Residual congestion at discharge in acute heart failure (AHF) is a primary driver of readmission and mortality. Inferior vena cava (IVC) ultrasound provides a noninvasive bedside assessment of volume status, yet its clinical impact on guiding therapy remains underdefined. This systematic review evaluated the efficacy of IVC ultrasound-guided therapy compared to standard clinical assessment in AHF decongestion.

Following PRISMA guidelines (PROSPERO: CRD420251171323), a systematic search was conducted across PubMed, EMBASE, and other major databases through October 2025. We included randomized controlled trials (RCTs) and nonrandomized studies focusing on IVC-guided management in adults with AHF. Outcomes included congestion markers, NT-proBNP levels, hospitalization duration, and mortality.

Four studies involving 629 patients met the inclusion criteria. Most studies showed improved decongestion with IVC ultrasound guidance, evidenced by lower residual congestion and improved IVC metrics (diameter/collapsibility). While NT-proBNP levels decreased in all cohorts, between-group differences were not statistically significant. Clinical outcomes improved in 50% of studies, showing shorter hospital stays and reduced mortality. Notably, one trial reported a significant mortality benefit (3.3% vs. 33.3%; p = 0.003). Adverse events were either similar or significantly fewer (p < 0.05) in the ultrasound-guided groups.

IVC ultrasound is an effective bedside tool for individualized volume management in AHF, potentially enhancing treatment precision and clinical outcomes. While current evidence is promising, larger multicenter trials are necessary to standardize its implementation in routine heart failure care.

The utilization of stress perfusion cardiac magnetic resonance (CMR) in patients with cardiac implantable electronic devices (CIEDs) is still limited.

The study was registered in the Prospective Register of Systematic Reviews (PROSPERO) with ID CRD42023457308. PubMed, Scopus, Embase, Web of Science, ProQuest, and CINAHL databases were searched using the Mesh and related terms of CMR imaging, stress, and CIEDs.

Out of the 1695 papers we found, eight met our inclusion criteria. We reviewed the included studies and provided a concluding remark concerning (a) image quality; (b) CMR compatibility, scanner, and safety; (c) device protocols and exclusion criteria; (d) vasodilator choices, effects, and safety; and (e) clinical outcomes.

This study has demonstrated a positive trend in the utilization of stress CMR in MR-conditional devices. However, the review has identified multiple research gaps that warrant further investigation.

Orthodontic tooth movement (OTM) is a complex process involving periodontal tissue remodeling, and safe strategies to accelerate OTM remain a research focus. DMXAA (Vadimezan), a non-toxic immune-modulating drug with established clinical trial data, stimulates the secretion of pro-inflammatory cytokines potentially relevant to OTM, which involves immune-mediated bone remodeling.

A murine OTM model was established in C57BL/6 mice, receiving local subperiosteal injections of DMXAA. Tooth movement distance, bone volume fraction, and osteoclast parameters were quantified via Micro-CT and histology. The mechanism was dissected using RNA-sequencing of bone marrow-derived macrophages (BMDMs), sEV proteomics, and functional osteoclastogenesis assays. Macrophage depletion and Rab13 knockdown models were employed to verify specificity.

Local DMXAA administration significantly enhance orthodontic tooth movement and rate in mice under orthodontic force application, accompanied by reduced alveolar bone volume and increased osteoclast numbers on the compressive force side. DMXAA induced macrophage accumulation at the force-applied site, polarizing them toward M1-like pro-inflammatory phenotypes characterized by high secretion of CCL5 and CXCL10. Furthermore, small extracellular vesicles derived from DMXAA-treated macrophages, which were enriched with Rab13 protein, contributed to osteoclast fusion and maturation, thereby accelerating OTM.

DMXAA accelerates OTM through a dual mechanism: chemokine-driven osteoclast differentiation and sEV-Rab13-mediated osteoclast fusion. These findings highlight the Rab13-sEV axis as a novel therapeutic target for modulating the periodontal microenvironment and enhancing orthodontic efficiency. Our results elucidated a novel mechanism by which DMXAA accelerated orthodontic tooth movement and suggested it as a potential therapeutic agent to optimize orthodontic treatment.

The pathological features of cerebral ischemia-reperfusion (CIR) include necroptosis activation. This study investigated how healthy fecal microbiota transplantation (H-FMT) improves CIR and intestinal barrier damage. Rats subjected to middle cerebral artery occlusion and reperfusion (MCAO/R) were treated with H-FMT and/or a Cysteine-aspartic acid protease-8 (Caspase-8) inhibitor. Survival and body weight were monitored throughout the experiment. Neurological function, tissue damage, inflammatory cytokines, and Caspase-8/Receptor-interacting protein kinase 1 (RIPK1)-Receptor-interacting protein kinase 3 (RIPK3)-Mixed lineage kinase domain-like protein (MLKL) expression were assessed. Ultrastructural changes were examined by transmission electron microscopy (TEM), p-RIPK1/p-RIPK3 expression by immunohistochemistry (IHC), and gut microbiota by 16 S sequencing. H-FMT significantly ameliorated neurological deficits and intestinal barrier disruption, reduced infarct volume and neuronal loss, and attenuated mitochondrial damage. These effects were accompanied by reduced apoptosis and inflammation, increased Caspase-8 activation, and suppressed RIPK1-RIPK3-MLKL phosphorylation. IHC confirmed reduced p-RIPK1/p-RIPK3 signals after H-FMT. 16 S sequencing revealed that H-FMT restored microbial diversity, reduced pathogenic Proteobacteria, and enriched beneficial Lactobacillus, which positively correlated with Caspase-8 activation. Our findings suggest that H-FMT alleviates CIR injury by activating Caspase-8 and suppressing necroptosis. However, due to the small sample size, these results should be considered preliminary.

Feline Hypertrophic Cardiomyopathy (HCM) is a significant health issue, with a current prevalence of 14.7% in cats. The mammalian target of rapamycin (mTOR) is an atypical serine/threonine protein kinase system that also participates in the control of structural and functional remodeling of the heart in relation to haemodynamic stress and non-hemodynamic stimuli. Here, we sought to discover candidate feline-specific inhibitors of mTOR for the treatment of HCM using an integrated computational pipeline combining homology modeling, virtual screening, and molecular dynamics simulations. Using this pipeline, we screened the DrugBank database and identified 17 candidate compounds that bind significantly better than rapamycin, serving as a control mTOR inhibitor. Both molecular dynamics (MD) simulation and MM/PBSA calculations indicated that the screened compound, dihydro-alpha-ergocryptine, exhibited a higher binding affinity and stability with feline mTOR compared to rapamycin. Moreover, ADMET analysis further demonstrated that the compound had good drug-like properties.

Homologous models of feline mTOR were built using publicly available software MODELLER (version 10.5) and the SWISS-MODEL webserver. Homologous templates were used to predict the active binding sites. Structure-based virtual screening of high-affinity small molecule compounds from the DrugBank database was carried out using AutoDock Vina (version 1.2.0). Molecular dynamics (MD) simulations were performed using the GROMACS software version 2021.4. The CHARMM36 all-atom force field parameterised the protein, and the ligand's parameters were taken from the GAFF force field. The simulations were equilibrated under NVT and NPT conditions. During trajectory analysis (RMSD, RMSF, radius of gyration, SASA and hydrogen bonding), the complex stability was evaluated to identify the best potential mTOR inhibitor candidates using OriginPro (version 2024).

Neutrophils are key in acute and chronic cardiovascular diseases (CVD) by mediating inflammation during myocardial infarction, stroke, and heart failure. Reactive oxygen species (ROS) generated by neutrophil NADPH oxidase 2 (NOX2) have been linked to CVD pathology by inducing tissue injury via oxidative stress. There is, however, only limited data investigating the impact of neutrophil-derived ROS on clinical outcome in patients with CVD. This study measured neutrophil oxidative burst capacity (NOBC) in patients with CVD and evaluated its association with major adverse cardiac events (MACE) and infection.

In a population of 201 (median age 69 years (interquartile range (IQR) = 61-80 years); 33.4% female) out of 1128 patients from the prospective all-comer Essen Coronary Artery Registry II (ECAD II registry), NOBC was measured using a Seahorse XF analyzer with phorbol-12-myristat-13-acetat (PMA) stimulation. Based on NOBC values, the study collective was divided by median split. The primary endpoint was MACE, comprising of acute myocardial infarction, acute ischemic stroke, or hospitalization for heart failure, with a median follow-up time of 287 days (IQR = 225-349 days). A secondary endpoint occurrence of infection was assessed with a median follow-up time of 273 days (IQR = 214-332 days).

Patients with low NOBC showed 20% lower values (98.8 nmol (IQR = 92.9-104.2 nmol; high NOBC) vs. 79.4 nmol (IQR = 71.8-84.9 nmol; low NOBC); p < 0,001). In this group, we observed a significantly higher portion of females (26.7% (high NOBC) vs. 41.0% (low NOBC); p = 0.03). Despite lower CCL2 and hemoglobin levels in patients with low NOBC, further inflammatory markers were unaltered. Occurrence of MACE (hazard ratio (HR) = 2.78; 95% confidence interval (CI) 1.17-6.63; p = 0.02) and infection (HR = 3.67; 95% CI = 1.16-11.62; p = 0.03) was significantly increased in patients with low NOBC. The latter remained significant, while the association between low NOBC and incidence of MACE lost its significance after adjustment for anemia and further confounders.

Incidence of MACE and infection was increased in patients with low NOBC. Whether low NOBC is directly associated with patient outcome or acts in combination with other factors remains unclear.

We report a case of muscular polyarteritis nodosa in a 23-year-old man with no past medical history presenting with diffuse myalgias, weight loss, fatigue, hypertension, and elevated C-reactive protein. Normal creatine kinase and electromyography contributed to a delayed diagnosis. MRI-guided muscular biopsy confirmed necrotizing vasculitis. Corticosteroid therapy led to rapid improvement.

Sarcoidosis is a systemic granulomatous disorder with variable prognosis. Mortality arises from both organ-specific and demographic factors, but reliable baseline predictors remain incompletely defined. We aimed to describe long-term survival and causes of death, and to identify demographic, radiological, and clinical predictors of mortality in national cohort of patients with sarcoidosis.

Retrospective multicentre cohort study within the Spanish SARCOGEAS registry. Adults diagnosed according to the ATS/ERS/WASOG criteria were consecutively enrolled across 36 hospitals. Demographic, clinical, and radiological variables were collected at baseline, including pulmonary involvement classified by the Scadding Scale and extrapulmonary disease defined by the WASOG criteria. The primary outcome was all-cause mortality. Survival was estimated with Kaplan-Meier analysis, and predictors were assessed using Cox regression.

A total of 2,187 patients were included (48.6 ± 15.2 years; 61.4% women). Median follow-up was 5.93 years. Overall, 225 patients died (10.29%). Survival was 99.2% at 1 year, 88.3% at 10 years, 73.2% at 20 years. In multivariable Cox proportional hazards analysis, independent predictors of mortality were older age (HR 1.11, 95% CI 1.10-1.13), male sex (HR 1.75, 95% CI 1.31-2.35, p<0.001), Scadding stages II-IV (HRs 1.42-2.73), and cardiac involvement (HR 1.84, 95% CI 1.05-3.21, p=0.033). Extrathoracic lymphadenopathy was associated with lower risk (HR 0.63, 95% CI 0.43-0.91, p=0.016). Main causes of death were pulmonary (n=92, 40.9%), malignancies (n=47, 20.9%), extrapulmonary (n=39, 17.3%), cardiovascular (n=24, 10.7%), and other causes (n=23, 10.2%).

n this nationwide, multicentre cohort, mortality was 10.29%. Mortality was independently associated with age, male sex, cardiac and pulmonary parenchymal involvement, while extrathoracic lymphadenopathy was linked to lower mortality.

Myocardial ischemia/reperfusion (I/R) injury remains a major clinical challenge characterized by cardiomyocyte loss and adverse remodeling after reperfusion. Ubiquitin-Specific Peptidase 20 (USP20), a deubiquitinase involved in cellular stress responses, has not been fully characterized in the ischemic heart. This study aimed to investigate the function and mechanism of cardiomyocyte-derived USP20 in myocardial I/R injury.

Myocardial I/R models and hypoxia/reoxygenation (H/R)-treated cardiomyocytes were used to evaluate USP20 expression and function. Single-cell transcriptomic analysis, cardiomyocyte-specific USP20 knockout, and USP20 overexpression models were applied. Co-immunoprecipitation, LC-MS/MS, ubiquitination assays, site-directed mutagenesis, and rescue experiments were performed to define the underlying mechanism.

USP20 expression was markedly decreased in I/R-injured mouse hearts and H/R-treated cardiomyocytes, and USP20 was predominantly localized in cardiomyocytes. Cardiomyocyte-specific USP20 deletion aggravated myocardial injury, adverse cardiac remodeling, and cardiac dysfunction after I/R, whereas USP20 overexpression conferred significant cardioprotection. Mechanistically, USP20 directly interacted with glucose-regulated protein 78 (GRP78) and removed K63-linked polyubiquitin chains from GRP78 at K602 through its C154 active site. This deubiquitination activated GRP78, promoted adaptive endoplasmic reticulum stress responses, and reduced myocardial injury.

These findings identify a previously unrecognized USP20-GRP78 regulatory axis that regulates endoplasmic reticulum stress responses and limits myocardial damage during I/R. USP20 may represent a potential therapeutic target for myocardial I/R injury.

The pathogenesis of myocardial ischemia-reperfusion (MI/R) injury is intricately linked to mitochondrial dysfunction occurring during both the ischemic and reperfusion phases. Through single-cell transcriptome analysis, we identified a subpopulation of HEY1-high expressing cardiomyocytes (HEY1⁺ CMs) characterized by superior mitochondrial homeostasis. To leverage this, we isolated P5CS-type or ATP5B-type functional mitochondria from a ΔΨ_m-high subpopulation, which was obtained via membrane potential sorting following dual overexpression in HEY1⁺ CMs, and subsequently encapsulated them within HEY1⁺ CM-derived exosomes to achieve stable, targeted delivery. We designed a responsive microneedle patch based on local copper/iron ion dynamics to enable the stage-specific release of these mitochondria within the ischemic or reperfusion microenvironments. In a Bama minipig MI/R model, this system significantly ameliorated cardiac function, reduced infarct size, and attenuated cardiomyocyte death. Mechanistically, the therapeutic strategy enhanced mitochondrial structural integrity and energy metabolic function. This study establishes a responsive, stage-specific mitochondrial delivery platform, offering a promising strategy for the precision treatment of ischemic heart disease.