Against the backdrop of escalating global plastic pollution, there is an urgent need to elucidate the systemic health risks posed by nanoplastics (NPs) as emerging environmental contaminants that enter higher organisms through the food chain. This study employed a three-level trophic transfer model, examining the pathway from polystyrene nanoparticles to Tenebrio molitor larvae and subsequently to mice, offering a comprehensive elucidation of the mechanisms behind the multiorgan toxicity associated with food chain-transferred nanoplastics (FCT-NPs). Our results demonstrated extensive accumulation of FCT-NPs across multiple organs via systemic circulation. Integrative multiorgan omics analysis revealed that FCT-NPs primarily induced two major categories of multiorgan comorbidities: cardiovascular diseases and metabolic disorders, with the liver identified as a central metabolic hub that potentially regulates other organs through bile acid-mediated metabolic crosstalk. Mechanistically, dysregulation of key genes, such as MTOR and FN1, activated Wnt and TGF-β signaling pathways, which in turn promoted organ fibrosis. Additionally, aberrant expression of critical regulators─including CAT, LPL, NQO1, and APOE─was found to drive oxidative stress and disrupt lipid metabolism. These findings provide crucial scientific evidence for FCT-NPs risk assessment and underscore the imperative for enhanced plastic pollution control and further investigation into long-term exposure effects.

A 45 year old patient presented with left upper visual field defect and decreased vision on the first postoperative day following "stent-assisted endovascular embolization for a ruptured left middle cerebral artery aneurysm with subarachnoid hemorrhage" performed in the neurology department. Lumbar puncture showed normal cerebrospinal fluid pressure initially, but repeated follow-up measurements during hospitalization indicated elevated intracranial pressure. The patient exhibited unequal pupil size, with a positive relative afferent pupillary defect (RAPD) in the left eye and slight pallor of the left optic disc. Half a month later, the patient developed decreased vision in the right eye. Fundus examination revealed optic disc hyperemia, edema with blurred margins, multiple peripapillary cotton-wool spots accompanied by small patchy hemorrhages, and scattered microaneurysms in the macular area. Based on the medical history, the diagnosis was confirmed as: left eye surgery-associated posterior ischemic optic neuropathy, and right eye Purtscher retinopathy. After treatment with mecobalamin tablets, citicoline sodium capsules, and compound vitamin B tablets, the ocular symptoms in the right eye showed some improvement.

We reported a middle-aged man who initially presented with anhidrosis for 20 years and subsequently developed severe orthostatic hypotension, gastrointestinal dysmotility, and urogenital dysfunction. Due to progressive symptom aggravation, he was hospitalized and underwent comprehensive clinical assessment, neurophysiological studies, autonomic function tests, and multidisciplinary team (MDT) evaluation. The final diagnosis was pure autonomic failure (PAF). This case describes in detail the patient's long diagnostic course, differential diagnostic reasoning, the pivotal role of MDT management, and individualized treatment strategies and outcomes. The report aims to enhance the understanding of primary autonomic disorders characterized by neurogenic orthostatic hypotension for physicians, emphasizing the importance of systematic etiological screening and multidisciplinary collaboration in rare disease diagnosis and management to reduce misdiagnosis and improve prognosis and quality of life.

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.