The gut microbiome supports digestion, immunity, and metabolism; its imbalance (dysbiosis) drives inflammation and metabolic dysfunction, contributing to chronic diseases such as diabetes, cardiovascular disease, inflammatory bowel disease, and autoimmune disorders. Medicinal plants provide a wide range of phytochemicals (such as polyphenols, flavonoids, alkaloids, saponins), which reach the colon and undergo two-sided interactions with microbes in the gut, acting as potential microbiome modulators and substrates of biotransformation into bioactive metabolites. This structured narrative review synthesises evidence from peer-reviewed studies indexed in PubMed, Scopus, and Web of Science over the last 10 years on the role of medicinal plants in microbiome-mediated chronic disease modulation. This literature is organised into three mechanistic axes: (i) perturbations, defined here as measurable shifts in microbial diversity or taxonomic composition relative to a baseline or healthy reference state, together with beneficial taxa enrichment; (ii) alterations in microbial metabolite output, especially short-chain fatty acids (SCFAs) and other immunometabolic mediators; and (iii) downstream host metabolic and immune signalling. Rather than broad descriptive summaries, the literature is organised using an axis-based mechanistic framework, highlighting key translational constraints such as botanical heterogeneity, dose/formulation variability, and inconsistent microbiome endpoint standardisation, that must be addressed to strengthen human evidence and clinical relevance. Illustrative microbiome-mediated processes involve botanicals such as turmeric (curcumin), ginseng (ginsenosides), and green tea (catechins), though evidence strength varies by study design. Future progress requires standardised phytochemical characterisation, microbiome-stratified trials, and integration of multi-omics with artificial intelligence analytics to enhance mechanistic insight, identify responders, and enable personalised plant-based microbiome therapies.

Children born small for gestational age (SGA) face elevated risks of metabolic, cardiovascular, respiratory, and neurodevelopmental disorders, as well as premature mortality, yet the underlying mechanisms remain only partly understood. We analyze blood proteomic data from multiple birth cohorts to identify molecular pathways linked to SGA and to later-life lung function. We find that approximately one-third of SGA children exhibit a distinct molecular endotype marked by dysregulation of axon-guidance proteins in cord blood. In peripheral blood collected later in life, these proteins are inversely associated with contemporaneous spirometric restriction. Using GWAS data and an experimental sheep model, we obtain convergent evidence that axon-guidance genes are associated with spirometric indices (FEV₁/FVC) at genome-wide significance and are broadly expressed during fetal development across multiple organs. These findings offer new insight into the developmental origins of chronic disease and highlight axon-guidance pathways as promising targets for investigating multiorgan morbidity.

Centenarian patients constitute a rapidly growing yet understudied population in emergency medicine. Evidence regarding prognostic factors and one-year outcomes in individuals aged 100 years and older presenting to the emergency department remains limited.

This retrospective observational study was conducted in the emergency department of Giresun Training and Research Hospital and included centenarian patients presenting between 2010 and 2023. A total of 160 emergency department visits from 83 unique patients were evaluated. Demographic characteristics, clinical variables, comorbidities, frailty indices, and laboratory parameters obtained at admission were recorded. Frailty was assessed using a modified frailty index excluding functional dependence (mFI-4) and the Clinical Frailty Scale (CFS). The primary outcome was one-year all-cause mortality. Kaplan-Meier survival analysis and Cox proportional hazards regression analysis were performed at the patient level using the index emergency department visit.

In the descriptive visit-level analysis, non-survivor visits showed higher hospitalization frequency and less favorable inflammatory and renal function marker profiles than survivor visits, while pulmonary diseases were more frequent among non-survivors and cardiovascular diseases were more common among survivors. Modified frailty index scores did not differ significantly between groups. Higher CFS categories were associated with shorter median survival times, although Kaplan-Meier analysis showed no statistically significant separation between frailty categories. In Cox regression analysis, hospitalization at the index emergency department visit and higher blood urea nitrogen levels remained independently associated with one-year mortality.

In centenarian patients presenting to the emergency department, traditional comorbidity-based frailty indices show limited discriminatory value for one-year mortality. Acute clinical presentation and laboratory parameters reflecting inflammatory burden, renal function, and physiological reserve appear to be more closely associated with outcomes.

The study is not registered in a clinical trial registry.

People living with HIV (PLWH) face an increased CardioVascular (CV) risk due to the interaction between risk factors, chronic inflammation and AntiRetroviral Therapies (ART) metabolic effects. However, standard risk models often underestimate this burden. Our study aims to evaluate: (i) the CV risk category and the relative LDL-C targets; (ii) the achievement of these targets; and (iii) factors associated with target achievement and HIV-related variables.

A retrospective analysis was conducted on 246 PLWH, aged ≥40, on ART followed at the Niguarda Hospital. Clinical and laboratory data were extracted from the hospital's electronic registries and ten-year CV risk was assessed using SCORE2. Only 27.2% of the analyzed cohort achieved the recommended LDL-C targets with further lower prevalence in patients in the "high" or "very high" risk categories. Patients who achieved their LDL-C target had a more favorable cardiovascular risk profile (LDL-C: 75.8 ± 18.1 vs 121.1 ± 33.4 mg/dL, p < 0.001; systolic blood pressure: 116.9 ± 12.4 vs 123.4 ± 15.7 mmHg, p = 0.001), and CV risk categories, being less frequently classified as high and very-high risk (20.8 vs 52.4%, p < 0.0001). No significant relation was found between LDL-C target achievement and HIV-specific variables.

LDL-C target achievement remains suboptimal and may not reflect adequate cardiovascular risk control in PLWH, supporting the need for more aggressive and HIV-tailored prevention strategies.

The Mediterranean Diet (MD) is a dietary pattern associated with reduced chronic disease risk and increased longevity. This systematic review and meta-analysis aimed to evaluate the association between adherence to the MD and frailty and disability among older people.

A comprehensive literature search was conducted in PubMed/MEDLINE, Cochrane Library, Embase, and Scopus (search date: February 28, 2024) without date restrictions. Observational and interventional studies examining the association between MD adherence (measured by any validated score) and frailty or disability, using any definition, and their complications were included. Study selection and data extraction were performed independently by pairs of reviewers using Covidence. Risk of bias was assessed using the Newcastle-Ottawa Scale. Random-effects meta-analysis was conducted, estimating pooled relative risks (RRs) per 1-point increment in MD adherence score. Heterogeneity was assessed using the I² statistic, and publication bias was evaluated by funnel plot. Certainty of evidence was graded using the NUTRIGRADE approach.

Out of 1361 screened records, 19 observational studies were included. Higher MD adherence was associated with a lower incidence (9 cohort studies, n = 94 072 participants; OR = 0.95, 95% CI: 0.93-0.97; moderate certainty of evidence) and prevalence (6 cross-sectional studies, n = 12 277participants; OR = 0.94, 95% CI: 0.90-0.98; low certainty of evidence) of frailty. The association with disability was present only for prevalence (OR = 0.98; 95% CI: 0.97-0.98).

Higher adherence to the MD is associated with a reduced presence of frailty and disability in older adults. These findings support public health strategies promoting the MD as a sustainable dietary model for healthy longevity.

This paper reviews the existing literature supporting a role for fatty acid ethanolamides including oleoylethanolamide and palmitoylethanolamide in regulating cholesterol and triglyceride metabolism and the mechanisms underlying these effects.

Deletion of various fatty acid ethanolamide biosynthesis genes in cellular models and small animal models have provided additional evidence that endogenous biosynthesis of fatty acid ethanolamides regulates cholesterol and triglyceride metabolism, while new clinical trials using oleoylethanolamide and palmitoylethanolamide support their therapeutic potential to normalize lipid levels in individuals with cardiometabolic disease. Fatty acid ethanolamides are biosynthesized in the intestine, liver, and adipose tissue in response to metabolic stimuli like fasting and feeding. These fatty acid ethanolamides then act via receptors including PPARα, GPR119, and GPR55 to regulate cholesterol and triglyceride levels and promote the resolution of inflammation, thereby protecting against cardiometabolic diseases including metabolic-dysfunction associated steatotic liver disease and atherosclerotic cardiovascular disease.

Primary percutaneous coronary intervention (PPCI) is the preferred treatment for ST-segment elevation myocardial infarction (STEMI). Treatment delay significantly affects the prognosis of STEMI patients.

The aim of this study was to investigate the treatment delay and its influencing factors for STEMI in Beijing.

STEMI patients undergoing PPCI at 65 hospitals between 2018 and 2022 were enrolled. Treatment delays were collected and analyzed using mixed-effects models to assess the impact of admission time, arrival mode, and hospital level.

Among 13,445 individuals, median total ischemic time (TIT), symptom onset-to-door time (S2D), and door-to-balloon time (D2B) were 188 minutes (Q1-Q3: 133-288 minutes), 116 minutes (Q1-Q3: 60-200 minutes), and 72 minutes (Q1-Q3: 58-89 minutes), respectively. Compared with off-hours admissions, S2D was longer and D2B was shorter for on-hours admissions (P < 0.001 for both). Median TIT, S2D, and D2B were longer for self-transported patients than for ambulance-transported patients (P < 0.001 for all). Median TIT and S2D were shorter and D2B was longer at nontertiary hospitals than at tertiary hospitals (P < 0.001 for all). According to linear mixed-effects models adjusting for confounders, off-hours admission was linked to 6.6% shorter S2D but 11.6% longer D2B. Ambulance transport was independently associated with 9.0% shorter S2D and 10.3% shorter D2B. Treatment at tertiary hospitals was associated with 19.0% longer S2D.

Despite advances in STEMI management, prehospital delay remains the dominant component of TIT in Beijing. Future strategies should focus on improving hospital preparedness, increasing ambulance use, and minimizing interhospital disparities to reduce treatment delay.

Endothelial dysfunction induced by lipotoxicity is a critical initiating factor in atherosclerosis. Sweroside, a bioactive iridoid glycoside, possesses significant anti-inflammatory activities; however, its therapeutic potential in regulating vascular endothelial inflammation and dysfunction remains unexplored. This study aimed to investigate the protective effects of Sweroside against endothelial injury and to elucidate the underlying molecular mechanisms, specifically focusing on the transcriptional regulation of inflammatory cascades.

Human umbilical vein endothelial cells (HUVECs) and mouse aortic endothelial cells (MAECs) stimulated with palmitic acid (PA), along with C57BL/6J mice fed a high-fat diet (HFD), served as the in vitro and in vivo models, respectively. Transcriptome sequencing (RNA-seq) was employed to screen for potential therapeutic targets. Molecular mechanisms were validated using small interfering RNA (siRNA) knockdown, Western blotting, and dual-luciferase reporter assays. Vascular function was evaluated via wire myograph to assess endothelium-dependent relaxation and pulse wave velocity (PWV) to measure arterial stiffness.

Sweroside treatment significantly attenuated PA-induced cytotoxicity, oxidative stress, inflammation, and cytoskeletal disruption in ECs. RNA-seq identified Krüppel-like Factor 2 (KLF2) as a core target up-regulated by Sweroside. Mechanistically, Sweroside restored KLF2 expression, which subsequently functioned as a transcriptional repressor by directly binding to the promoter of Fatty Acid Binding Protein 4 (FABP4). This repression reduced FABP4 levels, thereby alleviating the suppression of PPAR-γ and blocking the NF-κB-dependent induction of the downstream chemokine CCL20. In vivo, Sweroside administration effectively improved endothelium-dependent relaxation, and reduced aortic stiffness and vascular inflammation in HFD-fed mice.

Sweroside ameliorates endothelial dysfunction and vascular remodeling by activating the KLF2-mediated signaling axis to repress FABP4 and the downstream CCL20 inflammatory cascade. These findings highlight Sweroside as a promising therapeutic candidate for the treatment of atherosclerosis and cardiovascular diseases associated with metabolic inflammation.

It is analyzed whether differences in how the daily usage time is determined in a population exposed to hand-transmitted vibration are the cause of discrepancies between exposure-response models constructed for vibration-induced white finger (VWF). The predictions of the models are then used to evaluate the one in ISO 5349-1:2001.

Pooled analyses employing data from epidemiologic studies of vibration-exposed occupations deemed the most reliable, together with published ratios between daily tool or machine usage times determined by questionnaire or interview and measured values, are used to construct exposure-response relations. These models are compared to those in which the daily usage time is not compensated.

Of 17 data points, for 7 the usage time ratio is greater than 1, and for the rest the ratio is equal to 1. Adjusting daily vibration exposures, expressed as A(8)-values, by means of such ratios, results in reductions of varying magnitude. However, the exposure-response models show minor changes, and the scatter in the data points previously observed remains.

Methods for estimating 10% prevalence of VWF from the prevalence recorded in a population study are found to have more effect on the models than different methods for estimating the daily usage time. Yet, the spread and clustering in the data remain and point to issues in the constituents of the A(8)-value. The ISO relation is generally consistent with the lower 95-percentile confidence limit of the models and so provides a conservative exposure limit at least for A(8)-values greater than about 3 [Formula: see text].