[Linear nevus sebaceous syndrome: report of a case and a review of the literature].
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Biomedical subjects
Publications and source records attributed to T Okada.
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Panendoscopic examination, performed in 4,130 healthy males older than 50 years, detected 9 esophageal cancers (0.22%). Of these, 6 were classified as early esophageal cancer, and 3 of these 6 had intraepithelial cancers. In efforts to detect early esophageal cancers, especially at the intraepithelial cancer stage, panendoscopic examination seems to be highly useful.
The neurons in the substantia gelatinosa of the spinal cord of the rat and Japanese monkey were investigated electron microscopically and ultracytochemically. The confronting cisternae observed in the cytoplasm of the majority of gelatinosal neurons in both species were composed of closely apposed parallel cisternae with electron-dense flocculent material, and a continuity with the cisternae of the rough endoplasmic reticulum was often observed. Ultracytochemically, the p-nitrophenylphosphatase (p-NPPase) activity was present in the confronting cisternae, but thiamine monophosphatase (TMPase) and thiamine pyrophosphatase (TPPase) activities were absent. These results indicate that the confronting cisternae are a variant of the rough endoplasmic reticulum.
Amino acids and thiobarbituric acid reactive substances (TBARs) in the cerebrospinal fluid (CSF) and plasma were identified and assayed in 5 patients with septic encephalopathy. Levels of all the high molecular weight neutral amino acids (LNAAs) appeared to increase in the CSF. CSF levels of phenylalanine (PHE) and methionine (MET) increased significantly by factors of 20.9 and 9.5, respectively, and the plasma PHE level increased 7.5-fold. No significant changes in branched-chain amino acids were observed in either the CSF or plasma. The CSF/plasma ratios of valine (VAL), tyrosine (TYR), PHE, and MET significantly increased to 0.21, 0.46, 0.52, and 0.52, respectively. TBAR levels increased 4-fold in the CSF and also were slightly increased in the plasma, suggesting that lipid peroxidation in the central nervous tissues is markedly increased. We conclude that increases in LNAA levels and in lipid peroxidation in the central nervous tissues may play important roles in the development of septic encephalopathy.
We studied 57 patients admitted to hospital with ischaemic heart disease, including nine patients with variant angina, to evaluate platelet reactivity and its dependence on alpha-adrenergic receptor function. The threshold concentration for biphasic platelet aggregation in response to adrenaline and adenosine diphosphate was measured in fresh platelet rich plasma. There were age related alterations in platelet responsiveness to adrenaline. In 27 age matched control subjects platelets showed adrenaline induced aggregation at a concentration higher than 0.1 mumol. The threshold concentrations for adrenaline and adenosine diphosphate were 0.91 mumol and 4.68 mumol. In 16 patients with acute infarction, 14 with old infarction, nine with effort angina, and nine with rest angina, mean values of platelet aggregation threshold for both adrenaline and adenosine diphosphate were not altered significantly when compared with control subjects. In contrast, the values for adrenaline and adenosine diphosphate in nine patients with variant angina were 0.012 mumol and 2.24 mumol and seven of them showed obvious platelet hyperactivity to adrenaline at a concentration lower than 0.1 mumol. The threshold concentration for adrenaline induced aggregation did not correlate with serum cholesterol and triglyceride levels.
The effect of picrotoxin (PT) on catecholamine (CA) secretion was investigated in perfused bovine adrenal glands. A low dose of PT (3 microM) enhanced the CA secretion evoked by a 15-min exposure to 1,1-dimethyl-4-phenylpiperazinium (DMPP, a nicotinic agonist; 0.1 mM), but a higher dose (0.3 mM) of PT inhibited the DMPP-evoked CA secretion. The rate of decline of secretory response to the prolonged DMPP stimulation was also accelerated by a higher dose (0.1 mM) of PT. In the dose-response curves for DMPP-evoked CA secretion, the inhibitory action of PT (0.3-1 mM) was more prominent at high doses than at low doses of DMPP. The inhibition pattern was similar to the pattern of a barbiturates blockade. In separate experiments, PT (0.1 mM) augmented calcium (10 mM)- and high potassium (56 mM)-evoked secretory responses. Spontaneous CA secretion was unaffected by PT at the concentrations indicated above. These results indicate that a low dose of PT potentiates, but higher doses inhibit, the adrenal CA secretion by a nicotinic agonist and that the inhibitory effect of PT resembles that of barbiturates.
This study was designed to determine whether coronary collaterals have preventive effects on tachycardia-induced myocardial ischemia under partial restriction of proximal coronary artery inflow. Studies were carried out in dogs with developed coronary collaterals and control dogs. ST-elevation in epicardial and intramyocardial electrograms was used for assessing the degree of regional myocardial ischemia. In control dogs with coronary constriction (80% reduction of i.d.) pacing-induced tachycardia produced significant ST-elevation, 1.48 +/- 0.17 mV in the inner layer and 0.79 +/- 0.29 mV in the middle layer at a cardiac rate of 150/min, 3.58 +/- 0.38 mV in the inner layer, 2.73 +/- 0.38 mV in the middle layer, and 1.93 +/- 0.36 mV in the outer layer at a rate of 180/min. In dogs with moderate collaterals ST-segment elevation was only 1.41 +/- 0.18 mV in the inner layer and 0.96 +/- 0.24 mV in the middle layer at a rate of 180/min. In dogs with abundant collaterals there was no significant ST-elevation during tachycardia. These findings indicate that blood supply to the affected myocardium via developed collaterals is sufficient to meet graded increases in metabolic requirements under the condition of limited coronary flow reserve in an experimental model simulating angina pectoris.
We developed a canine model with coronary stenosis produced by intraluminal obstruction with a micro-balloon occluder to assess the role of vasomotor tone of a large coronary artery with a preexisting fixed stenosis in the genesis of myocardial ischemia. Hemodynamic and electrocardiographic responses to ergonovine, an agent capable of provoking coronary spasm, were evaluated. In the absence of coronary stenosis, intracoronary infusion of 4 micrograms/min ergonovine had no systemic and coronary hemodynamic effects. Similarly, with various degrees of external obstruction created by a screw-type metal constrictor, ergonovine had little hemodynamic effects. By contrast, with a stenosis greater than 28.4 +/- 5.0 mmHg in pressure gradient, created by intraluminal obstruction which preserved active arterial vasomotion, ergonovine-induced vasoconstriction produced a marked decrease in coronary blood flow and distal coronary pressure, followed by ST-elevation. These deleterious effects of ergonovine on coronary hemodynamics were reversed completely by intracoronary infusion of nitroglycerin. Our results indicate that the effects of normal coronary arterial vasomotor activity on a stenosed vessel can cause myocardial ischemia.
A balloon was introduced into the isolated rabbit left ventricle with intraventricular volume being controlled by a feedback amplifier. Pressure-volume and stiffness-pressure relations were determined as intraventricular volume was changed. These ventricular relations were explained according to the theory of wall muscle mechanics.