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Background Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder characterized by obesity, hyperandrogenism, and insulin resistance. Intercellular adhesion molecule-1 (ICAM-1) is a proinflammatory and proatherogenic cytokine which is associated with atherosclerosis, insulin resistance, and cardiovascular disease (CVD). The pathogenesis of PCOS is not precisely known. Thus, the purpose of this study was to investigate the potential role of ICAM-1 expression and serum ICAM-1 concentrations in pathogenesis of PCOS. Moreover, we aimed to evaluate the possible relationship between ICAM-1 gene expression with carotid intima-media thickness as well as clinic-morphological features of PCOS. Methods This case control study enrolled 180 patients with PCOS and 120 controls groups and they were stratified according to their fasting plasma glucose (FPG) into three subgroups; normal glucose tolerance (NGT) [n = 75], those with impaired glucose tolerance (IGT) [n = 65], and 40 patients with type 2 diabetes mellitus (T2DM). Circulating ICAM-1 expression levels were determined by real time polymerase chain reaction (RT-PCR). Serum ICAM-1 concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Results Our results revealed that PCOS patients had higher values of ICAM-1expression and serum levels. Among PCOS patients, T2DM patients had the highest values of ICAM-1 expression and serum levels compared to IGT and NGT subgroups. The ICAM-1 expression and serum levels were significantly positive correlated with cardiovascular risk and PCOS phenotypes. Linear regression test showed that HOMA-IR was the main predictors of serum ICAM-1 levels in PCOS. Receiver operating characteristic curve (ROC) analysis revealed that, the power of ICAM-1 expression levels was higher than serum ICAM-1 in diagnosis of PCOS and in differentiating T2DM from IGT and NGT subgroups. Interestingly, combination of both ICAM-1 expression and serum levels improved the diagnostic role of serum ICAM-1. Conclusion ICAM-1 expression and serum levels were higher in women with PCOS compared to control group also, there was a strong independent association between higher ICAM-1 expression and serum levels with cardiovascular risks in PCOS group.

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Background: Preeclampsia, a hypertensive disorder of pregnancy, is detrimental to both mother and fetus. Sildenafil been proposed as a potential therapy to reduce blood pressure and improve uteroplacental perfusion in preeclamptic patients. Adropin is a novel secreted energy homeostasis protein regulating carbohydrate, lipid and protein metabolism, maternal adropin levels in Preeclampsia were still controversy. Aim of the Work: To evaluate serum levels of adropin in preeclampsia-like rat model and in preeclamptic rats treated with Sildenafil and to investigate their associations with some inflammatory, oxidative stress, and metabolic parameters. Material and Methods: 32 pregnant rats were divided randomly into four groups (n=8): Control group, sildenafil treated group, L-NAME group to induce pre-eclampsia and L-NAME with sildenafil treated group. In all groups, maternal Body Mass Index (BMI), placental weights, fetal weights, maternal mean arterial blood pressure (MAP), total urinary proteins, serum glucose, insulin and calculated Homeostatic Model Assessment of Insulin Resistance index (HOMA-IR), serum urea, creatinine, Triglycerides (TGs), Total Cholesterol (TC), Low Density Lipoproteins-cholesterol (LDL-c), High Density Lipoproteins-cholesterol (HDL-c), C Reactive Protein (CRP), Endothelin-1 (ET-1), and adropin were measured, also placental Malondialdehyde (MDA) levels, and activities of the antioxidant enzymes Superoxide Dismutase (SOD) and glutathione peroxidase (GSH) in placental homogenates were determined plus histopathological examination of placental sections were done. Results: L-NAME induced preeclampsia in rats and they showed significant increase in MAP, total urinary proteins, serum levels of glucose, insulin, calculated HOMA-IR, serum urea, creatinine, CRP, ET-1, TGs, TC, LDL-c, adropin and placental tissue MDA with significant reduction in maternal BMI, placental weights, fetal weights, serum HDL-c and placental tissue SOD and GSH activities as compared to other groups, additionally, L-NAME treated and L-NAME + SILD treated groups revealed positive significant correlations between adropin levels and MAP, total urinary proteins, serum levels of urea, creatinine, CRP, ET-1, TGs, TC, LDL-c, and placental tissue MDA, however they showed negative correlations between adropin and BMI, placental weights, fetal

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Background Diabetic peripheral neuropathy (DPN) is the major microvascular complication of type 2 diabetes mellitus (T2DM). Adropin is a peptide hormone that has essential roles in metabolic homeostasis and the pathogenesis of T2DM and its complications. This study was designed to estimate serum adropin levels in patients with T2DM in correlation with risk factors of DPN. The authors also aimed to investigate the association between serum adropin level and clinical and electrophysiological tests of DPN. Patients and methods This case–control study enrolled 100 patients with T2DM (40 diabetic cases without DPN and 60 diabetic cases with DPN) and 50 controls. All participants were subjected to a complete neurological examination. The motor and sensory conduction velocities of the median nerve, ulnar nerve, and common peroneal nerve were measured. The severity of DPN was assessed by Toronto clinical scoring system (TCSS). Serum adropin levels were assessed using an enzyme-linked immunosorbent assay. Results Our results revealed decreased circulating serum adropin levels in patients with T2DM (3.5±1.2), especially diabetic patients with DPN (3.1±1.07), compared with controls (6.1±0.89). There is a negative correlation between serum adropin level and TCSS as well as electrophysiological tests: motor nerve conduction velocity of median and ulnar nerve, sensory nerve conduction velocity of median and ulnar nerve, compound muscle action potential amplitude (median and ulnar nerve), and sensory nerve action potential amplitude (median, ulnar, and perception threshold nerve) (P<0.001*). Conclusion Diabetic patients with DPN had lower values of serum adropin than diabetic patients without DPN, and serum adropin levels were negatively correlated with metabolic risk factors, TCSS, as well as electrophysiological tests of DPN.

Background: Chronic renal failure (CRF) is usually associated with abnormal coagulation profile. Hepcidin is a major regulator of iron metabolism and was reported to have an impact on anemia, insulin resistance, dyslipidemia, inflammation and oxidative stress which were all reported to play a potential role in CRF induced coagulopathy. Renin angiotensin system (RAS) is involved in the pathophysiology of CRF and can affect coagulation profile. Aim of Study: To evaluate changes in coagulation profile in a rat model of chronic renal failure and the possible association of these changes with serum hepcidin level in relation to some metabolic, inflammatory and oxidative stress parameters and to evaluate whether changes in these parameters induced by inhibition of angiotensin converting enzyme (ACE) can affect serum hepcidin level. Material and Methods: Forty adult male albino rats divided into: Group I (n=8): Control group: Rats received subcutaneous injection with the vehicle (0.3M NaHCO3, 5ml/Kg) once weekly for 5 weeks. Group II (n=16): Chronic renal failureinduced group (CRF): Rats received subcutaneous injection with folic acid (300mg/kg in 5ml) once weekly (dissolved in 0.3M NaHCO3) for 5 weeks. Group III (n=16): (CRF + captopril): Chronic renal failure was induced by folic acid as in group II with concomitant administration of the ACE inhibitor; captopril in a daily dose of (100mg/kg/day) orally by gastric gavage. The following was measured in all groups: Blood pressure, Kidney function, haematological and haemostatic parameters, HOMA-IR, lipid profile, CRP, IL6, MDA, SOD and histopathological examination was made. Results: There was a significant increase in serum hepcidin level in group II compared to control which was correlated positively with serum creatinine, blood urea and negatively with creatinine clearance, while its level decreased significantly in group III compared to group II. A significant increase in bleeding time, WBCT, PT, APTT, INR, FDPs, D dimer and protein C was found in group II compared to control with an increase in HOMA-IR, CRP, IL6, MDA, systolic and diastolic blood pressure and a significant decrease in Hb, MCV, MCH, platelet count, MPV and SOD. In group III, bleeding time, WBCT and protein C remained significantly elevated versus

Background An epidemic of obesity has spread across the globe. Obesity has numerous comorbidities, including airway disease, insulin resistance, type 2 diabetes, cardiovascular disease, atherosclerosis, degenerative neurological disease, cognitive dysfunction, and cancer. Inflammatory cytokine is suggested to play a role in obesity and its complications. The current study aimed to estimate the expression and serum visfatin concentrations in obese Egyptian women. Moreover, we aimed to evaluate the possible association of visfatin gene expression and its serum levels with idiopathic intracranial hypertension (IIH) and cognitive dysfunction Participants and methods This cross-sectional study enrolled 60 obese women and 40 lean healthy women as controls. Obese women were classified according to grades of obesity into three groups. All participants underwent full clinical, neurological, and psychiatric examination. IIH group included patients with intracranial pressure greater than 25 cm H2O (opening pressure measured during lumber puncture in lateral decubitus position). Cognitive function was evaluated by using Montreal Cognitive Assessment scale (MoCA), Arabic version. Estimation of visfatin expression levels was determined by real-time PCR, and serum visfatin concentrations were measured using enzyme-linked immunosorbent assay. Results Our results revealed that obese women had higher values of visfatin expression (1.44±0.29) and serum levels (124.1±) compared with lean women (1.01±0.3 and 46.1±33.8, respectively). The visfatin expression and serum levels were significantly positively correlated with obesity indices, metabolic risks, MoCA, cerebrospinal fluid opening pressure, and cognitive dysfunction. Linear regression test showed that BMI, cerebrospinal fluid opening pressure, and MoCA were the main predictors of both serum and expression levels of visfatin in obese women. The receiver operating characteristic curve analysis revealed that the power of serum visfatin levels was higher than visfatin expression in differentiating obese women from lean ones. Conclusion There was a strong independent association between both higher visfatin expression and serum levels and obesity indices, metabolic risks, IIH, and cognitive dysfunction in obese Egyptian women.