CD40-CD40L interaction plays an important role in the pathology of certain autoimmune diseases. ITP is an autoimmune disease characterized by increased platelet destruction caused by anti-platelet autoantibodies, which mainly target a platelet surface antigen. It is speculated that platelet-associated CD154 is competent to induce the CD40-dependent proliferation of B lymphocytes. Therefore, platelet-associated CD154 expression is increased in ITP patients and is able to drive the activation of autoreactive B lymphocytes in this disease. These findings are particularly useful for clarifying the pathogenic process in ITP patients and for developing a therapeutic approach that blocks pathogenic anti-platelet antibody production. Blockade of the CD40/CD154 signal is a potential immunomodulatory strategy for T cell-mediated diseases, and many findings suggest that CD40/CD154 blockade therapy is potentially effective for ITP through selective suppression of autoreactive T and B lymphocytes to platelet antigens.
Mini-pool intravenous immunoglobulin G was well tolerated, presented no safety issues, and was effective in the treatment of immune thrombocytopenia, with efficacy comparable to that of the standard intravenous immunoglobulin G group, and it was significantly more effective than no treatment.
Introduction Nasal colonization with coagulase-negative staphylococci (CoNS) may be a preliminary risk factor for systemic infection. The aim of this study was to assess the frequency of ica A and D genes and biofilm formation among hospital-acquired nasal colonizing CoNS strains isolated from neonates in the neonatal intensive care units (NICUs). Antibiotic sensitivity patterns and some relevant risk factors were estimated.Methods This study assessed nasal colonization with CoNS among neonates at days one and three of admission to NICUs of Beni-Suef University Hospital and Beni-Suef General Hospital from November 2015 to May 2016. The isolates were screened and identified; susceptibility testing was performed. Biofilm formation was examined using the Congo red agar method. Isolates identified as CoNS were tested by polymerase chain reaction (PCR) for the presence of mecA and icaA and icaD genes.Results A total of 340 nasal swabs were collected from 170 neonates. The incidence of nasal colonization with CoNS was 50%. The species most frequently isolated were S. haemolyticus and S. epidermidis. Multidrug resistance (MDR) was detected in 86% of isolates. It was found that there was a strong association between the presence of mecA gene and phenotypic resistance to methicillin and also the presence of the icaA gene and biofilm formation.Conclusions Neonates admitted to NICUs can become reservoirs for CoNS strains, leading to potential dissemination of MDR strains into the community.
Beta-thalassemia is a genetic disorder characterized by the impaired synthesis of the betaglobin
chain of adult hemoglobin. The disorder has a complex pathophysiology that affects multiple
organ systems. The main complications of beta thalassemia are ineffective erythropoiesis, chronic hemolytic
anemia and hemosiderosis-induced organ dysfunction. Regular blood transfusions are the
main therapy for beta thalassemia major; however, this treatment can cause cardiac and hepatic hemosiderosis
– the most common cause of death in these patients. This review focuses on unique future
therapeutic interventions for thalassemia that reverse splenomegaly, reduce transfusion frequency, decrease
iron toxicity in organs, and correct chronic anemia. The targeted effective protocols include
hemoglobin fetal inducers, ineffective erythropoiesis correctors, antioxidants, vitamins, and natural
products. Resveratrol is a new herbal therapeutic approach which serves as fetal Hb inducer in beta
thalassemia. Hematopoietic stem cell transplantation (HSCT) is the only curative therapy for beta thalassemia
major and is preferred over iron chelation and blood transfusion for ensuring long life in these
patients. Meanwhile, several molecular therapies, such as ActRIIB/IgG1 Fc recombinant protein,
have emerged to address complications of beta thalassemia or the adverse effects of current drugs. Regarding
gene correction strategies, a phase III trial called HGB-207 (Northstar-2; NCT02906202) is
evaluating the efficacy and safety of autologous cell transplantation with LentiGlobin. Advanced
gene-editing approaches aim to cut DNA at a targeted site and convert HbF to HbA during infancy,
such as the suppression of BCL11A (B cell lymphoma 11A), HPFH (hereditary persistence of fetal
hemoglobin) and zinc-finger nucleases. Gene therapy is progressing rapidly, with multiple clinical trials
being conducted in many countries and the promise of commercial products to be available in the
near future.
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