Circulating Apolipoprotein E (ApoE) plays key roles in lipoprotein metabolism, but its clinical utility in cardiovascular risk assessment and its relationship with incident heart failure remain unclear. This study aims to evaluate the association of serum ApoE concentration with incident cardiovascular outcomes.

This retrospective cohort study used electronic health records from a multi-specialty outpatient population in Shenzhen, China. Adults who had serum ApoE measured and did not have prior ischemic heart disease, stroke, or heart failure were included (N=14,852). The outcomes were incident major adverse cardiovascular events (MACE), ischemic heart disease, stroke, and heart failure. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard models.

During a median follow-up of 4.0 years, we observed 491 MACE, 515 ischemic heart disease, 293 stroke, and 181 heart failure incident events. Higher ApoE concentrations were significantly associated with increased risks of incident MACE (HR[95%CI] per 1mg/dL increment: 1.09[1.04-1.15]), ischemic heart disease (1.07[1.02-1.13]), and heart failure (1.14[1.07-1.22]), but not stroke (1.03[0.96-1.11]). These associations were independent of low-density lipoprotein cholesterol (LDL-C), small and dense LDL-C, high-density lipoprotein cholesterol, and neutrophil-to-lymphocyte ratio. However, adjustment for triglycerides attenuated the associations. Individuals with elevations in both ApoE and triglycerides had disproportionately higher risks of cardiovascular events.

Elevated circulating ApoE concentrations are risk factors for incident MACE, ischemic heart disease, and heart failure, and may signal the residual risk of cardiovascular disease beyond cholesterol markers. Concurrent elevation in ApoE and triglycerides may represent a high-risk clinical phenotype, suggesting the joint assessment of ApoE and triglycerides may improve risk stratification for hypertriglyceridemic individuals.

Statistical models used to estimate the cardiovascular disease (CVD) risk often present methodological constraints leading to overestimate or underestimate the total CVD risk. The aim of this study was to develop and implement a web-based Machine Learning (ML) platform to predict the personalized 10-year CVD risk for the Greek population.

The retrospective study included clinical and demographic data from 3,290 CVD-free participants. The CVD risk prediction model was based on two classifiers. The first was a binary classifier to estimate the occurrence of CVD, and the second was a multiclass classifier designed to replicate SCORE2 risk stratification categories. The selection of appropriate algorithms for integration into the platform was based on the evaluation metric ROC-AUC. To support the clinicians, the platform was integrated with scientific libraries to retrieve the most relevant literature based on the features that most influence the model decision-making.

The Voting Ensemble algorithm was selected for the binary classifier, achieving an AUC-ROC of 0.78. For the multiclass classifier, the selection algorithm was Stacking Ensemble, which yielded a 0.97 AUC-ROC. The comparison between ML and statistical model HellenicScore showed that the binary classifier was better in all metrics except accuracy in which HellenicSCORE had a higher value. The CVD risk prediction model and the integration with scientific libraries were successfully developed and deployed as a web-based platform.

The pilot run of the platform showed that it could be used as a reliable tool for CVD risk assessment, outperforming the traditional statistical models.

Aortic dissection (AD) is a fatal cardiovascular emergency for which effective pharmacological treatments are lacking. Increasing evidence suggests that spicy diets exert beneficial effects on cardiovascular diseases. However, whether a spicy diet can attenuate AD, and the mechanisms by which it might do so, remain unclear.

This study was performed to investigate the role of dietary capsaicin in AD and to elucidate its underlying mechanisms.

Fifty patients with AD (AD group) and 50 volunteers with risk factors for AD (NP group) were enrolled to examine associations among spicy food consumption, serum capsaicin levels, and AD. In addition, a β-aminopropionitrile-induced AD mouse model and a lipopolysaccharide-induced M1 macrophage polarisation model were established to investigate the impact of capsaicin on AD and elucidate its underlying mechanisms.

Patients with AD exhibited lower spicy food consumption, reduced serum capsaicin concentrations, and gut microbiota dysbiosis compared with the NP group. Dietary capsaicin attenuated AD pathogenesis in mice, suppressed M1 macrophage polarisation, and restored gut microbiota homeostasis. Mechanistically, in vitro transcriptomic sequencing and small interfering RNA experiments demonstrated that capsaicin activates TRPV1 to suppress TLR4/MyD88/NF-κB signalling, thereby inhibiting M1 macrophage polarisation. Importantly, the TRPV1 antagonist capsazepine abrogated the protective effects of capsaicin in vivo, confirming TRPV1 dependence.

These findings elucidate the mechanistic basis of the protective effects of dietary capsaicin against AD and provide the first evidence that dietary capsaicin attenuates AD by inhibiting M1 macrophage polarisation, an effect accompanied by the restoration of gut microbiota homeostasis and improved intestinal barrier function. Collectively, this work supports dietary capsaicin as a promising therapeutic strategy for AD.

Protein inhibitor of activated STAT 1 (PIAS1) functions as a SUMO E3 ligase, regulating cardiovascular diseases by promoting the SUMOylation of target proteins; however, its role in abdominal aortic aneurysm (AAA) remains unclear. Currently, molecular targeted therapies for AAA are still very limited. This study aimed to clarify whether PIAS1 regulates the stability of the PPARγ protein through SUMOylation to elucidate its molecular mechanisms in AAA formation and to evaluate its potential as a novel therapeutic target.

AAA rat models were established via the infusion of porcine pancreatic elastase, and an in vitro cell model was constructed by treating human umbilical vein endothelial cells (HUVECs) with Ang II. Flow cytometry, ELISA, H&E staining, and EVG staining were used to assess cell and abdominal aortic tissue damage, while RT-qPCR and Western blotting were used to detect the expression of relevant genes and proteins.

This study revealed that PIAS1 is expressed at low levels in AAA. The overexpression of PIAS1 effectively inhibited Ang II-induced lipid accumulation and inflammatory responses in HUVECs and AAA rats, alleviated pathological damage and apoptosis in the abdominal aorta, and alleviated the progression of AAA. With respect to the regulatory mechanism, the SUMOylation and expression levels of PPARγ are downregulated in AAA. PIAS1 primarily stabilizes PPARγ expression by promoting its SUMOylation, thereby inhibiting lipid accumulation and inflammatory responses. Further studies revealed that SENP3 is highly expressed in AAA and that PIAS1 can downregulate SENP3 levels, thereby attenuating its deSUMOylation effect on PPARγ and ultimately promoting the SUMOylation and expression of PPARγ.

PIAS1 alleviates the progression of AAA by inhibiting SENP3 expression, thereby promoting PPARγ SUMOylation and protein expression, which in turn reduces lipid accumulation and inflammatory responses.

Anthracyclines such as doxorubicin (DOX) are widely used in cancer chemotherapy but their clinical utility is severely limited by cumulative, dose-dependent, and largely irreversible cardiotoxicity. Mounting evidence suggests that DOX disrupts intestinal barrier integrity and microbial homeostasis, aggravating systemic oxidative stress and accelerating myocardial injury through the gut-heart axis. Probiotics offer a potential strategy to stabilize the intestinal microenvironment, yet their fragile nature and poor survival in the gastrointestinal tract hinder clinical translation. Here, we present an orally administrable bioinspired peroxisome engineered probiotic (BPEP) as a safe and effective therapeutic platform. Ruthenium-based nanozymes with superoxide dismutase-like and catalase-like activities were encapsulated in a lipid shell to form bioinspired peroxisomes (BP) and covalently anchored onto Escherichia coli Nissle 1917. The lipid shell enhances probiotic resistance to gastric acid, bile salts, and reactive oxygen species, improving gastrointestinal survival and colonization. Acting as a living carrier, probiotics deliver BPs to the intestinal barrier, where they synergistically scavenge reactive oxygen and nitrogen species, restore tight junction integrity, and remodel microbial communities. In a chronic DOX-induced cardiotoxicity mouse model, oral administration of BPEP effectively alleviated oxidative stress, preserved intestinal barrier function, stabilized microbial homeostasis, and ultimately improved cardiac function. This work establishes a bioinspired probiotic-nanozyme hybrid strategy that overcomes the intrinsic limitations of natural probiotics and provides a promising approach for mitigating chemotherapy-related cardiotoxicity via the gut-heart axis.

Moyamoya disease is a rare progressive cerebrovascular disorder involving stenosis of major intracranial arteries and the formation of fragile collateral vessels. Patients face lifelong risks of ischemic and hemorrhagic stroke. Surgical revascularization is the definitive treatment, aimed at restoring cerebral perfusion and reducing neurologic injury. Postoperative care is among the most complex in neuroscience nursing. Critical care nurses play a vital role in managing cerebral perfusion, conducting frequent neuro assessments, regulating blood pressure, and preventing seizures. Success requires individualized hemodynamic targets, early detection of complications like hyperperfusion or ischemia, psychosocial support, and close interdisciplinary collaboration.

Inflammation and immune response significantly contribute to brain injury following subarachnoid hemorrhage (SAH), a severe neurological condition. This study employed Mendelian randomization, colocalization, and multi-omics analysis to examine potential causal connections between inflammatory proteins, immune cells, and SAH, aiming to elucidate its pathogenesis.

This study utilized publicly available data from genome-wide association studies (GWAS), including protein QTL (pQTL) and RNA sequencing data. Bidirectional two-sample Mendelian Randomization (MR) analysis was initially employed to evaluate the cause-and-effect relationships among inflammatory proteins, immune cells, and SAH. A comprehensive multi-omics approach, encompassing transcriptome, colocalization, mediation MR, was employed to identify specific inflammatory proteins, immune cells, and potential drug targets.

A causal relationship between five inflammatory proteins and SAH was identified through MR analysis (CD6, FGF23, TGFB-1, LIFR, and TGF-α). Moreover, a causal relationship with SAH was identified in 22 types of immune cells. Subsequent multi-omics analysis showed that FGF23 was a hub inflammatory protein, and its expression level was closely linked to the amount of CD4 Treg cells. Meta-analysis and replication studies identified FGF23 as a risk factor for SAH, with a colocalization score of 0.74.

This study successfully identified inflammatory proteins and immune cells associated with SAH, and revealed the complex genetic causality and drug targets of SAH.

Human trafficking poses a major public health challenge to the international community, with significant health and social consequences for those affected. Forced migrants are particularly vulnerable to becoming victims of human trafficking due to language barriers and migration-related hardships. These include social and economic deprivation. To better understand the lived experiences within this already vulnerable group, it is essential to examine individual cases in relation to risk factors, experiences of exploitation and exit, and resilience.

Using a qualitative approach, this study examines social determinants and risk factors of forced migrants who survived human trafficking. It explores their experiences, eventual escape, and sheds light on their resilience. For this purpose, semi-structured interviews regarding the trafficking experiences were conducted with newly arrived forced migrants at a reception and registration centre in Germany. The presence of human trafficking was determined through an initial screening procedure and then confirmed in a personal interview. Additionally, we assessed the refugees' mental health burden with brief screening questionnaires for post-traumatic stress disorder, depression, anxiety, and the overall stress level (PC-PTSD-5, GAD-2, PHQ-2, RHS-15 distress thermometer).

A total of 20 interviews were conducted with 14 female and 6 male participants. The participants came from 9 different countries. Most of them experienced sexual exploitation (N = 11), labour exploitation (N = 7). Few were trafficked but not exploited (N = 3). Participants reported that financial hardship was the main benefitting exploitation risk, and in many cases, they had been recruited by individuals they already knew. Spiritual rituals were sometimes used to increase pressure and control. Various forms of violence were inherent to the trafficking situations. In most cases, those affected managed to free themselves. Interpersonal connections and religious beliefs played a crucial role in coping with these experiences, however the screening for common mental disorders among refugees still indicated high levels of psychological distress. The results are discussed in relation to existing literature and implications for support and intervention are presented.