Background: Critically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk. Although platelet activation is critical for thrombosis and is responsible for the thrombotic events and cardiovascular complications, the role of platelets in the pathogenesis of COVID-19 remains unclear. Methods: Using platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl 3-induced thrombus formation in vivo, and thrombus formation under flow conditions ex vivo.

Dimethylsulphoniopropionate (DMSP) is one of the Earth’s most abundant organosulphur molecules, a signalling molecule, a key nutrient for marine microorganisms, and the major precursor for gaseous dimethyl sulphide (DMS). DMS, another infochemical in signalling pathways, is important in global sulphur cycling2, and affects the Earth’s albedo, and potentially climate, via sulphate aerosol and cloud condensation nuclei production. It was thought that only eukaryotes produce significant amounts of DMSP, but here we demonstrate that many marine heterotrophic bacteria also produce DMSP, likely using the same methionine (Met) transamination pathway as macroalgae and phytoplankton10. We identify the first DMSP synthesis gene in any organism, dsyB, which encodes the key methyltransferase enzyme of this pathway and is a reliable reporter for bacterial DMSP synthesis in marine alphaproteobacteria. DMSP production and dsyB transcription are upregulated by increased salinity, nitrogen limitation and lower temperatures in our model DMSP-producing bacterium Labrenzia aggregata LZB033. With significant numbers of dsyB homologues in marine metagenomes, we propose that bacteria likely make a significant contribution to oceanic DMSP production. Furthermore, since DMSP production is not solely associated with obligate phototrophs, the process need not be confined to the photic zones of marine environments, and as such may have been underestimate

Global polarization of Λ hyperons has been measured to be of the order of a few tenths of a percent in Au+Au collisions at √ s N N = 200 GeV, with no significant difference between Λ andΛ.These new results reveal the collision energy dependence of the global polarization together with the results previously observed at √ s N N = 7.7 -62.4 GeV and indicate noticeable vorticity of the medium created in non-central heavy-ion collisions at the highest RHIC collision energy. The signal is in rough quantitative agreement with the theoretical predictions from a hydrodynamic model and from the AMPT (A Multi-Phase Transport) model. The polarization is larger in more peripheral collisions, and depends weakly on the hyperon's transverse momentum and pseudorapidity η H within |η H | < 1. An indication of the polarization dependence on the event-by-event charge asymmetry 3 is observed at the 2σ level, suggesting a possible contribution to the polarization from the axial current induced by the initial magnetic field. PACS numbers: 25.75.-q, 25.75.Ld

Regulatory T cells (Treg) mediate amelioration of disease and immune homeostasis by inhibiting immune activation and maintaining peripheral immune tolerance. The suppressive mechanisms and clinical significance of Treg have not been completely elucidated in patients with acute myeloid leukemia (AML). Here, we demonstrated that CD127 in combination with CD4 and CD25 can identify FoxP3+ Treg in peripheral blood (PB) and bone marrow (BM) using multicolor flow cytometry. We showed that the CD4+CD25+CD127lo Treg frequencies were significantly increased and their phenotypes were different in PB from newly diagnosed AML patients compared to those from healthy volunteers (HVs). Moreover, the Treg frequencies were significantly higher in BM than those from PB in the same patients. The Treg frequencies were reduced when patients achieved complete remission (CR) and were increased when patients relapsed. The Treg frequencies at diagnosis in PB and BM of patients who had achieved CR were lower than those of patients who had persistent leukemia or died, respectively. CD4+CD25+ Treg were isolated by magnetic‐activated cell sorting and tested for suppressive functions in coculture with allogeneic carboxyfluorescein diacetate succinimidylester‐labeled CD4+CD25− responder cells. Suppression mediated by Treg was higher in AML patients compared to HVs. No significant differences were observed in the cytokines production of Treg, including interferon‐gamma (IFN‐γ), interleukin (IL)‐4,IL‐2 and IL‐10, between patients with AML and HVs. Our study suggests that Treg may play a role in the pathogenesis of AML, and sequential measurements of Treg frequency may have clinical value in the evaluation of therapeutic effects and clinical outcome.