β-thalassemia is an inherited blood disorder in which the body cannot produce hemoglobin normally. Since patients with this condition receive blood transfusions regularly, iron builds up primarily in organs such as the heart, liver and endocrine glands. Accumulation of iron in the organs necessitates chelation therapy. These patients must visit the hospital frequently to assess and follow up on their health condition. Physician intervention is required after each regular assessment to adjust the treatment. Lifelong healthcare support using a web-based expert system with a quick response code is designed for β-thalassemia management in order to deliver benefits to patients, physicians, and other healthcare providers. The aim of this study is to implement a web-based expert system for β-thalassemia management in order to provide treatment recommendations and support the lifelong healthcare of patients. The system provides patient-related details, such as medical history, medicines, and appointments, in real-time. It has been also tested in real-life cases and shown to enhance β-thalassemia management.

Introduction: Studies assessing immune responses following Pfizer-BioNTech BNT162b2 mRNA COVID-19 (Pfizer) and ChAdOx1 nCoV-19 AZD1222 (AstraZeneca) vaccines in patients with hemoglobinopathy are non-existent in the literature despite being thought at high risk of infection. Methods: Prospectively, we collected serum from patients with hemoglobinopathies at least 14 days post vaccine and measured neutralizing antibodies (nAb) in addition to binding antibodies using in-house assays. Results: All 66 participants mounted a significant binding antibody response (100%), but nAbs were detected in (56/66) post-vaccine with a rate of 84.5%. Age, gender, vaccine type, spleen status, hydroxyurea use, and hyperferritinemia did not affect the rate significantly. While 23/32 (71.8%) patients receiving only one dose of the vaccine were able to mount a positive response, 33/34 (97.05%) of those who had two doses of any vaccine type had a significant nAbs response. Patients who had anti-nucleocapsid (N), signifying asymptomatic infection in the past, were able to produce nAbs (31/31). No nAbs were detected in 10/35 (28.5%) patients with no anti-N antibodies. Conclusion: Our results provide supportive data when advising patients with hemoglobinopathy to receive COVID-19 vaccines and ensure booster doses are available for better immunity. Whenever available, measurement of nAb is recommended.

Introduction The development of anti‐platelet factor 4 (PF4) antibodies is linked to a rare thrombotic complication described now as vaccine‐induced immune thrombotic thrombocytopenia (VITT). This clinical syndrome with thrombosis and thrombocytopenia was reported after exposure to the Oxford‐AstraZeneca COVID‐19 vaccine, ChAdOx1 nCoV‐19 vaccine (AZD1222), and Ad26.COV2.S vaccine (Janssen/Johnson & Johnson). In the absence of the clinical features, the incidence of positive anti‐PF4 antibodies in asymptomatic individuals post‐vaccination is unclear. Methods The aim of this study was to evaluate the development of anti‐PF4 antibodies in asymptomatic individuals 14–21 days after receiving the first dose of ChAdOx1 nCoV‐19 vaccine (AZD1222) and BNT162b2 vaccine. Prospectively, we collected serum from individuals before and after ChAdOx1 nCoV‐19 vaccine and BNT162b2 vaccine and measured anti‐PF4 antibodies using the Asserachrom HPIA IgG ELISA (Stago, Asnieres, France). Results We detected positive anti‐PF4 antibodies in 5 of 94 asymptomatic individuals post‐vaccine with a rate of 5.3% with low titers (OD 0.3–0.7). Four of 5 individuals who tested positive after the vaccine had also positive anti‐PF4 antibodies before the vaccine, which indicates that a majority of the positive results are due to preexisting anti‐PF4 antibodies. We did not find a relation between the development of anti‐PF4 antibodies and the immune response to the vaccine, status of prior COVID‐19 infection, and baseline characteristics of participants. None of the participants developed thrombosis nor thrombocytopenia. Conclusion Our results provide new evidence to guide the diagnostic algorithm of suspected cases of VITT. In the absence of thrombosis and thrombocytopenia, there is a low utility of testing for anti‐PF4 antibodies.

MicroRNA is a small non-coding RNA (sncRNA) involved in gene silencing and regulating post-transcriptional gene expression. miRNAs play an essential role in the pathogenesis of numerous diseases, including diabetes, cardiovascular diseases, viral diseases and cancer. Diffuse large B-cell lymphoma (DLBCL) is an aggressive non-Hodgkin’s lymphoma (NHL), arising from different stages of B-cell differentiation whose pathogenesis involves miRNAs. Various viral and non-viral vectors are used as a delivery vehicle for introducing specific miRNA inside the cell. Adenoviruses are linear, double-stranded DNA viruses with 35 kb genome size and are extensively used in gene therapy. Meanwhile, Adeno-associated viruses accommodate up to 4.8 kb foreign genetic material and are favorable for transferring miRNA due to small size of miRNA. The genetic material is integrated into the DNA of the host cell by retroviruses so that only dividing cells are infected and stable expression of miRNA is achieved. Over the years, remarkable progress was made to understand DLBCL biology using advanced genomics and epigenomics technologies enabling oncologists to uncover multiple genetic mutations in DLBCL patients. These genetic mutations are involved in epigenetic modification, ability to escape immunosurveillance, impaired BCL6 and NF-κβ signaling pathways and blocking terminal differentiation. These pathways have since been identified and used as therapeutic targets for the treatment of DLBCL. Recently miRNAs were also identified to act either as oncogenes or tumor suppressors in DLBCL pathology by altering the expression levels of some of the known DLBCL related oncogenes. i.e., miR-155, miR-17-92 and miR-21 act as oncogenes by altering the expression levels of MYC, SHIP and FOXO1, respectively, conversely; miR-34a, mir-144 and miR-181a act as tumor suppressors by altering the expression levels of SIRT1, BCL6 and CARD11, respectively. Hundreds of miRNAs have already been identified as biomarkers in the prognosis and diagnosis of DLBCL because of their significant roles in DLBCL pathogenesis. In conclusion, miRNAs in addition to their role as biomarkers of prognosis and diagnosis could also serve as potential therapeutic targets for treating DLBCL.