S-sulfhydration: Novel insights into the antioxidant and antiinflammation in age-related diseases.

Background: Hydrogen sulfide (HS) and hydrogen polysulfide-induced S-sulfhydration are critical posttranslational modifications that specifically target cysteine residues within proteins. Degenerative diseases are often characterized by oxidative stress and inflammaging, ultimately leading to progressive organ dysfunction. Emerging evidence underscores the essential role of S-sulfhydration in modulating mitochondrial synthesis, energy metabolism, and cellular homeostasis during aging.

Designing Natural Cell-Inspired Heme-Spurred Membrane Electrode Assembly for Fuel Cells.

Developing highly efficient and durable membrane electrode assemblies (MEAs) is imperative for the widespread implementation of proton exchange membrane fuel cells (PEMFCs). However, the poor mass transfer efficiency and sluggish oxygen reduction reaction (ORR) kinetics have significantly suppressed the power density and longevity of platinum (Pt)-based MEA in PEMFCs, particularly when using an ultralow Pt loading. Inspired by the functional principles of hemoglobin in red blood cells, we present a Heme-cofactor strategy to create a "respiratory proton-transfer chain" for PEMFCs.

Melatonin Promotes Cerebral Angiogenesis in Ischemic Mice via BMP6/Smad1/5/9 Pathway.

Angiogenesis facilitates the reinstatement of blood supply to cerebral tissues after stroke by reconstructing the vascular network, thereby rescuing the penumbra region and restoring neural functions. Melatonin can modulate angiogenesis under a variety of biological and disease-related states, and bone morphogenetic protein 6 (BMP6) targets regulators associated with angiogenesis. The specific functions of melatonin and BMP6 in angiogenesis following cerebral infarction, along with the potential intrinsic regulatory interactions between them, are currently unclear and need further investigation.

Chemical Affinity Capture of Plasma Extracellular Vesicles Enables Efficient and Large-Scale Proteomic Identification of Prostate Cancer Biomarkers.

The serum prostate-specific antigen (PSA) testing is widely used for prostate cancer (PCa) screening but suffers from poor specificity, leading to unnecessary biopsies and overtreatment. The significant potential of extracellular vesicles (EVs) in cancer diagnosis has driven the development of efficient methods to isolate and identify EV biomarkers from large-scale clinical samples. Here, we systematically evaluate five commonly used EV isolation techniques through proteomic profiling of plasma-derived EVs, endorsing TiO-based chemical affinity capture as a superior approach for analyzing EVs from complex clinical samples.

Trehalose activates autophagy to alleviate cisplatin-induced chronic kidney injury by targeting the mTOR-dependent TFEB signaling pathway.

Cisplatin is a potent chemotherapeutic agent limited by significant nephrotoxicity. Multiple cycles of cisplatin administration are necessary to confer chronic disease. Autophagy is a lysosomal degradation pathway that enables the clearance and reuse of cytoplasmic components and is essential for maintaining the integrity and normal physiological function of tissues and organs.

Inhibition of IRE-1α Alleviates Pyroptosis and Metabolic Dysfunction-Associated Steatohepatitis by Suppressing Gasdermin D.

Objectives: Metabolic dysfunction-associated steatohepatitis (MASH) is a significant risk factor for cirrhosis and hepatocellular carcinoma, for which there is currently no effective treatment. This study aimed to investigate the regulatory mechanism between endoplasmic reticulum stress (ER stress) and pyroptosis in the liver under the context of MASH.

Methods And Results: Pyroptosis was examined in both in vivo and in vitro ER stress models.

Trehalose Ameliorates Nonalcoholic Fatty Liver Disease by Regulating IRE1α-TFEB Signaling Pathway.

Nonalcoholic fatty liver disease (NAFLD), characterized by hepatic lipid deposition, is one of the most prevalent chronic metabolic disorders globally, and its pharmaceutical treatments are still limited. Excessive lipid accumulation triggers endoplasmic reticulum (ER) stress and autophagy flux dysfunction, which are important mechanisms for NAFLD. Trehalose (Tre), a natural disaccharide, has been identified to reduce hepatic steatosis and glucose intolerance.

Design Considerations and Fabrication Protocols of High-Performance Intrinsically Stretchable Transistors and Integrated Circuits.

Intrinsically stretchable electronics represent a significant advancement in wearable and implantable technologies, as they offer a unique advantage by maintaining intimate tissue contact while accommodating movements and size changes. This capability makes them exceptionally well-suited for applications in human-machine interfaces, wearables, and implantables, where seamless integration with the human body is essential. To realize this vision, it is important to develop soft integrated circuits for on-body signal processing and computing.

Ameliorating lung fibrosis and pulmonary function in diabetic mice: Therapeutic potential of mesenchymal stem cell.

This study aimed to investigate the potential of mesenchymal stem cells (MSCs) in alleviating diabetic lung injury by decreasing inflammation, fibrosis and recovering tissue macrophage homeostasis. To induce pulmonary injuries in an in vivo murine model, we utilized a streptozotocin (STZ), and high-fat diet (HFD) induced diabetic C57 mouse model. Subsequently, human umbilical cord-derived MSCs (hUC-MSCs) were administered through the tail vein on a weekly basis for a duration of 4 weeks.

Electrocatalytic ORR-coupled ammoximation for efficient oxime synthesis.

State-of-the-art technology for cyclohexanone oxime production typically demands elevated temperature and pressure, along with the utilization of expensive hydroxylamine sulfate or oxidants. Here, we propose an electrochemistry-assisted cascade strategy for the efficient cyclohexanone ammoximation under ambient conditions by using in situ cathode-generated green oxidants of reactive oxygen species (ROS) such as OOH* and HO. This electrochemical reaction can take place at the cathode, achieving over 95% yield, 99% selectivity of cyclohexanone oxime, and an electron-to-oxime (ETO) efficiency of 96%.

Autophagy-deficient macrophages exacerbate cisplatin-induced mitochondrial dysfunction and kidney injury via miR-195a-5p-SIRT3 axis.

Macrophages (Mφ) autophagy is a pivotal contributor to inflammation-related diseases. However, the mechanistic details of its direct role in acute kidney injury (AKI) were unclear. Here, we show that Mφ promote AKI progression via crosstalk with tubular epithelial cells (TECs), and autophagy of Mφ was activated and then inhibited in cisplatin-induced AKI mice.

STZ-induced diabetes exacerbates neurons ferroptosis after ischemic stroke by upregulating LCN2 in neutrophils.

Diabetic is a major contributor to the unfavorable prognosis of ischemic stroke. However, intensive hypoglycemic strategies do not improve stroke outcomes, implying that diabetes may affect stroke outcomes through other ways. Ferroptosis is a novel programmed cell death pathway associated with the development of diabetes and ischemic stroke.

High-speed and large-scale intrinsically stretchable integrated circuits.

Intrinsically stretchable electronics with skin-like mechanical properties have been identified as a promising platform for emerging applications ranging from continuous physiological monitoring to real-time analysis of health conditions, to closed-loop delivery of autonomous medical treatment. However, current technologies could only reach electrical performance at amorphous-silicon level (that is, charge-carrier mobility of about 1 cm V s), low integration scale (for example, 54 transistors per circuit) and limited functionalities. Here we report high-density, intrinsically stretchable transistors and integrated circuits with high driving ability, high operation speed and large-scale integration.

Th17 Cells and IL-17A in Ischemic Stroke.

The neurological injury and repair mechanisms after ischemic stroke are complex. The inflammatory response is present throughout stroke onset and functional recovery, in which CD4 + T helper(Th) cells play a non-negligible role. Th17 cells, differentiated from CD4 + Th cells, are regulated by various extracellular signals, transcription factors, RNA, and post-translational modifications.

Real-time continuous image guidance for endoscopic retrograde cholangiopancreatography based on 3D/2D registration and respiratory compensation.

Background: It has been confirmed that three-dimensional (3D) imaging allows easier identification of bile duct anatomy and intraoperative guidance of endoscopic retrograde cholangiopancreatography (ERCP), which reduces the radiation dose and procedure time with improved safety. However, current 3D biliary imaging does not have good real-time fusion with intraoperative imaging, a process meant to overcome the influence of intraoperative respiratory motion and guide navigation. The present study explored the feasibility of real-time continuous image-guided ERCP.

Oleic acid improves hepatic lipotoxicity injury by alleviating autophagy dysfunction.

Lipotoxicity caused by excess free fatty acids, particularly saturated fatty acids (SFAs) such as palmitic acid (PA), is one of the most important pathogenesis of nonalcoholic fatty liver disease (NAFLD). However, unsaturated fatty acids (UFAs), such as oleic acid (OA), are nontoxic and can combat SFA-induced toxicity through alleviation of cell apoptosis, endoplasmic reticulum stress (ER stress) and lipids metabolism disorder. However, whether OA is able to regulate autophagy is largely unknown.

S-sulfhydration of SIRT3 combats BMSC senescence and ameliorates osteoporosis via stabilizing heterochromatic and mitochondrial homeostasis.

Senescence of bone marrow mesenchymal stem cells (BMSCs) is one of the leading causes of osteoporosis. SIRT3, an essential NAD-dependent histone deacetylase, is highly correlated with BMSC senescence-mediated bone degradation and mitochondrial/heterochromatic disturbance. S-sulfhydration of cysteine residues favorably enhances SIRT3 activity by forming persulfides.

Macrophage-derived exosomal miR-195a-5p impairs tubular epithelial cells mitochondria in acute kidney injury mice.

Macrophages (Mφ) infiltration is a common characteristic of acute kidney injury (AKI). Exosomes-mediated cell communication between tubular epithelial cells (TECs) and Mφ has been suggested to be involved in AKI. Exosomes-derived from injured TECs could regulate Mφ polarization during AKI.

Molecular mechanisms and physiological functions of autophagy in kidney diseases.

Autophagy is a highly conserved cellular progress for the degradation of cytoplasmic contents including micromolecules, misfolded proteins, and damaged organelles that has recently captured attention in kidney diseases. Basal autophagy plays a pivotal role in maintaining cell survival and kidney homeostasis. Accordingly, dysregulation of autophagy has implicated in the pathologies of kidney diseases.

Matrine alleviates cisplatin-induced acute kidney injury by inhibiting mitochondrial dysfunction and inflammation via SIRT3/OPA1 pathway.

Cisplatin is extensively used to treat malignancies. However, its clinical use is always limited due to the serious side effects, especially the nephrotoxicity. Matrine (MAT), a tetracyclic quinolizine alkaloid found in sophora genus, exerts multiple pharmacological roles, including anti-oxidative stress, anti-inflammation and anti-apoptosis, but the role of MAT on acute kidney injury (AKI) has not been evaluated.