Common outcomes of childhood stroke include physical, cognitive, psychological and social difficulties. Evidence indicates young people with acquired brain injury have a range of community neuropsychological priorities impacting participation; however, less is known about priorities following childhood stroke specifically, and the demographic influences on these. This knowledge is essential to ensure rehabilitation services meet their needs.

Two-hundred twenty-two clinical priorities were extracted from the medical records of 59 children (66% male, 59% White, aged 1-17 years, median 7, all deprivation quintiles) attending an occupational therapy and neuropsychology Stroke Recovery Clinic: stroke type: 51% perinatal and 49% childhood. Priorities were coded using the International Classification of Functioning Disability and Health (ICF). Chi-square analysis identified associations between priorities and demographic factors.

On average, four priorities were raised per patient. Priorities were distributed across ICF components, with 47% classified as activities and participation, 25% as body functions, 23% as environmental factors and 5% as body structures. Key concerns included behaviour/emotion, health/education navigation, fine hand use and societal attitudes. No significant demographic differences were found. A nonsignificant trend showed more body function and environmental priorities in primary and high school. Males and non-White patients continued clinic access into adolescence, with fewer non-White individuals in preschool.

Children and their families have a range of priorities post-stroke, requiring patient and family centred, interdisciplinary and context specific approaches. These findings support longitudinal, integrated hospital, community and school care systems, which focus on children and young people's participation in their homes and communities well beyond the time of their stroke. Services must ensure interdisciplinary post-stroke care for children and young people is equitable and accessible, with priorities addressed in a timely manner.

Ischemic mitral regurgitation (IMR) reflects left ventricular (LV) remodeling, but its within-patient trajectory during sequential medical therapy and coronary revascularization remains incompletely characterized.

To compare within-patient changes in LV remodeling and IMR severity during the medical-therapy and subsequent post-revascularization intervals and examine the association between LV reverse remodeling and IMR regression.

In this single-center retrospective complete-case serial-imaging cohort, 125 adults with significant IMR underwent quantitative echocardiography at baseline, after medical therapy, and 2-3 months after PCI or CABG. The primary endpoint was ≥1-grade IMR improvement from baseline to final follow-up. Patient-level changes during the medical-therapy and subsequent post-revascularization intervals were compared using Wilcoxon signed-rank tests with Holm adjustment.

Median LVEDV reduction was 3 mL (IQR -4 to 19) during the medical-therapy interval versus 22 mL (IQR 5-51) during the post-revascularization interval. Corresponding improvements were 1 versus 8 percentage points for LVEF, 0.02 versus 0.16 cm² for EROA, and 2 versus 21 mL/beat for regurgitant volume (Holm-adjusted p < 0.001 for all comparisons). Overall, 93 patients (74.4%) achieved ≥1-grade IMR improvement. LV reverse remodeling occurred in 80 (64.0%) and was strongly associated with IMR improvement. Excluding 25 patients with >50% LVEDV reduction yielded consistent findings.

Serial echocardiography demonstrated substantially greater ventricular and IMR improvement during the post-revascularization interval than during the preceding medical-therapy interval. These temporal associations do not establish an independent causal effect of revascularization but support serial echocardiographic assessment of ventricular remodeling and residual IMR.

We aimed to assess whether low-grade albuminuria, characterized by a low urinary albumin-to-creatinine ratio (UACR) within the normal range (<30 mg/g), could predict cardiovascular disease (CVD) risk in a low-risk general population, with an emphasis on sex- and menopause-specific differences.

We analyzed data from 1327 participants from the Korean Genome and Epidemiology Study, excluding individuals with known CVD or major chronic illnesses, who were followed up for a median of 6.37 years. The UACR was measured from spot urine samples and treated as a continuous variable. The cardiovascular outcomes included stroke, myocardial infarction, and angina. Cox proportional hazards models and restricted cubic spline analyses were used to assess the association between UACR and incident CVD, stratified by sex and menopausal status.

No significant association was observed between UACR and CVD in men or premenopausal women. However, in postmenopausal women, UACR was significantly associated with incident CVD (adjusted hazard ratio 1.09; 95% confidence interval: 1.01-1.18 per 1 mg/g increase). Spline analyses revealed a clear dose-response relationship in postmenopausal women, whereas no such pattern was observed in the other subgroups. Covariate-stratified analyses suggested a potential interaction effect of body mass index, blood pressure, and lipid profile.

Low-grade albuminuria may serve as an early biomarker of cardiovascular risk in otherwise healthy individuals, particularly in subgroups susceptible to hormonal or metabolic changes. Routine UACR screening may be a practical tool for early risk stratification and prevention of CVD.

Cardiac rehabilitation (CR) is central to tertiary prevention after acute myocardial infarction (AMI), but the prognostic impact of different education and therapy patterns in Asian real world practice is uncertain.

Using Korean National Health Insurance Service claims (2018-2022), we identified patients aged ≥40 years hospitalized for AMI who underwent thrombolysis, percutaneous coronary intervention, or coronary artery bypass grafting. CR exposure was classified into six groups by structured education and the number of supervised therapy sessions, and outcomes over 2 years included all cause readmission, readmission and emergency room (ER) visits for MI or unstable angina (UA), all cause mortality, repeat revascularization, and stroke. Multivariable Cox models estimated adjusted hazard ratios (HRs) with 95% confidence intervals (CIs).

Among 92968 patients, 85.5% received no CR, 3.2% had education only, and 11.3% received any therapy. Education only participants had the lowest crude rates of mortality, cardiovascular readmission, and repeat revascularization. All CR exposed groups showed lower all cause mortality, with the greatest benefit in education plus ≥4 therapy sessions (HR 0.257, 95% CI 0.123-0.539) and ≥4 therapy sessions without education (HR 0.291, 95% CI 0.203-0.417). Education focused CR was additionally associated with lower cardiovascular readmission and repeat revascularization, whereas readmission and ER visits varied across therapy intensive groups.

In this nationwide Korean AMI cohort, CR participation, especially with education, was associated with substantial mortality reduction, suggesting structured education as a pragmatic cornerstone of tertiary prevention, with supervised therapy providing incremental benefit when available.

Surgical stress, such as liver ischemia/reperfusion (I/R) injury characterized by robust neutrophil infiltration and immune activation, induces sterile inflammation that reshapes tissue immunity and contributes to organ dysfunction, yet the intercellular circuits that spatially orchestrate these responses within the hepatic immune microenvironment remain incompletely defined. Here, we integrate single-cell RNA sequencing, spatial transcriptomics, high-dimensional spectral flow cytometry, and metabolomics to resolve the hepatic immune landscape following I/R at cellular and spatial resolution. While confirming extensive immune remodeling, we identify a dominant neutrophil-Kupffer cell communication axis mediated by neutrophil-derived thrombospondin-1 (TSP-1), which selectively engages CD36 on Kupffer cells. This interaction drives coordinated immune-metabolic reprogramming in Kupffer cells, characterized by suppression of oxidative phosphorylation, enhanced glycolysis, and remodeling of sphingolipid metabolism, including accumulation of hexosylceramides. Spatial analyses reveal preferential neutrophil-Kupffer cell colocalization within necrotic niches, and cross-species integration with human liver transplant datasets demonstrates conserved upregulation of the TSP-1/CD36 axis following reperfusion. Pharmacologic inhibition of TSP-1 attenuates liver injury and inflammatory responses in vivo. Together, these findings define a spatially organized, neutrophil-driven immune-metabolic circuit that governs functional reprogramming of Kupffer cells during surgical stress and identify the TSP-1/CD36 pathway as a conserved and targetable mediator of sterile liver injury.

Fibroblast activation protein (FAP) has gained clinical interest as a target for imaging and therapy in a spectrum of oncologic diseases in recent years. Yet, FAP expression by activated fibroblasts is not specific to the tumor microenvironment but rather shows tight coupling to pathologic tissue remodeling, chronic inflammation, and fibrosis across a broad spectrum of nonmalignant diseases. This linkage provides a compelling biologic rationale for extending FAP-directed imaging beyond oncologic applications. Indeed, across various cardiac (ischemic heart disease, nonischemic cardiomyopathy, valvular pathology), vascular (atherosclerosis, vasculitis, aneurysm), rheumatologic (interstitial lung disease, inflammatory arthritis, IgG4-related disease), and other conditions, emerging data suggest that FAP-directed PET may serve as an imaging biomarker for active tissue remodeling. Nonetheless, the supporting clinical evidence is derived primarily from early-stage studies and remains largely exploratory at present. FAP-targeted therapies (e.g., FAP-targeting radiopharmaceutical therapies and chimeric antigen receptor T-cells) are also being actively explored outside of oncology in preclinical settings. While further investigation remains needed, FAP-directed PET has the potential to become a valuable addition to fibrosis-driven disease monitoring. Within this context, this Special Series Review highlights the current early evidence and future potential of FAP-directed PET across a variety of nononcologic conditions.

Elevated blood pressure is an established risk factor for abdominal aortic aneurysm (AAA), yet traditional measures inadequately capture dynamic hemodynamic stress. This study examined the association between visit-to-visit systolic blood pressure variability (SBPV) and incident AAA, assessed whether genetic susceptibility modified this association, and explored protein-specific indirect associations. Visit-to-visit SBPV was calculated from ≥3 systolic blood pressure measurements in 189,770 UK Biobank participants with linked primary care records. Cox proportional hazards models evaluated SBPV-AAA associations, adjusting for cardiovascular risk factors and mean systolic blood pressure. Polygenic risk scores stratified genetic susceptibility. Proteomic profiling was used for exploratory protein-specific indirect-effect analyses. Over median follow-up of 10.7 years, 1,036 incident AAA cases occurred. Higher SBPV was independently associated with increased AAA risk across all metrics (all P for trend ≤0.003), with 33%-54% increased risk comparing the highest versus lowest tertile. Dose-response relationships were approximately linear (all P for non-linearity >0.05). High SBPV conferred elevated risk even with mean systolic blood pressure <130 mmHg. Participants with both high SBPV and high genetic risk had more than two-fold increased AAA risk (hazard ratio 2.07-2.28, all P<0.001). Ten circulating proteins showed FDR-significant protein-specific indirect effects in separate exploratory models, with descriptive coefficient-attenuation estimates ranging from 6.7% to 30.4%; these protein-specific estimates are non-additive and do not establish causal mediation. Associations remained robust across multiple sensitivity analyses. Higher visit-to-visit SBPV was associated with increased AAA risk, particularly among genetically susceptible individuals. These findings support SBPV as a potential AAA risk marker and warrant external validation, but do not establish that reducing SBPV would prevent AAA.

Tetralogy of Fallot (ToF) is the most common cyanotic congenital heart disease, with an incidence of approximately 1 in 3,500 live births, accounting for 7-10% of all congenital heart defects. Advances in cardiac surgery and intensive care have increased survival into adulthood to over 85%, resulting in a growing population of adults with repaired congenital heart disease and, in resource-limited settings, adults with untreated or previously undiagnosed disease. In this context, specialist nursing care plays a pivotal role throughout the continuum of care.

To systematically review the available scientific evidence on nursing care for patients with tetralogy of Fallot, with particular emphasis on nursing interventions during the preoperative and postoperative phases and on the competencies required across different clinical settings.

A systematic literature review was conducted between November 2025 and March 2026 using PubMed, the Cochrane Library, and CINAHL, following the PRISMA methodology. The search strategy was: care AND tetralogy of Fallot AND nurs*. Of the 56 records initially identified, 33 articles were screened after duplicate removal. Following the application of the eligibility criteria and methodological quality assessment using the Joanna Briggs Institute (JBI) Critical Appraisal Checklist, with an inclusion threshold of ≥75%, four studies were included in the review. The selected studies comprised two case reports and two narrative reviews.

The four included studies collectively addressed the major stages of the care pathway for patients with ToF: neonatal preoperative stabilization (Tran et al., 2022), postoperative management in the pediatric intensive care unit (Forman et al., 2019), nursing management of adults with unrepaired ToF (Araújo et al., 2017), and peri-anesthetic assessment of an adult patient with previously undiagnosed ToF (Edwards et al., 2025). Four principal themes emerged: systematic clinical monitoring as a strategy for preventing complications; management of hypercyanotic (Tet) spells; implementation of the nursing process using the standardized NANDA-I, NIC, and NOC taxonomies; and family support as an integral component of comprehensive nursing care.

Comparison of the included studies demonstrated strong consistency regarding the core principles of nursing care for patients with ToF, including systematic monitoring, prevention of complications, individualized care, and family-centered support. These principles are adapted according to the stage of care, patient age, and clinical setting. Particular attention emerged regarding the management of adults with ToF, whether surgically repaired or previously undiagnosed, representing an increasingly important challenge for specialist nursing practice. The expanding population of adults with congenital heart disease requires nurses with advanced competencies in clinical assessment, critical thinking, and cultural sensitivity.

Nurses play a key and irreplaceable role in the care pathway of patients with tetralogy of Fallot. Specialist clinical expertise, an evidence-based systematic approach, early clinical assessment, and family-centered care constitute the cornerstones of high-quality nursing care for this complex condition. The development of specialized educational pathways in adult congenital cardiology nursing should be considered a priority to ensure safe, equitable, and high-quality care for this continuously growing patient population.

Angiogenesis plays a critical role in the progression of endometriosis, with enhanced glycolysis accelerating pathological angiogenesis. Prior research has identified a central role for N6-methyladenosine (m6A) modification in regulating glycolytic processes. This study investigates the involvement of m6A-mediated mechanisms in the regulation of glycolysis and angiogenesis in endometriosis. Here, we report that PFKFB3 is significantly upregulated in vascular endothelial cells of ectopic endometrial tissues from humans and mice, correlating with elevated expression of YTHDF3. Specific deletion of Ythdf3 in endothelial cells reduces PFKFB3 protein levels and suppresses angiogenesis in ectopic endometrial lesions. Mechanistically, PFKFB3 mRNA displays increased m6A modifications in endometrial microvascular endothelial cells (EMECs). METTL3 enhances m6A modification of PFKFB3 mRNA, which is recognized by YTHDF3, promoting PFKFB3 translation and glycolytic activity, thus facilitating tube formation, migration, and proliferation of ovarian microvascular endothelial cells (OMECs). Moreover, estrogen upregulates both METTL3 and PFKFB3 via the estrogen receptor ERα. Collectively, these findings establish the YTHDF3-m6A-PFKFB3 pathway as a critical driver of angiogenesis in endometriosis, suggesting that targeting this pathway represents a promising therapeutic strategy.