Micropipette aspiration of guinea pig megakaryocytes: absence of fragmentation and dependence on maturation stage

Platelet release has been alternatively viewed as a fragmentation of platelet territories demarcated within the cytoplasm of mature megakaryocytes or as a later event involving segmentation of proplatelet pseudopodia extended from the cell. The mechanical constraints on platelet release were evaluated by measuring the resistance of guinea pig megakaryocytes to aspiration into micropipettes of similar diameter to the width of naturally forming proplatelet projections. Application of increasing negative pressure to the surface of the cells resulted in progressively longer extensions being drawn into the pipette until maximal extension lengths were reached. None of the passively aspirated cytoplasmic extensions fragmented off the cells even at the highest aspiration pressure under physiologic study conditions. The longest extensions were aspirated from megakaryocytes of the most advanced maturation stage, and a proportion of the mature cells yielded very long extensions over 50 mu and up to 150 mu in length. Surprisingly, the ease of aspiration did not correlate to cell size during any stage of maturation. The mechanical behavior of guinea pig megakaryocytes indicates a large availability of surface for extension in mature cells ideal for active proplatelet projection. The lack of mechanical fragility suggests that platelet release is a very late maturational event not yet initiated in the "mature" megakaryocytes available for study from marrow harvests.     

Adult hemoglobins are synthesized in murine fetal hepatic erythropoietic cells

The hemoglobins present in murine fetal hepatic erythroblasts on days 12-15 of gestation were studied by biochemical and immunocytologic techniques. In addition, fetal hepatic hemopoietic progenitor cells obtained from normal and mutant f/f mouse fetuses on days 11-13 of gestation were cultured in vitro with added erythropoietin and adult spleen cell conditioned medium to form large erythroid colonies. In all instances, adult hemoglobin synthesis was detected in the fetal hepatic erythroblasts and in the erythroid cell cultures in vitro. The tumor promoter, 12-O-tetradecanoylphorbol 13-acetate, enhanced the fetal hepatic erythroid colony growth in vitro, but did not alter the hemoglobin phenotypic expression.     

Is COVID-19-induced liver injury different from other RNA viruses?‎

Coronavirus disease 2019 is a pandemic disease caused by a novel RNA coronavirus, SARS coronavirus 2 (SARS-CoV-2), which is implicated in the respiratory system. SARS-CoV-2 also targets extrapulmonary systems, including the gastrointestinal tract, liver, central nervous system and others. SARS-CoV-2, like other RNA viruses, targets the liver and produces liver injury. This literature review showed that SARS-CoV-2-induced liver injury is different from other RNA viruses by a transient elevation of hepatic enzymes and does not progress to liver fibrosis or other unfavorable events. Moreover, SARS-CoV-2-induced liver injury usually occurs in the presence of risk factors, such as nonalcoholic liver fatty disease. This review highlights the important differences between RNA viruses inducing liver injury taking into consideration the clinical, biochemical, histopathological, postmortem findings and the chronicity of liver injury that ultimately leads to liver fibrosis and hepatocellular carcinoma.