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Biomedical subjects

R Horton

Publications and source records attributed to R Horton.

At least 109 records · Page 6Linked to original sources
PubMed1998

Low dihydrotestosterone and weight loss in the AIDS wasting syndrome.

24 consecutive AIDS patients with wasting, and who had never received anabolic therapies, were evaluated to determine their profile of sex hormones and whether transformation of testosterone (T) to the nuclear androgen, dihydrotestosterone (DHT), was impaired. Eleven (46%) patients had normal testosterone and DHT (group I), 10 (42%) had normal testosterone but low DHT (group II), and 3 (12%) had low testosterone and low DHT (group III). Age, prior opportunistic complications, symptoms, serum albumin, hemoglobin levels, and CD4 lymphocyte counts were similar in the groups. DHT was significantly lower (22.2 +/- 6.8 microg/dl) in group II compared with group I (50.8 +/- 15.3 microg/dl). The ratio of T/DHT, a measure of the conversion of testosterone to DHT, in group I was 15.1 +/- 3.5, which was within the range for eugonadal young men. In group II, the ratio was 22.3 +/- 1.5, indicating a defect in generation of DHT. Patients in group II had lost 9.2 +/- 3.5 kg compared with 5.6 +/- 2.6 kg in group I (p = .015). Thus, a syndrome of low DHT with normal testosterone was associated with significantly greater weight loss than in patients with normal testosterone and DHT. Further studies are needed to clarify whether low DHT is a result of AIDS wasting or is causally related to weight loss and whether androgen therapy in the form of DHT could reverse some of the metabolic changes associated with AIDS wasting.

Adult↗
PubMed1998

Coronary artery bypass surgery as treatment for ischemic heart failure: the predictive value of viability assessment with quantitative positron emission tomography for symptomatic and functional outcome.

OBJECTIVES: To determine the predictive value of quantitative evaluation of myocardial viability on changes in left ventricular function, exercise capacity, and quality of life after coronary artery bypass grafting in patients with ischemic heart failure (congestive heart failure, New York Heart Association class > or = III) with and without angina. METHODS: Thirty-five patients, 14 with congestive heart failure and angina (CHF-angina) and 21 with congestive heart failure without angina (CHF-no angina) were studied at baseline and 6 months after coronary bypass grafting. Left ventricular function was evaluated with transthoracic echocardiography and radionuclide ventriculography. Myocardial viability was assessed with [18F]-2-fluoro-2-deoxy-D-glucose using positron emission tomography. Peak aerobic capacity (peak oxygen consumption) and anaerobic threshold were assessed with treadmill exercise test and quality of life with a questionnaire. RESULTS: A total of 286 of 336 dysfunctional left ventricular segments were viable. There were two perioperative deaths (5.7%) and three late deaths. Left ventricular ejection fraction increased from 23% +/- 7% to 32% +/- 9% (p < 0.0001), and a linear correlation was found between the number of viable segments and the changes in ejection fraction (r = 0.65; p = 0.0001). Receiver operating characteristics curve identified eight viable segments as the best predictor for increase of ejection fraction more than 5 percentage points. Peak oxygen consumption increased from 15 +/- 4 to 22 +/- 5 ml/kg per minute (p < 0.0001). Preoperatively, anaerobic threshold was identified in one patient from the CHF-angina group and in all from the CHF-no angina group and increased from 13 +/- 4 to 19 +/- 4 ml/kg per minute (p < 0.0001). Quality of life scores improved significantly in both groups. No correlation was found between the amount of viable dysfunctional myocardium and changes in exercise capacity or quality of life. CONCLUSIONS: In patients with postischemic congestive heart failure the amount of viable myocardium dictates the degree of improvement in left ventricular function after revascularization.

Angina Pectoris↗
PubMed1998

Effect of projective aspects variations on estimates of changes in bone mass using digital subtraction radiography.

This study tests the hypothesis that estimates of changes in bone mass derived from subtraction data obtained in accord with published methods are independent of the spatial aspect of the lesion being evaluated when calibrations are performed independently. Nineteen sliver-shaped bone chips ranging in mass from approximately 1 to 35 mg were orientated with broad side parallel to the facial surface of a hemisectioned dry human mandible and radiographed using conventional exposure parameters on conventional E-speed dental X-ray film. Also attached to the film was a standardized aluminium calibration wedge that facilitated quantitative analysis of resulting subtraction data using established methodology. The effects of scatter were simulated by the addition of a 1-cm-thick slab of tissue-equivalent plastic. A second series of exposures then was produced using the same respective spatial chip locations and projection geometries but each chip was reorientated such that its broad side was now positioned perpendicular to the mandibular facial surface. Finally, a comparable series of control exposures was produced without any chips or calibration wedge to facilitate subtraction. When paired bone estimates derived from the two chip orientations were compared (paired comparisons) using Student's t-test, a statistically significant difference (p < 0.05) was observed. These results also were tested for statistical significance using the non-parametric Wilcoxon test. As with the parametric analysis, the discrepancy between the parallel and perpendicular mass estimates was found to statistically significant (p < 0.05). The methods employed in this investigation thus resulted in bone mass estimates that varied significantly depending upon lesion orientation.

Absorptiometry, Photon↗
PubMed1998

Stroke: therapeutic approaches.

Speakers at the Society for Medicines Research Symposium on Stroke, held July 9, 1998, in Windlesham, U.K., covered topics ranging from reasons for failure of drugs in late-stage clinical trials to in vitro and in vivo models of ischemia to therapeutic approaches to this disorder. The take-home message was that the side effect profile in humans needs to be closely examined, with emphasis on the pharmacokinetics and distribution to minimize the cardiovascular effects.

Journal Article↗
PubMed1998

Lysosomal lipid accumulation from oxidized low density lipoprotein is correlated with hypertrophy of the Golgi apparatus and trans-Golgi network.

Lipid accumulation within macrophages is a major sequelae of atherosclerosis. Much of this lipid accumulation occurs within large, swollen lysosomes. We analyzed lipid accumulation in cultured macrophages using oxidized or acetylated low density lipoprotein (LDL) as the loading agent. Pigeon macrophages incubated for 48 h with mildly oxidized pigeon LDL (TBARS = 5-10 nmol/mg protein) showed significant increases in cellular cholesterol compared with untreated controls. Forty-eight percent of the increased cholesterol occurred as unesterified cholesterol. Treated cells had lipid-swollen lysosomes similar to those of atherosclerotic foam cells. The increase in lysosomal lipid was accompanied (correlation coefficient of 0.96) by increases in acid phosphatase staining cisternae of the Golgi and trans-Golgi network (TGN). THP-1 macrophages incubated with oxidized LDL showed similar lysosomal loading and Golgi/TGN hypertrophy. In contrast, macrophages incubated with acetylated LDL accumulated significant amounts of cholesterol but the increase occurred as cholesteryl ester (81% in pigeons) within cytoplasmic droplets and there was no associated increase in acid phosphatase-containing cisternae of Golgi or TGN. The correlation in both pigeon and THP-1 macrophages of oxidized LDL-induced lysosomal lipid accumulation and Golgi hypertrophy suggests a linkage of these two phenomena. This implicates intracellular membrane trafficking as a possible defect in foam cells of the atherosclerotic lesion.

Acid Phosphatase↗
PubMed1997

Vaccines 1997.

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Humans↗