For all cycles, median times to recover to grade 0 were 56 and 20 days, respectively. The furosemide arm was characterized by relatively high urine output after cisplatin administration (900 vs 550mL/h), low frequency of unplanned additional hydration (14%vs 32%), and high incidence of hyponatremia (18% and 5%) compared with the mannitol arm. Both arms showed similar progression-free survival and overall survival. The preventive effect of the two forced diuretics on cisplatin-induced nephrotoxicity was not significantly different. However, the two diuretics have some distinct types of clinical presentations.The preventive effect of the two forced diuretics on cisplatin-induced nephrotoxicity was not significantly different. However, the two diuretics have some distinct types of clinical presentations.Right aortic arch (RAA) is one of congenital cardiovascular anomalies associated with esophageal atresia (EA). The surgical treatment for EA with RAA is still challenging. Although most pediatric surgeons are familiar with the right-sided approach, the division of the tracheoesophageal fistula and the anastomosis of the esophagus through right thorax are often difficult in cases of RAA. There are a few reports on thoracoscopic repair for EA with RAA. We report a case of EA with RAA treated by left-sided thoracoscopic approach. With left-sided thoracoscopic approach, identification and anastomosis of the esophagus could be safely performed without obstruction by the right-sided descending aorta. There was no leakage or stricture. Thoracoscopic repair of EA with RAA through the left thorax is feasible and safe without obstruction by the right-sided descending aorta.Chronic lung allograft dysfunction (CLAD) is the major barrier to long-term survival following lung transplantation, and new mechanistic biomarkers are needed. BYL719 Lymphocytic bronchitis (LB) precedes CLAD and has a defined molecular signature. We hypothesized that this LB molecular signature would be associated with CLAD in small airway brushings independent of infection. We quantified RNA expression from small airway brushings and transbronchial biopsies, using RNAseq and digital RNA counting, respectively, for 22 CLAD cases and 27 matched controls. LB metagene scores were compared across CLAD strata by Wilcoxon rank sum test. We performed unbiased host transcriptome pathway and microbial metagenome analysis in airway brushes and compared machine-learning classifiers between the two tissue types. This LB metagene score was increased in CLAD airway brushes (p = .002) and improved prediction of graft failure (p = .02). Gene expression classifiers based on airway brushes outperformed those using transbronchial biopsies. While infection was associated with decreased microbial alpha-diversity (p ≤ .04), neither infection nor alpha-diversity was associated with LB gene expression. In summary, CLAD was associated with small airway gene expression changes not apparent in transbronchial biopsies in this cohort. Molecular analysis of airway brushings for diagnosing CLAD merits further examination in multicenter cohorts. Seaweeds are rich sources of anti-oxidants and anti-inflammatory properties, which are beneficial to non-alcoholic fatty liver disease (NAFLD). However, whether seaweed consumption is associated with NAFLD is unknown. We investigated the association of seaweed consumption with newly diagnosed NAFLD in a large-scale adult population. This cross-sectional study involved 24572 participants aged over 18years. NAFLD was diagnosed by results of liver ultrasonography and alcohol intake. Dietary information was assessed using a validated and standardized 100-item food frequency questionnaire. Multivariate logistic analysis was used to evaluate the association between seaweed consumption and NAFLD. The prevalence of newly diagnosed NAFLD was 20.1%. After adjustment for sociodemographic characteristics, lifestyle factors, and other dietary intakes, the multivariable adjusted odds ratios (95% confidence intervals) of newly diagnosed NAFLD across seaweed consumption were 1.00 (reference) for almost never, 1.03 (0.93, 1.15) for <1 time/wk, 1.01 (0.90, 1.13) for 1 time/wk, and 0.84 (0.73, 0.96) for >1 times/wk (P for trend<.001). Stratified analyses suggested a potential effect modification by obesity status; the odds ratios (95% confidence intervals) across extreme quartiles was 0.77 (0.66, 0.91) in non-obese participants and 1.02 (0.79, 1.33) in obese participants (P for interaction<.001). Seaweed consumption is negatively associated with NAFLD, especially in non-obese participants.Seaweed consumption is negatively associated with NAFLD, especially in non-obese participants.Atrial structural remodelling including atrial hypertrophy and fibrosis is a key mediator of atrial fibrillation (AF). We previously demonstrated that the matricellular protein CCN5 elicits anti-fibrotic and anti-hypertrophic effects in left ventricles under pressure overload. We here determined the utility of CCN5 in ameliorating adverse atrial remodelling and arrhythmias in a murine model of angiotensin II (AngII) infusion. Advanced atrial structural remodelling was induced by AngII infusion in control mice and mice overexpressing CCN5 either through transgenesis (CCN5 Tg) or AAV9-mediated gene transfer (AAV9-CCN5). The mRNA levels of pro-fibrotic and pro-inflammatory genes were markedly up-regulated by AngII infusion, which was significantly normalized by CCN5 overexpression. In vitro studies in isolated atrial fibroblasts demonstrated a marked reduction in AngII-induced fibroblast trans-differentiation in CCN5-treated atria. Moreover, while AngII increased the expression of phosphorylated CaMKII and ryanodine receptor 2 levels in HL-1 cells, these molecular features of AF were prevented by CCN5. Electrophysiological studies in ex vivo perfused hearts revealed a blunted susceptibility of the AAV9-CCN5-treated hearts to rapid atrial pacing-induced arrhythmias and concomitant reversal in AngII-induced atrial action potential prolongation. These data demonstrate the utility of a gene transfer approach targeting CCN5 for reversal of adverse atrial structural and electrophysiological remodelling.