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B Healy

Publications and source records attributed to B Healy.

At least 55 records · Page 3Linked to original sources
PubMed1992

Hearing on the possible uses and misuses of genetic information.

In summary, I will reiterate the five points I would like to leave with you today: First, the biological revolution has extraordinary power to do good. As long as the use of our new genetic knowledge is guided by the traditional ideals of the healing professions--to help improve the human condition without doing harm--we can expect real benefits to come of it. Second, however, we need to prepare for the fact that, like all powerful tools, genetic information can be misused and abused. As I hope to have illustrated, NIH has the will and ability to work with the American public and the scientific community in preparing for the responsible use of genetic information for now and the future. To date, the best example of that will is the precedent-setting work being conducted in concert with the human genome program through our ELSI program. Third, as a part of that work, it will be imperative to continue to protect the voluntary nature of genetic services. The rights of people to determine for themselves whether or not to pursue genetic information about themselves must be defended, even from the forced choices that discriminatory social practices may create. Fourth, in order to allow those who choose to do so to benefit from our new genetic tools, discrimination based on genotype must be prohibited as a matter of basic civil rights. And finally, in the bright light of the Human Genome Project and its ELSI program, it is important not to let genetics eclipse the important ethical, legal and social issues that attend other biomedical advances. It is the purpose of NIH's new center for science policy studies to illuminate this broader view of the road ahead. Thank you. I will be happy to answer any questions you might have.

Biomedical Research↗
PubMed1991

The Yentl syndrome.

Explore the source record for details and available documents.

Coronary Disease↗
PubMed1991

The Monk Hard-Top prosthesis for displaced intracapsular fractures of the femoral neck.

The Monk Hard-Top prosthesis was inserted without operative mortality in 85 patients, with an average age of 81 years, presenting with Intracapsular Fracture of the Femoral Neck, Garden grade 3 or 4. At review, 60% of the patients walked unaided, without pain. Only 6% of those reviewed had a poor functional outcome. Fifty-three per cent of the patients returned to their previous environment and 47% had died 6 months postoperatively. The prosthesis is more difficult to dislocate, once inserted properly, than either a Thompson Hemiarthroplasty or a Primary Total Hip replacement. It is less likely to sustain Component Disassembly than other types of bipolar hemiarthroplasty. The Monk Hard Top Prosthesis is recommended for the treatment of Garden grade 3 or 4 Intracapsular Fractures of the Femoral Neck in elderly people.

Aged↗
PubMed1990

Myotrophin: purification of a novel peptide from spontaneously hypertensive rat heart that influences myocardial growth.

Mechanisms involved in the development or the regression of myocardial hypertrophy cannot be fully explained as responses to blood pressure control alone. We had hypothesized that the development of hypertrophy is initiated by a signal (mechanical or humoral) to the myocardium, which in turn produces a soluble factor that triggers protein synthesis and initiates myocardial growth. Using the stimulation of protein synthesis in isolated cardiac myocytes obtained from normal rat hearts as an assay system, we have identified a soluble factor from the hypertrophied myocardium of spontaneously hypertensive rats. This factor, which has been purified to apparent homogeneity, is a protein of 12 kDa. The sequence of three internally liberated peptides containing 7-24 residues was determined. Based on the determined amino acid sequences of these peptides, this factor (designated myotrophin) appears to be a novel protein that shows no homology with any previously described growth factors. Myotrophin is present in human, dog, and rat hypertrophied hearts (28-35% stimulation of protein synthesis over control) and in small amounts in normal hearts (5-6% stimulation). Myotrophin causes two dose-dependent effects in neonatal cardiac myocytes: an increase in the surface area of the myocyte and the appearance of organized myofibrils, which become apparent within 48 h. Myotrophin may play an important role in the pathogenesis of cardiac hypertrophy as well as in the normal development of cardiac myocytes.

Amino Acid Sequence↗
PubMed1990

Angiotensin II-forming pathways in normal and failing human hearts.

Reduced preload and afterload to the heart are important effects of angiotensin converting enzyme (ACE) inhibitors in the treatment of congestive heart failure. However, since angiotensin II (Ang II) directly increases the strength of myocardial contraction, suppression of Ang II formation by ACE inhibitors could potentially reduce the beneficial effects of Ang II on the failing heart. To study how ACE inhibition suppresses cardiac Ang II formation in man, we characterized ACE-dependent and ACE-independent Ang II-forming pathways in eight normal and 24 failing human hearts obtained at cardiac transplantation. Ang II-forming activity in left ventricular (LV) membrane preparations was assessed by measuring the conversion of [125I]angiotensin I (Ang I) to [125I]Ang II. LV [125I]Ang II-forming activity in normal hearts (35.5 +/- 2.7 fmol/min/mg, n = 8) was not different from that in hearts from patients with ischemic cardiomyopathy (25.5 +/- 2.9 fmol/min/mg, n = 9) and was 48% lower (p less than 0.001) in hearts from patients with idiopathic cardiomyopathy (18.5 +/- 1.9 fmol/min/mg, n = 15).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Angiotensins and the failing heart. Enhanced positive inotropic response to angiotensin I in cardiomyopathic hamster heart in the presence of captopril.

We examined the hypothesis that the positive inotropic effect of angiotensin I (Ang I) may be retained in the presence of angiotensin converting enzyme inhibitors so that it may have a direct beneficial effect on the heart. Accordingly, isolated perfused hearts (Langendorff preparation) of 300-day-old cardiomyopathic hamsters (a model of spontaneous cardiomyopathy) and age-matched normal hamsters (controls) were infused with Ang I in the presence of captopril; propranolol was added to the perfusing medium to block catecholamine-mediated effects of angiotensins on the heart. Left ventricular developed pressure and the rate of increase in left ventricular developed pressure increased significantly (p less than 0.001) in both the cardiomyopathic and the normal hamster heart despite concomitant reduction in myocardial flow rate favoring a direct inotropic effect of Ang I in both normal and myopathic hearts; these changes were significantly higher by almost threefold in the cardiomyopathic than in the normal hamsters (p less than 0.01) and were blocked by the angiotensin II (Ang II) antagonist [Sar1,Thr8]Ang II. Comparing dose-left ventricular contractility response curves for Ang I and Ang II, ED50 for responses was identical in both normal and myopathic hearts, whereas peak responses to Ang II were double those to Ang I in normal hearts but were almost identical in the myopathic hearts. Binding of [125I]Ang II in six cardiomyopathic and four normal hamster hearts was of high affinity, but there was no evidence for Ang I-saturable high-affinity binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗