The GPIbα-VWF A1 domain interaction is essential for platelet tethering under high shear. Synergy between GPIbα and GPVI signaling machineries has been suggested previously, however its molecular mechanism remains unclear. Generation of a novel GPIbα transgenic mouse allowed the authors of this study to identify a new role for the intracellular tail of GPIbα in transducing both VWF-GPIbα and collagen-GPVI signaling events in platelets.
This study analyzed the ChAdOx1 nCoV-19 (AstraZeneca) and Ad26.COV2.S (Johnson & Johnson) vaccines. ChAdOx1 nCoV-19 contains significant amounts of host cell protein impurities, including functionally active proteasomes, and adenoviral proteins. A much smaller amount of impurities was found in Ad26.COV2.S. These differences in impurities together with EDTA-induced capillary leakage might contribute to the higher incidence rate of vaccine-induced immune thrombotic thrombocytopenia associated with ChAdOx1 nCoV-19.
This study investigated 59 patients with sickle cell anemia by a multimodal approach and found that those with silent cerebral infarcts (SCI) had a distinctive profile characterized by decreased blood pressure, impaired blood rheology, increased P-selectin levels, and marked anemia. Magnetic resonance imaging and arterial spin labeling were effective screening tools for SCI. Early treatment targeting hemolysis, anemia and endothelial dysfunction should reduce the risk of this under diagnosed and serious complication.
VEXAS syndrome is a newly defined autoinflammatory disorder that arises from somatic mutations affecting UBA1. This gene lies on the X-chromosome, making VEXAS an X-linked syndrome affecting only males. This case report describes the occurrence of VEXAS in a female with Turner syndrome. It is important to be alert to the presence of disorders that result in the inactivation of the X-chromosome when assessing female patients with a possible X-linked disorder, such as VEXAS syndrome.
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