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The purpose of this study was to examine the relationship between serum selenium (Se) levels and lipid subfraction among Egyptian type 2 diabetes patients and their association with the severity of the disease. The study was conducted on 60 type 2 diabetic adults with BMI

Diabetic nephropathy (DN) is a major cause of end-stage renal disease. Epidemiological studies suggest genetic predisposition to DN. Apolipoprotein A5 (ApoA5) plays an important role in the triglyceride (TG) metabolism, accelerating the catabolism of the TG-rich lipoproteins. Studies revealed that the ApoA5-1131 polymorphism is strongly associated with TG levels affecting DN risk. Patients with DN have increased fasting plasma TG levels, and studies report that elevated TG precedes DN. To test the effect of polymorphism ApoA5-1131T→C on the elevated TG levels contributing to the development of DN on type 2 diabetes patients, the study was conducted on 40 diabetic patients divided into two groups according to the presence or absence of diabetic nephropathy (DN+ and DN−), com- pared to 20 age- and sex-matched apparently healthy con- trols. DNA analysis was performed using polymerase chain reaction-restriction fragment length polymorphism. ApoA5-1131 CC carriers had a higher mean TG in the DN +, DN−, and control groups (TG 224, 201, and 204 mg/dl, respectively) (p00.001) compared to TT and TC carriers. Genotype distribution between controls and patients revealed CC carriers in the DN− and DN+ to be 55 and 45 %, respectively, compared to only 15 % in the control group (p00.001). Association between DN and the poly- morphism (CC) that affects fasting TG is seen in this study (OR04.6, 95 % CI01.02-21, p00.001). ApoA5-1131 CC carriers are more susceptible to a higher fasting TG level and the development of DN.

Hypertension (HTN) is a chronic condition of concern due to its role in the causation of coronary artery disease (CAD), stroke, and other vascular complications. Essential hypertension (EH) is a multifactorial disorder arising from the influence of several susceptibility genes and environmental stimuli. Apolipoprotein E (Apo E) plays an essential role in clearance of chylomicron remnants and very low-density lipoproteins (VLDL). Apo E gene has three alleles (E2, E3, and E4) that give rise to six different genotypes. A significant association of E4 allele has been observed with HTN in addition to the other well-known risk factors and positive family history. Carriers of E4 allele form a higher risk group showing greater susceptibility to CAD. These observations emphasize the need of genotyping Apo E in patients with EH as an important molecular tool in personalized medicine. The aim of this work was to study the association between Apo E gene polymorphism and EH in Egyptian patients as well as correlating different Apo E genotypes with serum lipids. The study was conducted on 50 patients with EH and 50 age-matched controls. DNA analysis was performed using polymerase chain reaction restriction fragment length polymorphism. The E3/E3 genotype was found in 85.42 % of patients, compared to 80 % in controls. E3/E4 (8.33 %) and E2/E3 (6.25 %) were lower in patients compared to controls 12 and 8 %, respectively. E4/E4 and E2/E2 genotypes were only found in two patients (4 %). Total cholesterol and low-density lipoprotein were significantly higher in E3/E4 as compared to E3/E3 and E2/E3. However, there was no significant difference in triglyceride, high-density lipoprotein, and VLDL.

Cardiovascular disease is the leading cause of death in Chronic kidney disease patients. This study tries to identify circulating endothelial microparticles {MPs} [such as Cadherin 5 and Anexin V] in CKD patients with and without IHD as potential new risk factors of atherosclerotic vascular disease. This study was carried out in Theodor Bilharz Research Institute [TBRI] on 60 patients with chronic kidney disease on maintenance hemodialysis. They were 41 male and 19 females selected from hemodialysis unit in TBRI. They were further subclassified into the following two groups according to the Echocardiography and Electrocardiogram (ECG) to 25 patients of chronic kidney disease without cardiac complications (17 males, 8 females and ages were 53.5 ± 9.9 years) and 35 patients of chronic kidney disease with cardiac complications (24 males, 11 females and ages were 57.5 ± 7.4 years). Twenty healthy subjects were selected as healthy control, their age 50 ± 9 years. Cadherin 5 & Annexin V Were done by enzyme linked immunosorbant assay (ELISA). The mean cadherin 5 levels in CKD with ischemic HD, CKD without ischemic HD and control group were 86.99 ± 21.51, 33.21 ± 8.65 and 2.63 ± 1.47 respectively which significantly higher in CKD with ischemic HD and CKD without ischemic HD than control group (p < 0.01) and significantly higher in CKD with ischemic HD than CKD without ischemic HD (p < 0.01). As regard to the mean annexin v levels in CKD with ischemic HD, CKD without ischemic HD and control group were 83.73 ± 22.64, 28.51 ± 9.73 and 0.47 ± 0.36 respectively which significantly higher in CKD with ischemic HD and CKD without ischemic HD than control group (p < 0.01) and significantly higher in CKD with ischemic HD than CKD without ischemic HD (p < 0.01). Endothelial dysfunction leading to atherosclerotic vascular disease in patients with CKD can be assessed quantitatively by measurement of plasma levels of endothelial microparticles such as CD144-EMP (Cadherin 5) and Annexin V.

Background and study aims The transforming growth factor (TGF)-β signalling pathway plays a dual role in hepatocarcinogenesis. It has been recognised for its role as a tumour suppressor as well as a tumour promoter depending on the cellular context. The aim of this study was to investigate the clinical significance of serum TGF-β1 level and TGF-β1 messenger RNA (mRNA) in the peripheral blood of liver cirrhosis and hepatocellular carcinoma (HCC) patients as noninvasive biomarkers in diagnosing HCC. Patients and methods Twenty patients were allocated to each of the liver cirrhosis and HCC groups, in addition to 20 healthy volunteers. TGF-β1 gene expression in peripheral blood was quantitated using real-time polymerase chain reaction (PCR), while serum TGF-β1 was analysed using enzyme-linked immunosorbent assay (ELISA). Results TGF-β1 gene expression was significantly lower in HCC patients (median 0.401 (0.241–0.699) fold change) than in liver cirrhosis patients (median 0.595 (0.464–0.816)) ( p = 0.042) and normal controls (median 1.00 (0.706–1.426) fold change) ( p = 0.001). TGF-β1 gene expression showed significant positive correlation with serum TGF-β1 ( r = 0.272, p = 0.036) and significant negative correlation with alpha-fetoprotein (AFP) ( r = −0.528, p = 0.001). Receiver operating characteristic (ROC) analysis was conducted for TGF-β1 gene expression in comparison with AFP. The area under the curve for TGF-β1 gene expression was 0.688 (95% CI = 0.517–0.858) ( p = 0.042) and AFP was 0.869 (95% CI = 0.761–0.976) ( p = 0.001). The sensitivity and specificity of TGF-β1 gene expression were 65% and 75%, respectively, at a cutoff value of 0.462 fold change. Conclusion TGF-β1 gene expression in the peripheral blood may be used as a molecular marker for the diagnosis of HCC. Additional studies on a large-scale population are necessary to gain greater insight into the impact of TGF-β1 gene expression in the pathogenesis of HCC.

Two common polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene, the thermolabile C677T and A1298C polymorphism may contribute to hyperhomocysteinemia, a known risk factor for vascular diseases. Twenty with coronary artery disease (CAD) and 20 patients with cerebro-vascular stroke (CVS) were compared with 20 controls. Using PCR and restriction fragment length polymorphism (RFLP) analysis, we studied C677T and A 1298C MTHFR genotypes and their combined effect on homocysteine, measured by chemiluminescent enzymatic immunometric assay. Homocysteine values were significantly higher in CAD (16.12±5.09μmol/L) and in CVS (16.79±5.93μmol/L) compared with controls (10.43±2.57μmol/L, P0.05). A significant positive correlation between plasma homocysteine and cholesterol (r=0.37, P