journal of cardiovascular nursing articles

: National Heart, Lung, and Blood Institute, February 2003. New York: McGraw-Hill, 2001:2863-913. ), 3. Cooper R, Cutler J, Desvignes-Nickens P, et al. Koster T, Rosendaal FR, de Ronde H, Briet E, Vandenbroucke JP, Bertina RM. 7. Mohlke KL, Erdos MR, Scott LJ, et al. Sesti F, Abbott GW, Wei J, et al. Ridker PM, Hennekens CH, Lindpaintner K, Stampfer MJ, Eisenberg PR, Miletich JP. Gene expression profiling of human stent-induced neointima by cDNA array analysis of microscopic specimens retrieved by helix cutter atherectomy: detection of FK506-binding protein 12 upregulation. This peer-reviewed journal of the European Society of Cardiology's Association of Cardiovascular Nursing and Allied Professions (ACNAP) covers the broad field of cardiovascular nursing and care including chronic and acute care, cardiac rehabilitation, primary and secondary prevention, heart failure, acute coronary syndromes, interventional cardiology… Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2. The proliferation gene expression signature is a quantitative integrator of oncogenic events that predicts survival in mantle cell lymphoma. Finding genes that underlie complex traits. Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel. Nature 1996;384:80-83, 57. Studies examining polymorphisms in the genes encoding angiotensin II, aldosterone, and endothelin that may modify the phenotype of hypertrophic cardiomyopathy have not yielded consistent results.40-43 Interestingly, clinically affected persons with two mutations in the same gene or different genes (compound heterozygotes) have also been described.44. Nat Genet 1996;13:183-188, 20. Bowles, Kathryn H. The Journal of Cardiovascular Nursing. 2. Mutations in the cardiac troponin I gene associated with hypertrophic cardiomyopathy. Rosenwald A, Wright G, Wiestner A, et al. With regard to complex traits in more common cardiovascular diseases, current research is identifying functionally significant variations in DNA sequences that can establish a molecular diagnosis and influence patients' outcome. NHLBI morbidity and mortality chartbook, 2002. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. 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Effect of angiotensin-converting enzyme (ACE) gene polymorphism on progression of renal disease and the influence of ACE inhibition in IDDM patients: findings from the EUCLID Randomized Controlled Trial: EURODIAB Controlled Trial of Lisinopril in IDDM. Angiotensin-I converting enzyme genotypes and left ventricular hypertrophy in patients with hypertrophic cardiomyopathy. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs. diuretic: the Hypertensive and Lipid-Lowering Treatment to Prevent Heart Attack (ALLHAT). cardiovascular disease mechanisms, translational and clinical research, cardiac electrophysiology, cardiovascular surgery, resuscitation, hypertension, Hypertrophic cardiomyopathy. 10/8C103, 10 Center Dr., Bethesda, MD 20892, or at [email protected]. The cholesterol quartet. The blood-clotting system requires precise control of factors within and outside the coagulation cascade to prevent fatal bleeding or unwanted thrombosis. Lifton RP, Dluhy RG, Powers M, et al. Activated protein C resistance as an additional risk factor for the thrombosis in protein C-deficient families. Capillaries in muscle and adipose tissue remove the triglycerides, and the lipid particle is modified into an LDL, with its cholesteryl ester core and apolipoprotein B-100 coat. Address reprint requests to Dr. Nabel at the National Heart, Lung, and Blood Institute, Bldg. Vol. Small KM, Wagoner LE, Levin AM, Kardia SLR, Liggett SB. Br J Haematol 2001;113:630-635. Gain-of-function mutations in SCN5A cause the long-QT syndrome, whereas loss-of-function mutations in the cardiac sodium channel cause idiopathic ventricular fibrillation. Circulation 1995;92:1808-1812, 41. Circulation 1994;89:22-32, 39. (Adapted from Kamisago et al.32). Join us on December 1-2, 2020 and earn 4.0 CE contact hours at our virtual learning event all about heart failure. Concise summaries and expert physician commentary that busy clinicians need to enhance patient care. In 2001, about 450,000 people in the United States died suddenly from cardiac arrhythmias.1,2 Genetic factors may modify the risk of arrhythmia in the setting of common environmental risks. Polymorphism-association studies compare the prevalence of a genetic marker in unrelated people with a given disease to the prevalence in a control population. Simon DB, Karet FE, Hamdan JM, DiPietro A, Sanjad SA, Lifton RP. Circulation 2000;102:1950-1955, 45. (Accessed June 10, 2003, at Mutations in the gene for cardiac myosin-binding protein C and late-onset familial hypertrophic cardiomyopathy. J Clin Invest 1995;96:2162-2169, 76. Prevalence of hypertrophic cardiomyopathy in a general population of young adults: echocardiographic analysis of 4111 subjects in the CARDIA Study: Coronary Artery Risk Development in (Young) Adults. Mutations that cause a loss of aldosterone synthase activity impair renal salt retention and the secretion of potassium and hydrogen ions in the distal nephrons and lead to severe hypotension as a result of reduced intravascular volume.15. This study also highlights the importance of taking into account haplotypes, rather than a single polymorphism, when defining biologic function. Oliphant A, Barker DL, Stuelpnagel JR, Chee MS. BeadArray technology: enabling an accurate, cost-effective approach to high-throughput genotyping. Hansson JH, Schild L, Lu Y, et al. Hereditary hypertension caused by chimaeric gene duplications and ectopic expression of aldosterone synthase. Information and tools for librarians about site license offerings. This point can be illustrated by a description of the genetic basis of specific diseases. Science 2001;292:1310-1312. The findings of this study suggest that the α2cDel322–325 and β1Arg389 receptors act synergistically in blacks to increase the risk of heart failure. Genotyping at these two loci may identify persons at risk for the development or progression of heart failure and may predict their response to therapy. Cell 1994;79:407-414, 17. Wilson and colleagues identified two genes causing pseudohypoaldosteronism type II; both encode proteins in the WNK family of serine–threonine kinases.12 Mutations in WNK1 are intronic deletions on chromosome 12p. Niimura H, Bachinski LL, Sangwatanaroj S, et al. Rosendaal FR, Koster T, Vandenbroucke JP, Reitsma PH. N Engl J Med 2002;347:1135-1142, 65. Hypertension 2000;36:371-375, 82. Tan HL, Bink-Boelkens MT, Bezzina CR, et al. The apolipoprotein epsilon4 allele determines prognosis and the effect on prognosis of simvastatin in survivors of myocardial infarction: a substudy of the Scandinavian Simvastatin Survival Study.

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