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Biomedical subjects

R S Riley

Publications and source records attributed to R S Riley.

27 records · Page 2Linked to original sources
PubMed1982

Clinical results of early stage prostatic cancer treated by pelvic lymphadenectomy and 125iodine implants.

Eighty patients with clinically early stage adenocarcinoma of the prostate were treated with pelvic lymphadenectomy and interstitial implantation of 125iodine seeds. A new applicator that permits greater accuracy in spacing the seeds has been developed. Postoperative complications were minimal, with urinary irritability being the most common. Multiple transrectal needle biopsies were performed 12 and 18 months after treatment in 46 patients. The prostatic biopsies were negative for carcinoma in 61 per cent and positive in 39 per cent of the patients. Long-term followup is needed to correlate post-treatment biopsies with survival and to determine if patients with positive biopsies should receive further treatment.

Aged↗
PubMed1981

Evaluation of the role of coronary angioplasty in patients with unstable angina pectoris.

Seventeen patients presenting with unstable angina pectoris underwent percutaneous transluminal coronary angioplasty (PTCA). Despite vigorous medical therapy, all patients were disabled with 10 experiencing refractory in-hospital angina. PTCA was judged successful in 13 patients and resulted in decreased coronary diameter narrowing from 80 +/- 16% to 34 +/- 13% and reduced transstenotic pressure gradient from 69 +/- 13 to 23 +/- 12 mm Hg. Regional coronary blood flow (CBF) and myocardial metabolism were assessed at rest and during pacing tachycardia in six patients with left anterior descending coronary stenosis. Prior to PTCA, neither regional CBF increased nor coronary vascular resistance declined during rapid pacing; myocardial lactate extraction fell, indicating a shift from aerobic to anerobic metabolism. Following PTCA, however, rapid pacing resulted in increased regional CBF, decreased coronary vascular resistance, and preservation of aerobic metabolism. Following PTCA, successfully dilated patients demonstrated marked relief of angina symptoms, increase in functional capacity, and objective exercise ECG and thallium scintigraphic evidence of relief of previously ischemic myocardium. This investigation demonstrates that PTCA, when combined with medical therapy, can be performed safely and successfully in selected patients who present with otherwise refractory unstable angina, and indicates the procedure deserves further study as a therapeutic alternative in this condition.

Adult↗
PubMed1980

Restoration of normal coronary hemodynamics and myocardial metabolism after percutaneous transluminal coronary angioplasty.

Regional coronary blood flow and myocardial metabolism were evaluated in a patient who underwent percutaneous transluminal coronary angioplasty (PTCA). Angioplasty increased coronary luminal diameter and reduced trans-stenotic gradient. Before PTCA, angina pectoris developed during sustained rapid atrial pacing and was associated with abnormal lactate metabolism and a mild increase in coronary flow and myocardial oxygen consumption. After PTCA, angina was absent during pacing and lactate extraction was preserved. Coronary flow and oxygen consumption were increased to a greater degree than before PTCA. The temporal response of changes in coronary blood flow due to an abrupt increase in heart rate was also evaluated. Floow reached peak value more rapidly after PTCA. These observations suggest that PTCA may result in improved regional coronary blood flow and restoration of normal flow regulatory mechanism and myocardial metabolism.

Angina Pectoris↗
PubMed1977

Complete heart block as a cause of syncope in asymmetric septal hypertrophy.

This case report presents a young adult with asymmetric septal hypertrophy (ASH) and syncope. Infranodal complete heart block was demonstrated as his cause for syncope. Therapy consisted of implantation of a A-V sequential pacemaker. Cardiac output determinations and systolic time intervals demonstrated the beneficial effects of properly timed atrial contractions.

Adult↗
PubMed1975

Further studies on the activation of microsomal (Na+ + k+)-atpase by a leukocytic product.

Previous studies showed that microsomal (Na+ + K+)ATPase (ATP phosphohydrolase, EC 3.6.1.3) is activated by a proteinaeous material released by polymorphonuclear leukocytes. Investigations on the mode of action of the activator have been conducted by the siolation of 32P-labeled phosphoenzyme intermediates formed in the reaction of ATP and (Na+ + K)-ATPase, which has been postulated to occur through the formation and hydrolysis of acyl phosphate intermediates. The activator caused a concentration-dependent decrease in the recovery of phosphoenzyme intermediates that was not quantitatively altered by the Na+ or K+ concentration of the reaction mixture of by the presence of 1 mM oubain. A decline in phosphoenzyme intermediate recovery was promoted by the addition of the activator to preformed phosphoenzyme intermediates but not by activator that had been pretreated with protease or phenol. In addition, the activator caused a concentration-dependent stimulation of the p-nitrophenyl phosphatase and acetyl phosphatase activities of microsomal (Na+ + K+)-ATPase. It was proposed that the activator stimulates the dephosphorylation step of the (Na+ + K+)-ATPase reaction sequence.

Adenosine Triphosphatases↗
PubMed1975

Activation of rabbit brain microsomal (Na+ plus K+)-dependent ATPase by a leukocytic product.

The properties of a (Na+ plus K+)-dependent ATPase (ATP phosphohydrolase, EC 3.6.1.3) activator contained in leukocytic extracts was investigated. Intact polymorphonuclear leukocytes release the activator in a time- and temperature-dependent process. It is non-dialyzable through cellophane; inactivated by protease, trypsin, or phenol; contains essential sulfhydryl groups; and is heat and acid labile. Treatment of ATPase with the activator and subsequent removable of the activator from mixtures did not reverse the ATPase activation.

Adenosine Triphosphatases↗