Rapidity and charge correlations of centrally produced charged particles in events with a high-momentum pi 0 near 11 degrees.
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Biomedical subjects
Publications and source records attributed to M Sullivan.
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Using a kinetic turbidimetric assay based on the binding of serum glycoprotein to concanavalin A the acute phase reaction has been detected in dogs. Raised levels of glycoprotein were found in dogs which had undergone surgery, had been treated with bacterial endotoxin and had various inflammatory conditions.
Out of 156 patients with stable coronary heart disease randomized to either an exercise intervention group or a control group, 41 had complete gas analysis data. Continuous gas exchange data, including the ventilatory threshold, and selected heart rates were determined initially and at 1 year. The mean attendance for the exercise group was 2.2 +/- 0.7 days a week at an intensity of 60 +/- 9% of estimated peak oxygen uptake for 1 year of the study. Statistically significant differences (p less than 0.05) were observed between the exercise group (n = 19) and the control group (n = 22) for peak oxygen uptake (L/min), total treadmill time, and supine rest and submaximal heart rates after 1 year. The most remarkable change was a 16% increase in treadmill time. There was no difference between groups for the ventilatory threshold expressed either as an absolute oxygen uptake or as a percentage of peak oxygen uptake at 1 year. However, there was a significant correlation (r = 0.45; p less than 0.05) between the absolute change in peak oxygen uptake and the absolute change in the ventilatory threshold. These results indicate that a moderate exercise program is inadequate to alter the ventilatory threshold in patients with coronary heart disease and that changes in ventilatory threshold do not explain the increase in treadmill time that usually occurs.
IgM rheumatoid factor (RF) elaboration by rheumatoid arthritis (RA) synovial, bone marrow, and blood mononuclear cells (MNC) is reported. IgM RF was prepared from RF-positive sera by sequential euglobulin precipitation, Sephacryl S300 gel filtration, and IgG-Sepharose affinity chromatography. Purified material, which contained no detectable IgG or IgA, was used in an enzyme-linked immunosorbent assay (ELISA) to quantitate cellular elaboration of IgM RF. Excellent standard curves (r2 = 0.98) were obtained without nonspecific binding of samples or antisera to IgG-coated microtiter plates and without cross-reactivity of standards with antisera other than anti-IgM. We found RA blood MNC (11 patients) spontaneously averaged 15 ng/ml IgM RF (6% of total IgM produced), but elaborated 254 ng/ml IgM RF following pokeweed mitogen (PWM) stimulation (22 patients), exceeding that of 13 normal controls. Bone marrow MNC spontaneously (4 patients) produced 71 ng/ml IgM RF and secreted 78 ng/ml IgM RF with PWM stimulation (9 patients). In contrast synovial fluid MNC (5 patients) spontaneously elaborated 6652 ng/ml IgM RF, significantly (P less than 0.05) more than blood or bone marrow MNC; PWM-stimulated synovial fluid MNC (5 patients) produced 5472 ng/ml IgM RF. These observations confirm selective localization of activated, IgM RF-producing cells to the rheumatoid synovial space.
Sixteen patients with stable angina pectoris were studied in a double blind crossover manner utilizing treadmill exercise testing with the direct measurement of total body oxygen uptake, 1 and 24 hours after application of a 20 cm2 transdermal nitroglycerin system and identical placebo. Testing was performed after a 3 day lead-in period of treatment with either an active patch or placebo. Points of analysis were peak angina and the submaximal work load occurring at 4 minutes of exercise. No statistically significant differences were observed between nitroglycerin and placebo treatment in any of the rest hemodynamic or peak angina variables at 1 or 24 hours. A significant increase in the rate-pressure product at the submaximal work load was observed 1 hour after transdermal nitroglycerin relative to placebo application. However, no significant differences were observed in any of the other measured variables at the submaximal work load, 1 or 24 hours after nitroglycerin application. The once daily application of a 20 cm2 transdermal nitroglycerin system was ineffective in altering the exercise capacity of patients with angina pectoris. The lack of efficacy at 1 hour appears to be due to inadequate nitroglycerin blood levels; at 24 hours it may be due to tolerance.
Thirty patients who exhibited increased and 65 patients decreased spatial R wave amplitude during exercise testing were compared for left ventricular function and ischemic variables. Spatial R wave amplitude was derived from the three-dimensional Frank X, Y, Z leads using computerized methods. All patients had stable coronary artery disease and they were classified into two groups: one that attained a higher (n = 48) and one a lower (n = 47) median value of maximal heart rate during exercise (161 beats/min). Within these two groups, patients with increasing or decreasing spatial R wave amplitude during exercise were analyzed for differences in oxygen consumption, exercise-induced changes in spatial R wave amplitude, ST segment depression laterally (ST60, lead X), ST displacement spatially, left ventricular ejection fraction at rest, change in left ventricular ejection fraction with exercise and thallium-201 ischemia during exercise. Significant differences were demonstrated only in exercise-induced spatial R wave amplitude changes (p less than 0.0001). There was no significant correlation between exercise-induced change in heart rate and change in spatial R wave amplitude in either the group with increasing or the group with decreasing spatial R wave amplitude. It is concluded that changes in spatial R wave amplitude during exercise are not related to ischemic electrocardiographic or thallium-201 imaging changes or to left ventricular ejection fraction determined at rest or during exercise.
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Fifty-three male volunteers who had undergone coronary artery bypass surgery were randomized to a medically supervised exercise program (N = 28) or to usual community care (N = 25). They were tested initially and at one year with exercise tests for thallium scintigraphy, maximal oxygen uptake, and electrocardiography. Approximately one third of the patients had signs and/or symptoms of ischemia consistent with incomplete or unsuccessful revascularization. Over the year there were five dropouts, but no major complications occurred. The exercisers attended an average of 82% of the sessions (three times a week) and trained at 80% of their maximal heart rate. Both the exercisers with and those without angina had significant increases in estimated and measured oxygen uptake and significant declines in submaximal and resting heart rate. There was a trend toward improved thallium scans in the exercised patients with angina.
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To study the emergence of attention deficits in early childhood, the diagnostic team of an early education program documented the occurrence of poor concentration, distractibility, behavioral disorganization, poor self-monitoring, and overactivity in a group of 174 children followed prospectively from birth to school entry. Persistent attentional problems were identified in 5% of the children; 8% had problems which abated before kindergarten. Over the period from birth to kindergarten, 40% of the preschool youngsters were found to have some attentional indicator, but many of the findings were minor or transient. This study points to (1) the clustering of persistent attentional concerns with other developmental and environmental concerns, (2) the substantial long-term consequences of early attentional problems and (3) the feasibility of early detection of some children with attentional disorders.
In order to determine whether or not regular exercise could alter myocardial perfusion or function, we randomized 146 male volunteers with stable coronary heart disease to either a supervised exercise program (n = 72) or to a usual care program (n = 74). Subjects underwent exercise tests initially and one year later. Significant differences between the two groups included improved aerobic capacity, thallium ischemia scores, and ventricular function in the exercise intervention group. It was not possible to classify the conditions of patients as to the likelihood of improvement or deterioration. This study demonstrated changes in myocardial perfusion and function in a select group of middle-aged men with coronary heart disease who underwent a medically appropriate exercise program lasting one year, but these changes were relatively modest.
Primary sequence differences have been found between two different ribosomal DNA (rDNA) units of the rodent malaria parasite, Plasmodium berghei, within the coding areas of both the small and large ribosomal RNAs (rRNA). The coding regions of rDNA unit A are protected from nuclease S1 digestion by rRNA isolated from asexual blood stage parasites. Under the same conditions of analysis, the comparable coding regions from unit C are cut into small pieces by nuclease S1, the largest being 1.1 kb. Analysis of heteroduplexes of the respective DNA clones from units A and C by electron microscopy reveals that the two units differ in the 5' flanking and internal transcribed sequences and that there are extensive sequence differences in the DNA coding for the mature large rRNA. No introns were detected in either rDNA unit. The data shows that unit A is transcribed in blood stage parasites and that unit C is not.
A cDNA library constructed from total chick embryo RNA was screened with an enriched fraction of type II collagen mRNA. Two overlapping cDNA clones were characterized and shown to encode the COOH propeptide of type II collagen. In addition, a type II collagen clone was isolated from a Charon 4A library of chick genomic fragments. Definitive identification of the clones was based on DNA sequence analysis. The 3' end of the type II collagen gene appears to be similar to that of other interstitial collagen genes. Northern hybridization data indicates that there is a marked decrease in type II collagen mRNA levels in chondrocytes treated with the dedifferentiating agent 5-bromodeoxyuridine. The major type II collagen mRNA species is 5300 bases long, similar to that of other interstitial collagen RNAs.
A nine-and-a-half-year-old three quarters thoroughbred gelding was presented with unilateral epistaxis. The cause was a destructive, progressive haematoma in the left maxillary sinus. In all previous reports of progressive haematomata in the equine nasal cavity, the site of origin has been the ethmoidal labyrinth. Surgical removal of the progressive haematoma resulted in an apparent cure.
Clinically, the modified Bruce protocol is widely used to predict functional capacity in postmyocardial infarction (post-MI) patients. However, it has been suggested that post-MI patients have lower oxygen uptakes for standard workloads. In order to study this, we measured oxygen uptake (VO2) and venous blood lactic acid concentration in 12 post-MI patients and 12 normal male subjects during a modified Bruce treadmill protocol. During the first four stages of the protocol, mean oxygen uptake was significantly lower (1.0 to 6.2 cc X kg-1 X min-1; p less than 0.001) for the post-MI patients than for the normal male subjects. Venous blood lactic acid concentrations were different only at stage 4. However, a higher respiratory exchange ratio was observed for post-MI patients (p less than 0.001 at stage 3), suggesting an increased anaerobic metabolism and adequate buffering of lactic acid. The post-MI patient's measured VO2 for three stages of the protocol ranged from 1.8 to 7.3 cc X kg-1 X min-1 lower than the Bruce prediction for cardiac patients. In addition, maximal measured VO2 for the post-MI patients ranged from 3.7 to 11.2 cc X kg-1 X min-1 lower than predicted VO2 derived from the normal subjects. These data suggest myocardial damage may slow oxygen uptake kinetics, thus increasing the oxygen deficit at standard workloads during progressive exercise. An increased respiratory exchange ratio secondary to the buffering of lactic acid suggests that anaerobic metabolism may compensate for this oxygen deficit.
In order to evaluate the clinical practice of estimating oxygen uptake from treadmill time, patients with coronary heart disease and normal subjects had their oxygen uptake measured during treadmill testing. Continuous expired gas analysis was performed in order to see if the gas exchange anaerobic threshold could explain the difference between measured and estimated oxygen uptake. Below the gas exchange anaerobic threshold, normal subjects and patients had similar oxygen uptakes for a given workload. However, at workloads above this threshold, patients had approximately 1 MET lower oxygen uptake than normal subjects. Regression equations relating treadmill time to oxygen uptake are specific to groups of patients or individuals due to differences in anaerobic threshold. In addition, the use of standard workloads to predict aerobic capacity depends on the rate at which oxygen uptake obtains a steady state value. These findings must be considered in clinical practice when attempting to estimate aerobic capacity from treadmill testing.
To investigate the cardiac determinants of treadmill performance in patients able to exercise to volitional fatigue, 88 patients with coronary heart disease free of angina pectoris were tested. The exercise tests included supine bicycle radionuclide ventriculography, thallium scintigraphy and treadmill testing with expired gas analysis. The number of abnormal Q wave locations, ejection fraction, end-diastolic volume, cardiac output, exercise-induced ST segment depression and thallium scar and ischemia scores were the cardiac variables considered. Rest and exercise ejection fractions were highly correlated to thallium scar score (r = -0.72 to -0.75, p less than 0.001), but not to maximal oxygen consumption (r = 0.19 to 0.25, p less than 0.05). Fifty-five percent of the variability in predicting treadmill time or estimated maximal oxygen consumption was explained by treadmill test-induced change in heart rate (39%), thallium ischemia score (12%) and cardiac output at rest (4%). The change in heart rate induced by the treadmill test explained only 27% of the variability in measured maximal oxygen consumption. Myocardial damage predicted ejection fraction at rest and the ability to increase heart rate with treadmill exercise appeared as an essential component of exercise capacity. Exercise capacity was only minimally affected by asymptomatic ischemia and was relatively independent of ventricular function.
As part of a randomized trial of the effects of 1 year of exercise training on patients with stable coronary artery disease, 48 patients who exercised and 59 control patients had computerized exercise electrocardiography performed initially and 1 year later. The patients who had exercise training as an intervention had a 9% increase in measured maximal oxygen consumption and significant decreases in heart rate at rest and during submaximal exercise. ST segment displacement was analyzed 60 ms after the end of the QRS complex in the three-dimensional X, Y and Z leads and utilizing the spatial amplitude derived from them. Statistical analysis by t testing yielded no significant differences between the groups except for less ST segment displacement at a matched work load, but this could be explained by a lowered heart rate. Analysis of variance yielded some minor differences within clinical subgroups, particularly in the spatial analysis. Obvious changes in exercise-induced ST segment depression could not be demonstrated in this heterogeneous group of selected volunteers with coronary artery disease secondary to an exercise program.