Non-contrast computed tomography (NCCT) is widely used for post-treatment monitoring of patients with ischemic stroke due to its rapid acquisition, low cost, and non-invasiveness. Segmentation of ischemic lesions on NCCT images is critical for assessing disease severity and guiding clinical decision-making.

We propose an ensemble-based semi-supervised segmentation (ESS) framework to reduce the dependence of convolutional neural networks (CNNs) on a large number of manual annotations. The proposed method mainly consists of two components: first, strong data augmentation is introduced to increase sample diversity and alleviate overfitting in the presence of limited labeled data; second, a parameter-free ensemble module is adopted to generate more stable supervision signals for unlabeled samples and improve the reliability of pseudo-labels by fusing the predictions of the two student models. The proposed ESS is evaluated on a manually annotated follow-up NCCT dataset consisting of 9,020 image slices.

ESS consistently achieves the highest Dice coefficient among all compared methods under all four labeled-data ratios, with a more pronounced performance advantage when labeled data are scarce.

These results demonstrate the effectiveness of ESS for semi-supervised segmentation of follow-up NCCT under limited annotation conditions.

Cardiac rehabilitation (CR) improves peak oxygen uptake (VO₂peak) and body composition in patients with cardiovascular disease. However, improvement in VO₂peak is not observed in all patients following a CR program, and whether VO₂peak non-responders also demonstrate limited changes in body composition remains unclear. This study aimed to examine the association between changes in VO₂peak and body composition in patients undergoing a CR program.

Retrospective analysis of patients who completed CR between 2015 and 2022 at Mayo Clinic. The study included 143 patients who completed cardiopulmonary exercise testing and dual-energy X-ray absorptiometry pre- and post-CR. Patients were grouped by the change in relative VO₂peak response to CR (responders= Δ>0 vs non-responders=Δ ≤0 mL/kg/min). Two-way repeated ANOVA was used to compare groups, and regression models were used to examine the associations between baseline body composition and changes in body composition with VO₂peak change.

Among the cohort, 26% were classified as non-responders based on relative VO₂peak measurements. Both groups exhibited a significant improvement in most body composition variables including body fat mass, body fat percentage, body lean percentage, and fat mass index (all p<0.001), with no differences in the percentage of change in body composition variables between groups (p>0.05). Regression models demonstrated that neither baseline body composition nor changes in body composition were significantly associated with changes in VO₂peak.

Our data suggest that baseline and change in body composition were not significantly associated with changes in VO₂peak in patients undergoing the CR program.

Health vulnerability (HV), an intrinsic multidimensional construct integrating physiological, psychological, and social domains, may be associated with cardiovascular disease (CVD) risk. However, existing HV assessments lack integration and temporal dynamics change. This study identifies the dynamic association between the HV and risk of CVD.

This longitudinal cohort study included 16,072 participants from the UK Biobank with HV assessments at baseline (2006-2010) and repeat assessment (2014). Latent class analysis and latent transition analysis were used to identify HV transition patterns. Cox proportional hazards models were applied to evaluate associations between HV transitions and incident CVD, with follow-up initiated from baseline assessment. Sensitivity analyses included alternative HV transitions classification, exclusion of hypertensive diseases from the composite outcome, and competing risk analyses considering non-CVD death.

During a median follow-up of 8.9 years, 3,033 incident CVD events were identified. Compared with persistently low vulnerability, increasing vulnerability and persistently elevated vulnerability were associated with higher CVD risk after multivariable adjustment (HR = 2.14, 95% CI: 1.74-2.63 and HR = 1.18, 95% CI: 1.08-1.29, respectively). Subgroup analyses identified significant effect modification by age and smoking status, indicating that the associations between HV transitions and CVD risk differed across these populations. The main findings remained consistent in sensitivity analyses.

Dynamic changes in HV were associated with subsequent CVD risk, with increasing and persistently elevated vulnerability showing higher risks. These findings highlight the potential importance of monitoring multidimensional vulnerability changes for cardiovascular risk assessment.

To evaluate the association of Platelet Function Testing (PFT)-guided intensified antiplatelet strategy with the incidence of thromboembolic events and bleeding rates in patients with Unruptured Intracranial Aneurysms (UIA) undergoing stent-assisted coil embolization, compared with standard fixed-dose Dual Antiplatelet Therapy (DAPT).

In this retrospective study, 368 patients from two centers between January 2019 and September 2024 were enrolled and categorized into a Monitored Group (n = 219) and a Non-monitored Group (n = 149). Both groups initially received a fixed-dose DAPT regimen of clopidogrel 75 mg and aspirin 100 mg daily. Within 24 h prior to the procedure, the Monitored Group underwent PFT. Patients exhibiting High On-Treatment Platelet Reactivity (HPR) to clopidogrel were administered a single 300 mg clopidogrel loading dose and received short-term perioperative tirofiban. For patients with HPR to aspirin, the aspirin dose was increased to 200 mg daily. The Non-monitored Group did not undergo platelet function testing and dose adjustment. To control for confounding, propensity score matching (PSM) and multivariable Cox regression were performed. The primary outcome was the composite thromboembolic event rate within 7 days post-procedure. Secondary outcomes included the composite thromboembolic event rate within 30 days, and the safety outcome was the composite bleeding event rate within 30 days.

In the original cohort, the monitored strategy was associated with a lower incidence of the primary 7-day composite thromboembolic outcome (3.20% vs. 8.05%; unadjusted HR = 0.388, 95%CI 0.153-0.985, p = 0.045; adjusted HR = 0.391, 95%CI 0.154-0.994, p = 0.048). The association remained directionally consistent in the propensity score-matched cohort (115 pairs, 4.35% vs. 8.70%; HR = 0.487, 95%CI 0.166-1.424, p = 0.189). The secondary 30-day composite thromboembolic outcome showed similar patterns (original cohort: adjusted HR = 0.412, 95%CI 0.187-0.909, p = 0.028; PSM cohort: HR = 0.446, 95%CI 0.169-1.172, p = 0.101). No statistically significant association was observed for the 30-day composite bleeding event rates between the two groups in either the original or matched analyses. Subgroup analyses identified no significant association modifiers.

A PFT-guided intensified antiplatelet strategy was associated with a lower incidence of early post-procedural thromboembolic events without a significant increase in major bleeding in UIA patients treated with EP2 stent-assisted coiling. These findings support the potential utility of this comprehensive strategy, although the independent contribution of each component requires further investigation in larger prospective studies.

A magnetic resonance image (MRI) study recently described greater improvements in gray matter volume and cortical thickness in post-stroke patients with upper-limb spasticity treated with surgery versus botulinum toxin-A (BoNT-A).

To compare changes in the white matter of these patients after surgical versus BoNT-A treatment and to relate findings to upper-limb function and quality-of-life.

In a two-arm randomized controlled clinical trial, 30 post-stroke patients (>12 months) with spastic upper limbs were recruited and randomly assigned (1:1) to surgery or BoNT-A treatment (controls). Functional and quality-of-life parameters were studied at baseline (pre-intervention) and at 6 months, while brain MRI scans of the white matter were taken at the same time points using a Siemens 3T Prisma MRI scanner. Although baseline MRI scans were obtained in all 30 participants, complete longitudinal MRI data were available for only 14 participants because of contraindications or refusal of follow-up imaging. Therefore, the imaging analyses were considered only exploratory and hypothesis-generating.

Increased post- versus pre-surgery fractional anisotropy (FA) values were associated with Carer Burden and House functional scale scores, and decreased FA values with Ashworth, Fugl-Meyer, pain visual analogue scale, and SF-36 scores. Reduced mean diffusivity (MD) values for inferior fronto-occipital fasciculus, cingulum parahippocampal parietal, uncinate fasciculus, and reticular tract were associated with improvements in Fugl-Meyer motor recovery scores.

The post-pre increase in FA of white matter tracts in the experimental versus control group may suggest differences in white matter microstructure between treatment groups, potentially reflecting neuroplastic changes. These findings suggest that changes in white matter microstructure might be associated with improvements in motor function, independence, and caregiver burden. However, given the small longitudinal MRI sample, the tract-specific findings should be considered hypothesis-generating and require confirmation in larger studies.

Lupus nephritis (LN) confers a disproportionate thrombotic risk in systemic lupus erythematosus (SLE) that is not fully explained by conventional cardiovascular risk factors. The underlying molecular mechanisms remain largely unknown. We aimed to characterize the thrombo-inflammatory profiles in LN compared with SLE without nephritis (SLE-NonLN), and contextualized these findings to primary antiphospholipid syndrome (APS), primary Sjögren's disease (SjD), and healthy controls. In a cross-sectional design, we included 325 patients with SLE from two Danish cohorts, 10 with primary APS, 45 with primary SjD, and 100 healthy controls. A predefined thrombo-inflammatory panel encompassing endothelial and platelet activation, coagulation, fibrinolysis, and complement pathways was assessed using immunoassays. Group differences were adjusted for clinical covariates and multiple testing. Multivariate patterns were examined using principal component analysis, correlation networks, and logistic regression. Thrombomodulin levels were higher in SLE-LN than in SLE-NonLN and remained associated with LN after multiple testing correction and adjustment for age, treatment exposure, and disease activity. Thrombomodulin showed a modest association with albuminuria but not with disease activity, anti-double-stranded DNA antibody levels, or secondary APS. Correlation networks demonstrated a dense, integrated thrombo-inflammatory structure in SLE-LN. In multivariable logistic regression, thrombomodulin and prednisolone use emerged as independent factors associated with LN. LN is characterized by a distinct thrombo-inflammatory profile dominated by endothelial activation, with thrombomodulin emerging as the most consistent biological marker of renal involvement in SLE. The coordinated alterations observed across multiple pathways highlight the potential value of systems-oriented approaches for advancing mechanistic understanding in LN.

Reversible cerebral vasoconstriction syndrome (RCVS) is an under-recognized clinical entity characterized by transient segmental vasoconstriction of cerebral arteries. It commonly presents with thunderclap headaches and can mimic other acute neurological conditions, often delaying diagnosis. Known risk factors include the female sex, postpartum state and exposure to vasoactive substances.

We report the case of a 26-year-old, white woman presenting ten days postpartum with severe, recurrent headaches. Her medical history included opioid maintenance therapy and past cocaine use. Initial laboratory findings, magnetic resonance imaging (MRI) and transcranial duplex sonography (TCD) were unremarkable leading to the assumption of a multifactorial etiology of the headaches. However, 11-12 days after symptom onset, the development of new focal neurological deficits prompted repeat imaging (MRI and TCD), finally revealing basal cerebral arteries vasoconstriction and increased flow velocity consistent with RCVS. Treatment with nimodipine resulted in rapid clinical and sonographic improvement, with complete resolution of symptoms and vascular findings at 1-month follow-up.

This case underlines the diagnostic challenges of RCVS. Clinicians should maintain a high index of suspicion for RCVS in patients presenting with acute-onset headaches and risk profiles, even in the absence of early imaging abnormalities. Early recognition and targeted treatment may improve outcomes in this potentially reversible condition.

This systematic review and meta-analysis aimed to compare the associations of four triglyceride-glucose (TyG)-derived indices (TyG, TyG-BMI, TyG-WC, TyG-WHtR) with incident cardiovascular disease (CVD) risk among individuals with stage 0-3 cardio-kidney-metabolic (CKM) syndrome, and explore potential sources of inter-study heterogeneity using pre-specified subgroup analyses and exploratory meta-regression analyses.

We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library from database inception to May 1, 2026. Two independent reviewers completed study screening, data extraction, and quality assessment using the Newcastle-Ottawa Scale (NOS). Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were synthesized using fixed- or random-effects models according to between-study heterogeneity, which was quantified by Cochran's Q test and the I² statistic. Subgroup analyses, exploratory univariable meta-regression analyses, leave-one-out sensitivity analyses, and publication bias assessments were performed to investigate potential sources of heterogeneity and evaluate the robustness of the findings.

Nine high-quality prospective cohort studies were ultimately included. Participants in the highest versus lowest quantiles of each index had significantly elevated CVD risk: TyG (HR = 1.24, 95% CI 1.16-1.33, I² = 76%), TyG-BMI (HR = 1.44, 95% CI 1.26-1.66, I² = 93%), TyG-WC (HR = 1.42, 95% CI 1.21-1.67, I² = 96%), and TyG-WHtR (HR = 1.45, 95% CI 1.28-1.65, I² = 91%). Exploratory meta-regression suggested that follow-up duration may contribute to heterogeneity in TyG, whereas age may contribute to heterogeneity in TyG-WHtR; substantial residual heterogeneity remained for TyG-WC and TyG-WHtR. Sensitivity analyses supported the robustness of the findings. No significant publication bias was detected, but statistical power was limited by fewer than 10 studies per index.

This meta-analysis suggests that elevated TyG-derived indices are significantly associated with increased incident CVD risk among individuals with stage 0-3 CKM syndrome. Composite TyG-derived indices showed numerically higher pooled effect estimates than the TyG index; however, overlapping confidence intervals and the absence of direct statistical comparisons prevent conclusions regarding the superiority of any specific index. Given the observational nature of the included studies, limited population diversity, and substantial residual heterogeneity, these findings should be interpreted cautiously. TyG-derived indices may represent potential auxiliary markers for CVD risk stratification, and further large-scale multi-ethnic prospective studies are warranted to evaluate their clinical utility.

To investigate the role of the RIPK1 inhibitor GFH312 in ischemic stroke and identify its potential mechanisms.

GFH312 was administered to adult mice in an ischemic stroke model. To ascertain the effectiveness of treatment, neurobehavioral tests and assessments of brain damage were carried out. Brain tissues were examined using immunofluorescence as well as western blot and real-time quantitative PCR at various intervals following ischemia to evaluate inflammatory gene expression and signaling pathways linked to apoptosis and necroptosis.

Temporal analysis revealed that necroptosis and apoptosis were rapidly activated following ischemia, peaking at 1-3 days. GFH312 significantly improved neurological function and reduced brain injury in stroke mice. Mechanistically, GFH312 markedly inhibited apoptosis and necroptosis via suppression of the RIPK1-related signaling pathway (RIPK1-RIPK3-MLKL). In addition, GFH312 greatly decreased inflammatory gene expression in the brain.

Apoptosis and necrotic apoptosis occur primarily during the acute poststroke phase. GFH312 exerts neuroprotective effects after ischemic stroke, which are associated with suppression of RIPK1-related apoptosis, necroptosis, and neuroinflammation.

Xeroderma pigmentosum group A (XPA) serves as a core nucleotide excision repair (NER) factor essential for the repair process triggered by UV irradiation. Lactylation, a newly identified post-translational modification, plays a key role in tumorigenesis and cancer progression. Herein, we discovered that XPA was lactylated in the DNA-binding domain by the acyl-transferase KAT5. In addition, UV irradiation promoted XPA lactylation, thereby increasing the chromatin recruitment of XPA and NER. However, the mutation of XPA to a lactylation-deficient form impeded XPA chromatin recruitment under UV irradiation, impaired NER, and rendered cancer cells hypersensitive to UV irradiation. Our data demonstrate that the lactylation of XPA plays a crucial role in NER and reveals the link between metabolic reprogramming and DNA damage repair induced by UV irradiation.