Decoupled tin-silver batteries with long cycle life and power output stability based on dendrite-free tin anode and halide insertion cathode chemistry.

Conventional Ag-Zn batteries have historically faced the challenge of poor cycling stability, rooting in issues associated with Ag cathode dissolution and Zn anode dendrites. Herein, we present a pioneering decoupled Sn-Ag cell, which features two chambers separated by a cation-exchange membrane, containing a dendrite-free Sn metal anode immersed in an alkaline anolyte, and an Ag nanowires/carbon nanotube 3D thick-network cathode in a neutral catholyte. Benefiting from the achieved high electroplating/stripping stability of the metallic Sn anode in the alkaline electrolyte and the electrochemical reversibility of the Ag/AgCl cathode redox couple in the neutral electrolyte, the assembled decoupled Sn-Ag cell demonstrates superior cycling stability, retaining 82.4% of its initial capacity even after 4000 cycles (2 mA cm-2), significantly outperforming both the contrastive decoupled Ag-Zn cell (1500 cycles) and conventional alkaline Ag-Zn batteries (<100 cycles). Furthermore, through the integration of the decoupled Sn-Ag battery with solar cells and power management circuits, an intelligent power system of photovoltaic charging and energy storage was designed, demonstrating its practical viability through maintenance-free charging-discharging during day-night cycles. This research not only significantly increases the lifespan of Ag-batteries with an ultra-flat voltage platform but also opens avenues for the decoupled design of a wide variety of aqueous battery systems.

Hederagenol improves multiple sclerosis by modulating Th17 cell differentiation.

Multiple sclerosis (MS) is a common autoimmune illness that is difficult to treat. The upregulation of Th17 cells is critical in the pathological process of MS. Hederagenol (Hed) has been shown to lower IL-17 levels, although its role in MS pathophysiology is uncertain. In this study, we explore whether Hed could ameliorate MS by modulating Th17 cell differentiation, with the goal of identifying new treatment targets for MS. The experimental autoimmune encephalomyelitis (EAE) mouse model was conducted and Hed was intraperitoneally injected into mice. The weight was recorded and the clinical symptom grade was assessed. Hematoxylin-eosin staining was carried out to determine the extent of inflammation in the spinal cord and liver. The luxol Fast Blue staining was performed to detect the pathological changes in the myelin sheath. Nerve damage was detected using NeuN immunofluorescence staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. Immunohistology approaches were used to study alterations in immune cells in the spinal cord. The proportions of T cell subsets in the spleens were analyzed by flow cytometry. RORγt levels were measured using quantitative real-time PCR or Western blot. The activity of the RORγt promoter was analyzed by Chromatin immunoprecipitation. Hed administration reduced the clinical symptom grade of EAE mice, as well as the inflammatory infiltration, demyelination, and cell disorder of the spinal cord, while having no discernible effect on the mouse weight. In addition, Hed treatment significantly reduced the number of T cells, particularly Th17 cells in the spinal cord and spleen-isolated CD4+ T cells. Hed lowered the RORγt levels in spleens and CD4+ T cells and overexpression of RORγt reversed the inhibitory effect of Hed on Th17 differentiation. Hed decreased nerve injury by modulating Th17 differentiation through the RORγt promoter. Hed regulates Th17 differentiation by reducing RORγt promoter activity, which reduces nerve injury and alleviates EAE.

Automatic breast ultrasound (ABUS) tumor segmentation based on global and local feature fusion.

Accurate segmentation of tumor regions in automated breast ultrasound (ABUS) images is of paramount importance in computer-aided diagnosis system. However, the inherent diversity of tumors and the imaging interference pose great challenges to ABUS tumor segmentation. In this paper, we propose a global and local feature interaction model combined with graph fusion (GLGM), for 3D ABUS tumor segmentation. In GLGM, we construct a dual branch encoder-decoder, where both local and global features can be extracted. Besides, a global and local feature fusion module is designed, which employs the deepest semantic interaction to facilitate information exchange between local and global features. Additionally, to improve the segmentation performance for small tumors, a graph convolution-based shallow feature fusion module is designed. It exploits the shallow feature to enhance the feature expression of small tumors in both local and global domains. The proposed method is evaluated on a private ABUS dataset and a public ABUS dataset. For the private ABUS dataset, the small tumors (volume smaller than 1 cm3) account for over 50% of the entire dataset. Experimental results show that the proposed GLGM model outperforms several state-of-the-art segmentation models in 3D ABUS tumor segmentation, particularly in segmenting small tumors.

[Extraction of Extracelluar Vesicles Derived from Mycobacterium tuberculosis and Their Effect on the Production of Reactive Oxygen Species and Expression of Inflammatory Factors in Mouse Bone Marrow-Derived Dendritic Cells].

Objective: To isolate extracellular vesicles (EVs) from Mycobacterium tuberculosis ( Mtb), to examine their morphology, particle size, and distribution, to study the effect of EVs derived from Mtb ( Mtb-EVs) on intracellular reactive oxygen species (ROS) production and cytokine secretion in dendritic cells (DCs), and to make preliminary exploration of Mtb-EVs' effect on the immune regulation of DCs. Methods: Mtb-EVs were obtained by ultrafiltration concentration and the protein concentration was determined by BCA assay. The morphology of Mtb-EVs was observed through negative staining electron microscopy (EM). The particle size distribution and concentration of Mtb-EVs were determined by nanoparticle tracking analysis (NTA). Mouse bone marrow was isolated through sterile procedures and mice myeloid DCs were induced and amplified by the combined use of recombinant mouse granulocyte-macrophage colony-stimulating factor (rm GM-CSF) and recombinant mouse interleukin-4 (rm IL-4). Then, morphological and immunophenotypic characterization was performed. After that, the DCs were treated with Mtb-EVs at different concentrations and CCK-8 assay was done to measure their effect on the survival rate of DCs and to identify the appropriate stimulation concentration for subsequent experimental procedures. The intracellular ROS levels of DCs were evaluated with DCFH-DA fluorescence probe and the cytokine secretion of DCs was determined by ELISA. Results: EM observation showed that Mtb-EVs isolated by ultrafiltration concentration were spherical vesicles of varied sizes, all being approximately 100 nm in diameter and displaying typical morphology. NTA results from NanoSight nanoparticle tracker showed that the peak particle size was 98.5 nm, that the average particle size was 110.2 nm, and that the particle size was mainly distributed between 68.4-155.7 nm. Mtb-EVs that were smaller than 250 nm accounted for 98.39% of the total. Mouse myeloid DCs directionally induced and amplified in vitro displayed typical DC phenotype and morphology, and the purity exceeded 85%. EM verified the abundance of microvilli and radial protuberance on the surface of DCs, which had uniform cytoplasm and clear nuclear membrane. Loaded with Mtb-EVs at different concentrations, including 10 2, 10 3, and 10 4 particles/cell, the DCs had significantly upregulated levels of intracellular ROS ( P<0.05). In addition, Mtb-EVs induced the release of IL-1ß and IL-6 in a dose-dependent manner ( P<0.05). Conclusion: We established in the study a technical process for the extraction of Mtb-EVs by ultrafiltration concentration and obtained Mtb-EVs with sound morphology, high purity, and concentrated particle size distribution. Furthermore, Mtb-EVs can upregulate the intracellular ROS level in DCs and induce the release of IL-1ß and IL-6 in a dose-dependent manner.