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Coronary artery segmentation in X-ray angiography is clinically critical for percutaneous coronary intervention (PCI), as it offers essential morphological guidance for stent deployment, stenosis assessment, and hemodynamic optimization. Nevertheless, inherent angiographic limitations, including complex vasculature, low contrast, and fuzzy boundaries, persist as significant challenges. Current methodologies exhibit notable shortcomings, including fragmented output continuity, noise susceptibility, and computational inefficiency. This study proposes VM-CAGSeg, a novel U-shaped architecture integrating vessel structure-aware state space modeling, to address these limitations. The framework introduces three key innovations: ( 1 ) A Vessel Structure-Aware State Space (VSASS) block that synergizes geometric priors from a Multiscale Vessel Structure-Aware (MVSA) module with long-range contextual modeling via Kolmogorov–Arnold State Space (KASS) blocks. The MVSA module enhances tubular feature representation through Hessian eigenvalue-derived vesselness measures. ( 2 ) A Cross-Stage Feature Interaction Fusion (CSFIF) module that replaces conventional skip connections with cross-stage feature fusion strategies to enhance the variability of learned features, preserving long-range dependencies and fine-grained details. ( 3 ) A unified architecture that integrates the Vessel Structure-Aware State Space (VSASS) block and the Cross-Stage Feature Interaction Fusion (CSFIF) module to achieve comprehensive vessel segmentation by synergizing multiscale geometric awareness, long-range dependency modeling, and cross-stage feature refinement. Experiments demonstrate that VM-CAGSeg achieves state-of-the-art performance, surpassing CNN-based (e.g., UNet++), transformer-based (e.g., MISSFormer), and state space model (SSM)-based (e.g., H_vmunet) methods, with a Dice similarity coefficient (DSC) of 88.15%, mIoU of 79.19%, and a 95% Hausdorff distance (HD95) of 13.68 mm. The framework significantly improved boundary delineation, reducing HD95 by 49.8% compared to UNet++ (27.15 mm) and by 16.6% compared to TransUNet (15.85 mm). While its sensitivity (90.05%) was marginally lower than that of TransUNet (90.33%), the model's balanced performance in segmentation accuracy and edge precision confirmed its robustness. These findings validate the effectiveness of integrating multiscale vessel-aware modeling, long-range dependency learning, and cross-stage feature fusion, making VM-CAGSeg a reliable solution for clinical vascular segmentation tasks that require fine-grained detail preservation. The proposed method is available as an open-source project at https://github.com/GIT-HYQ/VM-CAGSeg .

Superselective adrenal arterial embolization (SAAE) appears to be beneficial in primary aldosteronism (PA) patients with lateralized aldosterone secretion (unilateral PA). As confirmed by adrenal vein sampling (AVS), nearly 40% of PA patients would be PA without lateralized aldosterone secretion (bilateral PA). We aimed to investigate the efficacy and safety of SAAE on bilateral PA. We identified 171 bilateral PA patients from 503 PA patients who completed AVS. Thirty-eight bilateral PA patients received SAAE, and 31 completed a median 12-month clinical follow-up. The blood pressure and biochemical improvements of these patients were carefully analyzed. 34% of patients were identified as bilateral PA. Plasma aldosterone concentration, plasma renin activity, and aldosterone/renin ratio (ARR) were significantly improved 24-h after SAAE. SAAE was associated with 38.7% and 58.6% of complete/partial clinical and biochemical success within a median 12-month follow-up. A significant reduction in left ventricular hypertrophy was shown in patients who obtained complete biochemical success compared with partial/absent biochemical success. SAAE was associated with a more apparent nighttime blood pressure reduction than daytime blood pressure reduction in patients with complete biochemical success. No major adverse safety events related to SAAE were reported during the intraoperative, postoperative, and follow-up periods. SAAE was associated with blood pressure and biochemical improvements in part of bilateral PA and appeared safe. The biochemistry success was accompanied by improved cardiac remodeling and a more prominent decrease in nocturnal blood pressure. This study was part of a trial registered with the Chinese Clinical Trial Registry, number ChiCTR2100047689.

Coronary microembolization (CME) refers to embolism in the coronary microcirculation. This study showed a reduction in succinyl transferase (CPT1A) and the succinylation substrate (succinyl-CoA) in cardiomyocytes in CME models, suppressing the succinylation of the mitochondrially localized protein TRMT10C. Suppression of succinylation promotes KPNA4 recognition of two nuclear localization signals (NLSs), KAKR and KKK(X) KVKK, in TRMT10C, which induces the transport of TRMT10C from the cytoplasm to the nucleus rather than to the mitochondria. Nuclear TRMT10C induces YTHDF2-mediated decay of TAFAZZIN and NLRX1 through m1A modifications. The reduction in TAFAZZIN and NLRX1 is associated with multiple detrimental effects, such as inflammation mediated by NF-κB and NLRP3, reactive oxygen species (ROS) production, and suppression of mitophagy. TRMT10C knockdown suppressed the accumulation of TRMT10C in the nucleus. It restored NLRX1 and TAFAZZIN protein levels in cardiomyocytes under hypoxia. However, the deficiency of TRMT10C in the mitochondria did not improve-or even worsened-with TRMT10C knockdown. Inducing TRMT10C succinylation via CPT1A overexpression led to the redistribution of TRMT10C to the mitochondria rather than the nucleus, which is likely a better approach for improving cardiomyocyte function under hypoxia than direct TRMT10C knockdown. This study reveals a novel pathological mechanism underlying CME and suggests potential therapeutic targets for this disease.

Coronary microembolization (CME) is a severe medical condition that occurs during acute coronary syndrome, leading to myocardial inflammation, apoptosis, and cardiac dysfunction. The research investigated SRSF1 biological functions during myocardial inflammation caused by CME and its underlying mechanisms. CME models were established in rats injected with microspheres in the left ventricle and oxygen-glucose deprivation (OGD)-exposed cardiomyocytes. RT-qPCR, Western blotting and immunohistochemical staining were used to evaluate the expression of target molecules. Myocardial apoptosis was detected by flow cytometry. The direct binding between SRSF1 and ectonucleotide pyrophosphatase/phosphodiesterase 3 (ENPP3) was verified by RIP and TRAP. Protein interaction was determined by Co-IP. The dual-luciferase reporter assay measured inflammatory cytokine transcription levels. Myocardial injury was assessed by HE staining and ultrasound examinations. The study used ELISA to measure inflammatory cytokines and cardiac troponin I (cTnI) levels. SRSF1 expression was strikingly enhanced in CME models. Knockdown of SRSF1 effectively restrained NF-κB-mediated myocardial inflammation through increasing ENPP3 mRNA/lncRNA ENPP3 ratio by regulating alternative splicing of ENPP3 pre-mRNA. The GlcNAcylation of bromodomain-containing protein 4 (BRD4) was reduced during CME, which increased BRD4 protein level to trigger NF-κB-mediated inflammation. SRSF1/ENPP3 axis inhibited the GlcNAcylation of BRD4 in CME. Myocardial-specific knockout of SRSF1 restored cardiac function and restrained myocardial inflammation in CME rats by inactivation of the ENPP3/BRD4/NF-κB pathway. SRSF1 facilitates CME-induced myocardial inflammation by up-regulating ENPP3/lncRNA ENPP3 ratio to suppress GlcNAcylation of BRD4, suggesting SRSF1 inhibition as a promising therapeutic strategy for CME.

Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers. The interaction of EZH2 with embryonic ectoderm development (EED) is required for EZH2's catalytic activity. Inhibition of the EZH2-EED complex thus represents a novel strategy for interfering with the oncogenic potentials of EZH2 by targeting both its catalytic and non-catalytic functions. To date, there have been no reported high-throughput screening (HTS) assays for inhibitors acting at the EZH2-EED interface. In this study, we developed a fluorescence polarization (FP)-based HTS system for the discovery of EZH2-EED interaction inhibitors. The tracer peptide sequences, positions of fluorescein labeling, and a variety of physicochemical conditions were optimized. The high Z' factors (>0.9) at a variety of DMSO concentrations suggested that this system is robust and suitable for HTS. The minimal sequence requirement for the EZH2-EED interaction was determined by using this system. A pilot screening of an in-house compound library containing 1600 FDA-approved drugs identified four compounds (apomorphine hydrochloride, oxyphenbutazone, nifedipine and ergonovine maleate) as potential EZH2-EED interaction inhibitors.

Denervation often results in skeletal muscle atrophy.Different mechanisms seem to be involved in the determination between denervated slow and fast skeletal muscle atrophy.At the epigenetic level,mi RNAs are thought to be highly involved in the pathophysiological progress of denervated muscles.We used mi RNA microarrays to determine mi RNA expression profiles from a typical slow muscle（soleus muscle） and a typical fast muscle（tibialis anterior muscle） at an early denervation stage in a rat model.Results showed that mi R-206,mi R-195,mi R-23 a,and mi R-30 e might be key factors in the transformation process from slow to fast muscle in denervated slow muscles.Additionally,certain mi RNA molecules（mi R-214,mi R-221,mi R-222,mi R-152,mi R-320,and Let-7e） could be key regulatory factors in the denervated atrophy process involved in fast muscle.Analysis of signaling pathway networks revealed the mi RNA molecules that were responsible for regulating certain signaling pathways,which were the final targets（e.g.,p38 MAPK pathway; Pax3/Pax7 regulates Utrophin and follistatin by HDAC4; IGF1/PI3K/Akt/m TOR pathway regulates atrogin-1 and Mu RF1 expression via Fox O phosphorylation）.Our results provide a better understanding of the mechanisms of denervated skeletal muscle pathophysiology.

The Thornthwaite moisture index, an index of the supply of water （precipitation） in an area relative to the climatic demand for water （potential evapotranspiration）, was used to examine the spatial and temporal variation of drought and to verify the influence of environmental factors on the drought in the Hengduan Mountains, China. Results indicate that the Thornthwaite moisture index in the Hengduan Mountains had been increasing since 1960 with a rate of 0.1938/yr. Annual Thomthwaite moisture index in Hengduan Mountains was between -97.47 and 67.43 and the spatial heterogeneity was obvious in different seasons. Thomthwaite moisture index was high in the north and low in the south, and the monsoon rainfall had a significant impact on its spatial distribution. The tendency rate of Thomthwaite moisture index variation varied in different seasons, and the increasing trends in spring were greater than that in summer and autumn. However, the Thomthwaite moisture index decreased in winter. Thomthwaite moisture index increased greatly in the north and there was a small growth in the south of Hengduan Mountains. The increase of precipitation and decrease of evaporation lead to the increase of Thomthwaite moisture index. Thornthwaite moisture index has strong correlation with vegetation coverage. It can be seen that the correlation between Normalized Difference Vegetation Index （NDVI） and Thomthwaite moisture index was positive in spring and summer, but negative in autumn and winter. Correlation between Thornthwaite moisture index and relative soil relative moisture content was positive in spring, summer and autumn, but negative in winter. The typical mountainous terrain affect the distribu- tion of temperature, precipitation, wind speed and other meteorological factors in this region, and then affect the spatial distribution of Thomthwaite moisture index. The unique ridge-gorge terrain caused the continuity of water-heat distribution from the north to south, and the water-heat was stronger than that from the east to west part, and thus determined the spatial distribution of Thornthwaite mois- ture index. The drought in the Hengduan Mountains area is mainly due to the unstable South Asian monsoon rainfall time.

Iron homeostasis disturbance has been implicated in Alzheimer’s disease (AD), and excess iron exacerbates oxidative damage and cognitive defects. Ferroptosis is a nonapoptotic form of cell death dependent upon intracellular iron. However, the involvement of ferroptosis in the pathogenesis of AD remains elusive. Here, we report that ferroportin1 (Fpn), the only identified mammalian nonheme iron exporter, was downregulated in the brains of APPswe/PS1dE9 mice as an Alzheimer’s mouse model and Alzheimer’s patients. Genetic deletion of Fpn in principal neurons of the neocortex and hippocampus by breeding Fpnfl/fl mice with NEX-Cre mice led to AD-like hippocampal atrophy and memory deficits. Interestingly, the canonical morphological and molecular characteristics of ferroptosis were observed in both Fpnfl/fl/NEXcre and AD mice. Gene set enrichment analysis (GSEA) of ferroptosis-related RNA-seq data showed that the differentially expressed genes were highly enriched in gene sets associated with AD. Furthermore, administration of specific inhibitors of ferroptosis effectively reduced the neuronal death and memory impairments induced by Aβ aggregation in vitro and in vivo. In addition, restoring Fpn ameliorated ferroptosis and memory impairment in APPswe/PS1dE9 mice. Our study demonstrates the critical role of Fpn and ferroptosis in the progression of AD, thus provides promising therapeutic approaches for this disease.

To tackle the challenge of the data accuracy issues of low-cost sensors (LCSs), the objective of this work was to obtain robust correction equations to convert LCS signals into data comparable to that of research-grade instruments using side-by-side comparisons. Limited sets of seed LCS devices, after laboratory evaluations, can be installed strategically in areas of interest without official monitoring stations to enable reading adjustments of other uncalibrated LCS devices to enhance the data quality of sensor networks. The robustness of these equations for LCS devices (AS-LUNG with PMS3003 sensor) under a hood and a chamber with two different burnt materials and before and after 1.5 years of field campaigns were evaluated. Correction equations with incense or mosquito coils burning inside a chamber with segmented regressions had a high R2 of 0.999, less than 6.0% variability in the slopes, and a mean RMSE of 1.18 µg/m3 for 0.1–200 µg/m3 of PM2.5, with a slightly higher RMSE for 0.1–400 µg/m3 compared to EDM-180. Similar results were obtained for PM1, with an upper limit of 200 µg/m3. Sensor signals drifted 19–24% after 1.5 years in the field. Practical recommendations are given to obtain equations for Federal-Equivalent-Method-comparable measurements considering variability and cost.

We aimed to fill the research gap between DII and herpes simplex virus infection among adults in the US by analyzing the association between dietary inflammatory index and herpes simplex virus and to provide new ideas for herpes simplex virus prevention and treatment. We used data from 8636 participants in NHANES 2007-2016, which were statistically analyzed by participant baseline study, one-way analysis of variance, multiple regression equations, smoothed curve fitting, and stratified analysis. In the fully adjusted model, the DII high concentration group was positively associated with the prevalence of herpes simplex (1.15 (0.89, 1.48), p = 0.0027), and the results of the stratified analyses indicated that the positive association between DII and herpes simplex virus type II was stable in the population. This study demonstrates a positive association between DII and herpes simplex virus II in US adults, suggesting that a proinflammatory diet may be an independent risk factor for herpes simplex virus II.