Activation of BNIP3-mediated mitophagy protects against renal ischemia-reperfusion injury

Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its pathophysiological role in AKI remains unclear. Here, we demonstrated an increase of BNIP3 expression in cultured renal proximal tubular epithelial cells following oxygen-glucose deprivation-reperfusion (OGD-R) and in renal tubules after renal ischemia-reperfusion (IR)-induced injury in mice. Functionally, silencing Bnip3 by specific short hairpin RNAs in cultured renal tubular cells reduced OGD-R-induced mitophagy, and potentiated OGD-R-induced cell death. In vivo, Bnip3 knockout worsened renal IR injury, as manifested by more severe renal dysfunction and tissue injury. We further showed that Bnip3 knockout reduced mitophagy, which resulted in the accumulation of damaged mitochondria, increased production of reactive oxygen species, and enhanced cell death and inflammatory response in kidneys following renal IR. Taken together, these findings suggest that BNIP3-mediated mitophagy has a critical role in mitochondrial quality control and tubular cell survival during AKI

Growth and reductive transformation of a gold shell around pyramidal cadmium selenide nanocrystals

We report the growth of an unstable shell-like gold structure around dihexagonal pyramidal CdSe nanocrystals in organic solution and the structural transformation to spherical domains by two means: i) electron beam irradiation (in situ) and (ii) addition of a strong reducing agent during synthesis. By varying the conditions of gold deposition, such as ligands present or the geometry of the CdSe nanocrystals, we were able to tune the gold domain size between 1.4 nm to 3.9 nm and gain important information on the role of surface chemistry in hetero nanoparticle synthesis and seed reactivity, both of which are crucial points regarding the chemical design of new materials for photocatalysis and optoelectronic applications.Comment: 5 pages, 4 figure

Field–effect transistors made of individual colloidal PbS nanosheets

Two-dimensional materials are considered for future quantum devices and are usually produced by extensive methods like molecular beam epitaxy. We report on the fabrication of field-effect transistors using individual ultra-thin lead sulfide nanostructures with lateral dimensions in the micrometer range and a height of a few nanometers as conductive channel produced by a comparatively fast, inexpensive, and scalable colloidal chemistry approach. Contacted with gold electrodes, such devices exhibit p-type behavior and temperature-dependent photoconductivity. Trap states play a crucial role in the conduction mechanism. The performance of the transistors is among the ones of the best devices based on colloidal nanostructures.Comment: 5 pages, 4 figure

Metal nanoparticle field-effect transistor

We demonstrate that by means of a local top-gate current oscillations can be observed in extended, monolayered films assembled from monodisperse metal nanocrystals -- realizing transistor function. The oscillations in this metal-based system are due to the occurrence of a Coulomb energy gap in the nanocrystals which is tunable via the nanocrystal size. The nanocrystal assembly by the Langmuir-Blodgett method yields homogeneous monolayered films over vast areas. The dielectric oxide layer protects the metal nanocrystal field-effect transistors from oxidation and leads to stable function for months. The transistor function can be reached due to the high monodispersity of the nanocrystals and the high super-crystallinity of the assembled films. Due to the fact that the film consists of only one monolayer of nanocrystals and all nanocrystals are simultaneously in the state of Coulomb blockade the energy levels can be influenced efficiently (limited screening).Comment: 15 pages, 6 figure

Association between Airborne Fine Particulate Matter and Residents’ Cardiovascular Diseases, Ischemic Heart Disease and Cerebral Vascular Disease Mortality in Areas with Lighter Air Pollution in China

Background: China began to carry out fine particulate matter (PM2.5) monitoring in 2013 and the amount of related research is low, especially in areas with lighter air pollution. This study aims to explore the association between PM2.5 and cardiovascular disease (CVD), ischemic heart disease (IHD) and cerebral vascular disease (EVD) mortality in areas with lighter air pollution. Methods: Data on resident mortality, air pollution and meteorology in Shenzhen during 2013–2015 were collected and analyzed using semi-parametric generalized additive models (GAM) with Poisson distribution of time series analysis. Results: Six pollutants were measured at seven air quality monitoring sites, including PM2.5, PM10, SO2, NO2, CO and O3. The PM2.5 daily average concentration was 35.0 ± 21.9 μg/m3; the daily average concentration range was from 7.1 μg/m3 to 137.1 μg/m3. PM2.5 concentration had significant effects on CVD, IHD and EVD mortality. While PM2.5 concentration of lag5 and lag02 rose by 10 μg/m3, the excess risk (ER) of CVD mortality were 1.50% (95% CI: 0.51–2.50%) and 2.09% (95% CI: 0.79–3.41%), respectively. While PM2.5 concentration of lag2 and lag02 rose by 10 μg/m3, the ER of IHD mortality were 2.87% (95% CI: 0.71–5.07%) and 3.86% (95% CI: 1.17–6.63%), respectively. While PM2.5 concentration of lag4 and lag04 rose by 10 μg/m3, the ER of EVD mortality were 2.09% (95% CI: 2.28–3.92%) and 3.08% (95% CI: 0.68–5.53%), respectively. Conclusions: PM2.5 increased CVD mortality. The government needs to strengthen the governance of air pollution in areas with a slight pollution

The negative feedback loop of NF-κB/miR-376b/NFKBIZ in septic acute kidney injury

Sepsis is the leading cause of acute kidney injury (AKI). However, the pathogenesis of septic AKI remains largely unclear. Here, we demonstrate a significant decrease of microRNA-376b (miR-376b) in renal tubular cells in mice with septic AKI. Urinary miR-376b in these mice was also dramatically decreased. Patients with sepsis with AKI also had significantly lower urinary miR-376b than patients with sepsis without AKI, supporting its diagnostic value for septic AKI. LPS treatment of renal tubular cells led to the activation of NF-κB, and inhibition of NF-κB prevented a decrease of miR-376b. ChIP assay further verified NF-κB binding to the miR-376b gene promoter upon LPS treatment. Functionally, miR-376b mimics exaggerated tubular cell death, kidney injury, and intrarenal production of inflammatory cytokines, while inhibiting miR-376b afforded protective effects in septic mice. Interestingly, miR-376b suppressed the expression of NF-κB inhibitor ζ (NFKBIZ) in both in vitro and in vivo models of septic AKI. Luciferase microRNA target reporter assay further verified NFKBIZ as a direct target of miR-376b. Collectively, these results illustrate the NF-κB/miR-376b/NFKBIZ negative feedback loop that regulates intrarenal inflammation and tubular damage in septic AKI. Moreover, urinary miR-376b is a potential biomarker for the diagnosis of AKI in patients with sepsis

The phase transition of ThFe

Differently from most of the other 1111-type iron-based superconductors, ThFeAsN itself shows superconductivity at 30 K without antiferromagnetism, even in the absence of chemical doping and other treating. In order to understand its peculiar behavior better, it is necessary to investigate the evolution of the superconducting phase through electron doping. Chemically, Co doping is a more effective way to introduce electrons, as carriers are doped directly into the FeAs planes. It also could provide information on how well the ThFeAsN tolerates in-plane disorder. Here we have substituted Co for Fe to synthesize ThFe1-xCoxAsN. It is found that the superconductivity of ThFeAsN parent compound is quickly suppressed upon Co doping. With a doping amount of $5\%\,x=0.05$ ), the superconductivity of ThFe1-xCoxAsN vanishes. ThCoAsN has been synthesized and characterized. It shows no superconductivity at 1.8 K. As both its crystal structure and transport behaviour are similar to those of itinerant ferromagnets LaCoAsO and LaCoPO, it is expected that ThCoAsN would be a kind of itinerant ferromagnet. However, until 1.8 K, the expected itinerant ferromagnetism could not be confirmed. The experimental data support that ThCoAsN is a kind of metallic paramagnet above 1.8 K