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atrial fibrillation/프롤린

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조항임상 시험특허
7 결과

Association of genetic variants with atrial fibrillation.

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Recent genome-wide association studies (GWASs) identified various genes and loci that confer susceptibility to coronary artery disease or myocardial infarction among Caucasian populations. As myocardial ischemia is an important risk factor for atrial fibrillation, we hypothesized that certain

Renin-angiotensin system component expression in the HL-1 atrial cell line and in a pig model of atrial fibrillation.

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OBJECTIVE Local atrial tissue angiotensin II (AngII) level is elevated in atrial fibrillation (AF), but the mechanism is unknown. We hypothesized that atrial myocytes express all components of the renin-angiotensin system (RAS) and investigated whether rapid depolarization alone is sufficient to

Novel KCNA5 mutation implicates tyrosine kinase signaling in human atrial fibrillation.

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BACKGROUND Emerging evidence has strongly implicated hereditary determinants for atrial fibrillation (AF). Loss-of-function mutations in KCNA5 encoding the ultrarapid delayed rectifier potassium current I(Kur) have been identified in AF families. OBJECTIVE The purpose of this study was to determine

Mutation in the S3 segment of KCNQ1 results in familial lone atrial fibrillation.

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BACKGROUND Mutations in several ion channel genes have been reported to cause rare cases of familial atrial fibrillation (AF). OBJECTIVE The purpose of this study was to determine the genetic basis for AF in a family with autosomal dominant AF. METHODS Family members were evaluated by 12-lead ECG,

Hypercoagulability causes atrial fibrosis and promotes atrial fibrillation.

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Atrial fibrillation (AF) produces a hypercoagulable state. Stimulation of protease-activated receptors by coagulation factors provokes pro-fibrotic, pro-hypertrophic, and pro-inflammatory responses in a variety of tissues. We studied the effects of thrombin on atrial fibroblasts and tested the

The Mutant Thyroid Hormone Receptor Beta R320P Causes Syndrome of Resistance to Thyroid Hormone.

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A 31-year-old Japanese male patient with a history of atrial fibrillation showed elevated serum levels of free thyroxine and triiodothyronine and a normal level of thyrotropin. The same abnormal hormone pattern was also found in his son. These data indicated that the index patient and the son have

Occlusion of left atrial appendage affects metabolomic profile: focus on glycolysis, tricarboxylic acid and urea metabolism.

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UNASSIGNED Left atrial appendage (LAA) closure (LAAC) by implantation of an occlusion device is an established cardiac intervention to reduce risk of stroke while avoiding intake of oral anticoagulation medication during atrial fibrillation. Cardiac interventions can alter local or systemic gene and
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