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Resuscitation Outcomes Consortium (ROC) Amiodarone, Lidocaine or Neither for Out-Of-Hospital Cardiac Arrest Due to Ventricular Fibrillation or Ventricular Tachycardia (ALPS)(ROC-ALPS-BioLINCC)

ABSTRACT: Resuscitation Outcomes Consortium (ROC) Amiodarone, Lidocaine or Neither for Out-Of-Hospital Cardiac Arrest Due to Ventricular Fibrillation or Ventricular Tachycardia (ALPS)(ROC-ALPS-BioLINCC)

PROVIDER: PRJNA1163441 | ENA |

REPOSITORIES: ENA

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Resuscitation Outcomes Consortium (ROC) Amiodarone, Lidocaine or Neither for Out-Of-Hospital Cardiac Arrest Due to Ventricular Fibrillation or Ventricular Tachycardia (ALPS)(ROC-ALPS-BioLINCC)

Project description:Resuscitation Outcomes Consortium (ROC) Amiodarone, Lidocaine or Neither for Out-Of-Hospital Cardiac Arrest Due to Ventricular Fibrillation or Ventricular Tachycardia (ALPS)(ROC-ALPS-BioLINCC)

| PRJNA1163442 | ENA

Transcriptional changes associated with advancing stages of heart failure underlie atrial and ventricular arrhythmogenesis underlie atrial and ventricular arrhythmogenesis

Project description:Heart failure (HF) is a leading cause of mortality and is associated with cardiac remodeling. Vulnerability to atrial fibrillation (AF) has been shown to be greater in the early stages of HF, whereas ventricular tachycardia/fibrillation develop during late stages. Here, we explore changes in gene expression that underlie the differential development of fibrosis and structural alterations that predispose to atrial and ventricular arrhythmias.

2019-01-01 | GSE123823 | GEO

The role of stretch, tachycardia and sodium-calcium exchanger in induction of early cardiac remodeling

Project description:Accute stretch and tachycardia are capable of inducing pathological excitation transcription coupling - an early invent before structural cardiac remodeling which transitions to heart failure. The sodium calcium exchanger is a key player in maintaining calcium homeostasis and is implicated in pathological signaling during heart failure. Neonatal rat ventricular cardiomyocytes (NRVCM) were subjected to mechanical stress and high freqency elecrical stimulation to study genes regulated during the early phase of trigger induced cardiac remodeling. Inhibition of the sodium calcium exchanger was used in an attempt to supress the early remodeling process and gain insight into the pathological signaling pathway.

2020-08-12 | GSE135172 | GEO

Tachycardia-induced metabolic rewiring as a driver of contractile dysfunction

Project description:Bulk RNA-Sequencing of EHTs subjected to tachypacing to probe the mechanism of tachycardia-induced cardiac dysfunction.

2023-11-17 | GSE242727 | GEO

Meta-analysis of the efficacies of amiodarone and nifekalant in shock-resistant ventricular fibrillation and pulseless ventricular tachycardia.

Project description: Not available

| S-EPMC5627292 | biostudies-literature

Net silencing by let-7i in Postural Tachycardia Syndrome

Project description:While strongly implicated in Postural Tachycardia Syndrome (POTS), considerable controversy exists regarding norepinephrine transporter (NET) loss-of-function. POTS is characterized by the clinical symptoms of orthostatic intolerance, light-headedness, tachycardia and syncope or near syncope with upright posture. Abnormal sympathetic nervous system activity is typical, of a type which suggests dysfunction of the NET, with evidence the gene responsible is under tight epigenetic control. Using RNA of isolated chromatin combined with sequencing (RICh-Seq) we show let7i miRNA suppresses NET by MeCP2. Vorinostat restores epigenetic control and NET expression in POTS.

2017-01-07 | GSE93235 | GEO

Resuscitation Outcomes Consortium-Amiodarone, Lidocaine or Placebo Study (ROC-ALPS): Rationale and methodology behind an out-of-hospital cardiac arrest antiarrhythmic drug trial.

Project description: Not available

| S-EPMC4014351 | biostudies-literature

Disruption of autophagic degradation with ROC-325 antagonizes renal cell carcinoma pathogenesis

Project description:Autophagy plays important roles in malignant pathogenesis and drug resistance. We used medicinal chemistry approaches to generate a series of novel agents that inhibit autophagic degradation. ROC-325 was selected as a lead compound for further evaluation. Comprehensive in vitro and in vivo studies were conducted to evaluate the selectivity, tolerability, and efficacy of ROC-325 in preclinical models of renal cell carcinoma (RCC). ROC-325 exhibited superior in vitro anticancer effects than the existing autophagy inhibitor hydroxychloroquine in 12 different tumor models with diverse genetic backgrounds. Focused studies of the mechanism of action and efficacy of ROC-325 in RCC cells showed that drug treatment induced hallmark characteristics of autophagy inhibition including accumulation of autophagosomes with undegraded cargo, lysosomal deacidification, p62 stabilization, and disruption of autophagic flux. Subsequent experiments showed that ROC-325 antagonized RCC growth and survival in an ATG5/7-dependent manner, induced apoptosis, and exhibited favorable selectivity. Oral administration of ROC-325 to mice bearing 786-0 RCC xenografts was well tolerated, significantly more effective at inhibiting tumor progression than HCQ, and inhibited autophagy in vivo. We used microarrays to determine gene expression changes following 24 h treatment with ROC-325 in RCC cell lines and identified differentially expressed genes.

2018-02-16 | GSE89766 | GEO

Resuscitation Outcomes Consortium (ROC) Prehospital Resuscitation on Helicopter Study (PROHS)(ROC-PROHS-BioLINCC)

Project description:Resuscitation Outcomes Consortium (ROC) Prehospital Resuscitation on Helicopter Study (PROHS)(ROC-PROHS-BioLINCC)

| PRJNA1181038 | ENA

Resuscitation Outcomes Consortium (ROC) Prehospital Resuscitation on Helicopter Study (PROHS)(ROC-PROHS-BioLINCC)

Project description:Resuscitation Outcomes Consortium (ROC) Prehospital Resuscitation on Helicopter Study (PROHS)(ROC-PROHS-BioLINCC)

| PRJNA1181039 | ENA