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Aims: Most dilated cardiomyopathies are either an ischemic dilated cardiomyopathy (IsDC) or an idiopathic dilated cardiomyopathy (IdDC). The treatments for both IsDC and IdDC are of a similar nature (upwards of 90%). Coronary revascularization, however, is only feasible for IsDC. The purpose of this study was to determine if microRNAs (miRNAs) could be used as biomarkers to distinguish between IsDC and IdDC. Materials and Methods: Patients were divided into two groups: IsDC and IdDC, with 25 patients in each group, and 10 healthy persons serving as a control group. In our study, the following miRNA expressions were detected using the Rotor Gene Q real-time polymerase chain reaction cycler (Qiagen) for all IsDC and IdDC subjects: let-7b-5p, let-7c-5p, miR-1-3p, miR-15b-5p, miR-17-5p, miR-19a-3p, miR-19b-3p, miR-20a-5p, miR-20b-5p, miR-23a-3p, miR-24-3p, miR-27a-3p, miR-28-5p, miR-30e-5p, miR-99b-5p, miR-100-5p, miR-101-3p, miR-103a-3p, miR-106a-5p, miR-125b-5p, miR-126-3p, miR-126-5p, miR-140-5p, miR-191-5p, miR-195-5p, miR-199a-3p, miR-214-3p, miR-222-3p, miR-342-3p, and miR-378a-3p. Results: We found that miR-24-3p, miR-28-5p, miR-100-5p, miR-103-3p, miR-125b5p, miR-214-3p, let-7b-5p, and let-7c-5p were each overexpressed by more than twofold in both the IsDC and IdDC groups when compared to the controls. We also found that miR-15b-5p and miR-106a-5p may be used to distinguish between patients with IsDC and IdDC. Conclusions: Our study has demonstrated that miR-15b-5p and miR-106a-5p expression levels could potentially serve as useful biomarkers for distinguishing between IsDC and IdDC. [ABSTRACT FROM AUTHOR]

Recent studies indicated that the Arg allele is preferentially mutated and retained in various human cancers arising in Pro/Arg heterozygotes and it may be an important biomarker in colon cancer prognosis. In this study, DNA was isolated from paraffine-embedded colon tumor tissue samples of 35 cases diagnosed as colon carcinoma. We have observed PCR-RFLP genotyping for the codon 72 exon 4 polymorphism (Arg72Pro) of the p53 gene. In this study, we detected that TP53 codon 72 polymorphism was present in 27 (77.1%) of 35 cases enrolled into the study. In 14 (51.9%) cases Arg/Arg, 11 (40.7%) cases Arg/Pro and 2 (7.4%) cases Pro/Pro genotype frequencies were found. In 8 (22.9%) cases DNA isolation were not obtained. Our results point out that individuals homozygous for the Arg allele have higher frequency than other alleles and that colon cancer may be related to Arg allele frequency. [ABSTRACT FROM AUTHOR]

Introduction: Carotid artery disease (CAD) is the narrowing of carotid arteries due to atherosclerosis. It can cause stroke. Some hereditary determinants can affect atherosclerosis formation.1 In present study, we investigated the hereditary thrombophilia on the formation of CAD. Patients and Methods: We evaluated the effects of Factor V LEIDEN, Factor V H1299R, Prothrombin G20210A, Factor XIII V34L, B-Fibrinogen -455 G>A, PAI-1 4G/5G, HPA1, MTHFR C677T, MTHFR A1298C, ACE I/D, APO B R3500Q, and APO E polymorphisms on CAD formation by using a ViennaLab CVD Strip Assay. Group A includes 41 patients (70.2 ± 8.6 years, 30 men) with CAD and Group B includes 39 healthy controls (67.3 ± 9.2 years, 28 men). Twenty patients had transient ischemic attack or stroke, 21 had carotid artery stenosis, more than 50 % in Group A. Hyperlipidemia is more frequent in Group A compared Group B (71%, 49 %; p<0.05). Hypertension, smoking habit and diabetes mellitus are similar in both groups. Results and Conclusion: Heterozygote form of Factor V H1299R, Factor XIII V34L, B-Fibrinogen -455 G>A, MTHFR C677T and MTHFR A1298C were more frequent in Group A compared with Group B significantly [(2.6%, 7.3% p<0.05), (12.8%, 19.5% p<0.05), (12.8%, 19.5% p<0.05), (20.5%, 34.1% p<0.05), (25.6%, 46.3% p<0.05)]. On the formation of CAD, Factor V H1299R, Factor XIII V34L, B-Fibrinogen -455 G>A, MTHFR C677T and MTHFR A1298C heterozygous mutation seems to be determinant (p<0.05). We have some difficulty on the explication that why heterozygous form is significant even though homozygous form is not significant. This is a pilot study. We will go on working on the project to evaluate the hereditary thrombophilia. [ABSTRACT FROM AUTHOR]