Systolic anterior motion (SAM) of the mitral valve remains a clinically relevant complication after mitral valve repair and may result in dynamic left ventricular outflow tract (LVOT) obstruction, SAM-associated mitral regurgitation, and hemodynamic instability. Despite advances in surgical techniques and perioperative imaging, SAM remains an important cause of difficult separation from cardiopulmonary bypass and postoperative circulatory compromise. The development of SAM is multifactorial and results from the interaction between mitral valve anatomy, ventricular geometry, surgical repair characteristics, and perioperative hemodynamic conditions. Contemporary evidence has identified several echocardiographic predictors, including excessive posterior leaflet height, elongated anterior leaflets, reduced coaptation-septal distance, a narrow mitro-aortic angle, basal septal hypertrophy, and small hyperdynamic left ventricles. Recognition of these risk factors facilitates perioperative risk assessment and pre-repair surgical planning. Transesophageal echocardiography plays a pivotal role throughout the perioperative period, enabling risk assessment before repair, early diagnosis after cardiopulmonary bypass, and guidance of therapeutic interventions. Initial treatment is based on preload optimization, afterload augmentation, withdrawal of inotropic stimulation, and heart rate control, whereas refractory cases may require surgical revision. This narrative review summarizes the current understanding of SAM after mitral valve repair, focusing on pathophysiological mechanisms, echocardiographic predictors, surgical prevention and perioperative management, with particular emphasis on the practical role of cardiac anesthesiologists and mitral valve surgeons.

Pesticides represent a significant threat to aquatic ecosystems due to their persistence and widespread use in agricultural areas, altering environments and exerting adverse effects on non-target organisms. Tebuthiuron is a phenylurea herbicide extensively used as an agrochemical to control pests and weeds in various crops, which often leads to contamination of aquatic environments. Despite its high water solubility and relatively long half-life in soil, studies on Tebuthiuron toxicity in fishes at environmental concentrations are limited. This study aimed to unravel the toxicity mechanisms of Tebuthiuron using the zebrafish model. Zebrafish embryos were exposed to Tebuthiuron (one concentration of either 0.1, 10, 1000 and 5000 µg/L) for 5 days and assessed for hatchability, heart rate, locomotor activity, oxygen reactive species, apoptosis and gene expression. There was no change in frequency of hatch, heart rate, or apoptosis. However, behavioral changes were noted, with hyperactivity in zebrafish larvae during the first light (at 10 µg/L), second light (at 10 and 1000 µg/L) and third dark (10 µg/L) periods of the Visual Motor Response assay. Biochemically, a significant depletion of basal ROS levels was observed at 1000 µg/L. At the molecular level, downregulation of oxidative stress-related genes (cat, sod1, and sod2) in larval fish was noted with exposure to 10 and 5000 µg/L Tebuthiuron, suggesting a depletion of antioxidant enzymes. In addition, some neurotoxicity-related genes were downregulated, such as acetylcholinesterase (ache), while some genes were upregulated, like microtubule-associated protein tau b (maptb) and synapsin 2 alpha (syn2a), with 5000 µg/L Tebuthiuron exposure. In conclusion, Tebuthiuron induces sublethal toxicity characterized by irregular, concentration-specific disruptions to photomotor behavior, basal ROS levels, and transcriptional markers of oxidative stress and synaptic function, even in the absence of acute morphological defects. Future research should prioritize functional assays targeting mitochondrial bioenergetics and antioxidant enzyme activities, alongside evaluations of later developmental stages, to fully elucidate the long-term ecological risks of phenylurea herbicides to non-target aquatic species.

Transition metal dichalcogenides (TMD) are attractive for adsorption-driven reactions, yet their activity is strongly site-dependent. Activity is concentrated at edge motifs, whereas most exposed area resides on inert basal planes. Dual-site designs that enrich edges while activating basal planes with catalysts remain challenging to realize without coarsening and metal aggregation during thermal processing. Here, an intense pulsed light-driven flash thermal synthesis route is demonstrated that directly converts ammonium tetrathiomolybdate ((NH4)2MoS4) into few-layer, edge-rich MoS2 nanoflakes (FTS-MoS2) within 10 ms pulse in ambient-air. Ultrafast photothermal shock (1192-1811°C; ∼10[5]/10[4]°C s[-] [1] heating/cooling rates) suppresses in-plane coarsening and out-of-plane stacking, while Pt, Ir, or Au single atoms are uniformly anchored on MoS2 via rapid metal-sulfur coordination without aggregation. As a proof-of-concept, FTS-MoS2 exhibits a 23.6-fold higher NO2 response at 5 ppm than solvothermally synthesized MoS2. Pt single atom functionalization (FTS-PtSA-MoS2, 1.2 wt%) further boosts the response by 22.8-fold versus pristine FTS-MoS2 and achieves 100.8% response toward 400 ppb NO2 at room temperature. Density functional theory supports enhanced NO2 adsorption and charge transfer on FTS-PtSA-MoS2. With a low electrical energy input (8.6 kJ g[-1]) and scalable irradiation, ultrafast FTS enables industrially relevant active-site and single-atom engineering in TMDs for high-performance gas sensors.

Coastal eutrophication is widely presumed to threaten filter-feeding bivalve aquaculture by inducing algal blooms, yet this relationship rarely follows a simple linear negative feedback in hydrodynamically complex areas. Based on multi-source data (2019-2022) from the Shengs Archipelago-a typical estuary-shelf system in East Asia-we investigated cascading effects of dynamic eutrophication on mussel yield. Results show that pulsed terrestrial inputs reshaped a "low-phosphorus, high nutrient stoichiometric ratio" habitat window, triggering summer blooms characterized by diatom-dinoflagellate alternation. Notably, the study area did not follow the traditional eutrophication-production decline trajectory; instead, unit-area mussel yield increased steadily from 124.97 to 153.17 t·ha[-1] over the study period, without clear evidence of basal ecosystem degradation. Bivalve aquaculture responses to eutrophication are thus highly context-dependent. Sustained production may reflect combined effects of nutrient structure optimization, functional group restructuring, management improvements, and system resilience, although direct causality requires further investigation.

Bilateral basal ganglia involvement is an uncommon but treatable manifestation of neuropsychiatric systemic lupus erythematosus (NPSLE) that is rarely described in pediatric patients and is frequently omitted from the standard differential diagnosis for bilateral basal ganglia lesions in childhood. We report an adolescent girl with a recent diagnosis of systemic lupus erythematosus who presented with acute neuropsychiatric deterioration, including altered mental status and seizures. Brain magnetic resonance imaging (MRI) demonstrated symmetrical T2-weighted/fluid-attenuated inversion recovery (T2/FLAIR) hyperintensity of the bilateral anterior basal ganglia without diffusion restriction, consistent with vasogenic edema. Concomitant findings included a left cerebellar subacute cortical infarct and diffuse leptomeningeal enhancement, a constellation postulated to reflect diffuse systemic lupus erythematosus-related endothelial dysfunction and blood-brain barrier disruption. Infectious and metabolic etiologies were excluded. The patient was managed with pulse methylprednisolone and azathioprine without significant improvement. Subsequent initiation of plasmapheresis resulted in clinical improvement, supporting a humorally mediated mechanism of injury. This case highlights the importance of including NPSLE in the differential diagnosis of symmetrical basal ganglia lesions in children, particularly when systemic autoimmune features are present, to ensure timely escalation of therapy.

Heart rate variability (HRV) is widely used as a non-invasive marker of cardiac autonomic regulation in human and experimental animal research. Its accessibility, repeatability, and applicability across clinical, psychophysiological, wearable, and preclinical settings make HRV a valuable translational tool. However, HRV indices are highly sensitive to physiological and methodological context, including recording duration, signal quality, respiratory pattern, posture, behavioral state, circadian timing, medication use, anesthesia, temperature, species, strain, artefact correction, frequency-band selection, and analytical method. Human HRV standards provide a strong methodological foundation, but they cannot be directly transferred to animal models without considering species-specific differences in basal heart rate, respiratory frequency, autonomic regulation, recording conditions, and experimental constraints. In animal studies, additional sources of heterogeneity include telemetry versus surface ECG recordings, conscious versus anesthetized states, handling and restraint, surgical recovery, body temperature control, and inconsistent frequency-domain definitions. This review synthesizes current methodological knowledge on HRV measurement in human and experimental animal studies and highlights major challenges that limit reproducibility and translational interpretation. Attention is given to common methodological pitfalls, and the risk of overinterpreting single indices such as LF/HF as direct measures of sympathovagal balance. We also propose a minimum reporting framework for human and experimental animal HRV studies, with shared translational items intended to support authors, reviewers, and editors. Transparent reporting of acquisition, preprocessing, analysis, and physiological context may improve comparability across studies and strengthen the role of HRV as a bridge between mechanistic animal research and human autonomic assessment.Clinical trial number: not applicable.

Although carotid-femoral pulse wave velocity (cf-PWV) is the non-invasive gold standard for assessing aortic stiffness, evidence linking cf-PWV to basal ganglia enlarged perivascular spaces (BG-EPVS) in the general population is limited. We aimed to evaluate this association and quantify the mediating role of blood pressure (BP) in community-based adults. This cross-sectional study included 485 participants from the Kailuan cohort. Cf-PWV was measured by ultrasound, and BG-EPVS were graded on 3.0-Tesla MRI. Logistic regression, restricted cubic spline, and mediation analyses were applied to quantify the indirect effects of systolic BP (SBP), diastolic BP (DBP), and pulse pressure (PP). BG-EPVS were identified in 59.4% of participants. After adjustment for cardiovascular risk factors other than BP, cf-PWV ≥ 10 m/s was independently associated with BG-EPVS (OR = 2.06, 95% CI: 1.27-3.36), with a linear dose-response relationship (p for non-linearity = 0.668). The association was stronger among participants aged ≤ 70 years and among males. SBP and PP mediated 43.0% and 43.6% of the total cf-PWV effect, respectively, whereas DBP did not function as a significant mediator. Higher cf-PWV was independently and dose-dependently associated with BG-EPVS, with pulsatile BP components mediating approximately 43% of this association.

Females with a normal body mass index (BMI) and high body fat percent (i.e., normal-weight obesity or NWO) are at increased risk for cardiometabolic diseases compared to normal-weight lean (NWL) counterparts. However, underlying mechanisms remain unclear. Here, we examined postprandial lipids, gut permeability biomarkers, and arterial stiffness outcomes as potential factors implicated in cardiometabolic disease development. Females (N=33) with a normal BMI were grouped as NWO (body fat percent ≥33.0%; n=18) or NWL (body fat percent <33.0; n=15). Following IV insertion and baseline blood collection, a high-fat meal was consumed. Additional blood samples were collected at 1-, 2-, 3-, and 4-hours post-meal for determination of lipids (triglycerides, HDL-C, apolipoprotein [apo] B) and intestinal permeability biomarkers (lipopolysaccharide binding protein [LBP], soluble cluster differentiation 14 [sCD14], LBP:sCD14). Pulse wave analysis and pulse wave velocity were measured as indicators of arterial stiffness at 0, 2, and 4 hours. Across both groups, the high-fat meal impacted triglycerides (increased), HDL-C (decreased), apolipoprotein-B (decreased; PTime≤0.001). The frequency of adverse postprandial triglyceride responses was higher in NWO compared to NWL females (p<0.05). Further, non-significant (PGroup≤0.08), medium effect sizes (ηp[2]≥0.12) were observed for triglycerides and apoB, consistent with NWO>NWL, regardless of time point. LBP and LBP:sCD14 increased, while sCD14 decreased, following the high-fat meal (PTime≤0.05). Additionally, NWO had higher LBP regardless of time point compared to NWL (PGroup<0.05). All arterial stiffness measures decreased post-meal (PTime≤0.05). In conclusion, this work provides early of evidence of postprandial dyslipidemia and basalintestinal hyperpermeability in females with NWO.

Electrical storm (ES) is a life-threatening clinical syndrome defined by recurrent episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF) within a short time frame. Although contemporary management relies on guideline-directed therapies, including antiarrhythmic drugs, deep sedation, sympathetic modulation, and catheter ablation in selected refractory cases, some patients remain unstable and require individualized treatment guided by the suspected electrophysiological substrate. We report the case of a 44-year-old previously healthy woman who presented with out-of-hospital cardiac arrest due to VF. Following successful resuscitation, she developed recurrent polymorphic VT apparently initiated by short-coupled premature ventricular complexes (PVCs). Despite implementation of several conventional and guideline-supported strategies for ES, ventricular arrhythmias continued to recur. The clinical pattern and electrocardiographic/telemetry recordings were considered compatible with a short-coupled ectopy-triggered mechanism, raising suspicion for a Purkinje-mediated substrate. Based on this hypothesis, a therapeutic strategy aimed at increasing the basal heart rate was adopted using continuous isoproterenol infusion. Following isoproterenol titration to achieve sinus tachycardia of approximately 120 beats per minute, no further VT was documented. Quinidine therapy was subsequently introduced, allowing withdrawal of isoproterenol with sustained arrhythmia suppression. This case illustrates how careful interpretation of arrhythmia patterns may guide therapeutic decisions in refractory ES and highlights the potential role of heart rate acceleration in selected patients with suspected short-coupled PVC-triggered ventricular arrhythmias.