47 research outputs found

    Plasma concentrations of soluble CD40 ligand in smokers with acute myocardial infarction: a pilot study

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    Coronary artery disease (CAD) is believed to be the single leading cause of death in both men and women in the world. Smoking is the most important risk factor for CAD. Smoking increases platelet aggregation and thrombus formation. CD40 ligand (CD40L) is a transmembrane glycoprotein derived from activated platelets. It participates in thrombus formation during the acute phase of acute myocardial infarction (MI). Elevation of CD40L identifies the patients who are at highest risk for cardiac events and who are likely to benefit from treatment with the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor antagonists. The purpose of this study was to evaluate levels of CD40L in smokers with acute MI. Fifty-seven patients with acute MI were enrolled in this study. Thirty-one smokers were compared with 26 non-smokers. Soluble CD40L level in the plasma was determined by a standard enzyme-linked immunosorbent assay. Circulating levels of CD40L were higher in the smokers’ group. Smokers with acute MI may have increased risk for thrombotic complications during acute MI, and optimal antiaggregant therapy should be administered

    Chemokine (C-C Motif) Ligand 2 (CCL2) in Sera of Patients with Type 1 Diabetes and Diabetic Complications

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    Chemokine (C-C motif) ligand 2 (CCL2), commonly known as monocyte chemoattractant protein-1 (MCP-1), has been implicated in the pathogenesis of many diseases characterized by monocytic infiltration. However, limited data have been reported on MCP-1 in type 1 diabetes (T1D) and the findings are inconclusive and inconsistent.In this study, MCP-1 was measured in the sera from 2,472 T1D patients and 2,654 healthy controls using a Luminex assay. The rs1024611 SNP in the promoter region of MCP-1 was genotyped for a subset of subjects (1764 T1D patients and 1323 controls) using the TaqMan-assay.Subject age, sex or genotypes of MCP-1 rs1024611SNP did not have a major impact on serum MCP-1 levels in either healthy controls or patients. While hemoglobin A1c levels did not have a major influence on serum MCP-1 levels, the mean serum MCP-1 levels are significantly higher in patients with multiple complications (mean = 242 ng/ml) compared to patients without any complications (mean = 201 ng/ml) (p = 3.5×10(-6)). Furthermore, mean serum MCP-1 is higher in controls (mean = 261 ng/ml) than T1D patients (mean = 208 ng/ml) (p<10(-23)). More importantly, the frequency of subjects with extremely high levels (>99(th) percentile of patients or 955 ng/ml) of serum MCP-1 is significantly lower in the T1D group compared to the control group (odds ratio = 0.11, p<10(-33)).MCP-1 may have a dual role in T1D and its complications. While very high levels of serum MCP-1 may be protective against the development of T1D, complications are associated with higher serum MCP-1 levels within the T1D group

    Vitamin D receptor gene BsmI, FokI, ApaI, TaqI polymorphisms and bone mineral density in a group of Turkish type 1 diabetic patients

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    PubMedID: 21538164Previous studies have suggested an influence of vitamin D receptor alleles on bone metabolism and on susceptibility to type 1 diabetes mellitus in different ethnic populations. We aimed to investigate the distribution of vitamin D receptor (VDR) alleles in relation to biochemical bone turnover parameters and bone densitometry measurements in a group of Turkish type 1 diabetic patients. One hundred and seventeen patients (M/F 57/60, 27.6 ± 7.3 y duration of diabetes 8.1 ± 6.3 y) and 134 healthy controls (M/F 61/73, 26.2 ± 5.3 y) were included in the study. Bone mineral density (BMD) was evaluated by dual-energy X-ray absorptiometry (DEXA). The vitamin D receptor gene (VDR) polymorphisms FokI, Bsm1, Apa1, and Taq1 were examined using a PCR-based restriction analysis. Serum levels of calcium, phosphor osteocalcin, intact parathyroid hormone, and C telopeptide were measured. Vitamin D receptor Bsm1 Fok1, Apa1, and Taq1 genotype distributions were not different between patient with diabetes and control groups. BMD was 0.77 ± 0.2 g/cm 2 vs. 0.97 ± 0.2 g/cm 2 (P = 0.0001) for the femur, 1.0 ± 0.1 g/cm 2 vs. 1.13 ± 0.1 g/cm 2 (P = 0.001) for type 1 diabetic patients and controls. Bone turnover markers were significantly lower in type 1 diabetic group. BMD measurements and bone metabolic markers were not different between the genotypes in either the patient with diabetes or the controls. The VDR gene polymorphisms, Bsm1, Fok 1, Apa1, and Taq1 showed no influence on bone metabolism in our group of type 1 diabetic patients. © 2011 Springer-Verlag
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