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Serum Hepcidin as a Diagnostic Marker of Severe Iron Overload in Beta-thalassemia Major

Posted by Ahmed Maher K, Amina A, Marwa Salah F, et al. on 2017-07-24 00:17:19



To investigate potential usefulness of serum hepcidin in the diagnosis of iron overload in children with β-thalassemia.


A study was conducted on 30 thalassemia major (TM), 30 thalassemia intermedia (TI) and 60 healthy children as controls. Serum hepcidin was measured by Human Hepcidin, ELISA Kit.


β-thalassemia patients had a higher serum hepcidin compared to the controls (p < 0.001). TM group had higher hepcidin and ferritin compared to the TI group (p = 0.034; < 0.001, respectively). Among controls, hepcidin did not correlate with age (r = 0.225, p = 0.084). Among β-thalassemia patients, it correlated positively with age (r = 0.4; p = 0.001), disease duration (r = 0.5; p < 0.001), transfusion frequency (r = 0.35; p = 0.007), total number of transfusions (r = 0.4; p = 0.003), and ferritin (r = 0.3; p = 0.027). Total hemoglobin and serum ferritin were significantly related to hepcidin, which tended to increase by 0.514 ng/ml with each 1 g/dl rise in hemoglobin (p = 0.023) and by 0.002 ng/ml with each 1 ng/ml rise in serum ferritin (p = 0.002). Iron overload [serum ferritin (SF) ≥ 1500 ng/ml] was independently associated with TM (p = 0.001) and elevated serum hepcidin (p = 0.02). The overall predictability of serum hepcidin in severe iron overload was statistically significant when compared to hepcidin to serum ferritin ratio.


Serum hepcidin is elevated in children with β-thalassemia; but this elevation is more evident in TM patients with severe iron overload. Thus, hepcidin can be a potential marker of severe iron overload in patients with TM. Further studies are recommended to compare serum hepcidin and serum ferritin in the prediction of severe iron overload in steady state and during infection or inflammation.


Hepcidin Iron overload β-thalassemia major β-thalassemia intermedia

The potential curative effect of rebamipide in hepatic ischemia/reperfusion injury

Posted by Abdallah M.G, Dalaal M.A, Hanan S.E. on 2017-07-24 00:58:45


Rebamipide (Reba), a gastroprotective drug, has signified its hepatoprotective activity; however, its possible post-therapeutic intervention in hepatic ischemia/reperfusion (I/R) remains elusive. Consequently, the intent of this study was to test Reba modulatory effect on nuclear factor (NF)-κB signaling in hepatic I/R model. Rats were randomized into sham, I/R, Reba 60, and Reba100 (60 and 100 mg/kg, respectively) groups. Ischemia was induced for 30 min followed by 3-day reperfusion to set up a model of partial (70%) warm hepatic ischemia. Post-treatment with Reba reduced the serum level of alanine transaminase, improved histopathological alterations of the liver, and elevated hepatic adenosine triphosphate. It also lowered hepatic lipid peroxides and increased both total antioxidant capacity and nitric oxide. Besides, Reba decreased tumor necrosis factor-α, interferon-γ, intercellular adhesion molecule-1, myeloperoxidase, prostaglandin E2, cyclooxygenase-2 expression/content, and caspase-3 activity. Reba also upregulated the gene expression/content of sirtuin 1 (SIRT-1), while it downregulated that of high mobility group box (HMGB)1 and reduced the expression/content of NF-κB p65/pS536-NF-κB and the content of pT180/Y182-p38MAPK. Reba provided tenable hepato-therapeutic mechanisms to mitigate events concomitant with hepatic I/R via inhibition of NF-κB p65 and modulation of its influential signals (SIRT-1, HMGB1, p38MAPK) associated with its antiinflammatory, antioxidant, and antiapoptotic impacts.


The efficacy of apitoxin (bee venom; BV) in ameliorating propionic acid (PPA) −induced neurobehavioral impacts was studied. Sixty rat pups were enrolled in a split litter design to six groups: a control group, a PPA-treated group, a BV-treated group, a BV/PPA protective group, a PPA/BV therapeutic group, and a BV/PPA/BV protective and therapeutic group. Exploratory, social, locomotor, and repetitive/stereotype-like activities were assessed and prosocial, empathy, and acquired behavior were evaluated. Levels of neurotransmitter including serotonin, dopamine, and gamma-aminobutyric acid (GABA) were determined and a quantitative analysis of Reelin gene expression was performed. PPA treatment induced several behavioral alterations, as reduced exploratory activity and social behaviors, increased repetitive/stereotypic behaviors, and hyperactivity. In addition, a marked decline of neurotransmitters and down-regulation of Reelin mRNA expression were observed. BV exhibited high efficiency in ameliorating the PPA-induced neurobehavioral alterations, particularly when applied both before and after PPA administration. Overall, the results implied that BV has merit as a candidate therapeutic treatment to alleviate PPA-induced neurobehavioral disorders.


Decabromodiphenyl ether (BDE-209) was one of most widely-used polybrominated diphenyl ether (PBDE) flame retardants and is frequently detected in both abiotic and biotic samples from environment. However, knowledge of its transgenerational risks is limited. Here, 4-month-old zebrafish were exposed to various concentrations of BDE-209 (0, 3, 30 or 300 μg/L) for 28 days and spawned in clean water without BDE-209. Concentrations of triiodothyronine (T3) and thyroxine (T4) as well as expressions of genes involved in the hypothalamic–pituitary–thyroid (HPT) axis were measured in offspring after exposure of adult zebrafish to BDE-209. BDE-209 was accumulated in adult fish and F1 eggs, which suggests transfer of this compound from adult fish to their offspring. Exposure of BDE-209 to parents resulted in developmental abnormalities in offspring and a significant decrease in T4 concentrations in F1 larvae 120 h post-fertilization (hpf). Furthermore, expressions of several genes involved in the HPT axis were also altered. Expressions of thyroid hormone receptor α (tr-α), thyrotropin releasing hormone (trh), thyroid stimulating hormone β (tsh-β) and deiodinase 1 (dio 1) were significantly down-regulated in F1 individuals, while expressions of thyroid stimulating hormone receptor (tshr) and transthyretin (ttr) were significantly up-regulated. These results suggest that exposure of parent zebrafish to BDE-209 can cause developmental toxicity in offspring and disruption of the thyroid endocrine system of offspring.


This work aimed to explore the link between angiopoietin-like protein 8 (ANGPTL8) and weight loss after metabolic surgery. In the cross-sectional study (n = 100), circulating ANGPTL8 concentrations were significantly lower in morbidly obese than in lean subjects, and strikingly lower in morbidly obese patients with type 2 diabetes mellitus (T2DM). Conversely, ANGPTL8 expression in subcutaneous adipose tissue (SAT) was higher in morbidly obese patients, particularly in those with T2DM, whereas its expression in visceral adipose tissue was unchanged. The main predictors for circulating levels of ANGPTL8 were BMI and T2DM, whereas ANGPTL8 expression in SAT was determined by the presence of T2DM. The prospective cohort studies before and 1 year after bariatric surgery in morbidly obese patients with (n = 45) and without (n = 30) T2DM, revealed a significant increase of circulating ANGPTL8 levels 1 year after the bariatric surgery. Intriguingly, this increment, which was predicted by basal ANGPTL8 concentrations, appeared as a determinant of T2DM remission. In conclusion, circulating ANGPTL8 levels have an inverse relationship with SAT expression. Low basal levels of ANGPTL8 rebound after bariatric surgery. The increment in ANGPTL8 concentrations at 1 month of follow-up after weight loss emerged as a significant predictor of the T2DM remission at 1 year of follow-up.

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