Overweight, (body mass index (BMI), kg/m2) 25-30 and obesity (BMI 30+) have long been linked to an increased risk of myocardial infarction and mortality. To better assess abdominal adiposity, several indices have been developed. However, the risk associated with each index can vary across different populations.

This study aims to investigate which body measurement, if any, exhibits the strongest associations with MI, and mortality. In 1993, a cohort of 1,000 randomly selected middle-aged Swedish men participated in a nurse-led health examination. Body measurements were recorded together alongside blood pressure readings, and a fasting blood test was conducted. A follow-up study, spanning 28 years, utilized data from the national Myocardial Infarction Register (Swedeheart) and mortality data from the Swedish Cause of Death Register. The obesity indices included body mass index, waist circumference (WC), waist-to-height ratio (WHtR), waist-to-hip ratio (WHR), sagittal abdominal diameter (SAD), and sagittal abdominal diameter-to-height ratio (SADHtR). Cox proportional hazard models were employed to analyze the z-scores of the six body measurements both before and after adjusting for covariates, with outcomes assessed for first-time myocardial infarction (MI) and mortality.

Data were collected for 959 men. Significant correlations were found between the six body measurements, all were associated with cardiovascular disease risk factors, myocardial infarction, and mortality. However, after adjusting for the traditional risk factors, the association with cardiovascular endpoints was diminished or vanished. WHtR emerged as a more reliable indicator, with hazard ratios (HR) of 1.31 (95% CI 1.07-1.62) for myocardial infarction and 1.27 (95% CI 1.08-1.49) for all-cause mortality although the differences were marginal.

There is currently no consensus on which obesity indicator should be the preferred predictor of cardiovascular risk. In this study, the WHtR emerged as the more reliable predictor, albeit with marginal clinical significance.

In this population, after adjustment for traditional risk factors, WHtR proved to be a more reliable predictor for MI and mortality.

Early risk stratification in acute pancreatitis (AP) is crucial for improving patient outcomes and guiding timely clinical management. D-dimer has emerged as a potential biomarker reflecting activation of coagulation and fibrinolysis and may assist in early risk stratification of patients with acute pancreatitis. However, its prognostic performance remains incompletely validated across different populations.

This retrospective cohort study included 200 adult patients diagnosed with acute pancreatitis between March 2023 and March 2024 at a tertiary care hospital. Disease severity was classified using the Revised Atlanta Classification. Admission serum D-dimer was measured within the first six hours after hospital presentation. Admission D-dimer levels were analyzed in relation to clinical severity, BISAP and Ranson scores, ICU admission, length of hospital stay, and in-hospital mortality. Statistical analyses included non-parametric tests, correlation analysis, logistic regression, and ROC curve analysis to evaluate predictive performance.

Two hundred consecutive patients, with a mean age of 58.1 ± 17.5 years and 54% male patients, were included in this study. Severity distribution showed 68.5% mild, 17% moderately severe, and 14.5% severe AP. Overall mortality was 7% (n = 14), and 56% (n = 112) required ICU admission. Admission D-dimer levels increased significantly with disease severity, with median values of 1534 ng/mL (mild), 1908.5 ng/mL (moderately severe), and 2960 ng/mL (severe). Non-survivors had markedly higher levels than survivors (3776.5 vs. 1663 ng/mL, p < 0.001). D-dimer showed significant positive correlations with BISAP (ρ = 0.6068), Ranson scores (ρ = 0.3425), and hospital length of stay. ROC analysis demonstrated good discriminatory ability for severe AP (AUC = 0.778; cutoff 2035 ng/mL) and good discriminatory performance for mortality prediction (AUC = 0.912; cutoff 2726 ng/mL, sensitivity 85.7%, specificity 80.1%). However, performance for predicting ICU admission was limited (AUC = 0.579). Multivariable analysis demonstrated that each 1-ng/mL increase in admission D-dimer level was independently associated with higher odds of severe AP (OR = 1.001, p < 0.001).

Admission D-dimer is a simple and rapid biomarker associated with disease severity and mortality in acute pancreatitis. While it should not replace established scoring systems, it can serve as a valuable adjunct for early risk stratification, particularly for identifying high-risk patients. Prospective multicenter studies are needed to validate its clinical utility and define standardized cutoff values.

Cardiac arrest (CA) is associated with high mortality and neurological morbidity, mainly due to hypoxic-ischemic encephalopathy. Accurate neurological prognostication in CA survivors is essential to guide therapeutic decisions and provide appropriate care.

To review the current evidence on neurological prognostication after CA and to propose an institutional protocol adapted to the resources of Hospital de Clínicas de Porto Alegre (HCPA).

The current narrative review was conducted in two stages: a literature review and the development of an institutional protocol. Articles were selected according to their clinical relevance and their contribution to current evidence on neurological prognostication after CA. The PubMed, Scopus, Web of Science, Embase, and SciELO databases were searched. The protocol was developed considering the clinical tools available at HCPA, including neurological examination, electroencephalography (EEG), and neuroimaging.

Brain injury after CA occurs in three stages: intra-arrest ischemia, immediate reperfusion, and delayed postreperfusion injury. Prognostic modalities include neurological examination, EEG, somatosensory-evoked potentials (SSEPs), serum biomarkers, and neuroimaging. Reliable predictors of poor outcome include absent brainstem reflexes at 72 hours, persistent EEG suppression, bilateral absence of cortical N20 potentials, and diffuse abnormalities on magnetic resonance imaging. The proposed protocol organizes assessments from admission to the Intensive Care Unit through day 5 after the return of spontaneous circulation.

A standardized post-CA neurological prognostication protocol at HCPA may improve care quality, enhance communication with families, and support ethically-sound decision-making.

Aneurysmal subarachnoid hemorrhage is a condition resulting from the rupture of a cerebral aneurysm, sometimes leading to delayed cerebral ischemia, primarily due to angiographic vasospasm; its prediction is crucial to improve patient management and outcomes.

To assess the predictive value of clinical, analytical and imaging parameters for vasospasm in aneurysmal subarachnoid hemorrhage and to develop a clinical practical score.

The current single-center retrospective study included 115 patients with aneurysmal subarachnoid hemorrhage who underwent a computed tomography scan within 24 hours of ictus. Clinical and analytical data were collected, and Hounsfield unit (HU) measurements were independently assessed. Statistical analyses were conducted to identify predictors of vasospasm.

Vasospasm occurred in 40% of patients (46/115). The multivariate analysis identified intracerebral hemorrhage (odds ratio [OR] = 2.482; 95%CI = 1.019-6.046; p = 0.045), interpeduncular HU value (per 5 HU increase: OR = 1.253; 95%CI = 1.044-1.504; p = 0.016), and serum chloride ≥ 106 mEq/L (OR = 3.545; 95%CI = 1.457-8.621; p = 0.005) as independent predictors (p < 0.05) of vasospasm. The model, combined as a simplified score including these 3 variables, demonstrated excellent discriminative capacity (area under the curve [AUC] = 0.886; bootstrapped AUC = 0.885).

We identified significant predictors of vasospasm in patients with aneurysmal subarachnoid hemorrhage, namely interpeduncular HU value, intracerebral hemorrhage, and serum chloride levels. A practical 5-point score based on these factors offers a potentially-robust, easy-to-use tool for early risk stratification, which may guide personalized follow-up and timely interventions. Further prospective multicenter studies are recommended to validate these findings.

To determine the effect of the timing of hyperbaric oxygen (HBO₂) treatment on functional and structural outcomes in central retinal artery occlusion (CRAO).

This single‑center retrospective cohort study analyzed 101 eyes with CRAO treated with HBO₂. Eyes were stratified by symptom‑to‑treatment interval: ≤12 hours (Group 1), 12-24 hours (Group 2), 24-36 hours (Group 3), and >36 hours (Group 4). Best‑corrected visual acuity (BCVA-logMAR), central macular thickness (CMT), and inner retinal hyperreflective band thickness (IRHBT) were recorded at presentation, week 1, and month 6.

Presentation BCVA was 2.16 ± 1.04, improving to 1.77 ± 1.02 at month 6 (p = 0.03). The mean BCVA gain was greatest in Group 1: -0.85 ± 0.96, and declined markedly with delayed treatment initiation (Group 2: -0.48 ± 1.38; Group 3: -0.10 ± 1.50; Group 4: -0.08 ± 1.77). In Group 1, the mean BCVA improved significantly from 2.04 ± 0.78 logMAR at presentation to 1.19 ± 0.56 logMAR at the 6-month follow-up (p = 0.02). Early treatment was also associated with more pronounced reductions in CMT and IRHBT, whereas anatomical changes were negligible when therapy was initiated beyond 24 hours. Baseline CMT and IRHBT showed modest but significant correlations with final BCVA (r = 0.37, p = 0.03 , and r=0.34, p=0.04, respectively).

HBO₂ provides a significant, time-sensitive benefit for CRAO; initiating treatment within 12-24 hours maximizes recovery and retinal remodeling, validating HBO₂ as a critical adjunct and necessitating rapid triage in ophthalmic emergencies.

Network pharmacology nominates targets but cannot show that they are altered in the relevant cell, distinguishable from a hypothesis-free analysis of the same data, or linked to disease. Taking the candidates nominated for Yangxin Decoction in dilated cardiomyopathy (DCM) and viral myocarditis, we asked how many survive independent functional-genomic testing. Few did. A direct-evidence intersection returned 61 genes, but across four bulk cardiac datasets the set was differentially expressed no more often than the transcriptome-wide background in any human cohort, and AKT1 was significant in none. Donor-pseudobulk single-nucleus RNA sequencing of 52 DCM and 18 control donors showed higher AKT1 (log2 fold change 0.351, adjusted P = 3.32 × 10^- 4), PIK3CA and GSK3B and lower STAT3 in cardiomyocytes; no fold-change threshold was applied, and the AKT1 difference is small. These differences were robust to nucleus depth, sex, age, ventricle and DCM genotype; in an independent single-nucleus DCM cohort AKT1 (0.530) and STAT3 (- 0.771) replicated at FDR < 0.05, PIK3CA was directionally consistent, and GSK3B did not replicate. Three further tests constrain the interpretation. A disease × cell-type interaction model showed that PIK3CA is altered in most cardiac lineages and significantly more in fibroblasts than in cardiomyocytes, endothelial or immune populations, whereas the AKT1 difference, although significant only in cardiomyocytes, could not be shown to differ from that in most other lineages, so it reflects detection rather than demonstrated restriction. A whole-heart pseudobulk of the same donors still detected AKT1 (adjusted P = 6.8 × 10^- 3), so cellular dilution does not explain the negative bulk-microarray result. Benchmarked against an unbiased genome-wide analysis of the same cardiomyocyte comparison, the nominated 61-gene set was not enriched (46.7% versus a 41.3% background, P = 0.281) and AKT1 ranked 2,182 of 14,586. A prespecified screen found no cis-eQTL instrument for AKT1; a single whole-blood MTOR Wald ratio was not supported by colocalization. These are cell-type-resolved transcriptional differences in dilated cardiomyopathy, not evidence that Yangxin Decoction engages PI3K-AKT signalling and not a validated therapeutic mechanism.

Panvascular intervention can restore lumen patency, exclude structural defects, or replace diseased valves, but procedural success does not reestablish ecological stability within the treated vessel. We propose eco-rebalancing as a tri-ecological framework in which durable device performance depends on coordinated recovery across three domains: the mechanical, cellular, and physicochemical-immune ecologies. Vascular-device suitcordance denotes the spatiotemporal match between a device's mechanical behavior, biological interface, and material persistence, and the healing trajectory of a specific vascular bed, lesion, and patient; we introduce the Suitcordance Score (Su-Score) as a conceptual metric of that match. This perspective reinterprets restenosis, thrombosis, fibrosis, calcification, and structural degeneration as signatures of incomplete eco-rebalancing, providing a translational basis for device design and patient-device matching.

This study aims to explore the action of the anoikis gene in the vascular endothelial cell injury.

The set of genes associated with anoikis was utilized for conducting enrichment analysis on the Gene Expression Omnibus (GEO: GSE100927) dataset to identify the common genes linked to Atherosclerosis. Subsequently, the expression levels and pathway enrichment of anoikis genes in the GSE100927 dataset were examined. The LASSO method was employed for reducing dimensionality in modeling to identify genes correlated with Atherosclerosis and to establish an anoikis score. The validation of the expression of neural precursor cell-expressed developmentally down-regulated 9 (NEDD9), FOSB, and ERCC1 in ox-LDL-induced bEnd.3 cells was carried out using RT-qPCR. Atherosclerotic mice were established to evaluate NEDD9 expression. The impact of overexpressing or silencing NEDD9 on anoikis in ox-LDL or detachment-induced bEnd.3 cells or Human Umbilical Vein Endothelial Cells (HUVEC) was assessed through CCK-8, EdU, and flow cytometry assays.

Based on anoikis gene analysis, NFIL3, NR4A3, ADAMTS4, NEDD9, STX17-AS1, and CSF3 were found to be under-expressed, while FOSB and ERCC1 were found to be over-expressed in the atherosclerosis group compared to the normal group. LASSO regression analysis yielded an anoikis score = -9.522^e-01 × NFIL3-3.410 × NEDD9 + 2.728^e-01 × ADAMTS4 + 1.178 × FOSB +5.896^e-15 × ERCC1 + 1.558^e+01. Compared with the blank group, NEDD9, FOSB, and ERCC1 were under-expressed in the ox-LDL intervention group. NEDD9 protein was significantly decreased in the arterial tissues of atherosclerotic mice. si-NEDD9 promoted an increase in ROS and apoptosis levels in the bEnd.3 cells intervened by ox-LDL. Transfection with oe-NEDD9 increased the viability of bEnd.3 cells, upregulated the ITGB1 and E-cadherin proteins level, while decreasing ROS and apoptosis levels induced by the ox-LDL and detachment. Overexpression of NEDD9 also reduced HUVEC anoikis induced by detachment.

A preliminary atherosclerotic anoikis model was established to predict endothelial cell injury. Overexpression of NEDD9 attenuated ox-LDL and detachment-induced endothelial cell anoikis in vitro, suggesting a potential protective role.

The Ostwald ripening phenomenon for gas bubbles in a liquid consists mainly in gas transfer from smaller to larger bubbles. While the phenomenon itself is well known, the consequence of the temporal evolution of bubbles in the bloodstream in human physiology lacks deeper investigation.

In this work, a series of direct experiments was carried out in which the Ostwald ripening for air bubbles in a viscous fluid was reproduced. There, the time evolution of the bubbles' mean radius, number of bubbles, and radius size distribution was measured, where the initial bubble distribution behaves like a Tsallis (q-Weibull) distribution.

The results show the usual behavior of wet foam, where smaller bubbles disappear, whereas the larger bubbles, potentially dangerous for the diver, grow, and the number of bubbles decreases in time. On the other hand, a long-time power-law regime was found with an exponent smaller than that of the LSW (Lifshitz-Slyozov-Wagner) model, and the radius size distribution showed positive asymmetry throughout the experiment.

From the results obtained, it is presumed that such a bubble broadening effect could contribute, even minimally, to decompression illness: decompression sickness and arterial gas embolism. This conjecture is reinforced by the preliminary results of Ostwald broadening to RGBM (Reduced Gradient Bubble Model) decompression schedules for a closed-circuit rebreather (CCR) dive to 420 feet of seawater (fsw) (128 meters of seawater (msw)) with a 21/79 Heliox gas mixture, where the first decompression stops lengthening time thanks to Ostwald ripening is at the Pyle-type deep stop, a stop at the half bottom depth, 210 fsw (64 msw).

Atherosclerosis (AS) is a lipid-driven chronic inflammatory disease in which pathological progression is profoundly regulated by macrophage fate determination mechanisms. This review explores how macrophages derived from hemogenic endothelial cells and bone marrow contribute to disease development, functioning either as tissue-resident cells or via systemic circulation. These macrophages drive the plaque progression via three major cellular fates: foam cell formation, polarization, and programmed cell death. Impaired cholesterol efflux, together with enhanced scavenger receptor expression induced by M1 macrophage polarization, are key features of macrophage-derived foam cells. The dichotomous polarization of macrophages into M1 and M2 phenotypes forms the basis of their complex regulatory roles within the plaque microenvironment. Moreover, recent advances in sequencing technologies have uncovered additional macrophage subsets, whose specific contributions to AS progression remain to be fully elucidated. Adopting a framework that links the macrophage life cycle with AS, this review discusses the critical roles of macrophages in AS progression from the perspectives of classical (M1/M2) and various non-classical cell classifications, by delineating the macrophage life cycle from origin to distinct cellular fates within the plaque environment. Concurrently, we summarize potential therapeutic strategies targeting these processes, including metabolic reprogramming, immunomodulation, epigenetic regulation, and innovative drug delivery systems, which provide multi-layered approaches for plaque stabilization while remaining subject to substantial limitations. Overall, we emphasize the unique fate trajectories of different macrophage lineages in AS progression, their multifaceted impact on AS pathological outcomes, and recent advances in potential targeted therapeutic strategies.