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Insulin is a vascular hormone and regulates vascular tone and reactivity. Muscle is a major insulin target that is responsible for the majority of insulin-stimulated glucose use. Evidence confirms that muscle microvasculature is an important insulin action site and critically regulates insulin delivery to muscle and action on myocytes, thereby affecting insulin-mediated glucose disposal. Insulin via activation of its signaling cascade in the endothelial cells increases muscle microvascular perfusion, which leads to an expansion of the endothelial exchange surface area. Insulin’s microvascular actions closely couple with its metabolic actions in muscle and blockade of insulin-mediated microvascular perfusion reduces insulin-stimulated muscle glucose disposal. Type 2 diabetes is associated with chronic low-grade inflammation, which engenders both metabolic and microvascular insulin resistance through endocrine, autocrine and paracrine actions of multiple pro-inflammatory factors. Here, we review the crucial role of muscle microvasculature in the regulation of insulin action in muscle and how inflammation in the muscle microvasculature affects insulin’s microvascular actions as well as metabolic actions. We propose that microvascular insulin resistance induced by inflammation is an early event in the development of metabolic insulin resistance and eventually type 2 diabetes and its related cardiovascular complications, and thus is a potential therapeutic target for the prevention or treatment of obesity and diabetes.

Background Caplacizumab, a nanobody targeting von Willebrand factor, has transformed the management of immune-mediated thrombotic thrombocytopenic purpura (iTTP) by rapidly restoring platelet counts and improving survival. However, comprehensive real-world evidence regarding its hematologic safety profile remains limited. Methods We conducted a post-marketing pharmacovigilance study using reports from the U.S. FDA Adverse Event Reporting System (FAERS) from 2019 to Q1 2025. Disproportionality analyses were performed using four signal-detection algorithms—reporting odds ratio (ROR), proportional reporting ratio (PRR), Bayesian confidence propagation neural network (BCPNN), and multi-item gamma Poisson shrinker (MGPS)—with false discovery rate adjustment. Time-to-onset was assessed among reports with available dates, and Weibull modeling was applied to characterize onset patterns. Results A total of 1,306 caplacizumab-related reports were identified, predominantly involving adult female patients with iTTP. Frequently reported adverse events included hematologic and hemorrhagic events (e.g., epistaxis and thrombocytopenia), as well as fatigue and laboratory abnormalities. Significant positive signals were consistently observed for bleeding-related preferred terms across multiple algorithms. The median time to onset was 10 days after treatment initiation, and Weibull modeling suggested an early-failure pattern, indicating greater susceptibility during the initial treatment cycles. Conclusions In FAERS post-marketing data, caplacizumab-associated adverse events were mainly bleeding-related, generally predictable, and tended to occur early during therapy. Close clinical and laboratory monitoring—particularly of hematologic parameters—during the initial treatment period is warranted to balance bleeding vigilance with therapeutic efficacy. These findings provide real-world evidence to inform hematologists about the safety profile of caplacizumab in iTTP management.

Methane-air explosion is one of the major disasters in industrial process. The explosion strength could be influenced by the crushed coal gangue, which is widely distributed in coal mine gob and roadway. To understand the influence of the coal gangue on gas explosion, an experimental system with a 0.2 × 0.2 × 3.0 m 3 pipeline was designed and explosion experiments of coal gangue with 5 blockage length-diameter ratios (ratio of axial blockage length to pipeline equivalent diameter) were carried out. The results show that coal gangue can cause significant disturbances to the flame front, resulting in a violent acceleration of the explosion flame. The overpressure ratio presents a negative exponential function distribution with the blockage length-diameter ratio. The influence range increases with the blockage length-diameter ratio under the condition of rich fuel, and reaches the maximum when equivalent ratio is 1.237. The explosion intensity is more sensitive to the blockage length-diameter ratio for the equivalent ratio equals 1.0 and 1.237. The formation of high-intensity explosion should be avoided by controlling the accumulation state of the overlying rock in coal mining.

Both type 1 and type 2 diabetes adversely affect the microvasculature in multiple organs. Our understanding of the genesis of this injury and of potential interventions to prevent, limit, or reverse injury/dysfunction is continuously evolving. This statement reviews biochemical/cellular pathways involved in facilitating and abrogating microvascular injury. The statement summarizes the types of injury/dysfunction that occur in the three classical diabetes microvascular target tissues, the eye, the kidney, and the peripheral nervous system; the statement also reviews information on the effects of diabetes and insulin resistance on the microvasculature of skin, brain, adipose tissue, and cardiac and skeletal muscle. Despite extensive and intensive research, it is disappointing that microvascular complications of diabetes continue to compromise the quantity and quality of life for patients with diabetes. Hopefully, by understanding and building on current research findings, we will discover new approaches for prevention and treatment that will be effective for future generations.This scientific statement reviews and discusses the microvascular complications of diabetes on an organ-by-organ basis.

Fatty acid metabolism, exercise, and insulin action play critical roles in maintaining vascular health, especially relevant in metabolic disorders such as obesity, type 2 diabetes, and cardiovascular disease. Insulin, a vasoactive hormone, induces arterial vasodilation throughout the arterial tree, increasing arterial compliance and enhancing tissue perfusion. These effects, however, are impaired in individuals with obesity and type 2 diabetes, and evidence suggests that vascular insulin resistance contributes to the pathogenesis of type 2 diabetes and its cardiovascular complications. Elevated plasma levels of free fatty acids in people with insulin resistance engender vascular inflammation, endothelial dysfunction, and vascular insulin resistance. Importantly, these effects are both functionally and structurally dependent, with saturated fatty acids as the primary culprits, while polyunsaturated fatty acids may support insulin sensitivity and endothelial function. Exercise enhances fatty acid oxidation, reduces circulating free fatty acids, and improves insulin sensitivity, thereby mitigating lipotoxicity and promoting endothelial function. Additionally, exercise induces beneficial vascular adaptations. This review examines the complex interplay among fatty acid metabolism, exercise training-induced vascular adaptations, and insulin-mediated vascular changes, highlighting their collective impact on vascular health and underlying mechanisms in both healthy and insulin-resistant states. It also explores the therapeutic potential of targeted exercise prescriptions and fatty acid-focused dietary strategies for enhancing vascular health, emphasizing tailored interventions to maximize metabolic benefits. Future research should investigate the pathways linking fatty acid metabolism to vascular insulin resistance, with a focus on how exercise and dietary modifications can be personalized to enhance vascular insulin sensitivity, optimize vascular health, and reduce the risks of type 2 diabetes and associated cardiovascular complications.

Precipitation plays a crucial role in the global hydrological cycle, and its irregular distribution contributes directly to natural hazards such as floods, waterlogging, and droughts. Satellite remote sensing has emerged as an effective tool for global precipitation monitoring. However, accurately estimating hourly precipitation from satellite observations remains a major challenge due to its high spatiotemporal variability. To address this challenge, we propose a novel framework—Geographically constrained multi‐source Fusion Network with cross Attention (GeoFNA)—designed to enhance the accuracy of hourly satellite precipitation estimates. GeoFNA integrates a spatiotemporal convolutional network with cross‐attention mechanisms to effectively capture complex spatiotemporal patterns and nonlinear relationships across multi‐source precipitation data sets and auxiliary variables. To further improve model robustness, geographically associated input constraints and weight constraints are incorporated to account for the skewed distribution and rapid variability of hourly precipitation. Results demonstrated that GeoFNA outperformed three baseline models, achieving significantly higher agreement with in situ measurements. Specifically, GeoFNA increased the Pearson Correlation Coefficient from 0.38 to 0.89 and reduced the Mean Squared Error from 2.39 to 0.50 (mm/h)2 compared to the original satellite precipitation data. Additionally, GeoFNA exhibited strong spatial robustness, underscoring its potential for accurate and reliable quantitative precipitation estimation. These advancements pave the way for improved hydrological modeling and meteorological research.

Thrombotic thrombocytopenic purpura (TTP) is a rare, life threatening thrombotic microangiopathy that requires prompt diagnosis to reduce mortality. However, its early identification is often hindered by delayed ADAMTS13 testing, particularly in low resource settings. In this study, we developed a machine learning–based model using readily available inflammatory markers, including systemic immune inflammation index (SII), platelet to lymphocyte ratio (PLR), and platelet neutrophil product (PPN), to distinguish TTP from immune thrombocytopenia (ITP). A retrospective analysis of 196 hospitalized patients was conducted, and eight machine learning models were trained and compared. Logistic regression achieved the best performance (AUC = 0.78), with SII identified as the most influential predictor. While the PLASMIC score remains a widely used tool with higher diagnostic accuracy (AUC = 0.92), our model relies only on routine blood tests and offers a fast, accessible alternative for early risk stratification. These findings suggest that composite inflammatory markers combined with machine learning can assist in the rapid triage of suspected TTP cases, especially in emergency or resource-limited environments.

Ferroelectrics are essential in memory devices for multi-bit storage and high-density integration. Ferroelectricity mainly exists in compounds but rare in single-element materials due to their lack of spontaneous polarization in the latter. However, we report a room-temperature ferroelectricity in quasi-one-dimensional Te nanowires. Piezoelectric characteristics, ferroelectric loops and domain reversals are clearly observed. We attribute the ferroelectricity to the ion displacement created by the interlayer interaction between lone-pair electrons. Ferroelectric polarization can induce a strong field effect on the transport along the Te chain, giving rise to a self-gated ferroelectric field-effect transistor. By utilizing ferroelectric Te nanowire as channel, the device exhibits high mobility (~220 cm 2 ·V −1 ·s −1 ), continuous-variable resistive states can be observed with long-term retention (>10 5 s), fast speed (<20 ns) and high-density storage (>1.92 TB/cm 2 ). Our work provides opportunities for single-element ferroelectrics and advances practical applications such as ultrahigh-density data storage and computing-in-memory devices. Authors find room-temperature ferroelectricity in single element Te nanowires, highlighting that reducing dimensions to 1D in low-dimensional piezoelectric materials with chain structures is an effective strategy to induce ferroelectricity absent in their 2D form.

Adult non-insulin requiring diabetes includes latent autoimmune diabetes of adults (LADA), distinguished from type 2 diabetes by the presence of islet autoantibodies. LADA China determined the characteristics of Chinese LADA. This nationwide, multicenter, clinic-based cross-sectional study was conducted in 46 university-affiliated hospitals in 25 Chinese cities. All 4,880 ketosis-free diabetic patients (<1 year postdiagnosis, without insulin therapy for >6 months, aged ≥30 years) had GAD antibody (GADA) and HLA-DQ genotype measured centrally with clinical data collected locally. GADA-positive subjects were classified as LADA. Of the patients, 5.9% were GADA positive with LADA. LADA showed a north-south gradient. Compared with GADA-negative type 2 diabetes, LADA patients were leaner, with lower fasting C-peptide and less metabolic syndrome. Patients with high GADA titers are phenotypically different from those with low GADA titers, while only a higher HDL distinguished the latter from those with type 2 diabetes. HLA diabetes-susceptible haplotypes were more frequent in LADA, even in those with low-titer GADA. HLA diabetes-protective haplotypes were less frequent in LADA. Our study implicates universal immunogenetic effects, with some ethnic differences, in adult-onset autoimmune diabetes. Autoantibody positivity and titer could be important for LADA risk stratification and accurate therapeutic choice in clinical practice.

Glucagon-like peptide 1 (GLP-1) increases tissue glucose uptake and causes vasodilation independent of insulin. We examined the effect of GLP-1 on muscle microvasculature and glucose uptake. After confirming that GLP-1 potently stimulates nitric oxide (NO) synthase (NOS) phosphorylation in endothelial cells, overnight-fasted adult male rats received continuous GLP-1 infusion (30 pmol/kg/min) for 2 h plus or minus NOS inhibition. Muscle microvascular blood volume (MBV), microvascular blood flow velocity (MFV), and microvascular blood flow (MBF) were determined. Additional rats received GLP-1 or saline for 30 min and muscle insulin clearance/uptake was determined. GLP-1 infusion acutely increased muscle MBV (P < 0.04) within 30 min without altering MFV or femoral blood flow. This effect persisted throughout the 120-min infusion period, leading to a greater than twofold increase in muscle MBF (P < 0.02). These changes were paralleled with increases in plasma NO levels, muscle interstitial oxygen saturation, hind leg glucose extraction, and muscle insulin clearance/uptake. NOS inhibition blocked GLP-1-mediated increases in muscle MBV, glucose disposal, NO production, and muscle insulin clearance/uptake. In conclusion, GLP-1 acutely recruits microvasculature and increases basal glucose uptake in muscle via a NO-dependent mechanism. Thus, GLP-1 may afford potential to improve muscle insulin action by expanding microvascular endothelial surface area.