.20-2.60) in the hs-CRP＞3 mg/L group when comparing with the hs-CRP＜ 1 mg/L group (trend test P=0.003).The HRs for all-cause mortality events were 1.76 (95％CI:1.23-2.54) and 2.64 (95％CI:1.74-4.01) (trend test P＜0.001),respectively.Conclusion Hs-CRP appeared an independent predictor for cardiovascular events and all-cause mortality events.
ABSTRACT
Objective To estimate the association between high-sensitivity C-reactive protein (hs-CRP) and cardiovascular events as well as all-cause mortality events.Methods During 2009-2010,out of the 11 623 individuals,1 000 participants aged 35-64 years,were recruited and divided into 12 age-groups,to have received a study on CVD risk factors.Information on the risk factors of cardiovascular diseases was also collected.Fasting blood sample was gathered for all the participants,with hs-CRP tested.Participants in 7 out of the 12 sites were followed,with 6.21 years (36 075 personyears) as the median follow-up period.Cardiovascular and all-cause mortality events were collected.A total of 6 177 participants had been followed after excluding participants who had baseline infections,or did not take hs-CRP test/physical examination at the baseline.Finally,5 984 participants were included for analysis.Participants were categorized into three groups based on the hs-CRP (mg/L) values:＜ 1,1-3 and ＞3,respectively.Cox proportional hazards regression model was used to analyze the relationships between hs-CRP with cardiovascular events or all-cause mortality events,after adjusting for confounding factors.Results Mean age of the participants was 50.2 years.The incidence rates of cardiovascular disease events were 3.6/1 000 person-years,7.1/1 000 person-years,and 10.4/1 000 person-years among three groups and 3.0/1 000 person-years,5.7/1 000 person-years,9.1/1 000 person-years for all-cause mortality events,respectively.After adjusting for confounding factors,the hazard risks (HR) for cardiovascular events were 1.33 (95％CI:0.95-1.84) in the hs-CRP 1-3 mg/L group and 1.76 (95％CI:1.20-2.60) in the hs-CRP＞3 mg/L group when comparing with the hs-CRP＜ 1 mg/L group (trend test P=0.003).The HRs for all-cause mortality events were 1.76 (95％CI:1.23-2.54) and 2.64 (95％CI:1.74-4.01) (trend test P＜0.001),respectively.Conclusion Hs-CRP appeared an independent predictor for cardiovascular events and all-cause mortality events.
ABSTRACT
Objective To analyze clinical manifestation and investigate therapy effect of re-operation of tricuspid regurgitation (TR) after mitral valve replacement with rheumatic heart disease.Methods Seventeen cases with rheumatic heart disease recurred TR after mitral valve replacement surgery,underwent tricuspid valve surgery again in the Third People's Hospital of Nanchang from January 2000 to December 2011.Of 17 cases,10cases underwent tricuspid valve annuloplasty including 1 case for pure De Vega plasty,9 cases for the valve leaflets forming + artificial valve ring forming.Another 7 cases underwent tricuspid valve replacement surgery including 4 cases for biological valve replacement and 3 cases for mechanical valve.Retrospective analyzed the clinical manifestations,treatment process and condition of prognosis.Results One case was with early postoperative deaths (5.88％,1717),and died of postoperative left ventricular failure.Three cases were postoperative low cardiac output syndrome,2 cases were renal insufficiency,and 2 cases were respiratory insufficiency,all those cases were successfully cured.Sixteen cases were followed up from 3 months to 9 years and 2 cases were lost.Of 14,2 cases were NYHA class Ⅰ,8 cases for grade Ⅱ,4 cases for grade Ⅲ.Conclusion After mitral valve replacement in patients with rheumatic heart disease,TR in patients with reoperation is a suitable choice.Reasonable surgical indications,timing of surgery and good perioperative management are the keys to improve the success rate of surgery.
ABSTRACT
To construct the eukaryotic expression plasmid of human PRX3 and measure its expression in the HEK-293FT cells, the full-length coding region of human PRX3 was cloned by PCR and inserted into the eukaryotic expression vector pcDNA4-Xpress (A). HEK-293FT cells were transiently transfected with the recombinant plasmid. Western blot and immuofluorescence were used to detect the expression of the fusion protein. In the experiment, restriction analysis identified the construction of the recombinant plasmid and the inserted sequence was identical with that published on GenBank. Western blot and immunofluorescence confirmed the expression of the recombinant protein in transfected HEK-293FT cells. It was concluded that the eukaryotic expression plasmid of human PRX3 was constructed successfully and the recombinant could be expressed efficiently in HEK-293FT cells, which provides a sound basis for the further study on human PRX3.
Subject(s)
Humans , Cell Line, Transformed , Cloning, Molecular , Embryo, Mammalian , Eukaryotic Cells , Metabolism , Gene Expression , Genetic Vectors , Kidney , Cell Biology , Metabolism , Peroxidases , Genetics , Peroxiredoxin III , Peroxiredoxins , Plasmids , Genetics , TransfectionABSTRACT
To construct the eukaryotic expression plasmid of human PRX3 and measure its expression in the HEK-293FT cells, the full-length coding region of human PRX3 was cloned by PCR and inserted into the eukaryotic expression vector pcDNA4-Xpress (A). HEK-293FT cells were transiently transfected with the recombinant plasmid. Western blot and immuofluorescence were used to detect the expression of the fusion protein. In the experiment, restriction analysis identified the construction of the recombinant plasmid and the inserted sequence was identical with that published on GenBank. Western blot and immunofluorescence confirmed the expression of the recombinant protein in transfected HEK-293FT cells. It was concluded that the eukaryotic expression plasmid of human PRX3 was constructed successfully and the recombinant could be expressed efficiently in HEK-293FT cells, which provides a sound basis for the further study on human PRX3.