As compared with epitaxial semiconductor devices, two-dimensional (2D) heterostructures offer alternative facile platforms for many optoelectronic devices. Among them, photovoltaic based photodetectors can give fast response, while the photogate devices can lead to high responsivity. Here, we report a 2D photogate photodiode, which combines the benefits of 2D black phosphorus/MoS2 photodiodes with the emerging potential of perovskite, to achieve both fast response and high responsivity. This device architecture is constructed based on the fast photovoltaic operation together with the high-gain photogating effect. Under reverse bias condition, the device exhibits high responsivity (11 A/W), impressive detectivity (1.3 × 1012 Jones), fast response (150/240 μs), and low dark current (3 × 10–11 A). All these results are already much better in nearly all aspects of performance than the previously reported 2D photodiodes operating in reverse bias, achieving the optimal balance between all figure-of-merits. Importantly, with a zero bias, the device can also yield high detectivity (3 × 1011 Jones), ultrahigh light on/off ratio (3 × 107), and extremely high external quantum efficiency (80%). This device architecture thus has a promise for high-efficiency photodetection and photovoltaic energy conversion.
Abstract-Cardiotrophin 1 (CT-1), a cytokine belonging to the interleukin 6 family, is increased in hypertension and in heart failure. We aimed to study the precise role of CT-1 on cardiac, vascular, and renal function; morphology; and remodeling in early stages without hypertension. CT-1 (20 g/kg per day) or vehicle was administrated to Wistar rats for 6 weeks. Cardiac and vascular functions were analyzed in vivo using M-mode echocardiography, Doppler, and echo tracking device and ex vivo using a scanning acoustic microscopy method. Cardiovascular and renal histomorphology were measured by immunohistochemistry, RT-PCR, and Western blot. Kidney functional properties were assessed by serum creatinine and neutrophile gelatinase-associated lipocalin and microalbuminuria/creatininuria ratio. Without alterations in blood pressure levels, CT-1 treatment increased left ventricular volumes, reduced fractional shortening and ejection fraction, and induced myocardial dilatation and myocardial fibrosis. In the carotid artery of CT-1-treated rats, the circumferential wall stress-incremental elastic modulus curve was shifted leftward, and the acoustic speed of sound in the aorta was augmented, indicating increased arterial stiffness. Vascular media thickness, collagen, and fibronectin content were increased by CT-1 treatment. CT-1-treated rats presented unaltered serum creatinine concentrations but increased urinary and serum neutrophile gelatinase-associated lipocalin and microalbuminuria/creatininuria ratio. This paralleled a glomerular and tubulointerstitial fibrosis accompanied by renal epithelial-mesenchymal transition. CT-1 is a new potent fibrotic agent in heart, vessels, and kidney able to induce cardiovascular-renal dysfunction independent from blood pressure. Thus, CT-1 could be a new target simultaneously integrating alterations of heart, vessels, and kidney in early stages of heart failure. 1-3 Cardiac hypertrophy is attributable to cardiomyocyte hypertrophy, the proliferation of interstitial fibroblasts, and increased depositions of extracellular matrix (ECM) components.4 Arterial stiffening is associated with decreased distensibility and modified wall structure mainly characterized by increased ECM. 5,6 Chronic kidney disease progression is generally associated with tubulointerstitial fibrosis. 7,8 Therefore, it is of paramount importance to identify common pathways able to trigger cardiovascular and renal fibrosis.Cardiotrophin 1 (CT-1) is an interleukin 6 superfamily member.9 Elevated CT-1 levels have been reported in HF and in hypertensive patients.10-12 Moreover, CT-1 positively correlates with left ventricular (LV) mass index and the serum concentration of carboxy-terminal propeptide of procollagen type I, a biomarker of collagen synthesis, 10 suggesting that CT-1 may contribute to the development of cardiomyocyte hypertrophy and fibrosis. Accordingly, CT-1 administration increases heart weight in mice. 13 Our group has characterized CT-1-induced cardiomyocyte survival and hypertrophy, 10,14 as well as CT-1...
Knowledge of how the elastic stiffness of a cell affects its communication with its environment is of fundamental importance for the understanding of tissue integrity in health and disease. For stiffness measurements, it has been customary to quote a single parameter quantity, e.g., Young's modulus, rather than the minimum of two terms of the stiffness tensor required by elasticity theory. In this study, we use two independent methods (acoustic microscopy and atomic force microscopy nanoindentation) to characterize the elastic properties of a cell and thus determine two independent elastic constants. This allows us to explore in detail how the mechanical properties of cells change in response to signaling pathways that are known to regulate the cell's cytoskeleton. In particular, we demonstrate that altering the tensioning of actin filaments in NIH3T3 cells has a strong influence on the cell's shear modulus but leaves its bulk modulus unchanged. In contrast, altering the polymerization state of actin filaments influences bulk and shear modulus in a similar manner. In addition, we can use the data to directly determine the Poisson ratio of a cell and show that in all cases studied, it is less than, but very close to, 0.5 in value.
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