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Background: Congenital heart diseases are abnormalities of the heart and/or great vessels present at birth. 1% of live births have a congenital heart defect. Cardiac Troponin, especially cardiac Troponin I (cTnI), are the preferred biomarkers for the detection of cardiac injury. International cardiology and laboratory medicine guidelines recommend highly sensitive Tn1 (hscTnI) that has excellent precision (

Background: Heart failure is one of the cardiovascular diseases that have high morbidity and mortality especially among children. It accounts for 2% of all pediatric inpatient admission. Cardiac Myosin Binding Protein-C (cMyBP-C) is cardiomyocyte specific sarcomeric protein that regulates sarcomeric structure and its function where it is released in circulation in response to cardiac injury. Objective: To explore the role of cMyBP-C as a biomarker in heart failure in children. Patients and Methods: This prospective cohort study was carried out during the period from October 2017 to October 2018 in Pediatric Cardiology Unit, Zagazig University Hospital. It included 26 selected patients with heart failure diagnosed clinically and by echocardiography. Results: The study revealed that the most common cause pf heart failure in our patients was VSD (30.8%) then DCM (26.9%). 57.7% of studied patients were grade III of ROSS classification while 30.8% were grade IV and 11.5% were grade II. In ECHO findings, mean EF% was 52.3% while mean FS% was 33 % with negative correlation between plasma level of cMyBP-C and EF% and FS%. There was high statistical significant difference in cMyBP-C plasma level at time of admission and after treatment (123.5 ng/ml and 78.8 ng/ml respectively). There was high statistical significant difference in level of cMyBP-C among improved cases before and after treatment. There was no statistical significant difference in level of cMyBP-C before and after treatment among cases with bad prognosis. Conclusion: cMyBP-C could be a prognostic biomarker in children with HF and may be used as a tool to help in HF diagnosis in children as a marker of disease severity.

Background: preeclampsia (PE) is a pregnancy related complication defined as a disease that begins in the placenta and ends at the maternal endothelium. It is a multi-stage disease that starts by utero-placental insufficiency and leads to generalized maternal endothelial dysfunction.Lipocalin2 (LCN2) is a 25kDasecretory glycoprotein implicated in many functions such as apoptosis and innate immunity. Also, it has been recognized to have potential effects in obesity, inflammation and insulin resistance in mice and humans. Many controversial studies about the changes in the plasma LCN2 levels in PE are reported. Aim: The current study was designed to perform an animal model of experimental PE in a trial to demonstrate the possible relationship between PE and the circulating LCN2 levels. Design: forty eight healthy adult female albino rats and eight adult male albino rats were used. The male rats were used for induction of pregnancy. The adult female rats (n=48) were divided into four equal groups: group I (control non-pregnant group), group II (non-pregnant treated with L-NAME), group III (normal pregnant group) and group IV (pregnant treated with L-NAME to induce a model of experimental PE). In all groups, body weight, body mass index (BMI), blood pressure, circulating levels of urea, creatinine, triglycerides (TGs), IL-6, endothelin-1(ET-1), vitamin D (VD), LCN2 and D-dimers in addition to total urinary proteins are measured. Histopathological examination of placental sections was done in group III and group IV. Results: The results of the present study revealed a significant increase in the body weight, BMI, MAP, total urinary proteins, circulating levels of urea, creatinine, TGs, IL-6, ET-1, LCN2 and D-dimers in both group II and IV. In addition to a significant decrease in VD in the same two groups. In group III, there was a significant increase in body weight, BMI, total urinary proteins and circulating levels of TGS, D-dimers and LCN2. There was a significant decrease in VD and MAP. Moreover, there was a positive significant correlation between LCN2 and all measured parameters except VD in group IV together with a positive significant correlation between LCN2 and MAP, IL-6, ET-1and D-dimers in group II.The results in group IV are supported by the histopathological examination results. Conclusion: L-NAME can be used for induction of experimental PE and plasma levels of LCN2 can be used as an indicator for the renal complications and coagulopathies in PE. Further studies are needed to ascertain this association.