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Background Human glucagon-like peptide-1 analogue, Liraglutide, has shown cardioprotective effects in animal and clinical studies of type 2 diabetes mellitus. This study was conducted to assess the effect of Liraglutide on diabetes-induced myocardial electrical remodeling. Materials and Methods A rat model of type 2 diabetes mellitus was induced by high-fat diet and low dose Streptozotocin (35 mg/kg). Diabetic rats were randomized into 4 subgroups (n=6–7): diabetic-untreated, diabetics treated with Liraglutide, diabetics treated with Ramipril, and diabetics treated with Metformin in addition to a control group. Changes in serum glucose, insulin, lipid profile and revised quantitative insulin sensitivity check index (QUICKI index) were assessed. QT and QTc intervals were measured and the degree of cardiac interstitial and perivascular fibrosis was examined. The expression of myocardial Ito channel α subunits, gap junction protein; Kv 4.2/4.3 and connexin 43 (Cx43) respectively, were assessed by western blotting and immunohistochemistry. Results Similar to Ramipril, both Liraglutide and Metformin effectively inhibited the diabetes-induced myocardial hypertrophy and fibrosis. However, Liraglutide treatment significantly improved Kv 4.2/4.3 and Cx43 expression/distribution and prevented diabetes-related QTc interval prolongation. Conclusions We have shown that pathological alterations in myocardial Cx43 expression and distribution, in addition to reduced Ito channel expression, may underlie the QTc interval prolongation in high-fat diet/STZ rat model of type 2 diabetes mellitus. The beneficial effects of Liraglutide, as those of Ramipril, on cardiac electrophysiology could be at least attributed to its direct ability to normalize expression and distribution of Cx43 and Ito channels in the diabetic rat heart.

Background: Adipokines are demonstrated to be associated with multiple cutaneous diseases. Leptin is mainly produced by the adipocytes that stem from the obese gene. In addition, it was reported that, secretion of leptin is a response to increased lipid uptake, thus, it might be regarded as a link between improper diet and the development of inflammatory acne. Objective: The aim of the current work wasto estimate serum leptin and adiponectin in both obese and non-obese patients with acne vulgaris and to evaluate adiponectin/leptin ratio (A/L) rates as a biomarker of insulin resistance and hence their role in pathogenesis of acne vulgaris in correlation with body weight and disease severity. Patients and methods: This prospective case-controlled study included a total of 60 patients with acne vulgaris, attending at the Dermatology, Andrology & STD Outpatient Clinic, Mansoura University Hospitals. Forty healthy subjects matched with the patients in age, sex were included. This study was conducted between April 2019 to January 2020. Results: Cases with acne vulgaris demonstrated significant increase in serum leptin level as well as significant decrease in serum adiponectin level compared to controls. No significant correlation was reported between both serum leptin and adiponectin levels and disease severity. Leptin could be used as reliable predictor in terms of the differentiation between cases of acne vulgaris and controls with high sensitivity, specificity and accuracy. Adiponectin could be used as reliable predictor in terms of the differentiation between cases of acne vulgaris and controls with high sensitivity, specificity and accuracy. Conclusion: Acne vulgaris was associated with significant elevation in leptin level, significant reduction in adiponectin level and significant decrease in A/L ratio. Thus, leptin, adiponectin and insulin resistance may be pathogenic cofactors contributing to the development of the disease and could be used as reliable predictors for development of acne vulgaris but not for severity of disease.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with a suggested genetic basis. The newly identified human programmed cell death 1 gene could be associated with SLE susceptibility. We aimed to investigate the association between programmed cell death 1 polymorphism (PD1.3G/A (rs11568821) and PD1.5C/T (rs2227981)) with the risk of SLE in the Egyptian female population. This retrospective case–control study included 150 Egyptian females; 70 patients diagnosed to have SLE and 80 age-matched healthy controls. The two single nucleotide polymorphisms of the pdcd1 gene were genotyped by allelic discrimination through TaqMan real-time polymerase chain reaction. The PD1.3GG genotype and G allele as well as the PD1.5CC genotype were significantly more frequent in SLE patients (67.1%; p = 0.023, 82.1%; p = 0.0021, 62.9%; p = 0.0287 respectively). The GC haplotype was the most common haplotype among SLE patients (70.77%) with a reported significant linkage disequilibrium between the two studied polymorphisms ( p = 0.0041). Although most of the studies showed significant association of SLE with the minor alleles, we reported a significant association between the dominant genotypes (PD1.3GG and PD1.5CC) as well as the major G allele with the risk of SLE among Egyptian females.

Background Androgenetic alopecia (AGA) is associated with a risk of coronary heart disease (CHD), although the causes underlying this association are not clear. Serum homocysteine (SH) is a known risk factor for CHD, and methylene tetrahydrofolate reductase enzyme (MTHFR) plays a crucial role in the remethylation of homocysteine to methionine. The polymorphism C677T that affects the catalytic domain of the MTHFR protein leads to a high levels of SH. Our hypothesis was that this polymorphism and SH level are risk factors for CHD in patients with AGA. Materials and methods A total of 106 patients with AGA and 100 well-matched healthy controls were enrolled in the study. SH levels were estimated. DNA was extracted and polymerase chain reaction amplification, followed by restriction enzyme digestion for MTHFR (C677T) gene, was conducted. Results SH levels were significantly higher in the patient group and highest in those with the TT genotype. The mutant T allele was associated with hyperhomocysteinemia and an increased risk of CHD in patients with AGA. Conclusions AGA is associated with a higher risk of developing CHD due to the associated higher level of SH that, in turn, depends on and is correlated with mutant MTHFR genotypes. Cardiac evaluation and follow-up of patients with AGA is recommended for early detection and treatment of CHD to avoid an overall detrimental course.

Introduction: Male factor is responsible for about half of infertility problems. However, the reasons for the decrease in male fertility are still broadly unclear. The mechanisms of how smoking may impact male fertility have not been established. However, with its influence on different semen parameters, it is regarded as a risk factor for infertility.Aim: To investigate the effect of chronic smoking on spermatozoa NRF2 expression and DNA fragmentation in infertile men with apparently normal seminogram and to determine if NRF2 expression and DNA fragmentation markers could be possible predictors of the impact of chronic cigarette smoking on male fertility.Methods: Semen samples were collected from 170 subjects; 65 nonsmokers (40 fertile and 25 infertile) and 105 smokers (25 fertile and 80 infertile). NRF2 gene expression, 8-OHdG and DNA fragmentation were assayed.Results: There were significant increases in 8-OHdG and %DNA fragmentation with a significant decrease in NRF2 gene expression in infertile smokers. ROC curve analysis of spermatozoa NRF2 gene expression showed 95% sensitivity 93.3% specificity at cutoff value ≤0. 931 (p 19.33 pg/ml predicting the detrimental effect of smoking on spermatozoa DNA.Conclusion: Chronic cigarette smoking may be a hidden causative mechanism of delayed fertility. Spermatozoa NRF2 gene expression and seminal 8-OHdG levels may serve as sensitive diagnostic indicators predicting smoking induced infertility. So, the presence of normal seminal parameters could not be an exclusion of potential effect of chronic smoking on male fertility.

Matrix metalloproteinase-9 is closely associated with the invasive and metastatic potential of most types of solid cancers. Our objective was to investigate the MMP-9 expression in lung cancer and to evaluate their relations to histopathologic types and prognosis.Bronchoscopic samples were obtained from tumor and normal bronchial mucosa in 25 patients with lung cancer. Total RNA was isolated from the tissues, and the relative expression as well as the activity of MMP-9 was evaluated.Non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) showed significantly higher MMP-9 expression (P0.0001) compared with normal tissues. MMP-9 activity in tissue and serum samples from both cancer groups were significantly higher than normal tissue and serum controls (P0.0001). Also, MMP-9 expression and tissue and serum activity were significantly higher in NSCLC than in SCLC (P=0.0167, 0.0454, and 0.004, respectively). As regards the pathologic types of NSCLC, similar results were found for the adenocarcinoma subgroup versus squamous cell lung cancer (P=0.0015, 0.0052, and 0.0011, respectively). MMP-9 expression and tissue activity were higher in stage III-IV NSCLC cases compared with early tumor stages (P=0.0120 and 0.0271, respectively).The expression and activity of MMP-9 are upregulated in NSCLC and are related to the pathologic type and clinical stage of NSCLC. Significantly higher expression and activity of MMP-9 in tumor tissue than in the surrounding tissue supports the important role of this metalloproteinase in the growth of lung cancer, and it could be used as a suggested therapeutic target.