ABSTRACT
The presence of elevated numbers of circulating microparticles (MPs) has been hypothesized to be responsible for the occurrence of thromboembolic events (TEEs) in thalassemic patients. Our aim is to evaluate the presence and the thrombotic risk of circulating MPs in thalassemia patients and to determine the difference in MPs between ß-thalassemia major (ß-TM) and thalassemia intermedia (TI). The percentage of the annexin-labeled MPs, platelet-derived MPs (PMPs), erythrocyte-derived MPs (RMPs), and endothelial-derived MPs (EMPs) was measured by flow cytometry, in 87 thalassemia patients (39 ß-TM and 48 TI). By multiple regression analysis, we then assessed the various independent risk factors for the occurrence of TEE. The thalassemic patients who experienced TEE had a significantly higher platelet count, higher percentage of annexin-labeled MPs, and higher percentage of PMPs (p value = 0.014, 0.003, and 0.014, respectively). There was no significant difference between ß-TM and TI patients at the level of any of the studied MPs. The predictive risk factors for TEE in thalassemic patients were splenectomy, total and direct bilirubin, the RMPs, and the EMPs (OR = 10.07 (CI = 3.7-27.1), 4.3 (CI = 2.1-8.7), 1.4 (CI = 1.5-6.2), 1.6 (CI = 1.1-2.2), 3.0 (CI = 1.9-4.9), respectively). In conclusion, the elevated numbers of circulating MPs is a risk factor for the TEE in thalassemia patients.
Subject(s)
Cell-Derived Microparticles/metabolism , Thromboembolism/blood , Thromboembolism/epidemiology , beta-Thalassemia/blood , beta-Thalassemia/epidemiology , Adolescent , Adult , Child , Child, Preschool , Cross-Sectional Studies , Egypt/epidemiology , Female , Humans , Infant , Male , Random Allocation , Risk Factors , Thromboembolism/diagnosis , Young Adult , beta-Thalassemia/diagnosisABSTRACT
BACKGROUND: Bronchopulmonary dysplasia (BPD) remains a leading cause of morbidity and mortality during infancy. Evidence suggests that the Toll-like receptor (TLR) signaling pathway plays an integral role in lung inflammation and injury. This study aimed to detect single nucleotide polymorphisms (SNPs) in TLR pathway genes [TLR5 and Toll-interleukin 1 receptor domain-containing adaptor protein (TIRAP)] among preterm neonates and to determine their association with the development and severity of bronchopulmonary dysplasia.
Subject(s)
Bronchopulmonary Dysplasia/genetics , Membrane Glycoproteins/genetics , Polymorphism, Single Nucleotide , Receptors, Interleukin-1/genetics , Toll-Like Receptor 5/genetics , Bronchopulmonary Dysplasia/pathology , Case-Control Studies , Female , Humans , Infant, Newborn , Infant, Premature , MaleABSTRACT
OBJECTIVE: The aim of this study was to investigate the possible relationship between angiotensin-converting enzyme (ACE) gene polymorphism (D/D and I/D genotypes) and respiratory distress syndrome (RDS) in preterm neonates. STUDY DESIGN: Our study included 120 preterm neonates (<37 weeks of gestation) with RDS (the patient group) and 120 preterm neonates without RDS (the control group). Blood samples were obtained from patients and control groups, and ACE gene polymorphism was analysed using the polymerase chain reaction method. RESULTS: D/D genotype was highly significant in the patient group compared with the control group (48.3% of RDS group vs 20% of the control group, P < 0.001). Meanwhile, I/D and I/I genotypes were significantly higher in the control group (75% and 5% of the control group vs 50% and 1.7% of the patient group, P < 0.001). D/D genotype was highly significant in neonates with bronchopulmonary dysplasia (BPD) compared with I/D genotype (P = 0.001). CONCLUSION: Our results may suggest that D/D genotype is associated with increased risk of RDS and BPD development in preterm neonates.
Subject(s)
Infant, Premature/physiology , Peptidyl-Dipeptidase A/genetics , Respiratory Distress Syndrome, Newborn/genetics , Case-Control Studies , Female , Genetic Predisposition to Disease , Genotype , Humans , Infant, Newborn , Male , Polymorphism, Genetic , Respiratory Distress Syndrome, Newborn/enzymology , Retrospective StudiesABSTRACT
BACKGROUND AND OBJECTIVES: It has become evident that fibromodulin and other members of the proteoglycan family are not only involved in collagen fibrillogenesis and cell adhesion but they also contribute to modulation of cytokine activity, suppression of tumor growth, and prevention of apoptosis. Fibromodulin has been characterized as one of the tumor associated antigens (TAA) in B cell chronic lymphocytic leukemia (B-CLL) with the potential to elicit specific antitumor response and it is considered as good candidate for immunotherapy. AIM OF WORK: to study the expression of fibromodulin at the gene level of B-cell chronic lymphocytic leukemia patients, in comparison to normal controls and to asses its role in the pathophysiology of CLL. PATIENTS AND METHODS: Fibromodulin gene expression was tested by one step reverse transcription-polymerase chain reaction (RT-PCR) in peripheral blood mononuclear cells of 30 patients with B-CLL as well as in 20 age and sex matched healthy volunteers. RESULTS: In this study, fibromodulin gene was expressed in 46.7% of patients with B-CLL which was significantly different from the control age and sex matched healthy volunteers in which none of them showed peripheral blood mononuclear cells positivity for fibromodulin gene expression (0%) (p-value =0.006). We also found significant associations between higher fibomodulin gene expression and some risk factors in the studied CLL cases such as hepatomegaly, lower haemoglobin level, lower RBCs count, lower platelet count and borderline significant associations with other risk factors as lymphadenopathy and splenomegaly. CONCLUSION: Our results suggest that fibromodulin can be used as a target for therapeutic intervention and it may play a role in the pathophysiology of CLL.
