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HighlightsA vanadium oxide (TMPA-VOH) is synthesized with trimethylphenylammonium cations chemically pre-inserted into hydrated vanadium oxide. The pre-intercalation of weakly polarized organic cations strategically utilizes both ionic and molecular pre-intercalation effects.TMPA-VOH, with modified crystal structure and morphology, increased V4+ content, and weakened electrostatic interactions between Zn2+ and the V-O lattice, demonstrates enhanced voltage, storage capacity, structural stability, and reaction kinetics. Vanadium oxides, particularly hydrated forms like V2O5·nH2O (VOH), stand out as promising cathode candidates for aqueous zinc ion batteries due to their adjustable layered structure, unique electronic characteristics, and high theoretical capacities. However, challenges such as vanadium dissolution, sluggish Zn2+ diffusion kinetics, and low operating voltage still hinder their direct application. In this study, we present a novel vanadium oxide ([C6H6N(CH3)3]1.08V8O20·0.06H2O, TMPA-VOH), developed by pre-inserting trimethylphenylammonium (TMPA+) cations into VOH. The incorporation of weakly polarized organic cations capitalizes on both ionic pre-intercalation and molecular pre-intercalation effects, resulting in a phase and morphology transition, an expansion of the interlayer distance, extrusion of weakly bonded interlayer water, and a substantial increase in V4+ content. These modifications synergistically reduce the electrostatic interactions between Zn2+ and the V–O lattice, enhancing structural stability and reaction kinetics during cycling. As a result, TMPA-VOH achieves an elevated open circuit voltage and operation voltage, exhibits a large specific capacity (451 mAh g–1 at 0.1 A g–1) coupled with high energy efficiency (89%), the significantly-reduced battery polarization, and outstanding rate capability and cycling stability. The concept introduced in this study holds great promise for the development of high-performance oxide-based energy storage materials.

In the endoplasmic reticulum (ER), defective proteins are cleaned via the ER-associated protein degradation (ERAD) pathway. The HRD1 ubiquitin ligase complex, with HRD1, SEL1L, XTP3B or OS9 and Derlin family proteins as the core components, plays essential roles in the recognition, retrotranslocation, and ubiquitination of luminal ERAD substrates. However, the molecular basis is unclear. Here, we determine the cryo-EM structure of the human HRD1-SEL1L-XTP3B complex at 3.3 Å resolution. HRD1 is a dimer, but only one protomer carries the SEL1L-XTP3B complex, forming a 2:1:1 complex. Careful inspection of the EM map reveals a trimmed N-glycan sandwiched by XTP3B and SEL1L, and SEL1L may also contribute to the recognition of the trimmed glycan. The complex undergoes dramatic conformational changes when coexpressed with Derlin proteins. The HRD1 dimer is broken, and two HRD1-SEL1L-XTP3B (1:1:1) units are joined together by a four-helix bundle formed by two SEL1L molecules. The four-helix bundle also touches the micelle, resulting in a bent transmembrane region. These findings indicate that Derlins engagement may induce local curvature in the ER membrane. Cell-based functional assays are conducted to verify the structural observations. Our work provides a structural basis for further mechanistic elucidation of mammalian HRD1 complex-mediated ERAD. The mammalian HRD1 ubiquitin ligase mediates ERAD of misfolded proteins in the ER. Here, the authors determined cryo-EM structures of human HRD1-SEL1L-XTP3B complexes with and without Derlins, offering insights into glycan recognition and revealing dramatic Derlin-induced conformational changes.

Mucosal associated invariant T (MAIT) cells are evolutionarily-conserved, innate-like lymphocytes which are abundant in human lungs and can contribute to protection against pulmonary bacterial infection. MAIT cells are also activated during human viral infections, yet it remains unknown whether MAIT cells play a significant protective or even detrimental role during viral infections in vivo. Using murine experimental challenge with two strains of influenza A virus, we show that MAIT cells accumulate and are activated early in infection, with upregulation of CD25, CD69 and Granzyme B, peaking at 5 days post-infection. Activation is modulated via cytokines independently of MR1. MAIT cell-deficient MR1 −/− mice show enhanced weight loss and mortality to severe (H1N1) influenza. This is ameliorated by prior adoptive transfer of pulmonary MAIT cells in both immunocompetent and immunodeficient RAG2 −/− γC −/− mice. Thus, MAIT cells contribute to protection during respiratory viral infections, and constitute a potential target for therapeutic manipulation. MAIT cells are abundant in the lungs and confer protection against bacterial pathogens. Whilst activation of these cells has been described during viral infections, here van Wilgenburg and colleagues show that in a murine model MAIT cells contribute to the protective host immune response to influenza virus infection.

Due to the inconsistent findings from various studies, the role of gene polymorphisms in the renin-angiotensin system in influencing the development of cardiomyopathy remains unclear. In this study, we conducted a systematic review and meta-analysis to summarize the findings regarding the impact of angiotensin converting enzyme (ACE) I/D, angiotensinogen (AGT) M235T, and angiotensin II Type 1 receptor (AGTR1) A1166C gene polymorphisms in patients with cardiomyopathy. We performed a comprehensive search of several electronic databases, including PubMed, Embase, the Cochrane Library, and Web of Science, covering articles published from the time of database creation to April 17, 2023. Studies on the assessment of genetic polymorphisms in genes related to the renin-angiotensin system in relation to cardiomyopathy were included. The primary outcome was cardiomyopathy. Risk of bias was assessed using the Newcastle-Ottawa Scale scale. The meta-analysis includes 19 studies with 4,052 cases and 5,592 controls. The ACE I/D polymorphisms were found to be associated with cardiomyopathy (allelic model D vs I: OR = 1.29, 95CI% = 1.08–1.52; dominant model DD+ID vs II: OR = 1.43, 95CI% = 1.01–2.02; recessive model DD vs ID+II: OR = 0.79, 95CI% = 0.64–0.98). AGT M235T polymorphism and cardiomyopathy were not significantly correlated (allelic model T vs M: OR = 1.26, 95CI% = 0.96–1.66; dominant model TT+MT vs MM: OR = 1.30, 95CI% = 0.98–1.73; recessive model TT vs MT+MM: OR = 0.63, 95CI% = 0.37–1.07). AGTR1 polymorphism and cardiomyopathy were not significantly associated under allelic model A vs C (OR = 0.69, 95CI% = 0.46–1.03) and recessive model AA vs CA+CC (OR = 0.89, 95CI% = 0.34–2.30), but under the dominant model AA+CA vs CC (OR = 0.51, 95CI% = 0.38–0.68). The current meta-analysis reveals that polymorphisms in ACE I/D may be a genetic risk factor for cardiomyopathy. There is an association between AGTR1 gene polymorphisms and risk of cardiomyopathy under the specific model.

YAP and TAZ are important co-activators of various biological processes in human body. YAP/TAZ plays a vital role in the development of pulmonary fibrosis. Dysregulation of the YAP/TAZ signaling pathway is one of the most important causes of pulmonary fibrosis. Therefore, considering its crucial role, summary of the signal mechanism of YAP/TAZ is of certain guiding significance for the research of YAP/TAZ as a therapeutic target. The present review provided a detailed introduction to various YAP/TAZ-related signaling pathways and clarified the specific role of YAP/TAZ in these pathways. In the meantime, we summarized and evaluated possible applications of YAP/TAZ in the treatment of pulmonary fibrosis. Overall, our study is of guiding significance for future research on the functional mechanism of YAP/TAZ underlying lung diseases as well as for identification of novel therapeutic targets specific to pulmonary fibrosis.

The structural analysis of shelterbelts forms the foundation of their planning and management, yet the scientific and effective quantification of shelterbelt structures requires further investigation. This study developed an innovative heterogeneous analytical framework, integrating three key methodologies: the LeWoS algorithm for wood–leaf separation, TreeQSM for structural reconstruction, and 3D alpha-shape spatial quantification, using terrestrial laser scanning (TLS) technology. This framework was applied to three typical farmland shelterbelts in the Ulan Buh Desert oasis, enabling the first precise quantitative characterization of structural components during the leaf-on stage. The results showed the following to be true: (1) The combined three-algorithm method achieved ≥90.774% relative accuracy in extracting structural parameters for all measured traits except leaf surface area. (2) Branch length, diameter, surface area, and volume decreased progressively from first- to fourth-order branches, while branch angles increased with ascending branch order. (3) The trunk, branch, and leaf components exhibited distinct vertical stratification. Trunk volume and surface area decreased linearly with height, while branch and leaf volumes and surface areas followed an inverted U-shaped distribution. (4) Horizontally, both surface area density (Scd) and volume density (Vcd) in each cube unit exhibited pronounced edge effects. Specifically, the Scd and Vcd were greatest between 0.33 and 0.60 times the shelterbelt’s height (H, i.e., mid-canopy). In contrast, the optical porosity (Op) was at a minimum of 0.43 H to 0.67 H, while the volumetric porosity (Vp) was at a minimum at 0.25 H to 0.50 H. (5) The proposed volumetric stratified porosity (Vsp) metric provides a scientific basis for regional farmland shelterbelt management strategies. This three-dimensional structural analytical framework enables precision silviculture, with particular relevance to strengthening ecological barrier efficacy in arid regions.

The verified text data of wheat varieties is an important component of wheat germplasm information. To automatically obtain a structured description of the phenotypic and genetic characteristics of wheat varieties, the aim at solve the issues of fuzzy entity boundaries and overlapping relationships in unstructured wheat variety approval data, WGIE-DCWF (joint extraction model of wheat germplasm information entity relationship based on deep character and word fusion) was proposed. The encoding layer of the model deeply fused word semantic information and character information using the Transformer encoder of BERT. This allowed for the cascading fusion of contextual semantic feature information to achieve rich character vector representation and improve the recognition ability of entity features. The triple extraction layer of the model established a cascading pointer network, extracted the head entity, extracted the tail entity according to the relationship category, and decoded the output triplet. This approach improved the model’s capability to extract overlapping relationships. The experimental results demonstrated that the WGIE-DCWF model performed exceptionally well on both the WGD (wheat germplasm dataset) and the public dataset DuIE. The WGIE-DCWF model not only achieved high performance on the evaluation datasets but also demonstrated good generalization. This provided valuable technical support for the construction of a wheat germplasm information knowledge base and is of great significance for wheat breeding, genetic research, cultivation management, and agricultural production.

Persistent and durable immunological memory forms the basis of any successful vaccination protocol. Generation of pre-existing memory B cell and T cell pools is thus the key for maintaining protective immunity to seasonal, pandemic and avian influenza viruses. Long-lived antibody secreting cells (ASCs) are responsible for maintaining antibody levels in peripheral blood. Generated with CD4 T help after naïve B cell precursors encounter their cognate antigen, the linked processes of differentiation (including Ig class switching) and proliferation also give rise to memory B cells, which then can change rapidly to ASC status after subsequent influenza encounters. Given that influenza viruses evolve rapidly as a consequence of antibody-driven mutational change (antigenic drift), the current influenza vaccines need to be reformulated frequently and annual vaccination is recommended. Without that process of regular renewal, they provide little protection against \"drifted\" (particularly H3N2) variants and are mainly ineffective when a novel pandemic (2009 A/H1N1 \"swine\" flu) strain suddenly emerges. Such limitation of antibody-mediated protection might be circumvented, at least in part, by adding a novel vaccine component that promotes cross-reactive CD8 T cells specific for conserved viral peptides, presented by widely distributed HLA types. Such \"memory\" cytotoxic T lymphocytes (CTLs) can rapidly be recalled to CTL effector status. Here, we review how B cells and follicular T cells are elicited following influenza vaccination and how they survive into a long-term memory. We describe how CD8 CTL memory is established following influenza virus infection, and how a robust CTL recall response can lead to more rapid virus elimination by destroying virus-infected cells, and recovery. Exploiting long-term, cross-reactive CTL against the continuously evolving and unpredictable influenza viruses provides a possible mechanism for preventing a disastrous pandemic comparable to the 1918-1919 H1N1 \"Spanish flu,\" which killed more than 50 million people worldwide.

Background Tobacco use is recognized as a major cause of cardiovascular disease, which is associated with endothelial dysfunction. Endothelial function is evaluated using flow-mediated dilation (FMD), which is a noninvasive method. This meta-analysis aimed to investigate the association between smoking exposure and endothelial function evaluated using FMD values. Methods We searched the PubMed, Embase, Web of Science, and Cochrane Library databases for cohort studies of smokers or passive smokers that used FMD to assess endothelial function. The primary outcome of the study was the change in the rate of FMD. The risk of bias was evaluated using the Cochrane Collaboration tool and Newcastle–Ottawa Scale. Further, the weighted mean difference was used to analyze the continuous data. Results Overall, 14 of 1426 articles were included in this study. The results of these articles indicated that smoking is a major cause of endothelial dysfunction and altered FMD; a pooled effect size of − 3.15 was obtained with a 95% confidence interval of (− 3.84, − 2.46). Notably, pregnancy status, Asian ethnicity, or health status did not affect heterogeneity. Conclusions We found that smoking has a significant negative impact on FMD, and measures such as medication or education for smoking cessation may improve endothelial function and reduce the risk of cardiovascular disease. Trial Registration The meta-analysis was registered with PROSPERO on April 5th, 2023 (CRD42023414654).