Computerization of anesthesia information management: yet another application.
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Biomedical subjects
Publications and source records attributed to J M Feldman.
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From 1970 until 1990, 8,958 cases of primary carcinoma of the lung were diagnosed at the Duke University Medical Center. During the same period, 126 patients (mean age, 53 +/- 13 years) were diagnosed with bronchial carcinoid. The overall survival was 78% for 5 years and 71% for 10 years. Surgical treatment in 106 patients included pneumonectomy (15), lobectomy (63 with 9 bronchoplastic procedures), stapled wedge resection (22), and bronchoscopic laser resection (6). The method of diagnosis was chest roentgenography (121), chest computed tomography (77), mediastinal tomography (31), bronchoscopy (81), bronchoscopic brushing and washing (50), bronchoscopic biopsy (40), transthoracic needle biopsy (27), thoracotomy (100), and autopsy (5). Univariate analysis of the medical history, presenting signs and symptoms, diagnostic test results, and pathologic data predicted improved survival (p less than 0.001) for: female sex (n = 58), asymptomatic presentation (n = 47), normal serum serotonin or urinary hydroxyindoleacetic acid levels (n = 76), peripheral location of the primary tumor (n = 50), pathologic stage I or II (n = 91), negative lymph nodes (n = 80), primary tumor 2 cm or less in diameter (n = 67), and typical histology (n = 80). No significance (p greater than 0.1) was observed for age, smoking history, race, family history of carcinoid, environmental exposure, or hemoptysis. The most important factors affecting survival defined by multivariate analysis were (p less than 0.01) pathologic stage, atypical histology, and asymptomatic presentation. Bronchial carcinoid tumors are unique, making up 1% to 2% of primary lung neoplasms and having an excellent prognosis after resection with a 95% 5-year and 93% 10-year survival for pathologic stage I disease.
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A questionnaire was used to evaluate asthenopia in 30 normal subjects (Ss). Then, each S experienced 3 min of continuous alternating convergent and divergent fusional vergence or a control condition which was identical to the experimental condition, but without any vergence demand, i.e., version. The stimulus was a computer-generated flat fusion red-blue anaglyph picture of a horse. The order of vergence and version conditions were randomized. Asthenopia measures and maximal fusional vergence ranges measures were repeated immediately after each condition. Results indicated a significantly higher rating of asthenopia after induced vergence than version. There were no differences in maximal fusional vergence ranges or recovery values after the two conditions. Correlations between pretreatment asthenopia scores and asthenopia scores after either induced vergence or version were also not significant. Post hoc analyses of Ss grouped as having either high or low asthenopia, according to baseline ratings, revealed no significant differences in vergence or version conditions. Alternative hypotheses for these results are presented.
We investigated the role of various stimulus parameters that influence motor fusion responses for peripheral as compared to central fusional stimuli. Results from the initial experiment indicated that a central stimulus equal in size to a peripheral fusion stimulus dominated the response independent of the amount of retinal eccentricity of the peripheral target. A second experiment indicated that the central stimulus dominated even when the peripheral stimulus was larger. However, when the peripheral stimulus was changed in shape so that it became an annulus surrounding the central stimulus, the peripheral stimulus was always stronger. In another phase of the experiment, we found that the extent to which a peripheral stimulus surrounded the central one determined which controlled the response. We concluded that the surrounding perceptual gestalt produced by the peripheral stimulus was the most significant variable determining the relative strengths of central and peripheral fusion stimuli. Clinical implications are discussed.
Platelet monoamine oxidase (MAO) activity and urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA), serotonin, tyramine and tryptamine were measured in patients with a variety of metastatic cancers and in healthy control subjects. The patients with cancer had higher platelet MAO activity and lower urinary excretion of 5-HIAA, sertonin and tyramine than the healthy subjects. The urinary tryptamine excretion was not significantly different in the two groups. At the present time it is unclear if the alterations in platelet MAO activity and monoamine excretion are casually related.
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Hamster and rat insulinomas were assayed for norepinephrine, dopamine and serotonin concentration and for monoamine oxidase and catechol-o-ethyltransferase (COMT) activity. The concentration of norepinephrine (mean 0.55 mumol/kg, range less than 0.20 to 2.64 mumol/kg) and serotonin (mean 5.22 mucol/kg, rang less than 0.6 to 26.5 mumol/kg) in hamster insulinomas were comparable to previously reported concentrations. Dopamine conentration (mean 0.34 mumol/kg, range less than 0.20 to 0.95 mumol/kg) was only 2 to 2.5% of that reported previously. Monoamine oxidase activity of the hamster and rat insulinomas were comparable to those of normal hamster islets. In contrast, the COMT activity of both insulinomas was much greater than the COMT activity of normal pancreatic islets of both species and was greater than in several other tissues and tumours. The tumour COMT, which was predominantly in the cytosol, was Mg2+ dependent and had a comparable sensitivity to inhibition by tropolone as purified beef-liver COMT. Hamster insulinoma monoamine oxidase was more sensitive than rat insulinoma monoamine oxidase to inhibition by tranylcypromine and deprenyl, while rat insulinoma monoamine oxidase was more sensitive to inhibition by clorgyline and was more heat labile.
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Medullary carcinoma of the thyroid (MCT) is reported to synthesize ACTH. This ACTH is believed to be responsible for the development of Cushing's syndrome in some patients with MCT. To determine the frequency of occurrence of adrenal cortical overactivity in patients with MCT, we measured plasma cortisol concentration and the urinary excretion of 17-hydroxycorticosteroids, 17-ketosteroids and urinary free cortisol in 22 patients with MCT and 7 patients with MCT plus pheochromocytomas. The patients with MCT and MCT plus pheochromocytoma had similar adrenal cortical function to age and sex matched normal subjects. We conclude that adrenal cortical function is usually normal in patients with MCT.
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To determine if patients with chronic hyperserotoninaemia from the carcinoid syndrome have increased basal adrenocortical function, I have determined the urinary free cortisol excretion of seventeen patients with carcinoid tumours and the carcinoid syndrome, twelve patients with carcinoid tumours without the carcinoid syndrome and seventeen normal subjects. There was no significant difference in the urinary free cortisol excretion of the patients with carcinoid tumours and the carcinoid syndrome (133 +/- 20.0 nmoles/24 h), patients with carcinoid tumours without the carcinoid syndrome (115 +/- 29 nmoles/24 h) and the normal subjects (96 +/- 9 nmoles/24 h). There was no correlation between the urinary free cortisol secretion and urinary 5-hydroxyindoleacetic acid or serum serotonin concentration in the patients with the carcinoid syndrome. There was a suggestion that patients with 5-hydroxytryptophan (5-HTP) secreting carcinoid tumours had higher urinary free cortisol excretion than patients with predominantly serotonin (5-HT) secreting carcinoid tumours. This may be due to the fact that the non-polar 5-HTP molecule penetrates the blood-brain barrier more effectively than the polar 5-HT molecule. 5-HTP is then converted to 5-HT within the brain. None of the twenty-nine patients with carcinoid tumours had clinical or laboratory evidence of the ectopic ACTH syndrome.
There is evidence that hypothalamic norepinephrine (NE) plays a role in the control of appetite in the rat. Using specific and sensitive radioenzymatic assays, we determined if there was a difference in the tissue (hypothalamus, cerebral cortex and kidney) concentration of NE or of dopamine (DA) in mice with the hereditary obese-hyperglycemic syndrome (ob/ob) and their normal weight littermates, both when they were in the rapid growth phase (2--3 months of age) and when they were mature (6--7 months of age). The concentration of NE was similar in the cerebral cortex of obese and normal mice and in the kidneys of obese and normal mice. The concentration of DA was similar in the hypothalamus of obese and normal mice. The concentration of DA was similar in the hypothalamus of obese and normal mice and in the cerebral cortex of obese and normal mice. These observations support the concept that alterations in hypothalamic NE may play a role in the obesity of ob/ob mice.
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Prior studies indicate that the monoamine oxidase inhibitors (MAOI) harmine and iproniazide inhibit N-acetyltransferase activity from liver. In this report we have demonstrated that harmine and harmaline are potent inhibitors of N-acetyltransferase, purified from hamster and rat liver. However, other MAOI such as deprenyl, clorgyline, methysergide, cyproheptadine, phenelzine, pargyline, methyltryptamine and tranylcypromine have either no effect, or only trivial effects on N-acetyltransferase. There is no correlation between a compound's properties as an MAO and N-acetyltransferase inhibitor. One must consider the inhibitory effect of harmine and harmaline on both MAO and N-acetyltransferase when evaluating the effects of these compounds on physiological processes.