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Objective:To analyze the value of minute ventilation to carbon dioxide production slope (VE/VCO 2 slope) combined with peak systolic blood pressure (SBP) in predicting prognosis for patients with chronic heart failure (CHF). Methods:A total of 170 patients with CHF who visited the Cardiac Rehabilitation Center of Tongji Hospital Affiliated to Tongji University and completed cardiopulmonary exercise test from March 2007 to December 2018 were enrolled in the study. The clinical data, cardiopulmonary exercise testing results and follow-up information of patients were collected to explore the predictors of all-cause mortality in patients with CHF.Results:The median follow-up time was 647 (182-1 764) days. All-cause death occurred in 34 patients. Compared with surviving patients, the proportion of diabetes and angiotensin-converting enzyme inhibitor/angiotensin Ⅱ receptor blocker (ACEI/ARB) use in fatal patients was significantly higher ( P<0.01). The VE/VCO 2 slope and peak SBP*VE/VCO 2 in the fatal patients were significantly higher, and the peak oxygen consumption (peak VO 2) was lower than those in the surviving patients ( P<0.01). The areas under the receiver operating characteristic curve (AUC) of VE/VCO 2 slope and peak SBP*VE/VCO 2 in predicting all-cause mortality in patients with CHF were 0.648 ( P=0.008) and 0.681 ( P=0.001), respectively; the optimal thresholds were >40.95 ( P=0.008) and > 5 423.50 mmHg (1 mmHg=0.133 kPa, P=0.006), the sensitivity was 0.559 and 0.588, and the specificity was 0.728 and 0.735, respectively. Multivariate Cox regression analysis showed that after adjusting for age, gender, diabetes and ACEI/ARB use, VE/VCO 2 slope ( HR=2.12, P=0.036) and peak SBP*VE/VCO 2 ( HR=2.42, P=0.016) were independent risk factors for all-cause mortality in patients with CHF. Conclusion:Compared to the traditional index VE/VCO 2 slope, a novel index peak SBP* VE/VCO 2 provides a relatively better predictive value for all-cause death of CHF patients.
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Objectives To explore the intrinsic factors related to the pathogenesis of acute arterial thrombosis (AAT) and to elucidate the patho-genesis of AAT on the basis of differentially expressed genes. Methods Patients with acute myocardial infarction (AMI), stable angina (SA) and healthy controls (n=20 per group) were recruited, and the whole human genome microarray analysis was performed to detect the dif-ferentially expressed genes among these subjects. Results Patients with AMI had disease-specific gene expression pattern. Biological func-tional analysis showed the function of T cells was significantly reduced, the mitochondrial metabolism significantly decreased, the ion me-tabolism was abnormal, the cell apoptosis and inflammatory reaction increased, the phagocytosis elevated, the neutrophil-mediated immunity increased and the post-traumatic repair of cells and tissues increased in AMI patients. The biological function in SA group and healthy con-trols remained stable and was comparable. Conclusions The reduced function of T cell gene models in AAT showed the dysfunction of the immune system. The pathogenesis of AAT may be related to the inflammatory reaction after arterial intima infection caused by potential pathogenic microorganisms.
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Objective To investigate expression differences of neutrophil and mononuclear phagocyte related gene mRNAs among acute myocar-dial infarction (AMI), stable angina (SA) and control groups, and then discuss their expression characteristics in the stable angina pectoris (SAP) and AMI stages of coronary artery disease (CAD). Methods Whole Human Genome Oligo Microarrays were applied to assess the differential expression characteristics of neutrophil and mononuclear phagocyte related mRNAs in patients with AMI (n=20), SA (n=20) and controls (n=20). Results (1) Almost all colony-stimulating factors (CSF) and their receptors related mRNAs was up-regulated in AMI and SA groups compared with the control group, and the expression of granulocyte-macrophage colony stimulating factor receptor (GM-CSFR) and granulocyte colony stimulating factor receptor (G-CSFR) mRNAs in the AMI group was significantly up-regulated com-pared with the other two groups (P<0.01). (2) The expression of mRNAs related to monocyte chemoattractant protein-1 (MCP-1), CCR2 (MCP-1 receptor) and CXCR2 (IL-8 receptor) was significantly up-regulated (P<0.01) in AMI group compared with SA and control groups. IL-8 mRNA expression in the AMI group was clearly higher than the controls (P<0.05). (3) All mRNAs expression related to opsonic re-ceptors (IgG FcR and C3bR/C4bR) was significantly up-regulated in AMI group compared with SA and control group (P<0.01), and the SA group showed an upward trend compared with controls. (4) Most pattern recognition receptor (PRR)-related mRNAs expression was up-regulated in AMI group compared with SA and control groups. Most toll-like receptor (TLR) mRNAs expression was significantly up-regulated (P<0.01) than the SA and control groups;macrophage scavenger receptor (MSR) mRNA was significantly up-regulated in AMI group compared with the control group (P<0.01), and the SA group showed an upward trend compared with the controls. Conclusions The expression of most neutrophil and mononuclear-macrophage function related genes mRNAs was significantly up-regulated by stages during the progression of CAD, suggesting that the adhesive, chemotactic and phagocytic functions of neutrophil and mononuclear-ma-crophage were strengthened in the occurrence and development of coronary atherosclerosis and AMI. This also showed a stepped up-ward trend as the disease progressed.
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Objective To observe the liver protection of Ginsenoside Rg1 and Oxymatrine and research its mechanisms.Methods Nonalcoholic fatty liver disease(NAFLD) model was induced by high-fat diet and hepatic fibrosis(HF) model was caused by CCl4 in rats. Protection effects of Ginsenoside Rg1, Oxymatrine and the combination were obsrved.ResultsBoth Rg1 and OMT significantly reduced serum total cholesterol(TC), triglyceride(TG), alanine aminotransferase(ALT) and aspartate amino transferase (AST) levels of NAFLD rats[Rg1 group (2.76±0.22) mmol/L,(1.24±0.17) mmol/L,(112.39±12.91)U/L, (195.16±12.99) U/L; OMT group (2.35±0.19) mmol/L,(1.09±0.09) mmol/L,(90.57±10.25) U/L, (186.45±13.14) U/L,P<0.05 or 0.01],elevated liver PPARα mRNA and PPARγ mRNA[Rg1 group: (0.64± 0.05),(0.77±0.07);OMT group(0.67±0.07),(0.73±0.06),P<0.05 or 0.01] and alleviated the degree of fatty liver. The effects of the combination group[(1.87±0.21) mmol/L, (0.77±0.10) mmol/L,(58.78± 8.87)U/L,(149.78±11.27)U/L,(0.81±0.09),(0.89±0.05) ] was better than single treatment group (P<0.05 or 0.01). Both Rg1 and OMT significantly reduced the serum ALT, AST levels and liver methane dicarboxylic aldehyde(MDA)content[Rg1 group: (46.75±5.11) U/L,(147.53±7.31) U/L,(5.54±1.06) nmol/g; OMT group:(148.24±4.32) U/L, (93.90±14.22) U/L,(5.85±0.91) nmol/g,P<0.01] in HF model[Rg1 group: (146.75±5.11) U/L,(147.53±7.31)U/L,(5.54±1.06)nmol/g; OMT group:(148.24±4.32) U/L,(93.90±14.22) U/L,(5.85±0.91) nmol/g,P<0.01], enhanced liver SOD activity[Rg1 group:(91.61±9.26) U/mg prot; OM group: (86.19±8.51) U/mg prot,P<0.01] and reduced the semi-quantitative score [Rg1 group:(2.7±0.4); OMT group:(2.9±0.5),P<0.05 or 0.01], the effect of the combination group[(92.21±4.36) U/L,(52.08±7.56) U/L,(3.68±0.54) nmol/g,(99.67±13.13) U/mg prot, (1.2±0.4)] was better than single treatment group.Conclusion Ginsenoside Rg1 and Oxymatrine had synergic of liver protection and the synergic regulation of liver PPARα, PPARγ and antioxidant effect, which should be the potential mechanisms.
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Objective To explore the role of T cell-mediated immunity in the pathogenesis of venous thromboembolism ( VTE ) by analyzing the differential expression of T cell immune-related gene mRNAs peripheral blood mononuclear cells (PBMCs) between VTE patients and controls with GeneChip Human Genome. Methods Human eDNA microarray analysis was employed in PBMCs from 20 VTE patients and 20 hypertensive controls,and random variant model (RVM) corrected t-test was used for statistical analysis of differential gene expression.Results Six mRNA stripes including CD247,CD3D,CD3G,Granzyme A (GzmA),Granzyme B (GzmB) and Zeta-chain-associated protein kinase 70 (ZAP70)were found to be associated with T cell-mediated immunity.Significant down-regulation of these six mRNAs was found in the VTE group compared with the controls ( 15.3050 ± 0.6346 vs 15.8053 ± 0.5567,13.7878 ±0.7731 vs 14.3820 ±0.4857,13.3299 ± 0.9104 vs 14.1246 ± 0.6011,14.8893 ± 0.8675 vs 15.5305 ±0.4624,15.9113 ±0.8123 vs 16.4553 ±0.5055,14.3652 ±0.7717 vs 14.3652 ±0.7717;all P values ＜ 0.05 ).Conclusions T cells' function including antigen recognition,signal transduction and cytotoxicity was impaired in VTE patients.T cell-mediated immunity dysfunction probably plays an important role in the pathogenesis of VTE.
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Objective To investigate the gene expression difference of IFN and their receptors in peripheral blood mononuclear cells (PBMC) of pulmonary embolism (PE) patients.Methods Twenty cases of PE patients and twenty sex and age matched controls were recruited into the study.Human cDNA microarray analysis was used to detect the gene expression difference of IFN associated genes between the two groups,and random variance model corrected t test was used to analyze the statistical data.Results In comparison with the control group, mRNA expression of type Ⅰ IFN, including IFNα5 mRNA,IFNα6 mRNA,IFNα8 mRNA,IFNα14 mRNA,IFNκ mRNA,IFNω1 mRNA,IFNε1 mRNA in PBMC of PE patients Were down-regulated (P ＜ 0.05 ).There was no significant difference in gene expression of type Ⅰ IFN receptors IFNαR1 and IFNαR2 between the PE and control groups (P ＞ 0.05 ).In comparison with the control group,mRNA expression of IFNγ gene was down-regulated ( P ＜ 0.05 ).The mRNA expression of IFNγR1 and IFNγR2 genes were upregulated compared with the control (P ＞ 0.05 ).Conclusion mRNA expression of type Ⅰ and type Ⅱ IFN in PE are significantly down-regulated,but not the IFN receptors.Reduced immune function may play an important role in the PE patients who are susceptible to virus,intracellular bacteria and parasites.
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ssociated genes,especially down-regulated expression of T cell mediated function genes,in patients with PE indicates that the etiology of PE might be related to viral infection.
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<p><b>OBJECTIVE</b>To establish a clinical classification of pulmonary embolism (PE), and to evaluate the optional treatment strategies for different types of PE.</p><p><b>METHODS</b>From December 1995 to July 2001, 45 patients with acute PE were hospitalized, of which 33 received intravenous thrombolytic therapy or interventional treatment.</p><p><b>RESULTS</b>Misdiagnostic rate in the 45 patients with acute PE during first visit was 62.2% and mortality rate was 28.9%. Misdiagnostic rate in acute PE patients who had undergone surgery was 82% and mortality rate was 73%. The effective rate of thrombolytic therapy was 77.7%. Clinical symptoms rapidly disappeared in massive PE patients treated with interventional therapies.</p><p><b>CONCLUSIONS</b>Intravenous thrombolytic therapy is one of the most effective methods for treating acute PE. Application of interventional therapy for severe acute PE is also promising.</p>