Biomedical subjects
J R Cooper
Publications and source records attributed to J R Cooper.
Case report: Sylvian fissure meningioma without dural attachment in a 4-year-old child.
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A case of cellulitis of the big toe?
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Preoperative risk stratification identifies low-risk candidates for early extubation after aortocoronary bypass grafting.
Early tracheal extubation has been the focus of recent attempts to accelerate the care of patients after aortocoronary bypass. Following the 1994 validation of a preoperative mortality risk mode based on the Society of Thoracic Surgeons National Cardiac Surgery Database, we examined the records of 328 aortocoronary bypass patients from our institution and identified 133 patients with low preoperative mortality risk. Their records were then analyzed for duration of tracheal intubation. One low-risk patient who did not survive was excluded from the analysis. Of the remaining 132 patients, 108 experienced no postoperative complications; nevertheless, 50 of these were intubated longer than 10 hours despite freedom from complications. In a 2nd group of 153 consecutive low-risk patients, we prospectively implemented a patient care protocol that designated low-risk patients as eligible for accelerated weaning. Compared were the 1st group, these patients with low preoperative mortality risk were weaned from mechanical ventilation in 40% less time. Thus, we found that low preoperative mortality risk predicts success in early tracheal extubation. Risk stratification appears to be a simple and useful means of identifying patients least likely to encounter postoperative complications. Risk-based accelerated recovery was successfully implemented without requiring a change in anesthetic or surgical management.
Measuring program performance in methadone treatment using in-treatment outcomes: an illustration.
Quality measurement and quality assurance in substance abuse treatment have, over the past few years, become a major policy issue. In addition, there is interest in the degree to which client outcomes can play a role in measuring treatment program performance. This article discusses the movement toward outcome-based performance measurement in substance abuse treatment. Examples of the products that such a performance measurement system might produce are provided. Why outcomes must be case-mix adjusted is discussed. In addition, using data from 18 methadone programs and more than 2,000 methadone clients from the Treatment Outcome Prospective Study, an illustration of case-mix-adjusted performance measurement is provided.
Regulation of ornithine decarboxylase mRNA levels in human breast cancer cells: pattern of expression and involvement of core enhancer promoter element.
Ornithine decarboxylase (ODC) expression is increased by growth factors and is obligatory for progression through the cell cycle in a wide variety of cell types. In this study, a variant human ODC cDNA was identified, sequenced, and used to probe mRNA levels in human breast tumor cell lines and xenografts. ODC mRNA was elevated about 3-fold in estrogen receptor-negative (ER-) tumors (MDA-MB-231) when compared with ER-positive (ER+) tumors (MCF-7), as assessed by quantitative autoradiographic analysis of in situ hybridization experiments. The pattern of ODC mRNA in MDA-MB-231 (ER-) xenografts was polarized to the extreme periphery of the tumor, whereas the distribution of ODC mRNA was more evenly distributed in MCF-7 (ER+) xenografts. This correlates with hematoxylin and eosin staining patterns, suggesting that ER+ and ER- xenografts have a differential dependence on host vasculature for growth factor supply. ODC mRNA was elevated 5-fold in MDA-MB-231 cells versus MCF-7 cells when analyzed in cell culture. These relative mRNA levels correlate with increased levels of "core" enhancer binding nuclear proteins in MDA-MB-231 cells over that detected in MCF-7 cells.
Over the counter H2 receptor antagonists. Increase the risks to offshore workers.
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DEA physician registration numbers: a need to know.
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Presynaptic modulation by eicosanoids in cortical synaptosomes.
In continuing experiments to determine the ionic basis of inhibitory presynaptic modulation, rat cortical synaptosomes were employed and receptor-activated K+ efflux was determined with a K+ sensitive electrode. When synaptosomes were sub-optimally depolarized by veratridine, the addition of agents that activated purinergic, alpha 2-adrenergic, muscarinic and opioid receptors all promoted K+ efflux. With 2-chloroadenosine as a model inhibitory presynaptic modulator, the increased K+ efflux evoked by this agent was blocked by the cyclooxygenase inhibitor indomethacin suggesting that arachidonic acid or its metabolites was an intermediary in opening the channel. When arachidonic acid and PGE2 were tested, both promoted K+ efflux that was inhibited by dendrotoxin and mast cell degranulating peptide, two agents that are known to inhibit a delayed rectifier K+ current. Our results suggest that via eicosanoid second messengers, inhibitory presynaptic modulators open a sub-class of K channels that hyperpolarize nerve terminals, therefore less Ca2+ would enter per nerve impulse and thus the evoked release of neurotransmitters would be decreased.
Presynaptic modulation by dopamine and GABA opens a potassium channel in rat cortical, striatal and hippocampal synaptosomes via eicosanoids.
Using a K(+)-sensitive electrode in synaptosomal preparations, the presynaptic modulating effect of dopamine and GABA in opening a K+ channel was investigated. In cortical, striatal and hippocampal synaptosomes dopamine D1 and D2 agonists and a GABAB agonist promoted the efflux of K+ in all three preparations. The effect was blocked by the cyclooxygenase inhibitor, indomethacin suggesting that eicosanoids act as second messengers in these systems. The inference in these studies is that dopamine and GABA hyperpolarize presynaptic terminals thereby reducing Ca2+ influx and thus inhibiting the evoked release of transmitters.
Unsolved problems in the cholinergic nervous system.
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Federal regulation of clinical practice in narcotic addiction treatment: purpose, status, and alternatives.
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Coping with reduced cost limits for home health agencies.
The Omnibus Budget Reconciliation Act of 1993, together with cost-limit reductions and wage-index changes published in the Federal Register, have resulted in a substantial reduction in Medicare cost limits, particularly as they apply to hospital-based home health agencies. This article examines specific changes in home health agency cost limits, reviews strategies to identify the bottom-line impact of the Medicare cost-limit reductions, and discusses methods that may be applied to minimize the negative impact of the reduced cost limits.
Dendrotoxin blocks a class of potassium channels that are opened by inhibitory presynaptic modulators in rat cortical synaptosomes and slices.
1. Rat cortical synaptosomes were prelabeled with radioactive acetylcholine and the release induced by veratridine was determined in the absence and presence of the inhibitory presynaptic modulators, 2-chloroadenosine, carbamylcholine, clonidine, and morphine. All four agents inhibited the evoked release of acetylcholine and this inhibition was reversed by dendrotoxin. 2. Using perfused cortical slices and an extracellular K-sensitive electrode, all modulators again increased K efflux that was blocked by dendrotoxin. In contrast, glybenclamide and tetraethylammonium did not block the modulator-induced efflux.
Receptor-activated modulation in rat cortical slices as measured with a K-sensitive electrode.
The effects of a variety of presynaptic receptor-activating modulating agents on potassium efflux have been investigated using a potassium (K)-sensitive extracellular electrode in rat brain cortical slices that are electrically stimulated. Purinergic, alpha 2-adrenergic, opioid and muscarinic drugs all increased K outflow. When these agents were used in combination at maximal concentrations, only morphine promoted a further increase in K efflux, suggesting that it utilized a different K channel or acted on cellular elements different from those of the other modulators.
An alternative mechanism for the inhibition of cholesterol biosynthesis in HepG2 cells by N-[(1,5,9)-trimethyldecyl]-4 alpha,10-dimethyl-8-aza-trans-decal-3 beta-ol (MDL 28,815).
Compounds that block hepatic cholesterol biosynthesis and secretion may be useful hypocholesterolemic agents. N-[(1,5,9)-trimethyldecyl]-4 alpha,10-dimethyl-8-aza-trans-decal-3 beta-ol (MDL 28,815) has been shown to block cholesterol biosynthesis in 3T3 fibroblasts and it causes cellular accumulation of squalene 2,3-epoxide and squalene 2,3:23,24-diepoxide (squalene epoxides), which suggests that it inhibits 2,3-oxidosqualene cyclase. The purpose of the present report was to determine whether MDL 28,815 acts only at the level of 2,3-oxidosqualene cyclase or whether other enzymes in the cholesterol biosynthetic pathway are affected. HepG2 cells, grown in lipoprotein-deficient serum, were incubated with MDL 28,815 and 14C-acetate to radiolabel cholesterol and the intermediates in the cholesterol biosynthetic pathway. Blockade of cholesterol biosynthesis by MDL 28,815 in these cells was associated with the accumulation of two metabolites, one of which was 5 alpha-cholest-8-en-3 beta-ol. The other metabolite was identified by a combination of ultraviolet spectrometry, gas chromatography, mass spectroscopy and analytical high-performance liquid chromatography as 5 alpha-cholest-8,14-dien-3 beta-ol. Maximal blockade of cholesterol biosynthesis was associated with the accumulation of these two metabolites and, in particular, 5 alpha-cholest-8,14-dien-3 beta-ol, rather than with squalene epoxides. These results suggest that MDL 28,815 blocks cholesterol biosynthesis primarily by the inhibition of sterol-delta 14-reductase, and possibly sterol-delta 8-ene isomerase, rather than 2,3-oxidosqualene cyclase.
Prescription drug diversion control and medical practice.
Concern about the role of prescription drug diversion in drug abuse has led to demands for more stringent regulation and for better ways to detect prescription drug diversion. Advances in technology now allow point-of-sale computer systems to report prescriptions filled by pharmacies to state agencies rapidly and possibly more economically. However, the advantages of more comprehensive control systems must be balanced against their possible effects on medical practice and patient care. Our limited knowledge about prescription drug diversion and the impact of diversion control systems on medical practice is summarized. Needed research is outlined together with the components of a diversion control program that balances reducing drug diversion with minimizing adverse effects on medical practice and patient care. We stress the need for broadly defined practice parameters and peer review by medical experts thoroughly familiar with the complexities of medical practice.
Ineffective use of psychoactive drugs. Methadone treatment is no exception.
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