Magnetic ground state of the one-dimensional ferromagnetic chain compounds M(NCS)(2)(thiourea)(2) (M = Ni, Co)

The magnetic properties of the two isostructural molecule-based magnets - Ni(NCS)2(thiourea)2, S=1 [thiourea=SC(NH2)2] and Co(NCS)2(thiourea)2, S=3/2 - are characterized using several techniques in order to rationalize their relationship with structural parameters and to ascertain magnetic changes caused by substitution of the spin. Zero-field heat capacity and muon-spin relaxation measurements reveal low-temperature long-range ordering in both compounds, in addition to Ising-like (D<0) single-ion anisotropy (DCo∼-100 K, DNi∼-10 K). Crystal and electronic structure, combined with dc-field magnetometry, affirm highly quasi-one-dimensional behavior, with ferromagnetic intrachain exchange interactions JCo≈+4 K and JNi∼+100 K and weak antiferromagnetic interchain exchange, on the order of J′∼-0.1 K. Electron charge- and spin-density mapping reveals through-space exchange as a mechanism to explain the large discrepancy in J-values despite, from a structural perspective, the highly similar exchange pathways in both materials. Both species can be compared to the similar compounds MCl2(thiourea)4, M = Ni(II) (DTN) and Co(II) (DTC), where DTN is known to harbor two magnetic-field-induced quantum critical points. Direct comparison of DTN and DTC with the compounds studied here shows that substituting the halide Cl- ion for the NCS- ion results in a dramatic change in both the structural and magnetic properties

Platelet GPIb alpha is a mediator and potential interventional target for NASH and subsequent liver cancer

Non-alcoholic fatty liver disease ranges from steatosis to non-alcoholic steatohepatitis (NASH), potentially progressing to cirrhosis and hepatocellular carcinoma (HCC). Here, we show that platelet number, platelet activation and platelet aggregation are increased in NASH but not in steatosis or insulin resistance. Antiplatelet therapy (APT; aspirin/clopidogrel, ticagrelor) but not nonsteroidal anti-inflammatory drug (NSAID) treatment with sulindac prevented NASH and subsequent HCC development. Intravital microscopy showed that liver colonization by platelets depended primarily on Kupffer cells at early and late stages of NASH, involving hyaluronan-CD44 binding. APT reduced intrahepatic platelet accumulation and the frequency of platelet–immune cell interaction, thereby limiting hepatic immune cell trafficking. Consequently, intrahepatic cytokine and chemokine release, macrovesicular steatosis and liver damage were attenuated. Platelet cargo, platelet adhesion and platelet activation but not platelet aggregation were identified as pivotal for NASH and subsequent hepatocarcinogenesis. In particular, platelet-derived GPIbα proved critical for development of NASH and subsequent HCC, independent of its reported cognate ligands vWF, P-selectin or Mac-1, offering a potential target against NASH