A cross-sectional study was conducted to evaluate the seroprevalence of and risk factors for Toxoplasma gondii antibodies in 260 blood donors seen at blood banks in Mansoura University Hospital, Egypt. Blood donors were interviewed about sociodemographic characteristics and risk factors for T. gondii infection. A blood sample was taken to document their T. gondii antibody status using enzyme-linked immunosorbent assay. Overall, 155 (59.6%) of 260 blood donors were positive for anti-T. gondii IgG antibodies. Multivariate logistic regression analysis showed a significant association between T. gondii seropositivity and eating meat by-products (luncheon/shawerma) (adjusted odds ratio [OR] 80.82 [95% CI 18.62-350.81], P < 0.0001) or being non-educated (adjusted OR 32.25 [95% CI 7.46-139.44], P < 0.0001). These findings highlight that T. gondii is prevalent among blood donors in Egypt.

The lymph node (LN) is the site of chronic lymphocytic leukemia (CLL) cell activation and proliferation. Aberrant microRNA (miRNA) expression has been shown to have a role in CLL pathogenesis; however, a comparison of miRNA expression between CLL cells in the LN and the peripheral blood (PB) has previously not been reported. On the basis of the analysis of 17 paired LN and PB samples from CLL patients, we identify a panel of miRNAs that are increased in LN CLL cells correlating with an activation phenotype. When evaluated in CLL cells from 38 patients pre and post treatment with ibrutinib, a subset of these miRNAs (miR-22, miR-34a, miR-146b and miR-181b) was significantly decreased in response to ibrutinib. A concomitant increase in putative miRNA target transcripts (ARID1B, ARID2, ATM, CYLD, FOXP1, HDAC1, IBTK, PTEN and SMAD4) was also observed. Functional studies confirmed targets of ibrutinib-responsive miRNAs to include messenger RNA transcripts of multiple tumor suppressors. Knockdown of endogenous miR-34a and miR146b resulted in increased transcription of tumor suppressors and inhibition of cell proliferation. These findings demonstrate that ibrutinib downregulates the expression of a subset of miRNAs related to B-cell activation leading to increased expression of miRNA targets including tumor suppressors and a reduction in cell proliferation.

Th17 cells and their effector cytokines have emerged as important mediators in inflammatory and autoimmune diseases and serve as an ambitious field in current immunology research. Recent studies suggest a potential impact of Th17 cells on solid tumors but relatively little is known about their contribution in hematological malignancies. The current study was designed to investigate the possible involvement and clinical significance of circulating Th17 cells in acute leukemia. Flow cytometry was used to analyze percentages of Th17 cells in peripheral blood mononuclear cells from 93 acute leukemia patients (ALL, n = 30; AML, n = 63) and 40 healthy volunteers. Serum levels of IL-17 and IL-21 were measured using enzyme-linked immunosorbent assay. Circulating Th17 cells were increased in patients with acute leukemia (2.88 ± 0.65 % and 2.90 ± 0.57 % in ALL and AML patients, respectively) and were significantly higher than in healthy controls (1.10 ± 0.28 %; P = 0.001). Furthermore, pretreatment Th17 cells were reduced significantly in patients who achieved complete remission after induction therapy (2.25 ± 0.44 % and 1.63 ± 0.27 % in ALL and AML patients, respectively, P < 0.0001). Serum levels of IL-17 and IL-21 were significantly elevated in acute leukemia patients. Kaplan–Meier curves revealed a significantly longer overall survival in patients with high Th17 levels (P = 0.029 and P = 0.027 for ALL and AML, respectively). In the multivariate analysis, Th17 cells retained statistical significance for overall survival in patients with ALL (OR 0.331; P = 0.043) and AML (OR 0.489; P = 0.032). These results strongly suggest Th17 cells as a powerful new prognostic determinant which could serve as a potential therapeutic target to modulate anti-tumor response in acute leukemia patients.

[ABS]Phospholipid asymmetry is well maintained in erythrocyte (RBC) membranes with phosphatidylserine (PS) exclusively present in the inner leaflet. Eryptosis, the suicidal death of RBCs, is characterized by cell shrinkage, membrane blebbing, and cell membrane phospholipids scrambling with PS exposure at the cell surface. Erythrocytes exposing PS are recognized, bound, engulfed, and degraded by macrophages. Eryptosis thus fosters clearance of affected RBCs from circulating blood, which may aggravate anemia in pathological conditions. Thalassemia patients are more sensitive to the eryptotic depletion and osmotic shock which may affect RBC membrane phospholipid asymmetry. We aimed in this work to determine the RBC PS exposure in splenectomized and nonsplenectomized β-thalassemia major (β-TM) patients and correlate it with the clinical presentation and laboratory data. RBCs were stained for annexin V to detect phosphatidylserine (PS) exposure in 46 β-TM patients (27 splenectomized and 19 nonsplenectomized) compared to 17 healthy subjects as a control group. We observed a significant increase in RBC PS exposure in β-TM patients compared to control group (P = .0001). Erythrocyte PS exposure was significantly higher in splenectomized β-TM patients compared with nonsplenectomized β-TM patients (P = .001). No correlation was found between RBC PS exposure and clinical or hematological data of β-TM patients, but there was a positive correlation between RBC PS exposure and ferritin level in β-TM patients have higher levels of RBC PS exposure, and splenectomy was shown to aggravate RBC PS exposure without aggravation of anemia.

Hemostatic and fibrinolytic parameters should be included in characterization of the insulin resistance syndrome. t-PA and vWf-antigen concentrations were increased in subjects with metabolic syndrome and correlated with the HOMA-IR measure of insulin sensitivity. Because both t-PA and vWf are mainly released from vascular endothelium, these findings could be an indicator of endothelial dysfunction in subjects with insulin resistance and metabolic syndrome.

Numerous prognostic markers were introduced to screen for patients with B-cell chronic lymphocytic leukemia (B-CLL) likely to have a progressive course, bearing the potential to facilitate risk-adapted treatment strategies. Extracellular adenosine triphosphate (ATP) functions as a "natural adjuvant" that boosts immune response in the tumor microenvironment. Ectonucleoside triphosphate diphosphohydrolase-1 (CD39/ENTPD1) is the ectonucleotidase that catalyzes the hydrolysis of ATP. The present study was conducted to analyze CD39 expression in T cells and B-CLL cells to evaluate its impact on the clinical course of patients with B-CLL and correlate its levels with well-established risk factors. T-cell CD39 expression was significantly increased in patients' peripheral blood compared to healthy controls. The higher levels were associated with advanced stages of disease and negatively interacted with time to first treatment. Overall, our data indicate that T-cell CD39 expression may identify subsets of patients with B-CLL with an unfavorable clinical outcome. Moreover, it can be incorporated into prognostic schema to improve the prediction of CLL disease progression.

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Occult hepatitis C virus (HCV) infection is a new entity that should be considered when diagnosing patients with abnormal liver functions of unknown origin. This work was carried out to evaluate T-helper liT-helper 2 (Thl/Th2) cytokine profiles in patients with occult HCV infection versus chronic hepatitis C (CHC) infection, also to investigate any association between theses cytokines and liver histological features in both groups. Serum levels of Thl cytokines (IL-2, IFN-y) and Th2 (IL-4 and IL-IO) were measured in 35 patients with occult HCV infection compared to 50 patients with chronic hepatitis C infection and 30 healthy controls. We have found that Thl cytokines were significantly increased in patients with CHC infection than in both occult HCV infection and control groups (p