Objective To investigate the serum levels of high sensitivity C-reactive protein (hsCRP),interleukin-1β (IL-1β) and lipoprotein-associated phospholipase A2 (Lp-PLA2),and investigate their clinical diagnostic value in acute coronary syndrome (ACS) patients.Methods Fifty three clinical serum samples of patients specifically diagnosed with acute coronary syndrome were collected.A total of 21 healthy subjects were enrolled as healthy controls.Serum IL-1β and Lp-PLA2 levels were determined by enzyme-linked immunosorbent assay.The concentration of hs-CRP was tested by immunoturbidimetry method.Results Compared to the healthy controls,the levels of serum hs-CRP,IL-1βand Lp-PLA2 were significantly higher in ACS and ACS subgroups (P ＜ 0.05),respectively.The level of Lp-PLA2 was gradually increased among healthy controls,angina pectoris (AP),ST-segment elevation myocardial infarction (STE-MI),non-ST-segment elevation myocardial infarction (NSTEMI) groups.The best cut-off value of hs-CRP,IL-1β and Lp-PLA2 was 7.44 mg/L,90.88 ng/L and 219.92 μg/L,respectively.The parallel test had better sensitivity (94.3％) and specificity (100％).Conclusions Serum hs-CRP,IL-1β and Lp-PLA2 play an important role in classifying the clinical types and monitoring the conditions of patients with ACS.Combination of hs-CRP,IL-1β and Lp-PLA2 is expected to be a new biomarker for ACS.

This study was aimed to observe the effect ofJia-Shen prescription (JSP) on angiotensinⅡ (AngⅡ) inhibition, ventricular remodeling in myocardial infarction (MI) rat model. The anterior descending coronary artery of Sprague-Dawley rat was ligated to establish the MI rat model. Rats were randomly divided into the 3 g JSP group, 6 g JSP group, losartan group, model group, and the sham-operation group. Intragastric administration of medication was given 24 h after MI. In the 3 g and 6 g JSP group, JSP was given at the dose of 3 g·kg-1·day-1 and 6 g·kg-1day-1, respectively. Losartan was given at the dose of 10 mg·kg-1·day-1 in the losartan group. Same volume of distilled water was given to the sham-operation and model group. Four weeks later, the left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), posterior wall thickness (PWT), left ventricular ejection fraction (LVEF), left ventricular fractional shorten (LVFS), left ventricular weight index (LVWI), the distribution and content of collagen, plasma brain natriuretic peptide (BNP) and the AngⅡ content in myocardial tissues homogenate were observed. The results showed that 4 weeks after MI, compared to the model group, 6 g PJP reduced myocardial infarct size, LVWI, LVEDD and LVESD, and enhanced LVEF and LVFS (P< 0.05). In ischemic regions, compared to the model group, JSP can obviously reduce the content of collagen (P < 0.05). This effect had dose-dependent relationship. Plasma BNP and AngⅡ content in myocardial tissues homogenate were also obviously lower than the model group (P< 0.05). It was concluded that JSP can improve the ventricular remodeling of MI rat model. Its action mechanism may be through the AngⅡ inhibition, in order to improve the early stage left ventricular morphological remodeling, myocardial fibrosis and cardiac contractile function.

ObjectiveTo investigate the serum concentration of 25-hydroxy vitamin D [25(OH)D] in the second-trimester women in winter and explore its correlation with age and blood hemoglobin level. Methods The blood samples of 78 second-trimester women were collected during the 24-28 gestational weeks. Serum 25 (OH) D and blood hemoglobin levels were measured. The correlations of serum 25 (OH) D with age and blood hemoglobin levels were analyzed by Pearson correlation. ResultsOf the 78 pregnant women, the rates of vitamin D deficiency ( ≤25.0 nmol/L), insufficiency [25.0 nmol/L ＜ 25(OH) D≤50.0 nmol/L], and sufficiency were 65.38％, 30.77％, and 3.85％, respectively. Serum concentration of 25 (OH) D was positively correlated with blood hemoglobin level ( r =0.2746, P =0.015 ). ConclusionVitamin D deficiency or insufficiency is common among the second-trimester women in winter, especially among those with low hemoglobin level.

Objective To quantifying the urine human cytomegalovirus(HCMV)DNA from the HCMV infection infants and its corresponding liver function indications,and investigate the relationship between their concentrations.Methods The u-rine samples were collected from HCMV infection infants.HCMV DNA was measured by fluorescence quantitative polymer-ase chain reaction (FQ-PCR).Serum ALT,AST,ALP,GGT,T-Bil and D-Bil liver function indications were detected and the positive rate was analyzed,simultaneously.The correlation between the logarithm urine HCMV DNA (log HCMV DNA) concentration and ALT,AST,ALP,GGT,T-Bil and D-Bil were analyzed by Spearman correlation analysis.Results The dis-tribution range ofurine log HCMV DNA in 444 HCMV infection infants was <2.70~7.90;the positive rate of serum ALT, AST,ALP,GGT,T-Bil and D-Bil were 24.8%,59.0%,95.7%,31.1%,16.7% and 16.3%,respectively.The urine log HC-MV DNA was associated with GGT and the correlation coefficient was 0.099 (P < 0.05),but no associated with ALT, AST,ALP,T-Bil and D-Bil.Conclusion The positive rate of liver function indications will rise in HCMV infection infants, the urine log HCMV DNA was associated with GGT,but not associated with other liver function indications.

This article was aimed to determine effects of Jia-Shen prescription (JSP) on infarct size (IS), cardiac function and myocardial cytokine in the early phase of myocardial infarction (MI) in rats. Acute MI models were induced by the ligation of left anterior descending coronary artery in Sprague-Dawley (SD) rats. The rats were ran-domly divided into five groups, which were the sham-operated group, model group, JSP-3 g (3 g·kg-1·day-1) group, JSP-6 g (6 g·kg-1·day-1) group, and the losartan (10 mg·kg-1·day-1) group. IS was determined by Evans blue and 2,3,5-Triphenyltetrazolium chloride (TTC) 3 days after MI. The left ventricular structure and contractility were measured by echocardiography performed 7 days after MI. And contents of myocardial inflammatory mediators in-cluding tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and monocyte chemoattractant protein-1 (MCP-1) were measured by ELISA. The results showed that compared with the model group, treatment with JSP at the dose of 6 g significantly reduced myocardial IS (P<0.05);left ventricular end diastolic diameter (LVEDD) and left ventricu-lar end systolic diameter (LVESD) were significantly decreased (P<0.05); left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were significantly increased (P<0.05).The results were similar as the losartan group. Compared with the model group, JSP can significantly reduce the production of TNF-α, IL-1βand MCP-1 in cardiac tissues (P<0.05). Except TNF-α, these effects of JSP were in a dose-dependent manner. JSP (6 g) had equal effectiveness with losartan. It was concluded that consistent with losartan-induced cardioprotection, JSP administered after MI reduced myocardial IS, improved cardiac function, and decreased inflammatory mediators in ischemic myocardium. The data indicated that JSP exerted its cardioprotection possibly via inhibiting inflammatory response.

This study was aimed to explore the method to improve the purity of primary myocardial cells from neonatal rats. The myocardial tissues of rats which were born 1-3 days were repeated digested by 0.08% myocardial cells digestive juices. And then, cells were neutralized with DMEM medium which containing 10% fetal bovine serum. The cells were separated with differential sidewall ion. The red blood cell cracking liquid was added to remove the red blood cells. Bromine deoxidization uracil (Brdu) was added to purify the myocardial cells. Then, cells were incubated in the CO2 incubator for two days. The serum-free synchronization was performed for one day. The results showed that the output of myocardial cells from one rat was about 1.2 × 106. The dynamic myocardial cells occupied more than 90%. The purity of myocardial cells was more than 90%. After 3 to 4 days, the cell fusion of myocardial cells was formed with spontaneous rhythm beats. It was concluded that the method can ensure the yield and the activity of the myocardial cells. At the same time, the purity of myocardial cells can also be improved greatly.

Objective This study was designed to determine the effect of transient receptor potential vanilloid type 4(TRPV4)on angiotensin Ⅱ(Ang Ⅱ)-induced renal injury in TRPV4-null mutant(TRPV4 -/-)mice. Methods The mice were divided into sham group and Ang Ⅱ-treated group. Ang Ⅱ was infused systemically into wild type(WT)and TRPV4 -/- mice via a miniosmotic pump for 4 weeks, and the sham mice were given with normal saline. Systolic blood pressure,urinary excretion of albumin and 8-isoprostane, serum creatinine, and the pathological changes in the kidney tissues were assayed after the 4-week treatment. Results Compared with corresponding sham mice,Ang Ⅱ infusion led to enhanced systolic blood pressure,increased urinary excretion of albumin and 8-isoprostane,increased serum creatinine(P< 0.05),and enhanced glomerulosclerosis degree and renal tubulointerstitial injury index(P< 0.05)in the WT and TRPV4 -/- mice. The result were associated with enhanced collagen levels in the kidney(P< 0.05). All of them were attenuated by the deletion of TRPV4 in the absence of alteration in blood pressure(P< 0.05). Conclusions Deletion of TRPV4 could alleviate renal injury during Ang Ⅱ-induced hypertension, suggesting that TRPV4 may contribute to the pathophysiology of angiotensin Ⅱ-induced renal injury.

BACKGROUND: Circulating levels of cell-free DNA increase in many pathologic conditions. However, notable discrepancies in the quantitative analysis of cell-free DNA from a large number of laboratories have become a considerable pitfall, hampering its clinical application. METHODS: We designed a novel recombinant DNA fragment that could be applied as an internal standard in a newly developed and validated duplex real-time PCR assay for the quantitative analysis of total cell-free plasma DNA, which was tested in 5,442 healthy adults and 200 trauma patients. RESULTS: Compared with two traditional methods, this novel assay showed a lower detection limit of 0.1 ng/mL, lower intra- and inter-assay CVs, and higher accuracy in the recovery test. The median plasma DNA concentration of healthy males (20.3 ng/mL, n=3,092) was significantly higher than that of healthy females (16.1 ng/mL, n=2,350) (Mann-Whitney two-sample rank sum test, P<0.0001). The reference intervals of plasma DNA concentration were 0-45.8 ng/mL and 0-52.5 ng/mL for healthy females and males, respectively. The plasma DNA concentrations of the majority of trauma patients (96%) were higher than the upper normal cutoff values and were closely related to the corresponding injury severity scores (R²=0.916, P<0.0001). CONCLUSIONS: This duplex real-time PCR assay with a new internal standard could eliminate variation and allow for more sensitive, repeatable, accurate, and stable quantitative measurements of plasma DNA, showing promising application in clinical diagnosis.
Adult ; DNA/*blood/standards ; Female ; Healthy Volunteers ; Humans ; Male ; Middle Aged ; Real-Time Polymerase Chain Reaction/*methods/standards ; Reference Values ; Wounds and Injuries/blood

Myocardial fibrosis is featured by excessive proliferation of cardiac fibroblast and collagen deposition. There is close relationship between myocardial fibrosis and various cardiovascular disease, and it is potential risk factor for sudden death. At present the precise mechanism remains unclear.Myocardial fibrosis has been found to relate with renin-angiotensin-aldosterone system,cell factor,oxidative stress,inflamatory factor,endothelial function obstacles,Intracellular calcium ion. These factors influences the occurrence of myocardial fibrosis by the same or different pathway.

AIM:Using bioinformatics analysis methods to identify the hub genes involved in myocardial isch-emia-reperfusion injury(MIRI).METHODS:Firstly,the rat MIRI related dataset GSE122020,E-MEXP-2098,and E-GEOD-4105 were downloaded from the database.Secondly,differentially expressed genes(DEGs)were screened from each dataset using the linear models for microarray data(limma)package,and robust DEGs were filtered using the robust rank aggregation(RRA)method.In addition,the surrogate variable analysis(SVA)package was used to merge all datas-ets into one,and merged DEGs were screened using the limma package.The common DEGs were obtained by taking the intersection of the two channels of DEGs.Next,the protein-protein interaction(PPI)network of common DEGs was con-structed,and the hub genes were identified using the density-maximizing neighborhood component(DMNC)algorithm.The receiver operating characteristic curve(ROC)was plotted to evaluate the diagnostic performance of the hub gene.Then,the mRNA and protein expression levels of hub genes were detected in the rat MIRI model,and the literature re-view analysis was carried out on the involvement of hub genes in MIRI.Finally,the gene set enrichment analysis(GSEA)was performed on hub gene to further reveal the possible mechanism in mediating MIRI.RESULTS:A total of 143 robust DEGs and 48 merged DEGs were identified.After taking the intersection of the two,48 common DEGs were obtained.In the PPI network of common DEGs,5 hub genes were screened out,namely MYC proto-oncogene bHLH transcription fac-tor(MYC),prostaglandin-endoperoxide synthase 2(PTGS2),heme oxygenase 1(HMOX1),caspase-3(CASP3),and plasminogen activator urokinase receptor(PLAUR).The ROC results showed that the area under the curve values for all hub genes were greater than 0.8.MYC,PTGS2,CASP3,and PLAUR showed high mRNA and protein expression in rat MIRI,while there was no difference in mRNA and protein expression for HMOX1.The literature review revealed that among the 5 hub genes,only PLAUR has not been reported to be involved in MIRI.The GSEA results for PLAUR indicat-ed that its functional enrichment mainly focused on pathways such as NOD-like receptor signaling pathway,P53 signaling pathway,Toll-like receptor signaling pathway,apoptosis,and fatty acid metabolism.CONCLUSION:MYC,PTGS2,CASP3,HMOX1,and PLAUR are involved in the pathological process of MIRI.PLAUR is a potential hub gene that can mediate MIRI by regulating pathways such as NOD like receptor signaling,P53 signaling,Toll like receptor signaling,cell apoptosis,and fatty acid metabolism.The results can provide reference for further investigation into the molecular mechanisms and therapeutic targets of MIRI.