Electrical and Thermoelectric Transport by Variable Range Hopping in Thin Black Phosphorus Devices.

The moderate band gap of black phosphorus (BP) in the range of 0.3-2 eV, along a high mobility of a few hundred cm(2) V(-1) s(-1) provides a bridge between the gapless graphene and relatively low-mobility transition metal dichalcogenides. Here, we study the mechanism of electrical and thermoelectric transport in 10-30 nm thick BP devices by measurements of electrical conductance and thermopower (S) with various temperatures (T) and gate-electric fields. The T dependences of S and the sheet conductance (σ□) of the BP devices show behaviors of T(1/3) and exp[-(1/T)(1/3)], respectively, where S reaches ∼0.4 mV/K near room T. This result indicates that two-dimensional (2D) Mott's variable range hopping (VRH) is a dominant mechanism in the thermoelectric and electrical transport in our examined thin BP devices. We consider the origin of the 2D Mott's VRH transport in our BPs as trapped charges at the surface of the underlying SiO2 based on the analysis with observed multiple quantum dots.

The mechanistic and structural role of von Willebrand factor in endotoxemia-enhanced deep vein thrombosis in mice.

BACKGROUND: Although the concept of immunothrombosis has established a link between inflammation and thrombosis, the role of inflammation in the pathogenesis of deep vein thrombosis remains to be fully elucidated. Further, although various constituents of venous thrombi have been identified, their localizations and cellular and molecular interactions are yet to be combined in a single, multiplexed analysis. OBJECTIVES: The objective of this study was to investigate the role of the von Willebrand factor (VWF) in inflammation-associated venous thrombosis. We also performed a proof-of-concept study of imaging mass cytometry to quantitatively and simultaneously analyze the localizations and interactions of 10 venous thrombus constituents. METHODS: We combined the murine inferior vena cava stenosis model of deep vein thrombosis with the lipopolysaccharide model of endotoxemia. We also performed a proof-of-concept study of imaging mass cytometry to assess the feasibility of this approach in analyzing the structural composition of thrombi. RESULTS: We found that lipopolysaccharide-treated mice had significantly higher incidences of venous thrombosis, an effect that was mitigated when VWF was inhibited using inhibitory αVWF antibodies. Our detailed structural analysis also showed that most thrombus components are localized in the white thrombus regardless of endotoxemia. Moreover, although endotoxemia modulated the relative representation and interactions of VWF with other thrombus constituents, the scaffolding network, comprised VWF, fibrin, and neutrophil extracellular traps, remained largely unaffected. CONCLUSIONS: We observe a key role for VWF in the pathogenesis of inflammation-associated venous thrombosis while providing a more comprehensive insight into the molecular interactions that constitute the architecture of venous thrombi.

A sticky proposition: The endothelial glycocalyx and von Willebrand factor.

Von Willebrand factor (VWF) is a critical component of the hemostatic system. Basal secretion of VWF from endothelial cells is the principal determinant of an individual's baseline plasma VWF levels, while endothelial VWF release can also be induced by several biochemical agonists and biomechanical forces such as increased shear stress. However, the mechanotransduction machinery responsible for this latter response is unclear. Here we propose that the endothelial glycocalyx (EGC), a dynamic layer of proteins and carbohydrates that covers the surface of the vascular endothelium, may play a key role in mediating this response. The EGC has previously been implicated in mediating the mechanotransduction of shear stress in other shear-responsive endothelial processes, such as nitric oxide production and stem cell differentiation. Here, we hypothesize that a similar mechanism may be responsible for the basal secretion of endothelial VWF, whereby the EGC mediates the mechanotransduction of physiological shear stress generated by flowing blood, that in turn contributes to the maintenance of physiological plasma VWF levels.