Background Due to their chronic hypercoagulable status, thalassemic individuals are at an elevated risk of developing thromboembolic sequence consequences. The goal of the current study is to assesses the EPCR gene polymorphism and soluble EPCR in Egyptian thalassemic children and its role in hypercoagulable state.Research design and methods Eighty children diagnosed as thalassemia major and 80 healthy youngsters as a control group. The EPCR gene was identified using a restriction fragment length polymerase chain reaction (RFLP PCR). Additionally, we assessed the soluble EPCR levels using an enzyme-linked immunosorbent assay (ELISA).Results Frequency of 1651C-G EPCR, the GC genotype was strongly related with an increased risk of coagulation (OR = 1.83 (0.64–5.26), P = 0.0.016). In addition, soluble EPCR was considerably higher in patients with thalassemia than in controls, P value <0.001. Our study revealed significance difference between soluble EPCR and different genotypes.Conclusion Polymorphisms in the EPCR gene and an elevated soluble EPCR level in patients with β-thalassemia major may contribute to these patients’ hemostatic derangement in thalassemic Egyptian children.
Introduction The detection of inflammatory mediators in the serum of children with have otitis media with effusion (OME) and their correspondence with clinical considerations may enable the use of a modern nonsurgical curative treatment for OME. Objective To determine the relation between interleukin-17 (IL-17) serum level and reactive oxygen species (ROS) serum levels in children suffering from OME and to disclose if any variation occurs in the level of IL-17 Will affect the ROS and antioxidant equilibrium in the serum, which indicates the entire body's reaction to OME. Methods The present study was a case-control study. A total of 24 children experienced OME, and 24 healthy controls were recruited. All participants in the study were subjected to a systematic clinical investigation including otoscopic, audiometric, and tympanometric examination. Also, venous blood samples were collected from all children to determine the levels of IL-17 and ROS. Results The mean ± standard deviation (SD) age ranges of the patients and the control group were 6.8 ± 2.7 and 6.2 ± 3.4 years, respectively. A stylistically significant difference in the levels of serum nitric oxide (NO), catalase (CT), myeloperoxidase (MPO), and malondialdehyde (MDA) ( p < 0.05) was detected between OME and control patients. No significant difference was found in serum levels of superoxide dismutase (SOD) and glutathione peroxidase (GPX) between OME and control patients. The serum levels of MDA, NO, and MPO positively correlated with the serum levels of IL-17 in OME patients. Conclusion In the present study, there is a reasonable role of the IL-17 pathway in OME pathogenesis through an increase in ROS levels.
Background: Omentin-1 an adipokine expressed in visceral fat, endothelium and gut. Its level was found lower in obesity and type II diabetes. It is expressed in placenta and was associated with insulin sensitivity during pregnancy. Materials & Methods: rats were divided into 4 groups; group I: control, group II: sham group (normal pregnant), group III: gestational diabetic group and group IV: omentin-1 treated gestational diabetic group. Blood glucose, insulin HOMA-IR, lipid profile, CRP and osteopontin (OPN) levels were measured and gene expression of PI3K, AKT, GSK-3, NF-κB and OPN Results: in group III, a significant increase in insulin resistance, CRP, OPN, increased mRNA expression of GSK-3, NF-κB, and OPN while PI3K and AKT expression decreased. Omentin-1 treatment in group IV attenuated insulin resistance, increased PI3K and AKT expression but decreased OPN, GSK-3, and NF-κB expression. Conclusion: Omentin-1 administration in gestational diabetic rats improved insulin sensitivity and attenuated inflammatory response through PI3K/AKT/GSK-3 pathway.
Spinal cord injury (SCI) is a devastating disease leading to motor disability. Metabolic dysfunction is another complication of SCI. Thus, we aimed to study the effect of SCI on the histological and biochemical structure of the liver in adult male rats and to delineate the role of post-injury administration of G-CSF. Thirty adult male Sprague-Dawley rats were assigned into three groups: Group I; control (18 rats subdivided equally into three subgroups), and 12 rats underwent SCI and were divided into an SCI group II and G-SCF-treated group III. Twenty-one days post-injury, liver sections were processed for light and electron microscopic examinations and immunohistochemical staining for PCNA and CD68 antibodies. The biochemical assay was carried out for detection of serum levels of ALT, AST, total proteins, albumin, total cholesterol, triglycerides, HDL-c, GSH and MDA. Liver tissue levels of GPx and MDA as well as semiquantitative RT-PCR analysis of hepatic cytokine expression were also conducted. In the SCI group, results showed liver tissue damage in the form of lipid infiltration, blood vessel congestion, vacuolated cells with apoptotic nuclei and increased collagen deposition. Increased CD68-positive macrophages and a decreased number of PCNA-positive cells was detected. Moreover, liver enzymes, total cholesterol and triglycerides were increased while serum albumin, total proteins and HDL-c were decreased in the SCI group. Oxidative stress and increased expression of inflammatory cytokines were detected. Administration of G-CSF induced significant liver improvement with retained liver function by anti-inflammatory, immune-modulatory and antioxidant mechanisms.
Perfluorooctane sulfonate (PFOS) is a man-made fluorinated compound employed in a variety of industrial and civilian applications. Due to its long elimination half-life and promotion of oxidative stress and inflammation, it is one of the most abundant organic contaminants. The present study was designed to determine the cytotoxic effect of PFOS on adult male rat cardiac tissue and to assess the cardioprotective role of the flavonoid quercetin (Que), which possesses antioxidant, anti-inflammatory, and anti-apoptotic properties. Twenty-four adult male Sprague-Dawley rats were randomly divided into four equal groups: Group I (Control). Group II (Que) received Que (75 mg/kg/day for 4 weeks) by oral gavage. Group III (PFOS group): supplemented orally with PFOS (20 mg/kg/day for 4 weeks) and Group IV (PF OS/Que). The rat heart was processed for histological, immunohistochemical, and gene expression studies. The PFOS group showed histological alterations in the myocardium that were partially reversed by the administration of Que. The inflammatory biomarkers (TNF, IL-6, and IL-1), lipid profile, TSH, MDA, and serum cardiac enzymes (LDH and CK-MB) were all altered. These findings collectively suggest that PFOS had adverse effects on the cardiac muscle structure, and these effects were alleviated by quercetin, which is a promising cardioprotective flavonoid.
Background: Indoxyl sulfate (IS) is a non-dialyzable gut-derived uremic toxin that is reported to be cardiotoxic in patients with advanced chronic kidney disease stages. Aim of the Work:The aim of this study was to investigate the role of IS as a risk factor for cardiovascular complications in children with end stage kidney disease (ESKD) on regular HD.Patients and Methods: This is a cross-sectional analytical study that included children with ESKD on regular hemodialysis (HD) for at least 6 months following at Nephrology Unit of Cairo University Pediatric Hospitals.Serum IS level was measured for all patients by the enzymelinked immunosorbent assay (ELISA).Cardiac complications was assessed using the M mode and 2D transthoracic echocardiography. Results:The study comprised 88 children with ESKD on regular HD for a mean ± SD of 31.94 ± 26.05 months, with a mean age ± SD of 9 ± 3.2 years (range 3.3-14 years).Of them 52 (59.1%) were males.Obstructive uropathy (28.4%), and focal segmental glomerulosclerosis (20.5%), were the main causes of ESKD in the study group.Cardiovascular complications were identified in 48 (54.5%) patients in the form of dilated cardiomyopathy in 44 (50%) children with decreased fractional shortening <30% and moderate to severe left ventricular hypertrophy above 95th for age and gender in 10 (11.4%).Cardiovascular affection correlated with duration of HD, hypertension, and IS serum level (p=<0.001for each).Hypertension was reported in 55 (62.5%) of patients, and vascular access related complications were evident in 40 (45.4%)patients with thrombosis being the commonest complication in 16 (18.1%).The mean IS was 29.14 ± 17.43 µg/ml in ESKD patients with normal cardiac function, and 77 ± 15.18 µg/ml among those with cardiac compromise (p < 0.001).The IS level correlated with longer duration of HD (p= 0.002), and older age (p= 0.043).IS level and duration of HD did not predict cardiomyopathy, (p=0.192), and (p=0.760)respectively.Conclusion: Cardiac complications are common among children on HD.Both cardiovascular complications and IS accumulation correlated positively with longer duration of HD, and age of children with ESKD.IS is non-dialysable and there is a need to control its production from the gut. Level of Evidence of Study: IV (1).