Doxorubicin-induced cardiotoxicity classically manifests as dose-dependent left ventricular systolic dysfunction. Herein, we describe an unusual case of acute mitral papillary muscle rupture following cumulative anthracycline therapy, presenting despite a preserved ejection fraction.

Doping represents a critical threat to the integrity of competitive sports, with diuretics frequently misused as masking agents to facilitate the urinary excretion of other prohibited substances. Torsemide (TSD), a widely misused loop diuretic, requires a sensitive and selective method for its determination in biological matrices to support efficient doping control. Herein, a sustainable fluorescent nanosensor based on multi-self-doped carbon quantum dots was synthesized for the first time from golden berry (GBQDs) via a rapid, one-step microwave-assisted approach at 800 W in just 7 min without additional surface passivation agents. Notably, these innovative CDs outperform previous traditional methods, as their preparation relies on minimum energy consumption and green natural substrate. The fabricated GBQDs exhibited intense blue fluorescence at λex/λem 350/423 nm, a quantum yield of 28.9%, nano-sized CDs (7.67 ± 1.02 nm), and a chemical composition of C (51.12%), N (22.8%), O (25.6%), S (0.02%), K (0.38%), Cl (0.04%), P (0.02%), and Cu (0.02%). The GBQDs demonstrated excellent aqueous solubility, remarkable photostability (3% fluorescence decrease after 60 min), and storage stability (in refrigerator) for 8 weeks. TSD selectively quenches GBQDs fluorescence via a combined inner filter effect and static quenching mechanism, forming the basis of a "turn-off" fluorescent nanosensor. Under optimized conditions, the method showed linearity over 0.5-30 μg/mL (r[2] = 0.9999), LOD of 0.110 μg/mL, LOQ of 0.335 μg/mL, high accuracy (99.75 ± 1.02%), precision (RSD < 1%), selectivity, and robustness. The proposed nanosensor was successfully applied for TSD determination in pharmaceutical dosage forms, human urine, and plasma with recoveries ranging from 99.43 to 100.29%. Greenness and blueness assessments using Complex-GAPI, BAGI (80), AGREE-Prep (0.79), and NAT (91) confirmed superior environmental sustainability and feasibility for on-site detection in doping regulation laboratories. This strategy offers a rapid, cost-effective, sensitive, and eco-friendly platform for anti-doping surveillance and therapeutic monitoring of TSD in biological matrices, guaranteeing fair competition and safeguarding athletes' health in the sports world.

Uromodulin (UMOD) regulates tubular sodium handling and modulates NKCC2, the molecular target of loop diuretics (LD). Although UMOD variants have been associated with blood pressure and hypertension, their pharmacogenetic relevance in heart failure (HF) remains unknown. We assessed whether the UMOD rs13333226 genotype is associated with clinical outcomes among patients with HF who initiated LD. We assembled a cohort of UK biobank (UKB) participants diagnosed with HF who initiated LD. Patients were followed in an intention-to-treat fashion for up to 12 months. Cox models estimated confounder-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) comparing rs13333226-AA versus rs13333226-AG/GG genotypes. The primary effectiveness outcome was worsening HF, defined as hospitalization for HF or death with HF as the primary cause. Additional effectiveness and safety outcomes were major adverse cardiovascular events (MACE), acute kidney injury (AKI), and all-cause mortality. Secondary analyses stratified by age and sex. Sensitivity analyses restricted follow-up to 3 and 6 months. Among 1,426 HF patients initiating LD (92% furosemide, mean age 68 years, 34% female), the rs13333226-AA genotype was not associated with worsening HF (HR, 0.95; 95% CI, 0.76-1.20), MACE (HR, 0.97; 95% CI, 0.62-1.52), AKI (HR, 1.05; 95% CI, 0.68-1.64), or all-cause mortality (HR, 1.17; 95% CI, 0.76-1.78). There was no effect modification by demographics. Shorter follow-up periods did not affect the results. In HF patients initiating LD, UMOD rs13333226 was not associated with effectiveness or safety outcomes. These findings do not support a clinically meaningful pharmacogenetic role for this variant.

The combined use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) and loop diuretics may reduce interstitial fluid (IF) retention without excessive plasma volume depletion; however, short-term effects compared with loop diuretic monotherapy remain unclear. This prospective, open-label observational study compared 7-day changes in body fluid status among patients with chronic kidney disease receiving loop diuretics alone (Loop group), SGLT2i alone (SGLT2i group), or SGLT2i plus loop diuretics (SGLT2i+Loop group). Body fluid status was assessed at baseline and day 7. In unadjusted analyses, percent change in estimated plasma volume (ePV) differed among groups (analysis of variance, p = 0.0076) and was lower in the SGLT2i+Loop group than in the Loop group (mean difference, -3.56%; 95% confidence interval, -6.22 to -0.90; p = 0.0059). However, this difference was not significant after adjustment for baseline imbalances and loop diuretic use. Percent change in IF differed overall (p = 0.0030) but did not differ between the SGLT2i+Loop and Loop groups in unadjusted or adjusted analyses. In group-specific analyses, baseline ePV was inversely correlated with percent change in ePV in the SGLT2i+Loop group (r = -0.4185, p = 0.0418), but exploratory interaction analyses showed no significant treatment-group difference in this association. Thus, early ePV and IF responses were comparable between loop diuretic monotherapy and combination therapy after adjustment. This finding supports the hypothesis that baseline intravascular volume status may be linked to early plasma volume responses to combination therapy, a relationship that warrants testing in larger prospective studies.