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The development of electrocatalysts capable of efficiently catalyzing the alkaline hydrogen evolution reaction (HER) is crucial for driving the advancement of sustainable energy. Herein, by altering the surface state of the support, we transformed the bulk W 5 N 4 into a porous structure and constructed a Ru/W 5 N 4 heterostructure. The transfer of electrons from Ru to W 5 N 4 can optimize the electronic structure of the catalyst, thereby effectively promoting electron transfer, accelerating reaction kinetics, and enhancing the activity of the catalyst. Furthermore, W 5 N 4 can serve as a protective shell to stabilize Ru0, which is regarded as the active center in HER. The resulting Ru/W 5 N 4 exhibits excellent HER activity, requiring only overpotentials of 43 and 156 mV to achieve current densities of −10 and −100 mA cm−2, respectively. This work provides valuable insights into the rational construction of heterostructures to optimize HER performance. • The Ru/W 5 N 4 /NF catalysts were synthesized by a conventional two-step method. • Electronic interaction between W 5 N 4 and Ru can enhance the catalytic activity. • Interface engineering is an effective method to regulate the interfacial charge. • The W 5 N 4 greatly enhances the hydrogen evolution efficiency of Ru in alkaline medium. [ABSTRACT FROM AUTHOR]

Biot's hydro-mechanical coupled consolidation theory has been widely used in Geotechnical Engineering for nearly 100 years. However, the Chemically Disturbed Zone (CDZ) generated in many geotechnical engineering applications (e.g. nuclear waste disposal, carbon capture and storage etc.) are not considered by Biot's theory, especially where there are highly swelling rocks (e.g. shale) and dissolving minerals. This paper presents a rigorous fundamental extension of Biots consolidation theory, with comprehensively considering the influence of molecular processes of coupled swelling and mineral dissolution, based on the newly developed Mixture Coupling Theory. A simple numerical example has been used for the demonstration purpose of the new constitutive equations, and the result shows that molecular influence can have a significant impact on the mechanical performance of the rocks. [ABSTRACT FROM AUTHOR]

Objective: To assess the reproducibility of 3.0T high-resolution magnetic resonance imaging for the identification and quantification of atherosclerotic plaques in the middle cerebral artery.Methods: Sixty-nine consecutive patients with ischemic stroke or asymptomatic stenosis (>30%) of the middle cerebral artery underwent 3.0T high-resolution magnetic resonance imaging examinations. Two independent investigators reviewed all images with 1 investigator re-evaluating all images 4 weeks later. Wall characteristics of the middle cerebral artery, including plaque surface morphology, plaque location, plaque components, and burden were identified and measured.Results: Intraobserver and interobserver agreement were all substantial in identifying plaque surface irregularity (k = 0.741, 0.555-0.897; k = 0.685, 0.490-0.843; respectively) and intraplaque hemorrhage (k = 0.654, 0.446-0.838; k = 0.605, 0.369-0.792; respectively). Intraobserver agreement was substantial (k = 0.654) and interobserver agreement was moderate (k = 0.553) for the identification of plaque fibrous caps. The total intraobserver and interobserver reproducibility was almost excellent for the identification of plaque position. With regards to vessel area measurement at the site of maximal lumen narrowing, intraobserver and interobserver reproducibility was excellent (intraclass correlation coefficient was 0.886 and 0.885, respectively) and moderate for lumen area at the site of maximal lumen narrowing (intraclass correlation coefficient was 0.695 and 0.558, respectively). In addition, intraobserver and interobserver reproducibility was excellent for vessel area and lumen area measurements at the reference sites.Conclusions: The reproducibility of 3.0T high-resolution magnetic resonance imaging for the identification and quantification of artery wall characteristics was overall acceptable. However, the reliability for lumen area measurement at the maximum narrowing site and identification of the fibrous cap needs to be improved. [ABSTRACT FROM AUTHOR]

Previous studies have reported that puerarin possesses cardioprotective, vasodilatory, anti-inflammatory, anti-apoptotic, and hypoglycemic properties. However, the impact of puerarin on sepsis-associated encephalopathy (SAE) remains unexplored. In this study, we explored whether puerarin can modulate microglia-mediated neuroinflammation for the treatment of SAE and delved into the underlying mechanisms. We established a murine model of SAE through intraperitoneal injection of lipopolysaccharide (LPS). The puerarin treatment group received pretreatment with puerarin. For in vitro experiments, BV2 cells were pre-incubated with puerarin for 2 h before LPS exposure. We employed network pharmacology, the Morris Water Maze (MWM) test, Novel Object Recognition (NOR) test, immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA), Western blotting, and quantitative real-time PCR (qRT-PCR) to elucidate the molecular mechanism of underlying puerarin's effects in SAE treatment. Our findings demonstrate that puerarin significantly reduced the production of inflammatory cytokines (TNF-α and IL-6) in the peripheral blood of LPS-treated mice. Moreover, puerarin treatment markedly ameliorated sepsis-associated cognitive impairment. Puerarin also exhibited inhibitory effects on the release of TNF-α and IL-6 from microglia, thereby preventing hippocampal neuronal cell death. Network pharmacology analysis identified AKT1 as a potential therapeutic target for puerarin in SAE treatment. Subsequently, we validated these results in both in vitro and in vitro experiments. Our study conclusively demonstrated that puerarin reduced LPS-induced phosphorylation of AKT1, with the AKT activator SC79 reversing puerarin's anti-inflammatory effects through the activation of the AKT1 signaling pathway. Puerarin exerts an anti-neuroinflammatory effect against SAE by modulating the AKT1 pathway in microglia. [ABSTRACT FROM AUTHOR]

Objective: The diagnosis of shock in patients presenting to the emergency department (ED) is often challenging. We aimed to compare the accuracy of experienced emergency physician gestalt against Li's pragmatic shock (LiPS) tool for predicting the likelihood of shock in the emergency department, using 30-day mortality as an objective standard.Method: In a prospective observational study conducted in an urban, academic ED in Hong Kong, adult patients aged 18years or older admitted to the resuscitation room or high dependency unit were recruited. Eligible patients had a standard ED workup for shock. The emergency physician treating the patient was asked whether he or she considered shock to be probable, and this was compared with LiPS. The proxy 'gold' or reference standard was 30-day mortality. The area under the receiver operating curve (AUROC) was used to predict prognosis. The primary outcome measure was 30-day mortality.Results: A total of 220 patients fulfilled the inclusion criteria and were included in the analysis. The AUROC for LiPS (0.722; sensitivity=0.733, specificity=0.711, P<0.0001) was greater than emergency physician gestalt (0.620, sensitivity=0.467, specificity=0.774, P=0.0137) for diagnosing shock using 30-day mortality as a proxy (difference P=0.0229). LiPS shock patients were 6.750 times (95%CI=2.834-16.076, P<0.0001) more likely to die within 30-days compared with non-shock patients. Patients diagnosed by emergency physicians were 2.991 times (95%CI=1.353-6.615, P=0.007) more likely to die compared with the same reference.Conclusions: LiPS has a higher diagnostic accuracy than emergency physician gestalt for shock when compared against an outcome of 30-day mortality. [ABSTRACT FROM AUTHOR]

Two novel strains GSK1Z-4-2T and MQZ15Z-1 were isolated from branches of mangrove plants collected from Guangxi Zhuang Autonomous Region, China. Both strains were Gram-negative, aerobic, non-flagellated and non-spore-forming bacteria. The comparison of 16S rRNA gene sequences initially indicated that the two strains were assigned to the genus Ancylobacter with sharing the highest similarity to Ancylobacter pratisalsi DSM 102029T (97.3%). The 16S rRNA gene sequence similarity, average nucleotide identity (ANI) and in silico DNA-DNA hybridization (is DDH) values between strains GSK1Z-4-2T and MQZ15Z-1 were 99.9%, 97.4% and 77.4%, respectively, which revealed that the two strains belonged to the same species. Phylogenetic analyses based on 16S rRNA gene sequences and the core proteome showed that the two strains formed a well-supported cluster with A. pratisalsi DSM 102029T. Moreover, the ANI and is DDH values between strain GSK1Z-4-2T and A. pratisalsi DSM 102029T were 83.0% and 25.8%, respectively, demonstrating that strain GSK1Z-4-2T was a previously undescribed species. Meanwhile, strains GSK1Z-4-2T and MQZ15Z-1 exhibited most of chemotaxonomic and phenotypic features consistent with the description of the genus Ancylobacter. Based on the polyphasic data, strains GSK1Z-4-2T and MQZ15Z-1 should represent a novel species of the genus Ancylobacter , for which the name Ancylobacter mangrovi sp. nov. is proposed. The type strain is GSK1Z-4-2T (=MCCC 1K07181T = JCM 34924T). [ABSTRACT FROM AUTHOR]

Accumulation of glutamate damages neurons via the reactive oxygen species (ROS) injury, which was involved in the development of neurodegenerative diseases. However, the mechanism of neuronal oxidative stress damage caused by glutamate and the intervention targets still needs to be further studied. This study explored whether 5′ adenosine monophosphate-activated protein kinase (AMPK)-induced glucose metabolic and mitochondrial dysfunction were related to glutamate-dependent ROS injury of the neuron. Neuronal oxidative stress injury was induced by glutamate treatment in HT-22 cells. Western blotting was used to evaluate the phosphorylation of the AMPK. The XF24 Flux Analyzer was used to measure the effect of glutamate and Compound C (a well-known pharmacological inhibitor of AMPK phosphorylation) on the cellular oxygen consumption rate (OCR) of HT-22 cells. Glucose uptake, intracellular ROS, mitochondrial potential, apoptosis and cell viability were quantified using biochemical assays. Glutamate caused the phosphorylation of AMPK and subsequently promoted the glucose uptake. Furthermore, AMPK-mediated glucose uptake enhanced OCR and increased the intracellular ROS levels in neurons. The pharmacological inhibition of AMPK phosphorylation by Compound C attenuated glutamate-induced toxicity in HT22 cells by regulating the glucose uptake/mitochondrial respiration/ROS pathway. The AMPK phosphorylation/glucose uptake/mitochondrial respiration/ROS pathway was involved in glutamate-induced excitotoxic injury in HT22 cells. The inhibition of AMPK phosphorylation may be a potential target for the development of therapeutic agents for treating the glutamate-induced neurotoxicity. [Display omitted] • Glutamate caused the phosphorylation of AMPK and subsequently promoted the glucose uptake in HT22 cells. • AMPK-mediated glucose uptake enhanced oxygen consumption rates and increased the intracellular ROS levels in HT22 cells. • Compound C attenuated glutamate-induced toxicity in HT22 cells via the glucose uptake/mitochondrial respiration/ROS pathway. [ABSTRACT FROM AUTHOR]

Interactions between the solidification front and the remaining suspended particles take place during solidification of particles reinforced composites. The particles are either engulfed by the solidification front or pushed by the solid–liquid interface. In this study, the relation of distribution and clustering degree of nano-Al 2 O 3 in Al7075 with the microstructure of alloy was investigated by conducting casting experiment. A hydrodynamic model for calculating the critical interface velocity required to push nano-particles by the interface was proposed. In addition, the influence of the nano-particles present ahead of solidification front on interface shape was discussed. Microstructural studies showed that the resulting microstructures of composites depended on the size and degree of nano-Al 2 O 3 clustering. Based on the model, it was found that for particles below approximately 36% of the critical radius, r < 0.36 r ⁎ = 0.9973 μm, the critical interface velocities were four orders of magnitude lower than those obtained by micron particles, suggesting that smaller particles are easily engulfed by the interface rather than pushed. The experimental results were validated by the prediction of the model. Result showed that the constitutional super-cooling of local melts and the accumulation of solute behind the particle caused formation of a cellular interface. [ABSTRACT FROM AUTHOR]

Complement activation is thought to underline the pathologic progression of obesity-related metabolic disorders; however, its role in adaptive thermogenesis has scarcely been explored. Here, we identify complement C3a receptor (C3aR) and C5a receptor (C5aR) as critical switches to control adipocyte browning and energy balance in male mice. Loss of C3aR and C5aR in combination, more than individually, increases cold-induced adipocyte browning and attenuates diet-induced obesity in male mice. Mechanistically, loss of C3aR and C5aR increases regulatory T cell (Treg) accumulation in the subcutaneous white adipose tissue during cold exposure or high-fat diet. Activated Tregs produce adenosine, which is converted to inosine by adipocyte-derived adenosine deaminases. Inosine promotes adipocyte browning in a manner dependent on activating adenosine A2a receptor. These data reveal a regulatory mechanism of complement in controlling adaptive thermogenesis and suggest that targeting the C3aR/C5aR pathways may represent a therapeutic strategy in treating obesity-related metabolic diseases. [Display omitted] • C3aR/C5aR DKO increases cold-induced adipose browning, improves diet-induced obesity • C3aR/C5aR DKO increases Treg accumulation in sWAT during cold exposure • C3aR/C5aR DKO Tregs increase adenosine in cold, adenosine converts to inosine in sWAT • C3aR/C5aR DKO promotes adipose browning via activating inosine/A2aR pathway Kong et al. provide a regulatory mechanism underlying the C3aR/C5aR pathway in cold-induced adipocyte browning and diet-induced obesity. C3aR/C5aR deficiency-mediated Treg accumulation promotes adenosine production. Activated Tregs produce adenosine, which is converted to inosine by ADA, and then the inosine promotes adipocyte browning via A2aR. [ABSTRACT FROM AUTHOR]