Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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Myocardial free wall rupture (MFWR) refers to laceration of the heart ventricle or atria, which is a rare but fatal complication of acute myocardial infarction (AMI). In this study, we aim to identify the clinical characteristics and protective factors of free wall rupture after myocardial infarction. This is a single-center, retrospective observational analysis. ⋯ The present study provides evidence for better understanding of the clinical characteristics and protective functions in MFWR after AMI. Reduced cardiac function is correlated with higher incidence of later phase free wall rupture. Higher ACEI/ARB and β-blocker coverage in the AMI treatment strategy is associated with lower MFWR incidence.
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Patients with hereditary spherocytosis (HS) have increased rates of erythropoiesis and higher folate requirements. In a case-control study of patients with HS, we evaluated the associations between the use of 5 mg folic acid (FA) daily and serum concentrations of folate, unmetabolized folic acid (UMFA), interleukin (IL)-6, IL-8, IL-10, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α); and mRNA expression of dihydrofolate reductase (DHFR), methylene tetrahydrofolate reductase (MTHFR), IL8, IFNG and TNFA genes. Total serum folate and folate forms were measured in 27 patients with HS (21 users [HS-U] and 6 non-users [HS-NU] of supplemental FA) and 54 healthy controls not consuming 5 mg/day supplemental FA. ⋯ DHFR mRNA expression was higher in HS-U than in HS-NU. The use of high daily doses of FA for treatment of patients with HS may be excessive and is associated with elevated serum UMFA and elevated DHFR mRNA expression. It is not known whether long-term high-dose FA use by patients with HS might have adverse health effects.
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Primary immune thrombocytopenia (ITP) is an autoimmune bleeding disorder which characterizes with platelet production impairment and platelet destruction increment. CD4+CD25+Foxp3+ Treg cells (Tregs) are involved in the immune pathogenesis of ITP. MicroRNAs (miRNAs) are also involved in ITP and their loss of function is shown to facilitate immune disorders. ⋯ Compared with the healthy controls, miRNAs expressed differentially in the Tregs of patients with ITP. The levels of expression of miR-155-5p, miR-146b-5p, and miR-142-3p were significantly decreased. Therefore, the deregulation of miRNAs may affect the function of Tregs in the course of ITP.
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T cell immunoglobulin and mucin domain 3 (TIM3) expression is associated with immunosuppression and clinical outcomes in many diseases. However, the specific mechanism of TIM3 in immune system has not been clarified. In order to illustrate the mechanism of TIM3 in immune system, we analyzed the expression, function and regulation of TIM3 in T helper (Th)1 cells, Th2 cells, Th17 cells and regulatory T cells (Treg) through flow cytometry in patients with myelodysplastic syndrom (MDS). ⋯ The secretion of transforming growth factor-β in TIM3+Treg cells decreased in patients with MDS. These findings suggested that TIM3 might affect immune helper systems by regulating Treg cells and related immune cells. Therefore, studying the role of the TIM3 pathway in MDS is necessary and may help to provide a new way to explore the pathogenesis and treatments of MDS.
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The varicose vein wall remodeling is a very complex process, which is controlled by numerous factors, including peptide growth factors. The aim of the study was to assess a/b FGF, IGF-1, TGF-β1, VEGF-A and their receptors in the vein wall. Varicose vein samples were taken from 24 patients undergoing varicose vein surgery. ⋯ There was no difference in VEGF R1 content between varicose and normal veins (p>0.05), whereas VEGF R2 content was significantly increased in varicose veins (p<0.05). Western blot demonstrated increased expression of TGF-β RII in varicose veins (p<0.05) and similar expression of FGF R1 in both groups (p>0.05). Demonstrated changes in peptide growth factors and their receptors may disturb metabolism of extracellular matrix in the varicose vein wall and contribute to the development of the disease to its more advanced stages.