Melatonin receptor 1A gene polymorphism rs13140012 and serum melatonin in atherosclerotic versus non-atherosclerotic Egyptian ESRD patients: pilot study.

AIM: To study the relationship between melatonin levels and Melatonin membrane receptor 1A (MTNR1A) SNP (rs13140012) in end-stage renal disease patients (ESRD) in Alexandria, Egypt on maintenance hemodialysis with or without atherosclerosis. MATERIALS AND METHODS: 40 end-stage renal disease patients on regular hemodialysis were divided into 2 subgroups, one with (n = 20) and one without atherosclerosis (n = 20) and normal subjects (n = 40). Serum melatonin, carotid intimal medial thickness (CIMT) were measured. Melatonin membrane receptor 1A (MTNR1A) SNP (rs13140012) genotyping was done using 5'nuclease Allelic discrimination. RESULTS: Serum melatonin was significantly lower in ESRD patients [1.6 to 11.30 (pg/mL) with a median of 2.5] than the control group [20.50 to 56.40 (pg/mL) with a median of 35.20]. Serum melatonin was significantly lower in atherosclerotic patients subgroup [1.6-2.50 (pg/mL) with a median value of 2.30] than non-atherosclerotic patients subgroup [2.0-11.30 (pg/mL) with a median of 4.9]. No significant association was found between serum melatonin and (MTNR1A) SNP (rs13140012) (p = 0.633). CONCLUSION: These results lead us to suggest that melatonin production is impaired in ESRD patients (included in this pilot study), and this impairment is more evident in atherosclerotic ESRD patients.

Study of Epstein-Barr virus serological profile in Egyptian patients with Hashimoto's thyroiditis: A case-control study.

BACKGROUND: Hashimoto's thyroiditis (HT) is now considered one of the most prevalent autoimmune diseases. The aim of the present study was to determine the prevalence of different types of EBV antibodies in patients with HT in comparison to healthy controls, and to detect any correlation between EBV serological markers and different laboratory findings in HT patients. SUBJECTS & METHODS: This case-control study was conducted on 120 subjects divided into two groups: Sixty patients with HT (patients group), and sixty age and sex matched healthy volunteers (control group). All the participants were subjected to: Thyroid ultrasound, laboratory assessment including: Serum thyroid -stimulating hormone (TSH), free tetraiodothyronine (FT4), free triiodothyronine (FT3), anti-thyroid peroxidase antibody (anti-TPO Ab) and anti-thyroglobulin antibody (anti-TG Ab). Four types of EBV antibodies (VCA IgM, VCA IgG, EA IgG, and EBNA-1IgG) were measured in serum using ELISA. RESULTS: The mean serum levels of EBV VCA IgG and EA IgG were significantly higher in HT patients group in comparison to control group. In euthyroid HT patients, a significant positive correlation was observed between the age and EBV EA IgG. While in hypothyroid HT patients, a significant positive correlation between thyroid isthmus and EBNA-1IgG was observed. A significant negative correlation was found between the serum FT3 and EBNA-1IgG and a significant positive correlation was observed between serum TSH and EBV VCA IgG. CONCLUSIONS: The high serum levels of EBV VCA IgG and EBV EA IgG in patients with HT suggest a possible association between EBV and HT.

Association of Tumor Necrosis Factor Alpha-Induced Protein 3 Interacting Protein 1 (TNIP1) Gene Polymorphism (rs7708392) with Lupus Nephritis in Egyptian Patients.

Lupus nephritis (LN) is a major cause of morbidity and mortality in systemic lupus erythematosus (SLE). Previous studies suggest that mutant A20 binding inhibitor of NF-κB 1 (ABIN1) protein encoded by tumor necrosis factor alpha-induced protein 3 interacting protein 1 (TNIP1) gene is associated with LN via NF-κB dysregulation. The aim of the current study was to evaluate the association of TNIP1 gene SNP rs7708392 with SLE and LN in Egyptian patients. 5' nuclease Allelic discrimination was used to evaluate the frequency of TNIP1 SNP rs7708392 in 53 patients with LN, 57 SLE patients without nephritis and 85 healthy controls. The genotyping analysis revealed that the CC genotype was more frequent in controls than SLE patients, while GC and GG genotypes were more common in SLE patients. Moreover, the GG genotype and the G allele were significantly more prevalent among LN patient than non-LN patients (P < 0.001). In LN patients, the most common genotype was GG (56.6%), while among the non-LN patients; the CG genotype was the most common (59.6%). Regression analysis demonstrated that SLE patients carrying only one G allele had a 3.4 folds increased risk for LN. Our results suggested that TNIP1 SNP (rs7708392) might be associated with the LN in Egyptian SLE patients. TNIP1 SNP (rs7708392) might be used to identify patients at risk of developing LN, which could help in early detection and treatment before progression to end-stage renal disease, improving patients' outcome and quality of life.

MicroRNA-200b Expression in the Vitreous Humor of Patients with Proliferative Diabetic Retinopathy.

BACKGROUND: The role of microRNA (miRNA)-200b in the pathogenesis of proliferative diabetic retinopathy (PDR) has been studied in diabetic animal models. The aim of this study was to assess miRNA-200b expression in the vitreous of patients with PDR and to determine its correlation with vascular endothelial growth factor (VEGF), one of the pathogenic mechanisms in PDR. METHODS: Quantitative reverse transcription polymerase chain reaction was used to measure miRNA-200b expression in the vitreous from 29 eyes with PDR and 30 eyes with idiopathic macular holes (IMH; control group). Vitreous VEGF was measured using an enzyme-linked immunosorbent assay. RESULTS: miRNA-200b expression was about 5-fold increased in the vitreous samples from eyes with PDR compared with the controls (p ≤ 0.001). Vitreous VEGF expression was also significantly higher in the PDR group than in the IMH group (p ≤ 0.001), but no significant correlation was found between miRNA-200b and VEGF. CONCLUSION: Both miRNA-200b and VEGF are increased in the vitreous of patients with PDR but in a noncorrelated pattern. miRNA-200b may be involved in the pathogenesis of PDR but through VEGF-independent mechanisms. Further studies are needed to identify the miRNA-200b-targeted genes involved in the pathogenesis of PDR and to examine the potential role of miRNA-200b as a target for PDR treatment.

Peroxisome proliferator-activated receptor-γ-coactivator 1α (PGC-1α) gene expression in chronic kidney disease patients on hemodialysis: relation to hemodialysis-related cardiovascular morbidity and mortality.

PURPOSE: The aim of the current study was to investigate some of the key regulators of mitochondrial oxidative metabolism in ESRD patients on hemodialysis (ESRD/HD) focusing on peroxisome proliferator-activated receptor-γ-coactivator 1α (PGC-1α) gene expression and its relation to ESRD/HD-related cardiovascular diseases (CVD) and mortality in an effort to identify new potential targets for pharmacological interventions. SUBJECTS AND METHODS: The expression of PGC-1α and one of its downstream genes: COX6C were evaluated in 49 ESRD/HD patients and in 33 age- and sex-matched healthy subjects as controls using quantitative real-time PCR. Malondialdehyde (MDA) was measured using colorimetric method as a marker of oxidative stress. Patients were followed up for 24 months for the development of HD-related cardiovascular complications and mortality. RESULTS: PGC-1α and COX6C expressions were significantly down-regulated in ESRD/HD patients compared to the controls (P ≤ 0.001 for both). Additionally, MDA level was higher in HD patients (P ≤ 0.001). Negative correlation was found between PGC-1α expression and MDA level (P ≤ 0.001). MDA was significantly higher, while PGC-1α expression was significantly lower in HD patients who developed CVD than in patients who did not. By using multivariate logistic regression analysis, it was found that down-regulated PGC-1α expression is independently associated with the development of CVD in HD patients. CONCLUSION: Our study suggests that ESRD/HD patients might have oxidative mitochondrial dysfunction, which may be partially responsible for CKD-related cardiovascular complications. Pharmacological modulation of PGC-1α might be a promising therapeutic tool to reduce oxidative stress-related complications in ESRD/HD patients.