The reactions of 1 nm plutonium dioxide particles with rat lung fluid.
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Biomedical subjects
Publications and source records attributed to J R Cooper.
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Forehead skin temperature measured by a stip of liquid-crystal material was compared to esophageal, rectal, and axillary temperatures measured by thermistor probes in patients having general anesthesia for coronary artery bypass grafting. Before extracorporeal circulation, forehead skin temperature was lower than axillary, rectal, and esophageal temperatures by approximately 2.2 C (4.0 F). During rapid warming, forehead skin temperature rose concurrently with the other temperatures measured but remained significantly different. The liquid-crystal strip may be useful as a safe, convenient method for routine monitoring of temperature trends during general anesthesia in patients whose exact core temperature need not be continuously monitored. We believe that infants, patients undergoing extracorporeal circulation, major abdominal, vascular, or neurosurgical procedures, or patients with a history of temperature regulatory problem are probably best monitored by a method which more exactly reflects core temperature.
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A case is presented of a baby in whom the abdominal catheter of a ventriculoperitoneal shunt entered the thoracic cavity. It is believed that the catheter migrated along the xiphocostal margin beneath the rectus abdominis muscle.
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The release of acetylcholine from synaptosomal preparations from bovine superior cervical ganglia and rat cortex was inhibited when the preparations were pretreated with collagenase. The inhibition of release could be overcome with the calcium ionophore A23187. Collagenase treatment was shown to inhibit the uptake of calcium into the preparations. In addition, gel electrophoresis of synaptosomal membranes revealed two missing high molecular weight proteins when either synaptosomes or synaptosomal membranes were incubated with collagenase.
Incubation of whole Chang liver cells with D-[1-14C]glucosamine results in incorporation of radioactivity into both proteins and lipids. A minor (approximately 3%) amount of the labelled lipid has the chromatographic, solubility and chemical properties of dolichol diphosphate N-acetylglucosamine. A similar compound is formed when membrane preparations of the cells are incubated with UDP-N-acetyl[14C]glucosamine. The same membrane fractions catalyse the transfer of [14C]-mannose from GDP-[14C]mannose to dolichol phosphate.
Thiamine pyrophosphate-ATP phosphoryltransferase, the enzyme that catalyzes the synthesis of thiamine triphosphate, has been found in the supernatant fraction of rat liver. The substrate for the enzyme is endogenous, bound thiamine pyrophosphate, since the addition of exogenous thiamine pyrophosphate had no effect. Thus, when a rat liver supernatant was incubated with gamma-labelled [32P]ATP, thiamine [32P]triphosphate was formed whereas the incubation of thiamine [32P]pyrophosphate with ATP did not produce thiamine [32P]triphosphate. The endogenous thiamine pyrophosphate was found to be bound to a high molecular weight protein which comes out in the void volume of Sephadex G-75, and is not dialyzable. The activity that catalyzes the formation of thiamine triphosphate has an optimum pH between 6 and 6.5, a linear time course of thiamine triphosphate synthesis up to 30 min, and is not affected by Ca2+, cyclic GMP and sulfhydryl reagents.
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Thiamine and thiamine triphosphate (TTP) values were assayed in various brain regions in 11 controls and 13 patients with subacute necrotizing encephalomyelopathy (SNE, Leigh disease). The TTP values of normal brain were 5% of the total thiamine value. The relative TTP (or % TTP) level was consistently low in the pons, midbrain, and cerebellum of all the SNE brains. Twenty-five percent of the SNE brains had normal TTP levels in the frontal region. The TTP values correlated with the degrees of pathologic involvement in all sampled regions of the brain except the cerebellum. The concentration of thiamine in the mammillary bodies exceeded its concentration elsewhere in both control and SNE brains. The finding of low TTP levels in morphologically abnormal regions supports the hypothesis that TTP deficiency is etiologically related to SNE.
The neurochemical activity of beta-bungarotoxin was investigated using a synaptosomal preparation of rat cerebral cortices. In preparations preincubated with [3H]choline in order to label acetylcholine the toxin caused a rapid release of the transmitter, which was calcium dependent but only a little affected by a depolarizing concentration of potassium. beta-Bungarotoxin was also shown to be a potent inhibitor of the high affinity transport system for choline, producing 50% inhibition at a concentration of 50 nM. These findings explain the observed electrophysiological effects of the toxin. Electron microscopy revealed no discernible effect of 0.1 muM beta-bungarotoxin on either synaptic vesicles or mitochondria. Neither the release of transmitter nor the inhibition of choline uptake by the toxin was affected by the presence of an inhibitor of phospholipase activity.
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To assess the hypothesis that thiamine is directly involved in the permeability changes at the sodium channel during nerve conduction, the effects of thiamine antagonists on lobster giant axon resting and action potentials were determined. Thiamine antimetabolites, in millimolar concentrations, reversibly decreased the maximum rate of rise and amplitude of the action potential while increasing its duration. In particular, thiamine tert-butyl disulfide (TTBD) elicited the formation of pronounced shoulders during repolarization, lengthening the action potential by 2-50 times, depending on dose. Antimetabolites also depolarized the resting membrane, but this change was poorly reversible and may indicate a dual mechanism for antimetabolite action. An extract of the fern, Pteris aquilina, reversibly decreased the maximum rate of rise of the action potential and depolarized the resting potential. It also elevated and prolonged the action potential after-depolarization, sometimes causing repetitive activity. The strength of these actions was correlated with the antithiamine potency of the extract, and was diminished by addition of thiamine to the extract.
Thiamine antimetabolites were externally applied to voltage clamped squid giant axons to investigate the possible role of thiamine in nerve conduction. Phenylthiazinothiamine, in concentrations as low as 250 muM, reduced peak early current and steady-state current, with the depression of the former being two to five times greater than that of the latter. Peak transient and steady-state conductances were about equally depressed by thiamine tert-butyl disulfide (2 mM) and L-586944-00P07 (5-10 mM). None of the antimetabolites produced an appreciable change in the kinetics of Na+ activation, K+ activation, or Na+ inactivation. Thiamine itself, applied externally up to 30 mM, had no appreciable effect on either the magnitude or time course of the ionic currents. Although these data are consistent with the hypothesis that thiamine may be involved in nerve conduction, they probably reflect a nonspecific stabilizing interaction of this class of compound with the axon membrane. Taken in this light, the hypothesis that thiamine plays a direct role in Na+ channel permeability changes must be reevaluated.
Dispersed cell cultures of guinea-pig epidermis have been maintained for up to 36 days. The progress of these cultures has been studied by phase contrast microscopy, the adenosine triphosphatase reaction, and cinephotomicrography. Langerhans cells have been identified and their behaviour studied, particularly in relation to keratinocytes.
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