NiO is a wide band gap p-type oxide semiconductor and has potential for applications in solar energy conversion as a hole-transporting layer (HTL). It also has good optical transparency and high chemical stability, and the capability of aligning the band edges to the perovskite (CH3NH3PbI3) layers. Ultra-thin and un-doped NiO films with much less absorption loss were prepared by atomic layer deposition (ALD) with highly precise control over thickness without any pinholes. Thin enough (5-7.5 nm in thickness) NiO films with the thickness of few time the Debye length (LD = 1-2 nm for NiO) show enough conductivities achieved by overlapping space charge regions. The inverted planar perovskite solar cells with NiO films as HTLs exhibited the highest energy conversion efficiency of 16.40% with high open circuit voltage (1.04 V) and fill factor (0.72) with negligible current-voltage hysteresis.

BackgroundRenal renin-angiotensin system (RAS) activation is one of the important pathogenic mechanisms in the development of diabetic nephropathy in type 2 diabetes. The aim of this study was to investigate the effects of a sodium-glucose co-transporter 2 (SGLT-2) inhibitor, dapagliflozin, on renal RAS in an animal model with type 2 diabetes.MethodsDapagliflozin (1.0 mg/kg, OL-DA) or voglibose (0.6 mg/kg, OL-VO, diabetic control) (n = 10 each) was administered to Otsuka Long-Evans Tokushima Fatty (OLETF) rats for 12 weeks. We used voglibose, an alpha-glucosidase inhibitor, as a comparable counterpart to SGLT2 inhibitor because of its postprandial glucose-lowering effect without proven renoprotective effects. Control Long-Evans Tokushima Otsuka (LT) and OLETF (OL-C) rats received saline (n = 10, each). Changes in blood glucose, urine albumin, creatinine clearance, and oxidative stress were measured. Inflammatory cell infiltration, mesangial widening, and interstitial fibrosis in the kidney were evaluated by histological analysis. The effects of dapagliflozin on renal expression of the RAS components were evaluated by quantitative RT-PCR in renal tissue.ResultsAfter treatment, hyperglycemia and urine microalbumin levels were attenuated in both OL-DA and OL-VO rather than in the OL-C group (P < 0.05). The urine angiotensin II (Ang II) and angiotensinogen levels were significantly decreased following treatment with dapagliflozin or voglibose, but suppression of urine Ang II level was more prominent in the OL-DA than the OL-VO group (P < 0.05). The expressions of angiotensin type 1 receptor and tissue oxidative stress markers were markedly increased in OL-C rats, which were reversed by dapagliflozin or voglibose (P < 0.05, both). Inflammatory cell infiltration, mesangial widening, interstitial fibrosis, and total collagen content were significantly increased in OL-C rats, which were attenuated in OL-DA group (P < 0.05).ConclusionDapagliflozin treatment showed beneficial effects on diabetic nephropathy, which might be via suppression of renal RAS component expression, oxidative stress and interstitial fibrosis in OLETF rats. We suggest that, in addition to control of hyperglycemia, partial suppression of renal RAS with an SGLT2 inhibitor would be a promising strategy for the prevention of treatment of diabetic nephropathy.

The edge sites of molybdenum disulfide (MoS 2 ) have been shown to be efficient electrocatalysts for the hydrogen evolution reaction (HER). To utilize these structures, two main strategies have been proposed. The first strategy is to use amorphous structures, which should be beneficial in maximizing the area of the edge-site moieties of MoS 2 . However, these structures experience structural instability during HER. The other strategy is nanostructuring, in which, to enhance the resulting HER performance, the exposed surfaces of MoS 2 cannot be inert basal planes. Therefore, MoS 2 may need critical nanocrystallinity to produce the desired facets. Here, we first describe that when atomic layer deposition (ALD) is applied to layered materials such as MoS 2 , MoS 2 exhibits the nonideal mode of ALD growth on planar surfaces. As a model system, the ALD of MoCl 5 and H 2 S was studied. This nonideality does not allow for the conventional linear relationship between the growth thickness and the number of cycles. Instead, it provides the ability to control the relative ratios of the edge sites and basal planes of MoS 2 to the exposed surfaces. The number of edge sites produced was carefully characterized in terms of the geometric surface area and effective work function and was correlated to the HER performance, including Tafel slopes and exchange current densities. We also discussed how, as a result of the low growth temperature, the incorporation of chlorine impurities affected the electron doping and formation of mixed 2H and 1T phases. Remarkably, the resulting 1T phase was stable even upon thermal annealing at 400 °C. With the simple, planar MoS 2 films, we monitored the resulting catalytic performance, finding current densities of up to 20 mA cm −2 at −0.3 V versus the reversible hydrogen electrode (RHE), a Tafel slope of 50−60 mV/decade, and an onset potential of 143 mV versus RHE.

We report the interface properties of atomic-layer-deposited Al2O3 thin films on ultraviolet/ozone (UV/O3)-treated multilayer MoS2 crystals. The formation of S-O bonds on MoS2 after low-power UV/O3 treatment increased the surface energy, allowing the subsequent deposition of uniform Al2O3 thin films. The capacitance-voltage measurement of Au-Al2O3-MoS2 metal oxide semiconductor capacitors indicated n-type MoS2 with an electron density of ∼10(17) cm(-3) and a minimum interface trap density of ∼10(11) cm(-2) eV(-1). These results demonstrate the possibility of forming a high-quality Al2O3-MoS2 interface by proper UV/O3 treatment, providing important implications for their integration into field-effect transistors.

Pancreatic stellate cells (PSCs) are involved in pancreatic inflammation and fibrosis. Recent studies have shown that blocking the renin-angiotensin system (RAS) attenuates pancreatic inflammation and fibrosis. However, there are few data about the direct effects of high glucose on extracellular matrix (ECM) protein synthesis and angiotensin II (Ang II) induction in PSCs. PSCs were isolated from male Sprague-Dawley rats and cultured in medium containing 5.5 mM (LG group) or 27 mM D-glucose (HG group). Levels of Ang II and transforming growth factor-beta (TGF-beta) in culture media were measured and Ang II-positive cells were counted. We used real-time polymerase chain reaction (PCR) to detect Ang II receptor expression and Western blot analysis for the expression of ECM proteins such as connective-tissue growth factor (CTGF) and collagen type IV. Cells were also treated with an Ang II-receptor antagonist (candesartan, 10 microM) or angiotensin-converting enzyme (ACE) inhibitor (ramiprilat, 100 nM). Thymidine uptake by PSCs increased fourfold with high glucose treatment. Ang II levels and the proportion of Ang II-positive PSCs were significantly increased after 6 h under high-glucose conditions. TGF-beta concentrations also increased significantly with high glucose. After 72 h, the expression of CTGF and collagen type IV proteins in high-glucose cultures increased significantly and this increase was effectively attenuated by the candesartan or the ramiprilat. All together, high glucose induced PSCs proliferation and ECM protein synthesis, and these effects were attenuated by an Ang II-receptor antagonist. The data suggest that pancreatic inflammation and fibrosis aggravated by hyperglycemia, and Ang II play an important role in this pathogenesis.