Background: Extreme obesity pathology is with a risk factor for heart failure (HF), whereas the obesity paradox in HF shows that obese subjects had a good prognosis. The mechanism underlying the obesity paradox in HF prognosis is unclear till now. We aimed to provide evidence for the molecular mechanisms of the obesity paradox in HF. Methods: Differentially expressed genes (DEGs) in ischemic HF samples were identified in the GSE57338 and GSE5406 datasets. Weighted gene co-expression network analysis (WGCNA) modules and a protein-protein interaction network (PPI) were constructed. HF-associated DEGs and pathways were screened in the Comparative Toxicogenomics Database (CTD). The expression of hub genes in adipose tissues from obese patients and LV samples from HF patients were validated in microarray datasets. Results: Three HF-associated WGCNA modules were identified and DEGs were associated with the ‘hsa04115: p53 signaling pathway’. SERPINE1 was the only common gene between DEGs and HF-associated genes in the CTD database. The SERPINE1 gene was downregulated in the white adipose tissues compared with brown adipose tissues (P = 3.90e-03) and was upregulated in the omental adipose tissues from obese patients compared with lean subjects (P = 3.85e-02). Conclusion: The downregulation of SERPINE1 expression might be responsible for the obesity paradox in HF via interacting with ESR1.

Background: Ectopic pregnancy is a type of pregnancy in which implantation of zygote occurs out of the uterine cavity. One of the most important problems is bleeding. On the other hand, Plasminogen Activator Inhibitor-1 (PAI-1) gene is one of the involved factors in unsuccessful pregnancies, and 4G/5G polymorphism is the most common changes of this gene. So, it is important to study the prevalence of these changes in this gene in women with ectopic pregnancy.Materials and Methods: In this case-control study, 100 Iranian women with ectopic pregnancy and 101 Iranian women with the normal pregnancy were selected. After blood sampling, ARMS PCR method has been used for detection 4G/5G polymorphism and data were analyzed by statistical analysis.Results: In this study, 4G allele with 70.79% prevalence and 5G allele with 63.5% prevalence are the most common alleles for the control and case group, respectively.4G/4G and 4G/5G genotypes in the control group and 4G/5G and 5G/5G genotypes in the case group are prevalent. An Armitage test found p<0.05 for both alleles, showing 4G allele (p=1.524e-10; OR=0.262) has decreasing effect and 5G allele (p=1.524e-10; OR=3.822) has increasing effect in ectopic pregnancy.Conclusion: According to the findings, 5G allele and 4G/5G and 5G/5G genotypes have increasing effect, 4G allele and 4G/4G genotype have decreasing effect in ectopic pregnancy. So, we could consider 5G allele as a risk factor of ectopic pregnancy in this study.

Background: The risk for unsuccessful reperfusion after streptokinase therapy may be caused by the antifibrinolytic effect of platelet-derived type 1 plasminogen activator inhibitor (PAI-1) and antistreptokinase antibodies. This study aims to show the relation of pretreatment PAI-1 levels of patients with acute myocardial infarction treated with streptokinase and the outcome of fibrinolysis, emphasizing on reperfusion with and without considering pretreatment antistreptokinase antibodies.Methods: Pretreatment PAI-1 and antistreptokinase antibodies levels of 61 patients with acute myocardial infarction, treated with streptokinase, were determined by an enzyme- linked immunosorbent assay kit method. Failure of thrombolysis with streptokinase was present when reperfusion was unsuccessful as assessed by noninvasive reperfusion criteria.Results: Mean pretreatment PAI-1 level of patients was 29.72±4.74 ng/ml. Thrombolysis with streptokinase failed significantly with higher pretreatment PAI-1 levels (p<0.05) in all patients and patients with negative pretreatment antistreptokinase antibodies.Conclusion: We showed that higher on reperfusion in patients with acute myocardial infarction, with and without considering pretreatment antistreptokinase pretreatment PAI-1 levels were associated with significant failure of streptokinase therapy with the emphasis antibodies (anti-SK). It seems that by estimating PAI-1>25 ng/1 and antistreptokinase antibodies higher than normal levels in patients before the start of streptokinase therapy, candidates for potentially unsuccessful streptokinase therapy (with failed reperfusion) can be identified in advance and an alternative therapy such as primary angioplasty with better immediate results can be started.

Background and Objectives Several hereditary and acquired risk factors for thrombosis are known. Among the genetic factors, PAI-1 4G/5G polymorphism can be noted. This study was done to investigate the association of 4G/5G polymorphism in PAI-1 gene and thrombosis in coronary arteries.Materials and Methods Sixty one patients with the history of thrombosis in coronary arteries and 92 healthy blood donors participated as the control in our study. After DNA extraction from leucocytes based on the selective detergent-mediated DNA precipitation from crude lysate, PCR was performed using ARMS technique. Single and multivariate analyses were applied to adjust for potentially confounding factors using SPSS 19 software. The data were also compared with those of the other similar studies.Results The results showed 61 patients with history of coronary artery thrombosis for PAI-1 with the values of 24.6%, 45.9%, and 29.5% for 4G/4G, 4G/5G, and 5G/5G, respectively; the values for 92 healthy blood donors were evaluated to be 20.7%, 42.2%, and 37% in order. The polymorphism studied was not significantly different between cases and controls. Single and multivariate analyses show a significant difference for the conventional risk factors for coronary artery disease between patients and healthy controls (P value: 0.001).Conclusions We found no association between arterial thrombosis and the 4G/4G genotype for PAI-1 gene in Iranian population of the current study.