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Biomedical subjects

E E Gordon

Publications and source records attributed to E E Gordon.

At least 19 recordsLinked to original sources
PubMed1998

Gender disparities in the attribution of cardiac-related symptoms: contribution of common sense models of illness.

The role of common sense models of heart disease in the attribution of cardiac-related symptoms was examined in a sample of healthy young adults (N = 224). Participants were less likely to attribute symptoms to possible cardiac causes for female victims reporting stressful life events (M = 5.14) than for female victims without such stressors (M = 6.82) or for male victims with (M = 6.23) or without (M = 6.48) concurrent stressors. Cardiac attributions remained lowest for female/high-stress victims in additional samples of undergraduates (N = 194), community-residing adults (N = 48), and physicians (N = 45), although this outcome sometimes appeared to reflect additive, rather than interactive, effects. Two final experiments with undergraduate samples (Ns = 48 and 60, respectively) indicated that stereotypes associating heart disease with male gender may account for gender disparities in the attribution of cardiac-related symptoms.

Adolescent↗
PubMed1997

Predictors of survival and the role of gender in postoperative myocardial infarction.

PURPOSE: To identify risk factors for mortality after postoperative myocardial infarction. METHOD: Retrospective study of 266 patients. RESULTS: The crude in-hospital mortality rate was 25%. This was more than twice as high as the mortality rate in patients admitted from home with an acute myocardial infarction. Women with postoperative infarction were the same age as men, but had a lower Acute Physiology and Chronic Health Evaluation (APACHE) II score prior to infarction (P = 0.03) and a higher crude mortality rate. Multivariate analysis showed that female gender (relative risk 2.2, 95% confidence limits 1.2 to 4.2), current cigarette smoking (relative risk 2.3 [1.2 to 4.7]), a history of congestive heart failure (relative risk 2.1 [1.04 to 4.1], resuscitation status (relative risk 8.1 [2.0 to 32.9]), and high preoperative APACHE II score were significant independent predictors of in-hospital mortality. CONCLUSION: Postoperative myocardial infarction is one of the most serious events a patient can experience. Women and current smokers are at especially high risk for mortality after postoperative myocardial infarction.

APACHE↗
PubMed1993

Coronary artery disease in women: the role of diagnostic imaging.

In the United States, coronary artery disease (CAD) kills equal numbers of men and women, and is the leading cause of death in women. Except at the oldest ages, the prevalence of disease is lower in women than in men. This low prevalence decreases the accuracy of all noninvasive testing methods, making the noninvasive diagnosis of CAD in women more difficult. Perhaps because of this increased difficulty in diagnosis and the prognosis of women with angina has been perceived to be "benign," invasive testing has been used less often in women. Since the morbidity and mortality are greater in women compared with men with manifest CAD (i.e., myocardial infarction and coronary artery bypass grafting), an understanding of the strengths and limitations of noninvasive testing in women is critical. Due to the lower prevalence of CAD in women, symptoms of CAD (i.e., chest pain) and noninvasive tests (graded exercise treadmill) are less reliable with lower positive predictive values. Recent studies suggest using imaging techniques to improve the diagnostic sensitivity and specificity of noninvasive testing. This article will review the current literature regarding noninvasive diagnosis of CAD in women, including the use of stress echocardiography and thallium imaging in women. Detailed statistical descriptions of study populations are necessary so that study results can be accurately applied and interpreted in the general population.

Coronary Disease↗
PubMed1993

Samarium-153-EDTMP in bone metastases of hormone refractory prostate carcinoma: a phase I/II trial.

Samarium-153-ethylenediaminetetramethylene phosphoric acid (EDTMP), a bone-seeking radiopharmaceutical, was given to prostate cancer patients in a dose escalation protocol for pain palliation to determine the maximally tolerated dose. Fifty-two patients with hormone refractory prostate cancer with bony metastases were treated with doses beginning at 0.5 mCi/kg (18.5 MBq/kg), escalating in 0.5-mCi (18.5 MBq) increments to 3.0 mCi/kg (111 MBq/kg). Pain response after treatment was assessed as well as hematologic and serum chemistry parameters. Pain palliation with a mean duration of 2.6 mo was present in 74% of the patients. Toxicity was exclusively hematologic at the highest dose levels. No infectious or bleeding complications occurred, with 45 of the 52 (86%) patients demonstrating complete hematologic recovery. Patients receiving higher doses had significantly greater reductions in serum prostate specific antigen and serum prostatic acid phosphatase levels. The patients receiving greater doses also showed a trend toward improved survival.

Aged↗
PubMed1991

HETEs and coronary artery endothelial cells: metabolic and functional interactions.

Porcine coronary artery endothelial cells have been established in culture. These cells produce prostaglandin (PG) I2, PGF2 alpha, and PGE2 when exposed to either arachidonic acid or ionophore A23187. PG formation was reduced when the cells were exposed to monohydroxy and dihydroxy unsaturated fatty acids. Although all of the hydroxyeicosatetraenoic acids (HETEs) produced reductions, 5-HETE caused the largest decrease in PGI2 formation. Therefore, these lipoxygenase products, especially 5-HETE, may impair the nonthrombogenic surface and some vasodilator responses of coronary endothelium. The cells took up each of the HETEs and incorporated them into phospholipids. Uptake was not affected by equimolar amounts of oleic or linoleic acids; even arachidonic acid reduced 12- and 15-HETE uptake by only 50-60%. Like other cells, the coronary endothelium converted 12- and 15-HETE to polar metabolites. As opposed to other cells, however, these cultures also converted 5-HETE to a more polar metabolite. Thus coronary artery endothelium can take up and metabolize all of the major HETEs, including 5-HETE, and thereby reduce their potentially injurious effects in the coronary circulation.

Animals↗
PubMed1987

DIABEDS: a randomized trial of the effects of physician and/or patient education on diabetes patient outcomes.

To examine the effects of intensive patient and/or physician diabetes education on patient health outcomes, a controlled trial was conducted in which internal medicine residents and their 532 diabetic patients were randomly assigned to: routine care; patient education; physician education; or both patient and physician education. Patient outcome data were analyzed either by analysis of covariance on post intervention values (2-hour post-prandial plasma glucose [PPG]; body weight [BW]; blood pressure [BP]; or analysis of variance conducted on change values (fasting plasma glucose [FPG] and glycosylated hemoglobin [A1Hgb]). After patient education, significant improvements were observed in FPG, A1Hgb, BW, and systolic and diastolic BP. Physician education resulted in significant decreases in FPG, A1Hgb and BW. The combination of patient plus physician education resulted in the greatest improvements in patients' health outcomes including FPG, A1Hgb, PPG, BW and diastolic BP. Adjusted systolic BPs were not significantly different in the two groups. While these physiologic improvements were statistically and probably clinically significant, hyperglycemia and obesity still persisted. Thus, achieving optimal patient outcomes for a chronic disease like diabetes mellitus may require a greater or more effective use of resources than currently estimated.

Clinical Trials as Topic↗
PubMed1987

Biochemical mechanisms of cardiac hypertrophy.

Rapid cardiac growth in adult rats and neonatal pigs involves more efficient use of existing components of the protein synthesis pathway and synthesis of new ribosomes and mRNA to increase the capacity for protein synthesis. Greater efficiency of synthesis can be induced by mechanical perturbations that stretch the ventricular wall, including increased cardiac work and increased ventricular pressure development in beating hearts, and increased aortic and intraventricular pressure in arrested-drained hearts. The biochemical signal linking stretch to more efficient protein synthesis has not been identified. Preferential synthesis of new ribosomes occurs in the first two hours of exposure of Langendorff preparations to high aortic pressure or within four hours after injection of thyroid hormone into normal rats. The rate of protein degradation is either accelerated or unchanged in hypertrophing hearts but is inhibited by induction of cardiac work or high aortic pressure in Langendorff preparations. Overall, increased capacity for, and efficiency of, protein synthesis are the major factors accounting for cardiac growth.

Aging↗
PubMed1987

Faster ribosome synthesis induced by elevated aortic pressure in rat heart.

An increase in aortic pressure from 60 to 120 mmHg accelerated ribosomal protein synthesis in rat hearts during 1 or 2 h of labeling with 0.4 mM [3H]phenylalanine. When hearts were perfused with buffer that contained 20 mM glucose and normal plasma concentrations of 19 other amino acids without added insulin, ribosomal protein synthesis relative to the rate of total protein synthesis increased from approximately 0.22 to 0.36 and 0.30 as aortic pressure was raised from 60 to 120 mmHg during 1 or 2 h of labeling, respectively. With the addition of insulin, the relative rate of ribosomal protein synthesis averaged 0.33 at an aortic pressure of 60 mmHg and increased to 0.42 when aortic pressure was raised to 120 mmHg. These results indicate that elevation of aortic pressure has a preferential effect on synthesis of new ribosomes. This response appears to be an early and physiologically significant event in cardiac hypertrophy.

Animals↗
PubMed1987

The effect of oral zindotrine (MDL-257), a bronchial smooth muscle relaxant, on histamine airways responsiveness in asymptomatic asthmatics.

We evaluated the efficacy of an oral dosage form of the investigational smooth muscle relaxant, zindotrine, a novel pyridazine derivative, in counteracting histamine-induced bronchospasm in a group of 12 non-medicated asymptomatic asthmatics. Histamine inhalation challenges were performed before (control) and 45, 150, and 300 minutes after zindotrine (200 and 300 mg), or the corresponding dose of placebo was administered orally in a randomized, double-blind crossover fashion. When compared to the control state, the 300-mg zindotrine dose markedly lowered histamine airway responsiveness as indicated by a significant (P less than .01) increase in the inhaled histamine dose necessary to provoke a 20% decrease in the forced expired volume in one second (PD20FEV1) 45 minutes after drug administration. The PD20FEV1 then decreased linearly over time but remained higher than the control PD20FEV1 value (P less than .05) during the entire observation period. The 200-mg zindotrine dose failed to affect the PD20FEV1. Our data indicate that orally administered zindotrine lowers airways responsiveness to inhaled histamine in asymptomatic asthmatics in a dose-dependent and time-dependent fashion.

Administration, Oral↗
PubMed1987

Aortic perfusion pressure, protein synthesis, and protein degradation.

An increase in aortic pressure from 60 to 120 mm Hg accelerated protein synthesis and inhibited protein degradation in isolated rat hearts perfused as Langendorff preparations. This elevation of aortic pressure raised intraventricular pressure development, coronary flow, and oxygen consumption. The effect of aortic pressure on protein turnover was dissociated from intraventricular pressure development, contractile activity, and oxygen consumption by use of beating-drained and arrested-drained preparations. Results of other experiments argued against coronary flow as a determinant of rates of protein synthesis and degradation. These results indicated that effects of elevated aortic pressure on protein turnover were caused by stretch of the ventricular wall via its engorgement with blood, the so-called erectile properties of the heart or "garden-hose effect." These effects on protein turnover may be of importance in initiating hypertrophy of the heart secondary to pressure or volume overload.

Animals↗
PubMed1986

Aortic pressure as a determinant of cardiac protein degradation.

Mechanical parameters and intracellular mediators that may control protein degradation were studied in isolated rat hearts subjected to increased aortic pressure. Elevation of aortic pressure from 60 to 120 mmHg in Langendorff preparations provided glucose or pyruvate as substrate decreased the rate of protein degradation during the second hour of perfusion. Intracellular contents of ATP or creatine phosphate or the creatine phosphate/creatine ratio did not indicate that energy depletion accounted for these effects. When ventricular pressure development was prevented by ventricular draining, and hearts were arrested with tetrodotoxin, protein degradation still decreased as aortic pressure was raised. The effect of elevated aortic pressure on proteolysis was unchanged when perfusate calcium concentrations were 0.6, 3.0, or 5.1 mM, or when indomethacin or meclofenamate was added to the perfusion buffer. These results provided no evidence to indicate that intraventricular pressure development or cardiac contraction was responsible for the inhibitory effect of increased aortic pressure on protein degradation. Instead, they suggested that stretch of the ventricular wall, as a consequence of increased aortic pressure, could be the mechanical parameter most closely related to the restraint on proteolysis. No evidence was obtained that the lower rate of degradation depended on energy or calcium availability or prostaglandin synthesis.

Adenosine Triphosphate↗
PubMed1986

Effect of intraventricular pressure on protein synthesis in arrested rat hearts.

A modification of the Langendorff technique for perfusion of rat hearts was developed to allow a constant intraventricular pressure to be imposed on the left ventricle of arrested-catheterized hearts. This model was used to assess effects of increased aortic (60 and 120 mmHg) and intraventricular (0 and 25 mmHg) pressures on the rate of protein synthesis between 70 and 130 min of perfusion and on contents of ATP and creatine phosphate (creatine-P) in ventricles. Rates of protein synthesis in atria also were measured. Increased intraventricular or aortic pressure elevated the rate of protein synthesis (41%) compared with hearts supplied an aortic pressure of 60 mmHg and an intraventricular pressure of 0 mmHg. Higher intraventricular pressure also decreased the ribosomal subunit content. No change in the rate of protein synthesis was observed when intraventricular pressure was raised in hearts supplied an aortic pressure of 120 mmHg. Rates of atrial protein synthesis and contents of ATP and creatine-P were unchanged by elevations of either intraventricular or aortic pressure. These experiments indicate that stretch of the ventricular wall due to higher intraventricular or aortic pressure accelerated protein synthesis by maintaining the in vivo balance between rates of peptide chain initiation and elongation.

Adenosine Triphosphate↗
PubMed1986

Mechanical factors affecting protein turnover in isolated rat hearts.

Induction of cardiac work increased protein synthesis in hearts supplied glucose or a mixture simulating normal plasma levels of glucose, insulin, glucagon, lactate, and beta-hydroxybutyrate. During 2 h of perfusion, cardiac work did not accelerate protein synthesis in hearts supplied a mixture of glucose, lactate, and higher concentrations of insulin. Protein degradation was decreased by work in hearts supplied glucose. Nitrogen balance was negative in Langendorff-perfused hearts provided glucose, but was less so in working preparations. Nitrogen balance was zero or positive in working hearts provided the mixture simulating plasma or the mixture of glucose, lactate, and insulin. In Langendorff preparations, increased aortic pressure accelerated protein synthesis during the second hour of perfusion in hearts supplied glucose, glucose plus insulin, or pyruvate. When ventricular pressure development was prevented by ventricular draining or when drained hearts were arrested with tetrodotoxin, protein synthesis still increased as perfusion pressure was raised from 60 to 120 mm Hg. Oxygen consumption increased as aortic pressure was increased in drained, beating hearts, but was unaffected in arrested, drained hearts. These studies indicated that increased aortic pressure and its attendant stretch of the ventricular wall were the mechanical parameter most closely associated with faster rates of protein synthesis.

Animals↗
PubMed1985

Dependence of protein synthesis on aortic pressure and calcium availability.

Increased aortic pressure accelerated protein synthesis in control-beating and arrested-drained hearts supplied with either glucose or pyruvate. Elevation of perfusion pressure from 60 to 120 mm Hg increased oxygen consumption in control-beating but not in arrested-drained preparations. Energy availability, as assessed by adenylate energy charge or creatine phosphate/creatine ratio, or both, was increased in arrested-drained hearts supplied with glucose and perfused at 60 and 120 mm Hg aortic pressure. In control-beating or arrested-drained hearts supplied with pyruvate, energy availability was not improved by elevation of aortic pressure from 60 to 120 mm Hg. An increase of perfusate calcium concentration from 0.5 to 5.0 mM in control-beating Langendorff preparations supplied with glucose and perfused at an aortic pressure of 90 mm Hg doubled oxygen consumption and decreased energy availability, but had no effect on the rate of protein synthesis. In arrested-drained hearts supplied with either glucose or pyruvate and calcium concentrations ranging from 0.5 to 5.0 mM, the rates at 120 mm Hg aortic pressure were 11-25% higher than at 60 mm Hg. These findings provide no evidence to implicate increased oxidative metabolism, energy availability, or extracellular calcium concentration as important factors in the mechanism that accounts for the effects of increased aortic pressure on protein synthesis.

Animals↗