Amany H. Mansour

Increased expression of costimulatory molecules CD86 and sCTLA-4 in patients with acute lymphoblastic leukemia

Abstract We herein evaluate the role of the B7-family molecule CD86 and the Cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) as a possible immunopathogenic factors in patients with ALL. The results of 60 patients with de novo ALL were compared to 40 controls. A significant statistical difference between CD86 expression and sCTLA-4 levels in patients versus their controls has been detected. During follow up period of 28 months, patients suffered from relapse (16 patients) had significantly higher CD86 expression and sCTL-4 levels compared to those remained in complete remission (44 patients) (p = 0.005 and 0.03 respectively). Patients who died from the disease (9 patients) showed significantly higher CD 86 expression and sCTLA-4 levels than surviving patients (51 patients) (p = 0.004 and 0.01 respectively). In conclusion, the higher levels of sCTLA-4 and CD86 in B-ALL patients might be candidate parameters for poor prognosis and may serve to refine treatment stratification with intensification of therapy in those patients prone to relapse.

Evaluation of the procoagulant potential of endothelial microparticles CD144 (VE-Cadherin) positive in coronary syndrome patients

Background Apoptotic microparticles are responsible for almost all tissue factor activity of the plaque lipid core. We hypothesized that elevated levels of procoagulant microparticles could also circulate in the peripheral blood of patients with recent clinical signs of plaque disruption and thrombosis. The present study included 60 acute coronary syndrome (ACS) adult patients. Group I included 30 patients with diabetes mellitus who presented with ACS. Group II included 30 nondiabetic patients complaining of ACS and 25 healthy individuals as controls. ACS patients were further classified according to laboratory and radiological findings (troponin test and ECG) as follows: group A included 16 ST-segment elevation myocardial infarction (STEMI) patients, group B included 19 non-ST-segment elevation myocardial infarction (NSTEMI) patients, and group C included 25 patients with unstable angina. Traditional laboratory investigations and special laboratory assessments of CD144 fluorescein isothiocyanate by flow cytometry were performed. Results The present study found highly elevated CD144 percentages in diabetic ACS patients compared with healthy controls (P≤0.0001(, and highly elevated creatine kinase-MB (CK-MB), fasting sugar, total cholesterol, triglyceride, HDL, and LDL (P = 0.0001, 0.0001, 0.0002, 0.0002, 0.0001, and 0.0001, respectively). In contrast, nondiabetic ACS patients had significantly elevated CD144, CK-MB, total cholesterol, triglyceride, HDL, and LDL (P = 0.0001, 0.0001, 0.0001, 0.0021, 0.0001, and 0.0021, respectively), whereas fasting sugar and HbA1c did not change significantly. However, the patients in group B (NSTEMI) had significantly elevated CD144% in comparison with patients with unstable angina (group C) ( P = 0.05), but patients with group A (STEMI) had significantly elevated CK-MB compared with patients with unstable angina (group C) (P = 0.02). Conclusion The high levels of circulating microparticles of endothelial origin are increased in diabetic patients with coronary artery disease, suggesting an important role for endothelial injury in the prediction of ACS. Hyperglycemia in ACS is associated with enhanced local thrombin generation and platelet activation, as well as unfavorably altered clot features in patients with and without a previous history of diabetes.

Analysis of human platelets brain-derived neurotrophic factor as a predictor of response in depressed patients

Background Despite the significant progress in the management of major depressive disorder, little is known about the biological alterations that underlie the pathophysiology or the treatment of depression. Previous studies show that the brain-derived neurotrophic factor (BDNF) may play a role in the pathophysiology of major depressive disorders. Assuming that BDNF may be implicated in the etiology of depression, we examined BDNF concentrations in patients with major depressive disorder and its correlation with therapeutic response to fluoxetine therapy. Patients and methods This study included 40 depressed patients (25 women and 15 men) and 20 healthy individuals (11 women and nine men) as a control group selected to match the study group in age and sex. All patients were subjected a semistructured clinical interview of DSM-IV-TR for the diagnosis of major depressive disorder, assessment of severity of depression using the 16-item Hamilton Rating Scale of Depression before treatment and 8 weeks after fluoxetine treatment, and estimation of the level of BDNF before treatment and 8 weeks after antidepressant treatment. Results Before treatment, the concentrations of BDNF were significantly lower in depressed patients than in the control participants. After treatment, a significant increase in the BDNF concentration occurred, with no significant difference from the control group. Serum BDNF levels in patients with poor response (17.58 ± 4.99 ng/ml) were significantly lower than those of the patients with good response (28.88 ± 7.81 ng/ml; t = 5.48, P = 0.001). However, there were no significant differences in both groups of patients compared with the normal controls (21.60 ± 8.04). Conclusion BDNFs drug-free depressed patients are lower than those of healthy controls and we propose that low BDNF levels might reflect failure of neuronal plasticity in depression. Also, The increase in BDNF after antidepressant therapy could be considered a good predictor of response to antidepressant therapy and might contribute toward the therapeutic response of patients with major depressive disorder.