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Biomedical subjects

A O'Donoghue

Publications and source records attributed to A O'Donoghue.

6 recordsLinked to original sources
PubMed1999

An evaluation of the nurse practitioner role in a major rural emergency department.

The purpose of this pilot study was to investigate whether nurse practitioners are able to provide a level of primary health service applicable to remote/isolated settings in wound management and treatment of blunt limb trauma. It was hypothesized that there would be no significant difference in the quality of care, or the level of client satisfaction, provided by the medical officers and the nurse practitioners in the study. Two groups participated in the study, nurse practitioners and medical officers. The study used a randomized trial design. Data were collected using quantitative and qualitative methods. Two hundred and thirty-two clients participated in the study. Of this number 63 were supervised cases in the pilot trial. In the randomized trial participants were distributed between nurse practitioners and medical officers (n = 169), of which 91 were randomized to medical officers and 78 to nurse practitioners. Telephone interviews were conducted to evaluate client satisfaction. The majority of study participants were surveyed for client satisfaction (n = 132). This represents approximately 78% of the randomized sample and multivariate analysis was carried out on the data. Study results indicate that there were no significant differences between the two groups in relation to client satisfaction. Very positive outcomes of treatment were consistent across groups in the study. The study also found that there was strong support for the role of the nurse practitioner in the rural emergency setting. Recommendations include further research to measure the efficacy of nurse practitioners utilizing the selected competencies in remote/isolated settings.

Adolescent↗
PubMed1998

Risk-taking and creative thinking pay off.

The Nursing Branch has taken more risks, thought more creatively and responded to needs that are both unique and long-standing and in this way continues to raise the profile of nursing.

Creativity↗
PubMed1997

Abnormal skeletal muscle bioenergetics in familial hypertrophic cardiomyopathy.

OBJECTIVE: To determine the skeletal muscle metabolic manifestations of familial hypertrophic cardiomyopathy. DESIGN: A case-control study. SETTING: 31P magnetic resonance spectroscopy of the calf muscle was performed on volunteers from a centre specialising in familial hypertrophic cardiomyopathy. PATIENTS: Five patients with abnormal beta myosin heavy chain protein in cardiac and skeletal muscle and five patients with a troponin T abnormality in cardiac muscle were compared with healthy controls. RESULTS: High energy phosphate metabolism in vivo was examined in a non-invasive manner. In resting muscle, the beta myosin heavy chain group had a higher ratio of phosphocreatine to ATP concentration (4.51 (SD 0.17)) than either the troponin T group (3.88 (0.42)) or controls (n = 16; 4.04 (0.40)). Exercise duration was reduced compared to controls, and during the fourth minute of exercise phosphocreatine depletion and muscle acidification were greater in both patient groups. After exercise, the recovery of phosphocreatine-an index of oxidative metabolic capacity of the muscle-was slower in the beta myosin heavy chain group (mean half time 0.65 (0.08) minutes) than in the troponin T group (0.60 (0.17) minutes) or controls (0.48 (0.14) minutes). CONCLUSIONS: Exercise metabolism was abnormal in both groups of subjects, and the affected contractile protein determined the metabolic changes in muscle at rest and during recovery. In patients with abnormal beta myosin heavy chain protein, there was a decrease in oxidative capacity consistent with the reduction in mitochondria reported in muscle biopsy studies of similar patients.

Adenosine Triphosphate↗
PubMed1995

Mutations in the genes for cardiac troponin T and alpha-tropomyosin in hypertrophic cardiomyopathy.

BACKGROUND: Familial hypertrophic cardiomyopathy can be caused by mutations in the genes for beta cardiac myosin heavy chain, alpha-tropomyosin, or cardiac troponin T. It is not known how often the disease is caused by mutations in the tropomyosin and troponin genes, and the associated clinical phenotypes have not been carefully studied. METHODS: Linkage between polymorphisms of the alpha-tropomyosin gene or the cardiac troponin T gene and hypertrophic cardiomyopathy was assessed in 27 families. In addition, 100 probands were screened for mutations in the alpha-tropomyosin gene, and 26 were screened for mutations in the cardiac troponin T gene. Life expectancy, the incidence of sudden death, and the extent of left ventricular hypertrophy were compared in patients with different mutations. RESULTS: Genetic analyses identified only one alpha-tropomyosin mutation, identical to one previously described. Five novel mutations in cardiac troponin were identified, as well as a further example of a previously described mutation. The clinical phenotype of four troponin T mutations in seven unrelated families was similar and was characterized by a poor prognosis (life expectancy, approximately 35 years) and a high incidence of sudden death. The mean (+/- SD) maximal thickness of the left ventricular wall in subjects with cardiac troponin T mutations (16.7 +/- 5.5 mm) was significantly less than that in subjects with beta cardiac myosin heavy-chain mutations (23.7 +/- 7.7 mm, P < 0.001). CONCLUSIONS: Mutations in alpha-tropomyosin are a rare cause of familial hypertrophic cardiomyopathy, accounting for approximately 3 percent of cases. Mutations in cardiac troponin T account for approximately 15 percent of cases of familial hypertrophic cardiomyopathy in this referral-center population. These mutations are characterized by relatively mild and sometimes subclinical hypertrophy but a high incidence of sudden death. Genetic testing may therefore be especially important in this group.

Adolescent↗