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An erythroid-specific lentiviral vector improves anemia and iron metabolism in a new model of XLSA.
Blood
January 2025
Department of Pediatrics, Hematology, The Children's Hospital of Philadelphia, Philadelphia, PA.
X-linked sideroblastic anemia (XLSA) is a congenital anemia caused by mutations in ALAS2, a gene responsible for heme synthesis. Treatments are limited to pyridoxine supplements and blood transfusions, offering no definitive cure except for allogeneic hematopoietic stem cell transplantation, only accessible to a subset of patients. The absence of a suitable animal model has hindered the development of gene therapy research for this disease.
View Article and Find Full Text PDFOcoxin Oral Solution Triggers DNA Damage and Cell Death in Ovarian Cancer.
Nutrients
July 2024
Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC), Instituto de Investigación Biomédica de Salamanca (IBSAL) and Centro de Investigación Biomédica en Red Cáncer (CIBERONC), Campus Miguel de Unamuno, 37007 Salamanca, Spain.
Ovarian cancer is the most fatal of all the reproductive cancers within the female population, mainly due to its late diagnosis that limits surgery and medical treatment. Classically, ovarian cancer therapy has included conventional chemotherapy, and other therapeutic approaches are now being used to treat these patients, but the outcomes of the disease are still poor. Therefore, new strategies are needed to improve life expectancy and life quality of ovarian cancer patients.
View Article and Find Full Text PDFLuspatercept enhances hemoglobin levels in a Chinese boy with congenital sideroblastic anemia: A case report.
World J Clin Cases
July 2024
Anemia Therapeutic Center, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Science, Peking Union Medical College, Tianjin 300020, China.
Background: Congenital sideroblastic anemia (CSA) is a rare and heterogeneous group of genetic disorders. Conventional treatment include pyridoxine (vitamin B6) and allogeneic hematopoietic stem cell transplantation (allo-HSCT), and can alleviate anemia in the majority of cases. Nevertheless, some CSA cases remain unresponsive to pyridoxine or are unable to undergo allo-HSCT.
View Article and Find Full Text PDFErythromycin, retapamulin, pyridoxine, folic acid, and ivermectin inhibit cytopathic effect, papain-like protease, and M enzymes of SARS-CoV-2.
Front Cell Infect Microbiol
December 2023
University of Nigeria Centre for Clinical Trials, University of Nigeria Teaching Hospital, Enugu, Nigeria.
Background: Although tremendous success has been achieved in the development and deployment of effective COVID-19 vaccines, developing effective therapeutics for the treatment of those who do come down with the disease has been with limited success. To repurpose existing drugs for COVID-19, we previously showed, qualitatively, that erythromycin, retapamulin, pyridoxine, folic acid, and ivermectin inhibit SARS-COV-2-induced cytopathic effect (CPE) in Vero cells.
Aim: This study aimed to quantitatively explore the inhibition of SARS-CoV-2-induced CPE by erythromycin, retapamulin, pyridoxine, folic acid, and ivermectin and to determine the effect of these drugs on SARS-CoV-2 papain-like protease and 3CL protease (M) enzymes.
Rapid Diagnostic Platform for Personalized Vitamin B6 Detection in Erythrocytes PLP Cofactor Mimics.
ACS Chem Biol
July 2023
TUM School of Natural Sciences, Department Biosciences, Chair of Organic Chemistry II, Center for Functional Protein Assemblies (CPA), Technical University Munich (TUM), Ernst-Otto-Fischer Str. 8, Garching 85748, Germany.
Personalized assessment of vitamin levels in point-of-care (POC) devices is urgently needed to advance the recognition of diseases associated with malnutrition and unbalanced diets. We here introduce a diagnostic platform, which showcases an easy and rapid readout of vitamin B6 (pyridoxal phosphate, PLP) levels in erythrocytes as a first step toward a home-use POC. The technology is based on fluorescent probes, which bind to PLP-dependent enzymes (PLP-DEs) and thereby indirectly report their occupancy with endogenous B6.
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