Introduction: Hepatic ischemic reperfusion injury occurs in multiple clinical settings. Novel potential protective agents are still needed to attenuate this injury. Apelin preconditioning protects against ischemic reperfusion injury in different organs. However, the protective mechanism of apelin on hepatic ischemic reperfusion injury is not yet clear. Aim: Evaluate the effect of apelin-13 preconditioning on hepatic ischemic reperfusion injury and clarify possible interactions between apelinergic, renin-angiotensin systems and endothelial nitric oxide synthase. Methods: In total, 60 rats were assigned to four groups: control sham-operated, ischemic reperfusion, apelin-treated ischemic reperfusion and apelin þ N-nitro-L-arginine methyl ester-treated ischemic reperfusion. Apelin 2 mg/kg/day and N-nitro-L-arginine methyl ester 10 mg/kg/day were injected intraperitoneally daily for 3 days and 2 weeks respectively before hepatic ischemic reperfusion. Serum aminotransferase, aspartate aminotransferase, hepatic malondialdehyde, apelin, gene expression of caspase-3, endothelial nitric oxide synthase and angiotensin type 1 receptor and liver histopathology were compared between groups. Results: Apelin significantly reduced serum aminotransferase, aspartate aminotransferase, hepatic malondialdehyde, caspase-3 and angiotensin type 1 receptor expression, whereas hepatic apelin and endothelial nitric oxide synthase expression were significantly increased with improved hepatic histopathology. N-nitro-L-arginine methyl ester co-administration partially reversed this hepatoprotective effect. Conclusion: Apelin-13 reduced hepatic ischemic reperfusion injury. This protection could be related to the suppression of hepatic angiotensin type 1 receptor expression and elevation of hepatic apelin level and endothelial nitric oxide synthase expression, which counteracts the pathologic effects of Ang II/angiotensin type 1 receptor. An interaction exists between apelinergic, renin-angiotensin systems and endothelial nitric oxide synthase in hepatic ischemic reperfusion pathophysiology.

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Introduction: There is growing evidence that genetic and environmental factors play an important role in the development and progression of non-alcoholic fatty liver disease (NAFLD). We investigated the association of single nucleotide polymorphism (SNP) rs738409 in PNPLA3 gene and TNF-α G238A polymorphism with the development and severity of NAFLD in an overweight and obese Egyptian population. Material and Methods: 100 overweight and obese patients with NAFLD and 30 control subjects were enrolled. All NAFLD patients underwent a confirmatory biopsy. Laboratory investigations included fasting plasma glucose, kidney and liver function tests, liver enzymes, lipid profile and hepatitis markers. Abdominal ultrasound was performed and all subjects were genotyped for (rs738409) PNPLA3 and (rs361525) TNF-α gene polymorphisms using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Results: The homozygous GG genotype of the PNPLA3 was most frequent among patients with NASH (26%) as compared to borderline NASH (20.5%) and simple steatosis (20%). Higher serum levels of transaminases were observed in NAFLD patients and controls who were carriers of the G allele of rs738409, but this was not statistically significant. Regarding the TNF-α G238A SNP; the frequency of the A allele was significantly higher in NAFLD patients (20%) compared to controls (5%) (p value = 0.006). The highest TNF G allele frequency was observed in the NASH group (88%) and this was statistically significant (p value = 0.009). Conclusion: Our study confirmed the association of the PNPLA3 (rs738409) and TNF-α promoter region G238A polymorphisms with susceptibility to NAFLD and its progression. M. A. Hegazy et al.54

Bisphenol S (BPS) is used as an alternative to bisphenol A (BPA) in polycarbonate plastics, epoxy resins and thermal receipt sheet manufacturing. We examined the toxic effects of BPS on gastric and renal functions, as well as the efficacy of allopurinol as a treatment. Albino rats were given only BPS (30 and 120 mg/kg BW/day), and some were treated with allopurinol prior to sacrifice. Gastric and renal specimens were evaluated histologically and immunohistochemically, and blood from the tail vein was analysed for levels of gastrin, uric acid (UA), erythropoietin and 8‐deoxyguanosine (8‐OHdG). Gastrin levels decreased while erythropoietin, UA and 8‐OHdG levels increased significantly. The severity of gastric and renal damage observed in BPS‐treated animals increased with increasing doses. The mean percentage of COX‐2 immunoreactivity and the mean number of CD45 immunoreactive cells were significantly increased in the stomach and kidney of BPS rats. Allopurinol ameliorated the biochemical, histological and immunohistochemical alterations induced by BPS, with superior protection at lower doses. Allopurinol can reverse the effects of BPS on the stomach and kidneys.

Background: it's well known that diabetic patients are more prone to infection. In these patients, chronic infections are frequent and severe due to impairment of their immune system. The relationship between H. pylori infection and diabetes mellitus have shown in some studies but the relationships remain controversial. Aim of The study: was to determine the prevalence of Helicobacter pylori infection (H. pylori) among diabetic patients (type1 and type 2 diabetes mellitus) and the relation of H. pylori infection to gastrointestinal (GI) complications in diabetics. Subjects and methods: the study included 100 subjects were divided into 2 groups. Group I 50 patients with diabetes mellitus and have dyspeptic symptoms, group II 50 non-diabetic with dyspeptic symptoms. This is a case and control study comparison of diabetic and non-diabetic groups. The study was conducted at Police Hospital Cairo during the period from (January-December 2012). Methods: H. pylori were assessed by H. pylori stool antigen (HpSAg) test among diabetic and non-diabetic group. Results: a positive cases for H. pylori infection by (HpSAg) test was 61.1% in type 1 diabetic patients and 65.6% in type 2 diabetic patients compared to 50% of the non-diabetic group (p 0.36) non significant (N.S). The prevalence of gastrointestinal symptoms in H. pylori positive diabetic patients as regarding dyspepsia (62.5%), early satiety (56.25%), heart burn (62.5%), bloating (25%), diarrhea (15.63%), constipation (25%), nausea (43.75%), vomiting (9.38%) and abdominal pain (53.13%), but by comparison with negative diabetic group these was statistically insignificant. Glycosylated Hb (HBA1c) was higher among positive cases, but yet not significant, (p 0.07). Also, FBS (p 0.08) and PPBS (p 0.1) were not significant. The Presence of H. pylori not associated with increase duration of diabetes. The mean age of diabetic patients positive for H. pylori was 48.750±11.09 years compared to 40.167±12.76 years in diabetic patients negative for H. pylori infection (p 0.017) significant (s). Age and BMI was higher among those positive for H. pylori in studied cases. Conclusion: the study reported no significant association between H. pylori infection and the prevalence of diabetes, but there is a borderline increased risk for H. pylori infection in diabetic among participants with a BMI greater than 25 kg/m².