Changes in the Hydrological Characteristics of the Attabad Landslide-Dammed Lake on the Karakoram Highway

Understanding the evolving hydrological characteristics of landslide-induced barrier lakes is crucial for flood control, forecasting, early warning, and safety measures in reservoir areas. This study examines the changes in the hydrological characteristics of the Attabad landslide-dammed lake over the past decade after the occurrence of the landslide, focusing on lake area dynamics and sediment concentration. High-resolution satellite images from QuickBird, Pleiades, and WorldView2 over seven periods were analyzed. The findings indicate that the lake area has gradually decreased, with the center of mass shifting towards the lake dam, indicating a trend towards stability. The suspended sediment in the barrier lake is distributed in a strip running from north to south, then northeast to southwest, with the sediment concentration decreasing from the lake entrance to the dam and from the lake bank to the center. Over time, the average sediment concentration has decreased from 2010 to 2020, with higher concentrations in summer than in winter. Notably, during the 2017–2020 period, the lower-middle parts of the lake experienced a higher sediment concentration, while the dam area witnessed lower concentrations, thereby reducing the sediment impact on the dam. Furthermore, the sediment content in the middle of the dammed lake is relatively high, which may lead to the formation of a new dammed dam in the middle and the division of the original dammed lake into two smaller lakes, which will affect the stability of the dammed lake

Performance of common buckwheat (Fagopyrum esculentum M.) supplied with selenite or selenate for selenium biofortification in northeastern China

Selenium (Se) deficiency commonly occurs in soils of northeastern China and leads to insufficient Se intake by humans. A two-year field study of Se biofortification of common buckwheat supplied with 40 g Se ha−1 as selenite (Se(IV)), selenate (Se(VI)), or a combination (1/2 Se(IV + VI)) was performed to investigate Se accumulation and translocation in plants and determine the effects of different forms of Se on the grain yield, biomass production, and Se use efficiency of plants and seeds. Se application increased seed Se concentrations to 47.1–265.1 μg kg−1. Seed Se concentrations following Se(VI) or 1/2 Se(IV + VI) treatment exceeded 100 μg kg−1, an amount suitable for crop Se biofortification. Se concentration in shoots and roots decreased with plant development, and Se translocation from root to shoot in Se(IV)-treated plants was lower than that in plants treated with 1/2 Se(IV + VI) and Se(VI). Both grain yield and biomass production increased under 1/2 Se(IV + VI) treatment, with grain yields reaching 1663.8 and 1558.5 kg ha−1 in 2015 and 2016, respectively, reflecting increases of 11.0% and 10.3% over those without Se application. The Se use efficiency of seeds and plants under Se(VI) treatment was significantly higher than those under 1/2 Se(IV + VI) and Se(IV) treatments. Thus, application of selenate could result in higher Se accumulation in buckwheat seeds than application of the other Se sources, but the combined application of selenate and selenite might be an alternative approach for improving buckwheat grain yield by Se biofortification in northeastern China. Keywords: Common buckwheat, Se uptake, Se accumulation, Se translocation, Se biofortificatio

Entry properties and entry inhibitors of a human H7N9 influenza virus.

The recently identified human infections with a novel avian influenza H7N9 virus in China raise important questions regarding possible risk to humans. However, the entry properties and tropism of this H7N9 virus were poorly understood. Moreover, neuraminidase inhibitor resistant H7N9 isolates were recently observed in two patients and correlated with poor clinical outcomes. In this study, we aimed to elucidate the entry properties of H7N9 virus, design and evaluate inhibitors for H7N9 virus entry. We optimized and developed an H7N9-pseudotyped particle system (H7N9pp) that could be neutralized by anti-H7 antibodies and closely mimicked the entry process of the H7N9 virus. Avian, human and mouse-derived cultured cells showed high, moderate and low permissiveness to H7N9pp, respectively. Based on influenza virus membrane fusion mechanisms, a potent anti-H7N9 peptide (P155-185-chol) corresponding to the C-terminal ectodomain of the H7N9 hemagglutinin protein was successfully identified. P155-185-chol demonstrated H7N9pp-specific inhibition of infection with IC50 of 0.19 µM. Importantly, P155-185-chol showed significant suppression of A/Anhui/1/2013 H7N9 live virus propagation in MDCK cells and additive effects with NA inhibitors Oseltamivir and Zanamivir. These findings expand our knowledge of the entry properties of the novel H7N9 viruses, and they highlight the potential for developing a new class of inhibitors targeting viral entry for use in the next pandemic

H3K27me3 of Rnf19a promotes neuroinflammatory response during Japanese encephalitis virus infection

Abstract Histone methylation is an important epigenetic modification that affects various biological processes, including the inflammatory response. In this study, we found that infection with Japanese encephalitis virus (JEV) leads to an increase in H3K27me3 in BV2 microglial cell line, primary mouse microglia and mouse brain. Inhibition of H3K27me3 modification through EZH2 knockdown and treatment with EZH2 inhibitor significantly reduces the production of pro-inflammatory cytokines during JEV infection, which suggests that H3K27me3 modification plays a crucial role in the neuroinflammatory response caused by JEV infection. The chromatin immunoprecipitation-sequencing (ChIP-sequencing) assay revealed an increase in H3K27me3 modification of E3 ubiquitin ligases Rnf19a following JEV infection, which leads to downregulation of Rnf19a expression. Furthermore, the results showed that Rnf19a negatively regulates the neuroinflammatory response induced by JEV. This is achieved through the degradation of RIG-I by mediating its ubiquitination. In conclusion, our findings reveal a novel mechanism by which JEV triggers extensive neuroinflammation from an epigenetic perspective

Cell permissiveness to H7N9pp and N9-mediated H7N9pp superinfection exclusion.

<p><b>(A)</b> Different subtypes of HANApp with equal amounts of p24 antigen were incubated with various cells derived from different species and tissues, and the transduction efficiencies were measured and normalized to that of MDCK cells. <b>(B)</b> N9 expression specifically inhibits H7N9pp infection. 293T cells were transfected with various amounts of pCAGGS-N9 (0 µg, 0.0375 µg, 0.075 µg and 0.15 µg) and then infected with equal amounts of H7N9pp at 24 h post-transfection. Pseudovirus infection was determined by a luciferase activity assay and normalized to that of cells transfected with vector alone. VSVGpp was included as negative control. <b>(C)</b> N9-mediated H7N9pp inhibition can be partially blocked with NA inhibitor Zanamivir (ZA). N9-expressing 293T cells were treated with the indicated concentrations of ZA and then infected with H7N9pp. Pseudovirus infection was determined by a luciferase activity assay and normalized to that of cells transfected with vector alone. VSVGpp was included as a negative control.</p

Inhibition of H7N9 virus by peptides.

<p><b>(A)</b> Amino acid sequences of the indicated synthetic peptides. <b>(B)</b> Location of P155-185. Structure of HA. HA1, green; HA2, red; fusion peptide, yellow; P155-185, cyan. <b>(C)</b> Characterization of the antiviral activity of the synthetic peptides. Viral entry without peptide treatment was set at 100%. A scrambled peptide was included as a negative control. Cytotoxicity of the peptides to MDCK cells was measured by a MTT assay. <b>(D)</b> The inhibitory effect of P155-185-chol against H7N9 influenza virus in combination with neuraminidase inhibitors. P155-185-chol 2 µM; P155-185 2 µM; scrambled peptide 2 µM; ZA, 100 nM Zanamivir hydrate; OS, 200 nM Oseltamivir carboxylate. <b>(E)</b> The same experiments as panel D were performed. H7N9-infected MDCK cells were fixed at 36 h after the indicated treatments and processed for immunostaining and observed under confocal microscope. Fixed cell monolayers were immunostained with an anti-influenza A nucleoprotein (NP) murine monoclonal antibody (MAB8251; Millipore) and Alexa 594 conjugated secondary antibody (red). Nuclei were stained with DAPI (blue). <b>(F)</b> The same experiments as panel D were performed. The cytopathic effect of H7N9-infected MDCK cells in the presence or absence of the indicated treatments was visually inspected under an inverted microscope at 48 h post-infection.</p

Inhibition of H7N9 virus by chemicals.

<p><b>(A)</b> Inhibition of HA-mediated infection by dynasore. Dynasore's concentrations range from 0 to 80 µM in the absence (left) or presence (right) of 10% fetal bovine serum (FBS). MDCK cells were kept at 37°C in Opti-MEM I Reduced Serum Medium with or without 10% FBS at all times. Dynasore was added 1 h prior to HANApp infection. Pseudovirus infection was determined by a luciferase activity assay 48 h post-infection. Viral entry in the 0 µM treatment control group was set at 100%. <b>(B)</b> The inhibitory effect of bafilomycin A1. MDCK cells were pretreated with bafilomycin A1 (concentration range 0 nM to 10 nM) for 1 h at 37°C followed by infection with HANApp. Pseudovirus infection was determined by a luciferase activity assay at 48 h post-infection. Viral entry in the 0 nM treatment control group was set at 100%. <b>(C)</b> Antiviral effects of bafilomycin A1, dynasore and chloroquine. Viral entry in the DMSO treated control group was set at 100%. The cytotoxicity of the chemicals at indicated concentrations for MDCK cells was also measured by a MTT assay.</p