Healable, adhesive, wearable, and soft human-motion sensors for ultrasensitive human-machine interaction and healthcare monitoring are successfully assembled from conductive and human-friendly hybrid hydrogels with reliable self-healing capability and robust self-adhesiveness. The conductive, healable, and self-adhesive hybrid network hydrogels are prepared from the delicate conformal coating of conductive functionalized single-wall carbon nanotube (FSWCNT) networks by dynamic supramolecular cross-linking among FSWCNT, biocompatible polyvinyl alcohol, and polydopamine. They exhibit fast self-healing ability (within 2 s), high self-healing efficiency (99%), and robust adhesiveness, and can be assembled as healable, adhesive, and soft human-motion sensors with tunable conducting channels of pores for ions and framework for electrons for real time and accurate detection of both large-scale and tiny human activities (including bending and relaxing of fingers, walking, chewing, and pulse). Furthermore, the soft humanmotion sensors can be enabled to wirelessly monitor the human activities by coupling to a wireless transmitter. Additionally, the in vitro cytotoxicity results suggest that the hydrogels show no cytotoxicity and can facilitate cell attachment and proliferation. Thus, the healable, adhesive, wearable, and soft human-motion sensors have promising potential in various wearable, wireless, and soft electronics for human-machine interfaces, human activity monitoring, personal healthcare diagnosis, and therapy.
Antiphospholipid antibodies reduce the levels of annexin V and accelerate the coagulation of plasma on cultured trophoblasts and endothelial cells. The reduction of annexin V levels on vascular cells may be an important mechanism of thrombosis and pregnancy loss in the antiphospholipid-antibody syndrome.
Annexin A5 (AnxA5) is a potent anticoagulant protein that crystallizes over phospholipid bilayers (PLBs), blocking their availability for coagulation reactions. Antiphospholipid antibodies disrupt AnxA5 binding, thereby accelerating coagulation reactions. This disruption may contribute to thrombosis and miscarriages in the antiphospholipid syndrome (APS). We investigated whether the antimalarial drug, hydroxychloroquine (HCQ), might affect this prothrombotic mechanism. Binding of AnxA5 to PLBs was measured with labeled AnxA5 and also imaged with atomic force microscopy. Immunoglobulin G levels, AnxA5, and plasma coagulation times were measured on cultured human umbilical vein endothelial cells and a syncytialized trophoblast cell line. AnxA5 anticoagulant activities of APS patient plasmas were also determined. HCQ reversed the effect of antiphospholipid antibodies on AnxA5 and restored AnxA5 binding to PLBs, an effect corroborated by atomic force microscopy. Similar reversals of antiphospholipid-induced abnormalities were measured on the surfaces of human umbilical vein endothelial cells and syncytialized trophoblast cell lines, wherein HCQ reduced the binding of antiphospholipid antibodies, increased cell-surface AnxA5 concentrations, and prolonged plasma coagulation to control levels. In addition, HCQ increased the AnxA5 anticoagulant activities of APS patient plasmas. In conclusion, HCQ reversed antiphospholipid-mediated disruptions of AnxA5 on PLBs and cultured cells, and in APS patient plasmas. These results support the concept of novel therapeutic approaches that address specific APS disease mechanisms.
Treatment with the antimalarial drug hydroxychloroquine (HCQ) has been associated with reduced risk of thrombosis in the antiphospholipid (aPL) syndrome (APS) and, in an animal model of APS, with reduction of experimentally induced thrombosis. Recognition of 2-glycoprotein I (2GPI) by aPL antibodies appears to play a major role in the disease process. We therefore used the techniques of ellipsometry and atomic force microscopy (AFM) to investigate whether HCQ directly affects the formation of aPL IgG-2GPI complexes on phospholipid bilayers. HCQ, at concentrations of 1 g/mL and greater, significantly reduced the binding of aPL-2GPI complexes to phospholipid surfaces and THP-1 (human acute monocytic leukemia cell line) monocytes. The drug also reduced the binding of the individual proteins to bilayers. This HCQmediated reduction of binding was completely reversed when the HCQ-protein solutions were dialyzed against buffer. HCQ also caused modest, but statistically significant, reductions of clinical antiphospholipid assays. In conclusion, HCQ reduces the formation of aPL-2GPI complexes to phospholipid bilayers and cells. This effect appears to be due to reversible interactions between HCQ and the proteins and may contribute to the observed reduction of thrombosis in human and experimental APS. These results support the possibility that HCQ, or analogous molecules, may offer novel nonanticoagulant therapeutic strategies for treating APS. (Blood. 2008;112:1687-1695) IntroductionThe antiphospholipid (aPL) syndrome (APS) is a thrombophilic disorder that is defined by the presence of autoantibodies against phospholipid-binding cofactor proteins in patients with vascular thrombosis and/or pregnancy complications. 1 Of the various phospholipid-binding proteins, aPL antibody recognition of the phospholipid-binding protein, 2-glycoprotein I (2GPI), appears to particularly correlate with thrombosis 2 and is associated with significantly increased risk of thrombosis. 3 Antiphospholipid antibodies have been demonstrated to play a causal role in the development of thrombosis in animal models (reviewed in Rand 4 ). Long-term anticoagulation with warfarin, a medication that carries a significant risk of bleeding complications, 5 is the standard treatment for APS-associated thrombosis. 6 Hydroxychloroquine (HCQ), an amphiphilic antimalarial compound, has proven to be an effective immunosuppressive treatment of systemic lupus erythematosus (SLE). [7][8][9][10][11] The Hopkins Lupus Cohort reported that the presence of aPL antibodies is an independent predictor of thrombosis in SLE, and that treatment of SLE patients with HCQ was associated with a reduced risk of thrombosis. 12 A cross-sectional study that compared aPL antibody-positive patients with thrombosis to a group of patients having the antibodies but who did not have thrombotic histories indicated that HCQ may be protective against thrombosis. 13 HCQ significantly reduced the extent of thrombosis in an animal model of injuryinduced thrombosis in APS, 14 and, in a si...
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