Biomedical subjects
Publications and source records attributed to R A Johnson.
A case is reported in which accumulation of Tc-99m sulfur colloid in one lung occurred following trauma, although the lung remained clear radiographically. Another trauma case is mentioned in which the uptake was bilateral. The cause of this phenomenon is unclear; several potential mechanisms are discussed.
Flexible sigmoidoscopy became available in 1976. To date, studies comparing it with rigid sigmoidoscopy support an increase of 2.5 to six times in the flexible sigmoidoscope's ability to detect polyps, and a two- to threefold increase in detection of colonic neoplasms in the same patients. This paper summarizes the current reported results of flexible sigmoidoscopy to date and describes the instrument and procedure as done at the UCLA Family Practice Residency Program. The flexible sigmoidoscope deserves evaluation for widespread primary care application.
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The flexible sigmoidoscope may represent a partial solution to the longstanding problem of physician and patient noncompliance with sigmoidoscopy for the detection of colorectal cancer. A three-year longitudinal audit of medical records revealed at least a sevenfold increase in the number of sigmoidoscopies performed after the introduction of flexible sigmoidoscopy to a salaried medical group. This procedure has made a significant contribution to patient care and resident education in the UCLA family practice residency program.
Ninety patients meeting the Research Diagnostic Criteria (RDC) for major depressive disorder were further diagnosed using the RDC depressive subtypes. Patients with specific RDC subtype diagnoses were compared to those who did not meet the subtype criteria on several variables, including family history, illness course, work history, social history, previous treatment, quality of remissions, and symptomatology. Several items significantly differentiated patients diagnosed as primary, psychotic, and situational from those not so diagnosed: this supports the validity of these subtype categories. However, the study did not support the validity of the incapacitated, agitated, and retarded subtypes. No conclusions could be drawn regarding the endogenous, simple, or recurrent unipolar depressive subtypes.
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Twenty-four schizophrenic outpatients in remission were compared with 21 medical outpatient controls on tasks designed to evaluate smooth pursuit of different frequency sinusoidal targets, saccadic eye tracking, and performance on psychomotor analogues of these tasks that require eye-hand coordination. The schizophrenics demonstrated impaired performance on all the smooth-pursuit and psychomotor tracking tasks. However, the oculomotor reaction times of schizophrenics during the saccadic eye-tracking tasks were equal to those of controls. This dissociation of smooth-pursuit and saccadic performance indicates that smooth-pursuit dysfunction cannot be attributed to a lack of motivation, simple inattention, or oculomotor control mechanisms for which the pursuit and saccadic systems share a common anatomy. The saccadic eye-tracking task is quite similar to a variable-foreperiod simple reaction-time task. That schizophrenics produce normal response latencies on this task raises important questions about the nature of the reaction-time deficit in schizophrenia.
The pharmacokinetics of furosemide in normal man reported from a number of investigators show great discrepancies. We have evaluated the effect on derived pharmacokinetic parameters of furosemide of using different weighting factors or fewer data points to fit the same set of data to an exponential equation, or using noncompartmental analysis. Terminal half-lives of furosemide differed vastly, as did the volume of distribution, but to a lesser extent. The plasma clearance was rather consistent with the different methods used. Thus the discrepancies of the pharmacokinetics of furosemide may, in large part, be due to different methods of analysis of the data. The terminal half-life was most subject to errors of method and the plasma clearance the least.
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Treatment of striatal washed particles with phospholipase A(2) or C abolished the activation of adenylate cyclase by dopamine but not by N(16)-phenylisopropyl adenosine (PIA). The inhibition of dopamine-sensitive cyclase was dependent on Ca2+ and increased with time and phospholipase concentration. F(-)-sensitive cyclase was not affected by phospholipase A(2) treatment, but was enhanced by phospholipase C treatment. Phospholipase D did not affect basal, PIA, dopamine, or F(-)-sensitive cyclase activities. The observed effects of phospholipase A(2) were not due to either the detergent effect of lysophospholipids or to contaminating proteases. Dopamine-sensitive cyclase, inactivated by pretreatment with phospholipase A(2), was restored by asolectin (a soybean mixed phospholipid), phosphatidylcholine, phosphatidylethanolamine, or phosphatidylserine, but not by phosphatidylinositol. Phosphatidylserine and phosphatidylcholine were equipotent in restoring dopamine-sensitive activity. Lubrol-PX, a nonionic detergent, abolished completely the dopamine-sensitive cyclase activity, whereas PIA-sensitive activity was slightly inhibited. In contrast, digitonin inhibited dopamine- and PIA-sensitive cyclase activity in a parallel fashion. Lubrol-PX released some adenylate cyclase into a 16,000 x g supernatant fraction that was stimulated by PIA but not by dopamine. Removal of most of the free detergent by Bio-bead SM 2 enhanced stimulation by PIA but did not restore sensitive cyclase. The data suggest that the requirement for phospholipids for the coupling of dopamine and adenosine receptors to the striatal adenylate cyclase may be different and that the adenosine receptors may be more tightly coupled to the enzyme than are dopamine receptors.
Three-hundred and thirty-five patients without left main stenosis or recent acute myocardial infarction underwent isolated aortocoronary bypass grafting during 1974 and 1975. The hospital mortality was 2 per cent for the four-year predicted survival is 94 per cent. Neither the preoperative presence or absence of a progressive or unstable angina pattern, the extent of coronary artery disease, nor the left ventricular ejection fraction predicted postoperative survival. None of the 25 patients whose ejection fraction was 0.30 or less died in the perioperative period, and no late deaths occurred in this subgroup until after 36 months of follow-up, giving a predicted four-year survival rate of 82 per cent. With only one exception, patients in this subgroup were operated on because of angina, which was unstable in three-quarters of them. We believe that this study shows that patients with a severely reduced ejection fraction should not be refused aortocoronary bypass grafting if symptoms of angina are severe and predominate over symptoms of heart failure.
Forty-one patients with postinfarction ventricular septal rupture were cared for in our hospital during 1971-1975. Cardiogenic shock developed after septal rupture in 55% of these patients. Shock was unrelated to site of infarction, extent of coronary artery disease, left ventricular ejection fraction, or pulmonary-to-systemic flow ratio, but mean pulmonary artery pressure was lower in shock than in nonshock patients. These observations suggest that shock was produced mainly by right ventricular impairment. Perioperative survival was much higher in patients who did not have shock preoperatively (14 of 17 [82+]) than in those who did (three of 11 [27%]). Magnitude of shunt, left ventricular ejection fraction, extent of coronary artery disease, and performance of aortocoronary bypass grafting were not distinctly correlated with perioperative survival. After a minimum 4-year follow-up, 76% of the perioperative survivors are alive, and none suffer more than New York Heart Association functional class II disability. All 13 unoperated patients (11 in shock) died within 3 months.
Decision-analytic techniques were used to evaluate the choice between an aortocoronary bypass operation and medical management in a set of hypothetical patients with coronary artery disease. The decision framework incorporates variables believed to have an important bearing on the choice of treatment. Probability estimates were obtained from two cardiologists and one cardiac surgeon. Patient preferences for the trade-off between years of survival and the quality of life as reflected by the severity of angina pectoris were made explicit by assigning utility values to alternative health outcomes. The results are expressed in terms of quality-adjusted years of life expectancy. Decision analysis favored operation for 13 of the 14 hypothetical patients, including patients with one- and two-vessel disease. The one patient for whom medical treatment was preferred had mild angina pectoris, severe left ventricular dysfunction, and a poor prognosis regardless of therapeutic modality. The results are sensitive to changes in the probability of long-term survival, but not to changes in operative mortality rates. In five patients, the physicians' clinical judgments favored medical treatment, whereas their decision-analysis-derived estimates of survival favored operation. Possible explanations for these discrepancies are discussed. A simplified cost-effectiveness analysis for patients in whom surgery was the optimal treatment indicated costs ranging from $1,500 to $250,000 per year of life gained and from $1,500 to $32,000 per quality-adjusted year of life gained.
Heart failure is frequently a result of impaired systolic ventricular performance. We describe a patient with heart failure and a systemic arteriovenous fistula who had left ventricular enlargement and a normal left ventricular ejection fraction, demonstrated by gated cardiac blood pool scanning. The heart failure was relieved by surgical repair of the fistula, but the left ventricular ejection fraction did not change. These observations show that volume overload rather than impaired systolic function was the mechanism by which heart failure occurred in this patient with a systemic high output state and illustrate the value of gated cardiac blood scanning in noninvasively elucidating the mechanism of heart failure.
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Pretreatment of isolated rat liver plasma membranes by washing with NaHCO3 buffer or by exposure to the chelator ethyleneglycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) with or without the ionophore A23187, produced a decrease in the sensitivity of adenylate cyclase (ATP pyrophosphate-lyase (cyclizing) EC 4.6.1.1) to subsequent stimulation by NaF or guanosine 5'-(beta-gamma-imino)triphosphate (GPP(NH)P). Sensitivity to activation by the nucleotide could be restored by addition of the lyophilized and ashed wash or by addition of Ca2+, Mg2+ or Mn2+. The factor extracted from the membranes by these various treatments which was responsible for loss of stimulation was identified as Ca2+. Determination of the metal ion content of isolated membranes by atomic absorption spectrometry indicated that Ca2+ was the only divalent cation present in sufficient concentration to support persistent activation by either NaF or GPP(NH)P. Pretreatment of liver plasma membranes with trifluoperazine, which inhibits the action of Ca2+-dependent regulator protein in other enzyme systems, reduced GPP(NH)P activation of adenylate cyclase and caused marked depletion of membrane Ca2+. The effects of low concentrations (less than 100 microM) of the phenothiazine could be reversed totally by Ca2+ and partly by regulator protein. At higher concentrations of trifluoperazine, slight restoration of enzyme activation was seen with either agent. The hypothesis is presented that Ca2+ interacts with the nucleotide (GTP or GDP) regulatory site(s) of the adenylate cyclase. This interaction may be regulator-protein-dependent and may be important in determining the sensitivity of the enzyme to nucleotide activation in vivo.