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The vascular endothelium is a layer of cells lining the inner surface of vessels, serving as a barrier that mediates microenvironment homeostasis. Deterioration of either the structure or function of endothelial cells (ECs) results in a variety of cardiovascular diseases. Previous studies have shown that reactive oxygen species (ROS) is a key factor that contributes to the impairment of ECs and the subsequent endothelial dysfunction. The longevity regulator Sirt1 is a NAD+-dependent deacetylase that has a potential antioxidative stress activity in vascular ECs. The mechanisms underlying the protective effects involve Sirt1/FOXOs, Sirt1/NF-κB, Sirt1/NOX, Sirt1/SOD, and Sirt1/eNOs pathways. In this review, we summarize the most recent reports in this field to recapitulate the potent mechanisms involving the protective role of Sirt1 in oxidative stress and to highlight the beneficial effects of Sirt1 on cardiovascular functions.

With strong reducibility and high redox potential, the hydride ion (H − ) is a reactive hydrogen species and an energy carrier. Materials that conduct pure H − at ambient conditions will be enablers of advanced clean energy storage and electrochemical conversion technologies 1 , 2 . However, rare earth trihydrides, known for fast H migration, also exhibit detrimental electronic conductivity 3 – 5 . Here we show that by creating nanosized grains and defects in the lattice, the electronic conductivity of LaH x can be suppressed by more than five orders of magnitude. This transforms LaH x to a superionic conductor at −40 °C with a record high H − conductivity of 1.0 × 10 −2  S cm −1 and a low diffusion barrier of 0.12 eV. A room-temperature all-solid-state hydride cell is demonstrated. By creating nanosized grains and defects in lanthanum trihydride, its electronic conductivity can be suppressed, transforming it into a superionic conductor at −40 °C with a record high H − conductivity.

Thermochemical treatment is a promising technique for biomass disposal and valorization. Recently, machine learning (ML) has been extensively used to predict yields, compositions, and properties of biochar, bio-oil, syngas, and aqueous phases produced by the thermochemical treatment of biomass. ML demonstrates great potential to aid the development of thermochemical processes. The present review aims to 1) introduce the ML schemes and strategies as well as descriptors of the input and output features in thermochemical processes; 2) summarize and compare the up-to-date research in both ML-aided wet (hydrothermal carbonization/liquefaction/gasification) and dry (torrefaction/pyrolysis/gasification) thermochemical treatment of biomass (i.e., predicting the yields, compositions, and properties of oil/char/gas/aqueous phases as well as thermal conversion behavior or kinetics); and 3) identify the gaps and provide guidance for future studies concerning how to improve predictive performance, increase generalizability, aid mechanistic and application studies, and effectively share data and models in the community. The development of biomass thermochemical treatment processes is envisaged to be greatly accelerated by ML in the near future.

Ammonia is a promising carbon-free energy carrier, but is currently synthesized industrially under harsh conditions. Synthesizing ammonia using lower temperatures and pressures could therefore improve its prospects as a chemical means to store and transport energy. Here we report that alkali and alkaline earth metal imides function as nitrogen carriers that mediate ammonia production via a two-step chemical looping process operating under mild conditions. Nitrogen is first fixed through the reduction of N 2 by alkali or alkaline earth metal hydrides to form imides and, subsequently, the imides are hydrogenated to produce NH 3 and regenerate the metal hydrides. The oxidation state of hydrogen therefore switches between −1 (hydride), 0 (H 2 ) and +1 (imide and NH 3 ). Late 3d metals accelerate the reaction rates of both steps. The chemical loop mediated by BaNH and catalysed by Ni produces NH 3 at 100 °C and atmospheric pressure. Reducing the severity of the conditions required to synthesize ammonia would increase the viability of its use as a carbon-free energy carrier. Here the authors use metal imides to mediate ammonia production via a two-step chemical looping process that operates under mild conditions.

Background Sulfate-reducing bacteria (SRB) is a potential pathogen usually detected in patients with gastrointestinal diseases. Hydrogen sulfide (H2S), a metabolic byproduct of SRB, was considered the main causative agent that disrupted the morphology and function of gut epithelial cells. Associated study also showed that flagellin from Desulfovibrio vulgaris (DVF), the representative bacterium of the Desulfovibrio genus, could exacerbate colitis due to the interaction of DVF and LRRC19, leading to the secretion of pro-inflammatory cytokines. However, we still have limited understanding about the change of gut microbiota (GM) composition caused by overgrowth of SRB and its exacerbating effects on colitis. Results In this study, we transplanted D. vulgaris into the mice treated with or without DSS, and set a one-week recovery period to investigate the impact of D. vulgaris on the mice model. The outcomes showed that transplanted D. vulgaris into the normal mice could cause the gut inflammation, disrupt gut barrier and reduce the level of short-chain fatty acids (SCFAs). Moreover, D. vulgaris also significantly augmented DSS-induced colitis by exacerbating the damage of gut barrier and the secretion of inflammatory cytokines, for instance, IL-1β, iNOS, and TNF-α. Furthermore, results also showed that D. vulgaris could markedly change GM composition, especially decrease the relative abundance of SCFAs-producing bacteria. Additionally, D. vulgaris significantly stimulated the growth of Akkermansia muciniphila probably via its metabolic byproduct, H2S, in vivo. Conclusions Collectively, this study indicated that transplantation of D. vulgaris could cause gut inflammation and aggravate the colitis induced by DSS.

Screening and follow-up of interstitial lung disease associated with rheumatoid arthritis (RA-ILD) is a challenge in clinical practice. In fact, the majority of RA-ILD patients are asymptomatic and optimal tools for early screening and regular follow-up are lacking. Furthermore, some patients may remain oligosymptomatic despite significant radiological abnormalities. In RA-ILD, usual interstitial pneumonia (UIP) is the most frequent radiological and pathological pattern, associated with a poor prognosis and a high risk to develop acute exacerbations and infections. If RA-ILD can be identified early, there may be an opportunity for an early treatment and close follow-up that might delay ILD progression and improve the long-term outcome. In connective tissue disease–associated interstitial lung disease (CTD-ILD), lung ultrasound (LUS) with the assessment of B-lines and serum Krebs von den Lungen-6 antigen (KL-6) has been recognized as sensitive biomarkers for the early detection of ILD. B-line number and serum KL-6 level were found to correlate with high-resolution computed tomography (HRCT), pulmonary function tests (PFTs), and other clinical parameters in systemic sclerosis–associated ILD (SSc-ILD). Recently, the significant correlation between B-lines and KL-6, two non-ionizing and non-invasive biomarkers, was demonstrated. Hence, the combined use of LUS and KL-6 to screen and follow up ILD in RA patients might be useful in clinical practice in addition to existing tools. Herein, we review relevant literature to support this concept, propose a preliminary screening algorithm, and present 2 cases where the algorithm was used.

In a previous study, we demonstrated the role of polydatin (PD) in protecting against multiple organ dysfunction in sepsis. The aim of this study is to investigate whether PD protects against lipopolysaccharide (LPS)-induced endothelial barrier disruption through SIRT3 activation and to disclose the underlying mechanisms. Wild-type mice were injected with LPS and Evans Blue assay was performed to evaluate vascular permeability. Primary human umbilical vein endothelial cells (HUVECs) were stimulated with LPS. Endothelial permeability was evaluated by transendothelial electrical resistance (TER) and FITC-dextran leakage. SIRT3 activity was determined by a Deacetylase Fluorometric kit, and protein expression level of SIRT3 was detected by western blotting. Mitochondrial function was evaluated by determination of ROS level, mitochondrial membrane potential and mPTP opening. In endotoxemic mice, PD pretreatment attenuated vascular leakage in multiple organs while SIRT3 inhibition with 3-TYP reversed the effects of PD. PD treatment in late sepsis also exhibited barrier protective effects. In HUVECs, PD alleviated LPS-induced F-actin rearrangement, cadherin–catenin complex dissociation and endothelial hyperpermeability, whereas 3-TYP or SIRT3 siRNA attenuated the protective effects of PD. PD enhanced SIRT3 deacetylase activity, and attenuated LPS-induced decrease in SIRT3 expression as well. Furthermore, gain-of-function and loss-of-function strategies also confirmed the role of SIRT3 in enhancing endothelial barrier integrity. It was further ascertained that PD enhanced SIRT3-mediated deacetylation of SOD2 and cyclophilin D (CypD), thus suppressing mitochondrial dysfunction and subsequent endothelial barrier dysfunction. In addition, it was revealed that RAGE was involved in LPS-regulated SIRT3 signaling. Our results suggest that polydatin protects against LPS-induced endothelial barrier disruption dependent on SIRT3 and can be applied as a potential therapy for sepsis.

Systemic autoimmune rheumatic diseases (SARDs) related pulmonary disease is highly prevalent, with variable clinical presentation and behavior, and thus is associated with poor outcomes and negatively impacts quality of life. Chest high resolution computed tomography (HRCT) is still considered a fundamental imaging tool in the screening, diagnosis, and follow-up of pulmonary disease in patients with SARDs. However, radiation exposure, economic burden, as well as lack of point-of-care CT equipment limits its application in some clinical situation. Ultrasound has found a place in numerous aspects of the rheumatic diseases, including the vasculature, skin, muscle, joints, kidneys and in screening for malignancies. Likewise it has found increasing use in the lungs. In the past two decades, lung ultrasound has started to be used for pulmonary parenchymal diseases such as pneumonia, pulmonary edema, lung fibrosis, pneumothorax, and pleural lesions, although the lung parenchymal was once considered off-limits to ultrasound. Lung ultrasound B-lines and irregularities of the pleural line are now regarded two important sonographic artefacts related to diffuse parenchymal lung disease and they could reflect the lesion extent and severity. However, its role in the management of SARDs related pulmonary involvement has not been fully investigated. This review article will focus on the potential applications of lung ultrasound in different pulmonary scenarios related with SARDs, such as interstitial lung disease, diffuse alveolar hemorrhage, diaphragmatic involvement, and pulmonary infection, in order to explore its value in clinical daily practice.

Antisynthetase syndrome-associated interstitial lung disease (ASS-ILD) exhibits clinical heterogeneity and progression, with unclear immunopathogenic mechanisms. This study aimed to define the cell type-specific interferon immune signatures and transcriptional networks underlying ASS-ILD. Single-cell RNA sequencing (scRNA-seq) was performed on peripheral blood mononuclear cells (PBMCs) from three treatment-naive ASS-ILD patients and three healthy controls (67,421 cells). A comprehensive analysis was conducted in conjunction with an external cohort, encompassing 126,026 cells. The analytical pipelines included the following: AUCell for interferon-stimulated gene (ISG) activity scoring, Seurat for clustering, Monocle for trajectory inference, and CellChat for cell-cell communication. The inference of transcription factor activity was facilitated using decoupleR software. Monocyte-specific ISG activity was identified and validated in an integrated cohort of 126,026 cells. Among the six monocyte subsets, mono2 exhibited elevated expressions and a preferential inflammatory trajectory, marked by upregulated innate and adaptive immune pathways. Cell-cell interaction modeling revealed dysregulated type II interferon (IFN-II) and tumor necrosis factor (TNF) signaling, with mono2, NK, and CD8 T cells as key signal transmitters. Regulatory network analysis revealed that the transcription factors , , , , , and drive inflammatory and profibrotic signatures via the IL-17, JAK-STAT, and TGF-β pathways. This study identifies monocytes as central orchestrators of immune dysregulation in ASS-ILD, highlighting IFN/TNF signaling and associated transcriptional regulators as therapeutic targets.

To date, the nitrogen metabolism pathways and salt-tolerance mechanisms of halophilic denitrifying bacteria have not been fully studied, and full-scale engineering trials with saline fly ash-washing wastewater have not been reported. In this study, we isolated and screened a halophilic denitrifying bacterium (Marinobacter sp.), GH-1, analyzed its nitrogen metabolism pathways and salt-tolerance mechanisms using whole-genome data, and explored its nitrogen removal characteristics under both aerobic and anaerobic conditions at different salinity levels. GH-1 was then applied in a full-scale engineering project to treat saline fly ash-washing leachate. The main results were as follows: (1) Based on the integration of whole-genome data, it is preliminarily hypothesized that the strain possesses complete nitrogen metabolism pathways, including denitrification, a dissimilatory nitrate reduction to ammonium (DNRA), and ammonium assimilation, as well as the following three synergistic strategies through which to counter hyperosmotic stress: inorganic ion homeostasis, organic osmolyte accumulation, and structural adaptations. (2) The strain demonstrated effective nitrogen removal under aerobic, anaerobic, and saline conditions (3–9%). (3) When applied in a full-scale engineering system treating saline fly ash-washing wastewater, it improved nitrate nitrogen (NO3−-N), total nitrogen (TN), and chemical oxygen demand (COD) removal efficiencies by 31.92%, 25.19%, and 31.8%, respectively. The proportion of Marinobacter sp. increased from 0.73% to 3.41% (aerobic stage) and 2.86% (anoxic stage). Overall, halophilic denitrifying bacterium GH-1 can significantly enhance the nitrogen removal efficiency of saline wastewater systems, providing crucial guidance for biological nitrogen removal treatment.