In-stent restenosis (ISR) after percutaneous coronary interventions (PCI) remains a significant challenge.

This study aimed to investigate the predictive ability of coronary CT angiography (CTA) derived plaque and hemodynamic characteristics for ISR.

In this retrospective study, we included stable patients who underwent coronary CTA prior to the index PCI and subsequently exhibited both ISR and non-ISR in different stented lesions during follow-up. The plaque and hemodynamic characteristics derived from coronary CTA were assessed. The incremental discriminant and reclassification abilities for ISR prediction were compared among 2 models (model 1: procedural characteristics; model 2: model 1 + plaque characteristics + hemodynamic characteristics).

A total of 52 patients with 120 lesions were included in the study, comprising 63 ISR lesions and 57 non-ISR lesions. The average age was 62.6 ± 9.9 years old and 67.3% (35/52) were male. The median interval between index PCI and ISR was 22 (14.3-66.8) months. Compared with non-ISR group, lesions in ISR group exhibited more adverse plaque characteristics (APC) and adverse hemodynamic characteristics (AHC). The risk of developing ISR in lesions with ≥ 2 APC and ≥ 3 AHC was significantly higher than that with < 2 APC and < 3 AHC (HR = 11.02, 95% CI = 1.63-16.32, p = 0.002). The C-index of Model 2 (0.858; 95% CI: 0.782-0.925) was higher than that of Model 1 (0.762; 95% CI: 0.670-0.845) (p = 0.017).

The noninvasive assessment of CTA-derived plaque characteristics and hemodynamic features enhanced the prediction of ISR after PCI in stable patients.

Moyamoya disease (MMD), historically termed spontaneous occlusion of the circle of Willis, is a rare steno-occlusive cerebrovascular disease. Its etiology and pathogenesis remain incompletely understood, and lipid metabolism has recently attracted attention as a potential correlate of its clinical and biological heterogeneity.

This scoping review summarizes evidence on lipid metabolic abnormalities in MMD, including clinical associations, lipid-related markers, multi-omics findings, potential mechanisms, and therapeutic implications of lipid-modulating approaches.

Epidemiological studies suggest that lipid abnormalities, including hypertriglyceridemia, low high-density lipoprotein cholesterol, and elevated lipoprotein(a), are common in MMD and are associated with disease phenotype, progression, stroke risk, and postoperative outcomes. Multi-omics studies reveal lipid metabolic alterations across peripheral blood, cerebrospinal fluid (CSF), and cerebrovascular tissue, suggesting a pattern of peripheral depletion, central enrichment, and tissue remodeling. Alterations in apolipoproteins such as APOE and lipid classes including sphingolipids, cardiolipins, and lysophosphatidylcholine may be associated with endothelial and vascular smooth muscle cell dysfunction, inflammatory responses, oxidative stress, and pathological vascular remodeling. Clinical studies suggest that statin use may be associated with improved collateral formation, although the underlying mechanisms remain uncertain.

This review maps emerging evidence linking lipid metabolism to MMD and highlights future directions for biomarker discovery, mechanistic validation, and therapeutic exploration.

Nesfatin-1 is a multifunctional peptide that integrates cardiovascular, metabolic, and immune regulation, particularly along the "Heart-Brain-Gut" axis. Accumulating evidence highlights its pivotal role in inter-organ communication under both physiological and pathological conditions. However, its underlying molecular mechanisms remain incompletely understood, and the prevailing orphan G protein-coupled receptor (GPCR) hypothesis is currently undergoing critical scrutiny due to accumulating data that contest its exclusivity and sufficiency in accounting for nesfatin-1's pleiotropic effects. This review provides a comprehensive synthesis of recent advances in these fields, with a focus on putative non-canonical signaling mechanisms and lipid rafts. By examining these non-canonical mechanisms and their implications for cellular cross-talk, we provide new insights into how nesfatin-1 coordinates multi-system integration. Furthermore, we discuss its translational relevance for precision medicine and targeted therapies against multi-organ diseases, proposing a comprehensive framework to guide future research and clinical applications.

Venous thromboembolism (VTE), including deep-vein thrombosis and pulmonary embolism, is the third most common cause of vascular death worldwide and a major contributor to costly and debilitating non-fatal complications. Despite the changing landscape of risk factors, preventive and diagnostic strategies, risk stratification and therapies, no contemporary global summary of the burden of VTE is available. In a collaborative, multinational effort, we provide a global overview of the incidence and outcomes of VTE. Reliable data were available for only a limited number of countries (predominantly in Northern America, Western Europe and Oceania), with notable regional differences. During 2012-2016, the global annual incidence of deep-vein thrombosis ranged from 25.1 to 131.5 per 100,000 of the population. The incidence of pulmonary embolism rose from 2012-2016 to 2017-2022 in Northern America and Asia but remained stable in Oceania. Among patients with pulmonary embolism, 30-day all-cause mortality ranged globally from 1.0% to 9.0%, and the 1-year cumulative incidence of recurrent VTE ranged from 2.9% to 8.1%. These findings reveal the substantial global burden of VTE, sources of heterogeneity and stark regional gaps in the data, demanding coordinated surveillance, standardized reporting and research into local and global drivers to curb worldwide morbidity and mortality.

Objective: To explore and discuss the protective effects of 5-carbonyl-8-hydroxyquinoline (IOX1) potential mechanisms in the mouse model of hepatic ischemia-reperfusion injury (IRI) and in vitro hepatocyte hypoxia-reoxygenation (H/R). Methods: In vivo and in vitro models of liver injury were established using a mouse hepatic ischemia-reperfusion model and a primary hepatocyte hypoxia-reoxygenation (H/R) model. In vivo experiments were divided into three groups: sham group, IRI group, and IRI+IOX1 group. In vitro experiments were divided into four groups: negative control group (CTRL), CTRL+IOX1 group, H/R group, and H/R+IOX1 group. Liver injury was assessed by measuring serum liver enzyme levels, hematoxylin-eosin (HE) staining, and immunohistochemistry. Apoptosis and oxidative stress were evaluated using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, flow cytometry, real-time quantitative PCR, and reactive oxygen species (ROS) fluorescence staining. Differentially expressed genes were screened by RNA sequencing of liver tissues, and the expression levels of differential proteins were validated by western blotting. Data were processed using GraphPad Prism 10.0. Results: Compared with the IRI group, the IRI+IOX1 group showed significantly lower levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). At an IOX1 dose of 2 mg/kg, ALT and AST levels decreased by 87.05% and 94.49%, respectively (P<0.000 1), and hepatic histopathological damage was markedly ameliorated. Immunohistochemical staining results revealed less inflammatory cell infiltration in the IRI+IOX1 group. TUNEL assay, western blotting, and real-time quantitative PCR results demonstrated that IOX1 treatment reduced apoptosis after hepatic I/R injury. In the in vitro model, flow cytometry and western blotting results showed that IOX1 reduced apoptosis in primary hepatocytes after H/R injury, and ROS staining results indicated that IOX1 decreased ROS production following H/R injury. RNA sequencing and western blotting results revealed that IOX1 regulated the mitogen-activated protein kinase signaling pathway in hepatocytes by inhibiting AlkB homolog 5 (ALKBH5). Conclusion: IOX1 regulates the extracellular signalregulated kinase (ERK)/p38 mitogen-activated protein kinase (MAPK) signaling pathway by inhibiting ALKBH5 in hepatocytes, thereby reducing hepatocyte apoptosis and inflammatory responses and attenuating liver injury following ischemia-reperfusion.

Health literacy is considered a prognostic determinant for patients with heart failure (HF), and the recognition of disease names could be fundamental to this. This study examined the proportion of patients with HF who recognized their disease name and its association with prognosis.

From January 2021 to June 2023, 188 hospitalized patients with HF (Stage B-D, median age 81 years) were asked to recall their disease name before discharge. Recognition accuracy was evaluated using a standardized scoring system, and interobserver agreement was confirmed. In a subset, communicative and critical health literacy (CCHL) was assessed. Prognostic outcomes included all-cause mortality and all-cause hospitalization after discharge.

The recognition score showed high interobserver reliability (κ = 0.85). Seventy-two patients (38%) failed to recognize their primary diagnosis. Those without recognition had significantly lower CCHL scores than those with recognition (p < 0.01). During a median follow-up of 280 days, 76 patients (40%) experienced adverse events. In univariate analyses, lack of diagnosis recognition was associated with an increased risk of adverse outcomes, but this association disappeared after adjustment for age, cognitive function, and HF severity.

A substantial number of older patients with HF did not recognize their primary diagnosis, but disease recognition was not an independent determinant of prognosis.

Myocardial ischemia/reperfusion (MI/R) injury remains a major clinical challenge characterized by inflammation and progressive cardiomyocyte loss. Although pyroptosis is known to drive this pathogenesis, the upstream molecular switches that trigger the pyroptotic cascade remain poorly understood. Here, we investigated the role of Keratin 19 (KRT19) and its regulation by the deubiquitinase USP14 in MI/R-induced pyroptosis.

In vivo mouse models of MI/R and in vitro neonatal mouse cardiomyocyte (NMCM) models of hypoxia/reoxygenation (H/R) were established. Following genetic manipulation of USP14 or KRT19, we evaluated cardiac function (via echocardiography), cell death (via flow cytometry and LDH release assays), mitochondrial function (via Seahorse analysis), and molecular interactions (via co-immunoprecipitation, domain-mapping, and ubiquitination assays).

Both USP14 and KRT19 expression levels are significantly elevated in MI/R mouse hearts and H/R-exposed NMCMs. Knockdown of either USP14 or KRT19 mitigated NLRP3/Caspase-1/GSDMD-mediated pyroptosis both in vivo and in vitro. Mechanistically, USP14 interacted with KRT19 to prevent its K48-linked proteasomal degradation. Domain-mapping assays revealed that the C-terminal USP catalytic domain of USP14 bound to the Coil1B domain of KRT19. The resulting stabilization and accumulation of KRT19 promoted mitochondrial dysfunction and reactive oxygen species (mtROS) generation, thereby activating the pyroptotic cascade.

The USP14-KRT19 axis is a critical driver of cardiomyocyte pyroptosis and MI/R injury. Targeting this deubiquitination-mediated cytoskeletal stabilization cascade represents a promising therapeutic strategy to mitigate reperfusion injury.

Chest X-ray (CXR) interpretation is hindered by the long-tailed distribution of pathologies and the open-world nature of clinical environments. Existing benchmarks often rely on closed-set classes from a single institution, failing to capture the prevalence of rare diseases or the appearance of novel findings. To address this, we present the CXR-LT challenge. The first event, CXR-LT 2023, established a large-scale benchmark for long-tailed multi-label CXR classification and identified key challenges in rare disease recognition. CXR-LT 2024 further expanded the label space and introduced a zero-shot task to study generalization to unseen findings. Building on the success of CXR-LT 2023 and 2024, this third iteration of the benchmark introduces a multi-center dataset comprising over 145,000 images from PadChest and NIH Chest X-ray datasets. Additionally, all development and test sets in CXR-LT 2026 are annotated by radiologists, providing a more reliable and clinically grounded evaluation than report-derived labels. The challenge defines two core tasks this year: (1) Robust Multi-Label Classification on 30 known classes and (2) Open-World Generalization to 6 unseen (out-of-distribution) rare disease classes. This paper summarizes the overview of the CXR-LT 2026 challenge. We describe the data collection and annotation procedures, analyze solution strategies adopted by participating teams, and evaluate head-versus-tail performance, calibration, and cross-center generalization gaps. Our results show that vision-language foundation models improve both in-distribution and zero-shot performance, but detecting rare findings under multi-center shift remains challenging. Our study provides a foundation for developing and evaluating AI systems in realistic long-tailed and open-world clinical conditions.

Intracerebral hemorrhage (ICH) remains one of the most severe stroke subtypes and requires continuous risk assessment across the acute, subacute, and rehabilitation-transition phases. This review summarizes established and emerging immune-related circulating biomarkers and discusses their relevance to nursing management and prognostic assessment. Markers with the highest current clinical readiness include peripheral blood cell counts and derived ratios, C-reactive protein (CRP), and procalcitonin (PCT), whereas cytokines, chemokines, broader immunometabolic mediators, and neuroinjury-inflammation cross-over markers remain mainly investigational. On the basis of the revised synthesis, we propose a stage-specific monitoring framework that emphasizes sampling at admission, approximately 24 hours, approximately 72 hours, and at clinically triggered reassessment points, together with interpretation of trajectories rather than isolated values. We further outline practice-oriented nursing scenarios in which biomarker trends may support escalation of neurologic observation, infection surveillance, airway care, glucose and nutrition management, structured handoff communication, and multidisciplinary coordination. Current evidence suggests that routinely available biomarkers may add value as adjunctive monitoring tools, but the literature remains limited by observational designs, heterogeneous assay platforms, inconsistent sampling windows, variable endpoints, incomplete confounder control, and uncertain action thresholds. At present, biomarkers should complement rather than replace imaging, neurological examination, and bedside nursing assessment. Future prospective studies should prioritize standardized sampling, trajectory-based analyses, integration into nursing workflows, and clinically interpretable multimodal models.

The association between kidney function and dementia remains inconsistent across studies, and its relationship in older adults is unclear. This study aimed to investigate the longitudinal associations between kidney dysfunction, assessed by estimated glomerular filtration rate (eGFR) and albuminuria, and cognitive impairment (CI) in a national cohort of Chinese older adults.

We included individuals aged ≥ 65 years from the 2011 and 2014 waves of the Chinese Longitudinal Healthy Longevity Survey (CLHLS). Cognitive function was assessed using the Chinese version of the Mini-Mental State Examination (MMSE). Kidney function was evaluated by eGFR (CKD-EPI equation) and the urinary albumin-to-creatinine ratio (ACR), classified by KDIGO categories and quartiles. Multivariable logistic regression models were used to assess cross-sectional (n = 3364) and prospective (n = 1195) associations, controlling for sociodemographic and clinical confounders. The false discovery rate was controlled for multiple comparisons.

In cross-sectional analysis, both lower eGFR and higher ACR were independently associated with higher odds of prevalent CI. Prospectively, over a 3-year follow-up, 143 of 1195 cognitively normal participants developed CI. Compared to those with normal kidney function, participants with impaired (eGFR < 60 mL/min/1.73 m²) kidney function had a significantly higher risk of incident CI (OR = 1.744, 95% CI: 1.162-2.616). Similarly, elevated ACR (categories A2 and A3) was associated with increased incident CI risk (A2: OR = 1.801, 95% CI: 1.111-2.920; A3: OR = 2.650, 95% CI: 1.541-4.557).

Impaired kidney function, indicated by reduced eGFR and elevated ACR, is independently associated with an increased risk of cognitive impairment in older adults. These findings support integrating cognitive screening into the clinical management of elderly patients with chronic kidney disease.