Biomedical subjects

Y Tamura

Publications and source records attributed to Y Tamura.

At least 361 records · Page 20Linked to original sources

PubMed1993

Erysipelothrix tonsillarum isolated from dogs with endocarditis in Belgium.

Five strains of Erysipelothrix tonsillarum were isolated from dogs with endocarditis in Belgium. The identity and validity of the species was proved by serotyping, and biochemical and pathogenicity tests. All the isolates belonged to serovar 7 (E tonsillarum serovars); they produced acid from saccharose but did not induce any clinical sign of erysipelas in swine. These results suggest that some strains of E tonsillarum are a canine pathogen.

Animals↗

PubMed1993

Premature closure of the distal radial physis.

Two cases of fracture of the radius treated by pinning resulted in severe wrist joint deformity due to premature closure of the epiphysial growth plate. Inappropriate pinning through the physis damaged the growth plate in both cases. They were treated by bone bridge resection with free fat interposition. The bone bar resection was effective in correcting the wrist joint deformity, and bone growth was expected without bone grafting.

Bone Wires↗

PubMed1993

Cholera toxin directly stimulates pregnenolone generation with increasing Ca2+ efflux in bovine adrenocortical mitochondria.

The present experiments demonstrated that the holotoxin as well as the A- and B-subunits of cholera toxin were able to directly enhance pregnenolone synthesis when isolated intact mitochondria, prepared from bovine adrenocortical tissue, were incubated; they were not, however, able to enhance pregnenolone synthesis when the inner mitochondrial fraction was similarly incubated, suggesting that the conformational structure of mitochondria is very important for activation of cholesterol side-chain cleavage by cholera toxin. Data are also presented demonstrating that cholera toxin can enhance Ca2+ release from isolated mitochondria, while pertussis toxin could activate neither pregnenolone generation nor increase Ca2+ efflux from mitochondria. Thus it is suggested that cholera toxin may activate pregnenolone synthesis by regulating Ca2+ movement in mitochondria.

Adrenal Cortex↗

PubMed1993

Adiabatic compressibility of myosin subfragment-1 and heavy meromyosin with or without nucleotide.

The partial specific adiabatic compressibilities of myosin subfragment-1 (S1) and heavy meromyosin (HMM) of skeletal muscle in solution were determined by measuring the density and the sound velocity of the solution. The partial specific volumes of S1 and HMM were 0.713 and 0.711 cm3/g, respectively. The partial specific adiabatic compressibilities of S1 and HMM were 4.2 x 10(-12) and 2.9 x 10(-12) cm2/dyn, respectively. These values are in the same range as the most of globular proteins so far studied. The result indicates that the flexibility of S1 region almost equals to that of HMM. After binding to ADP.orthovanadate, S1 and HMM became softer than their complexes with ADP. The bulk moduli of S1 and HMM were of the order of (4-6) x 10(10) dyn/cm2, which are very comparable with the bulk modulus of muscle fiber.

Adenine Nucleotides↗

PubMed1993

Altered electrical and metabolic response of reperfused myocardium to ischaemia after recovery from preceding ischaemia: evidence for ischaemia sensitised myocardium.

OBJECTIVE: The aim was to examine electrical and metabolic responses of myocardium to ischaemia after recovery from preceding ischaemia. METHODS: In 23 open chest dogs (5 min occlusion group), the left anterior descending coronary artery was occluded three times in the following order: 2 min occlusion (Trial 1) followed by 15 min reperfusion; then 5 min occlusion followed by 90 min reperfusion and 2 min occlusion (Trial 2). In 15 control dogs, the 2 min occlusion was performed twice at a 110 min reperfusion interval; the former occlusion was also referred to as Trial 1 and the latter as Trial 2. The dogs were monitored by epicardial surface ECG, while regional myocardial function was estimated by sonomicrometry. Continuous measurements of myocardial tissue PCO2, pH, and extracellular K+ concentration were made concurrently. RESULTS: Both trial occlusions produced a biphasic change in R wave amplitude characterised by a transient initial decrease succeeded by an increase with ST elevation. This biphasic change in R wave amplitude was indistinguishable between Trial 1 and Trial 2 in the control group. By contrast, in the 5 min group, the R wave amplitude initially decreased to a greater degree in Trial 2 than in Trial 1. More rapid contractile failure was also noticed in Trial 2, suggesting the possible involvement of mechanically induced electrical changes in the genesis of decreased R wave amplitude. After 45-60 s of occlusion, however, the R wave amplitude increased to a level much beyond the initial amplitude in Trial 1 [124.9(SEM 8.4)% at 120 s], whereas this level of increase was not observed in Trial 2 [106.5(7.8)%, p < 0.05 v Trial 1]. There was also reduced elevation of the ST segment in Trial 2: 3.6(0.8) mV v 6.5(0.8) mV in Trial 1 at 120 s (p < 0.05). This reduction in ST elevation was concomitant with decreased changes in PCO2, pH, and extracellular K+ concentration in Trial 2. These reduced changes in the ST segment and the metabolic variables were absent in the control group. CONCLUSIONS: These altered electrical responses of the myocardium may be the result of more rapid early contractile failure and attenuated metabolic changes during ischaemia occurring after recovery from preceding ischaemia.

Animals↗

PubMed1993

Mitochondrial NADPH-linked aquacobalamin reductase is distinct from the NADPH-linked enzyme from microsomal membranes in rat liver.

Mitochondrial NADPH-linked aquacobalamin reductase was purified and characterized to clarify its enzymatic properties. The enzyme was purified about 360-fold over rat liver mitochondrial membranes in a yield of 7.5%. The purified enzyme was homogenous in SDS-PAGE. The molecular mass (M(r)) of the enzyme was calculated to be 65 kDa by SDS-PAGE and by Toyopearl HW55 gel filtration, indicating that the enzyme is a monomeric polypeptide with M(r) of 65 kDa. The enzyme was a flavoprotein containing 1 mol of FAD and FMN per mole of the enzyme. The enzyme was specific for NADPH as electron donor and had the ability to reduce cytochrome c (15.4 mumol.min-1 x mg protein-1), potassium ferricyanide (4.9 mumol.min-1 x mg protein-1) and 2,6-dichlorophenolindophenol (16.8 mumol.min-1.mg protein-1) as well as aquacobalamin (6.4 mumol.min-1 x mg protein-1). Although the enzyme immunoreacted with an antibody against NADPH-cytochrome P-450 reductase, which had the activity of the NADPH-linked aquacobalamin reductase in rat liver microsomes, the mitochondrial enzyme and the microsomal enzyme had different enzymological properties.

Animals↗

PubMed1993

Corrinoid specificity of cytosolic cobalamin-binding protein of Euglena gracilis z.

To elucidate the corrinoid specificity of the cytosolic cobalamin-binding protein of Euglena gracilis, inhibition of the binding of radioactive cyanocobalamin to the cytosolic binding protein was studied with a variety of cobalamin analogues. The cytosolic cobalamin-binding protein showed an absolute requirement for the alpha-axial ligand (the cobalt-coordinated nucleotide) in cobalamin binding, but was not able to recognize certain differences in the base or ribose moiety. Regarding the contributions of the b-, d-, and e-propionamide side chains in the binding of cobalamin to the cytosolic protein, the order of the contributions was shown to be b > d > e; in particular the b-propionamide side chain was essential for the formation of the protein-cobalamin complex. No involvement of the beta-axial ligand or the alkanolamine group in the binding of cobalamin to the protein was found.

Animals↗

PubMed1993

Uptake of cobalamin by Euglena mitochondria.

Cobalamin uptake by Euglena mitochondria is a biphasic process, consisting of energy-independent cobalamin-binding to mitochondrial membranes and energy-dependent active transport. The energy-dependent phase of cobalamin uptake is not dependent on mitochondrial respiration, but on the presence of ATP within the mitochondrial matrix. The dissociation constant of the energy-independent cobalamin-binding reaction is estimated to be 0.45 nM. Inhibition of the mitochondrial cobalamin uptake by a variety of cobalamin analogues indicates that Euglena mitochondria have an absolute requirement for the complete cobalamin molecule with an alpha-axial ligand (the cobalt-coordinated nucleotide) and an intact b-propionamide side-chain. Thus, the Euglena mitochondrial cobalamin uptake system is highly specific for the cobalamin structure. The cobalamin taken up by the Euglena mitochondria cannot be exchanged with exogenous cobalamin. All of the mitochondrial cobalamin is associated with three proteins with molecular masses of > 700,000 (16.3%), 160,000 (7.4%), and 35,000 (76.3%). They occur in the soluble fraction of mitochondria, suggesting that these cobalamin-binding proteins or cobalamin-dependent enzymes play an important role in cobalamin accumulation and metabolism within the mitochondria.

Adenosine Triphosphate↗

PubMed1993

Coronary artery spasm is a major cause of sudden cardiac arrest in survivors without underlying heart disease.

BACKGROUND: The role of coronary spasm in underlying disease-free patients who were resuscitated from sudden cardiac arrest remained uncertain. This study investigated the cause of cardiac arrest, and the etiologic and prognostic differences were compared between patients with underlying heart disease (group I) and those patients without underlying heart disease (group II). METHODS: Twenty-five survivors of sudden cardiac arrest were classified into two groups according to the presence or absence of underlying heart disease. To investigate the cause of cardiac arrest, we performed ergonovine testing and electrophysiologic study. Fifteen of the patients had underlying heart disease, while 10 did not. RESULTS: Electrophysiologic abnormalities were found in 13 of the 15 patients in group I. In group II, spontaneous attack of coronary spasm occurred in four patients during the observation period, and coronary spasm was induced in three of the remaining six period of 32 +/- 23 months, whereas no patients in group II had recurrence of sudden cardiac arrest at a median follow-up of 32 months (range, 10 to 72 months). CONCLUSIONS: Electrophysiologic study identified a potential cause in 13 of 15 patients with underlying heart disease. Coronary spasm was involved in the pathogenesis of sudden cardiac arrest in survivors without identifiable underlying heart disease.

Adolescent↗

PubMed1993

Differentiation of Erysipelothrix rhusiopathiae and Erysipelothrix tonsillarum by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of cell proteins.

The protein patterns of whole cells of Erysipelothrix rhusiopathiae and Erysipelothrix tonsillarum were studied by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The protein patterns of the 16 strains of E. rhusiopathiae and E. tonsillarum studied, including the type strains of these two species, resembled each other, except that there were 71-, 41-, 34-, and 26-kDa proteins in the E. rhusiopathiae pattern and 74-, 44-, 36-, and 25-kDa proteins in the E. tonsillarum pattern. This observation indicates that there is some phenotypic heterogeneity in the genus Erysipelothrix. In addition, the protein patterns of E. rhusiopathiae serotype reference strains representing serotypes 1 through 23 and type N were compared. The protein patterns of serotype 1a, 1b, 2, 4, 5, 6, 8, 9, 11, 12, 15, 16, 19, and 21 and type N strains were similar to the pattern of the type strain of E. rhusiopathiae (strain ATCC 19414). Conversely, the protein patterns of serotype 3, 7, 10, 14, and 20 strains were very similar to the pattern of the type strain of E. tonsillarum (strain ATCC 43339). An atypical pattern was observed in serotype 13, 17, 18, 22, and 23 strains. These results suggest that this method may be used as an aid in studying the taxonomy of these bacteria.

Animals↗

PubMed1993

Electron microscopic study of intercellular junctions in human gastric mucosa with special reference to their relationship to gastric ulcer.

The development of gap junctions in the human gastric mucosa has been examined to see if there is any relation to gastric ulcer. Freeze fracture replicas were prepared from the endoscopic biopsy specimens of 20 patients with gastric ulcer (15 men and five women, aged 49 (13) years) and seven healthy volunteers (four men and three women, aged 41 (19) years). Large fractured areas of lateral cell membranes of surface mucous cells were observed randomly at a direct magnification of 15,000 using electron microscopy. Small gap junctions were observed between gastric surface mucous cells in all healthy volunteers. Gap junctions in the patients with gastric ulcer were significantly fewer than in the healthy volunteers. In addition, gap junctions in patients with recurrent ulcer were significantly fewer than in those with first onset ulcer. There was no obvious relationship between age and the development of gap junctions in patients with gastric ulcer or in healthy volunteers. In areas of intestinal metaplasia, gap junctions were occasionally seen between absorptive cells of the villi, but not in the lateral membranes of goblet cells. These findings suggest that loss of intercellular communication via gap junctions is associated with gastric ulcer formation.

Female↗

PubMed1993

Acute effect of percutaneous transvenous mitral commissurotomy on ventilatory and hemodynamic responses to exercise. Pathophysiological basis for early symptomatic improvement.

BACKGROUND: Improvement of exertional dyspnea occurs immediately after percutaneous transvenous mitral commissurotomy (PTMC), but the pathophysiological basis for this early symptomatic improvement has not been elucidated. METHODS AND RESULTS: Exercise hemodynamic measurement and exercise ventilatory measurement with arterial blood gas analysis were performed in 21 patients aged 50.4 +/- 9.5 years (mean +/- SD) with symptomatic mitral stenosis before and a few days after PTMC. Exercise ventilatory measurement were also performed in 14 normal control subjects aged 48.9 +/- 4.9 years. After PTMC, mitral valve area increased (from 1.0 +/- 0.3 to 1.7 +/- 0.3 cm2, P < .001), mean mitral gradient (from 12.2 +/- 5.2 to 5.2 +/- 2.2 mm Hg, P < .001), and mean left atrial pressure (from 18.7 +/- 6.1 to 12.1 +/- 4.0 mm Hg, P < .001) decreased. All patients experienced significant symptomatic improvement soon after PTMC. Comparison of hemodynamic parameters at the same ergometer work rate showed a significant decrease in pulmonary artery systolic pressure (from 77 +/- 18 to 67 +/- 14 mm Hg, P < .001) and diastolic pressure (from 36 +/- 10 to 28 +/- 7 mm Hg, P < .001) and a significant increase in cardiac output (from 6.4 +/- 1.4 to 8.1 +/- 1.9 L/min, P < .001). Despite the improvement in exercise hemodynamics and symptoms, exercise capacity determined by peak oxygen uptake (from 18.0 +/- 2.9 to 18.6 +/- 3.1 mL.kg-1 x min-1) and anaerobic threshold (from 11.7 +/- 2.4 to 12.0 +/- 2.4 mL.kg-1 x min-1) remained unchanged. Excessive exercise ventilation, as assessed by the slope of the regression line between expired minute ventilation and carbon dioxide output, decreased significantly from 37.2 +/- 6.7 to 33.9 +/- 5.8 (P < .001), but remained significantly higher than that in the normal subjects (27.9 +/- 3.6, P < .01). The ratio of total dead space to tidal volume and total dead space per breath during exercise decreased significantly after PTMC (P < .05). The change in excessive exercise ventilation after PTMC was correlated with the change in dead space to tidal volume ratio (r = .59). CONCLUSIONS: Significant relief of exertional dyspnea immediately after PTMC is not accompanied by an improvement in exercise capacity. A decrease in excessive ventilation due to a decrease in physiological dead space resulting from hemodynamic improvement partly contributes to the early relief of symptoms after PTMC. However, lung compliance, which was not measured in the present study, may have changed after PTMC. This change may also contribute to the symptomatic improvement.

Anaerobic Threshold↗

PubMed1993

Effects of protein kinase C on the muscarinic excitation of rat adrenal chromaffin cells.

The role of protein kinase C (PKC) in the muscarinic excitation of chromaffin cells freshly isolated from rat adrenal medullae was examined by the patch-clamp recording method. Acetylcholine and McN-A-343, a M1-receptor agonist, depolarized the cell and induced action potentials. Phorbol 12,13-dibutyrate (PDBu), an activator of PKC, increased acetylcholine-induced firing concomitant with a persistent depolarization. Under voltage-clamp recording, both McN-A-343 and PDBu decreased the cesium-sensitive K+ current, which was induced by shifting the membrane potential between -140 mV and -40 mV. These results suggested that the stimulation of muscarinic M1-receptors by cholinergic drugs activated phospholipase C to degrade phosphoinositide, consequently producing diacylglycerol, and diacylglycerol activates PKC to induce excitation of adrenal chromaffin cells.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1993

Blockade of retinal NMDA receptors by sodium nitroprusside is probably due to nitric oxide formation.

Effects of a nitric oxide (NO)-producing agent, sodium nitroprusside, on N-methyl-D-aspartate (NMDA) receptor activation in the cultured retinal neurons of rats were examined. NMDA in a Mg(2+)-free medium evoked inward currents at the resting membrane potential. Inward currents were also evoked by kainate. Sodium nitroprusside markedly reduced the NMDA-induced currents without affecting those induced by kainate. These results suggest the possible existence of a negative feed back system of NO which serves to regulate the activation of NMDA receptors in retinal neurons.

Animals↗

PubMed1993

The ability of Salmonella enteritidis isolated from chicks imported from England to cause transovarian infection.

S. Enteritidis HY-1 isolated during quarantine from chicks imported from England was used. Laying hens at the age of 34 weeks were inoculated orally with 10(10) organisms (10 birds), intramuscularly with 10(9) (5 birds), and intravenously with 10(9) (5 birds). Egg production did not change in hens infected orally, although it was reduced in hens infected intramuscularly for 2-3 weeks post inoculation. For one month, internally infected eggs of which the shells were not contaminated were found: one out of 65 eggs in hens infected orally and three out of 36 eggs in hens infected intramuscularly. This experiment demonstrated the ability of S. Enteritidis isolated from chicks imported from England to cause transovarian infection.

Animals↗

PubMed1993

Long-term shedding of Salmonella enteritidis in chickens which received a contact exposure within 24 hrs of hatching.

Rifampicin-resistant mutant of Salmonella Enteritidis was used for the experiment of long-term excretion in chickens. Thirty-five specific pathogen free chicks within 24 hrs of hatching were placed in contact with 18 chicks inoculated orally with 4 x 10(2) CFU of S. Enteritidis HY-1 Rif within 12 hrs of hatching. After 7 weeks of the contact exposure, samples of cecal droppings were examined for the isolation of S. Enteritidis weekly or biweekly. Twenty-five out of 35 chicks (71%) survived. S. Enteritidis was isolated intermittently at least until 28 weeks after the contact exposure for male chickens and 21 weeks for female chickens although this strain could be isolated only for one or two months from cecal droppings or internal organs of young chickens and laying hens. In order to prevent S. Enteritidis infection in poultry, it was concluded that (1) the contact exposure within 24 hrs of hatching or transovarian infection should be avoided because infection of chicks within 24 hrs of hatching with S. Enteritidis causes the prolonged cecal shedding, and that (2) the isolation of S. Enteritidis from cecal droppings should be repeated because of its intermittent shedding.

Animals↗

PubMed1993

Regulation of cholesterol metabolism in adrenal cortex: effects of apoproteins on cholesterol esterase in rat adrenal glands.

We have investigated the effects of apoproteins on cholesterol esterase (CEase) in rat adrenal glands in order to clarify the mechanism of synthesis of free cholesterol which is the most important substrate for steroidogenesis. We prepared lipid mixtures containing cholesteryl oleate plus apoproteins with and without phosphatidylcholine as a substrate for CEase in order to investigate the effect of the substrate state on CEase. The substrate containing only cholesteryl oleate and apo-HDL increased both acid and alkaline CEase activities. Both acid and alkaline CEase activities were also increased by a substrate containing apo-HDL plus cholesteryl oleate and phosphatidylcholine more than by a substrate containing cholesteryl oleate plus apo-LDL with phosphatidylcholine or cholesteryl oleate with phosphatidylcholine. We have already reported that phosphatidylcholine is an important factor for the regulation of adrenal CEase. Therefore, the present studies show that apoproteins as well as phosphatidylcholine may be important factors for the regulation of adrenal CEase.

Adrenal Cortex↗

PubMed1993

Regulation of cholesterol metabolism in adrenal cortex: comparative studies on cholesterol esterase in human adrenal glands.

We have studied the nature and characteristics of cholesterol esterase (CEase) in human adrenal adenoma and hyperplasia tissues showing Cushing's syndrome, comparing with those in normal tissue. Each tissue demonstrated that two pH optima were found at around 4.5 and 8.0. The results of a subcellular distribution study show that acid and alkaline CEase are mainly located in lysosomes and microsomes, respectively. Our previous data suggested that phosphatidylcholine which was sonicated with cholesteryl oleate as a substrate may play a crucial role in the regulation of CEase in rat adrenal. The effect of phosphatidylcholine was therefore investigated in the present study. Acid CEase in normal tissue was increased in a dose-dependent manner by phosphatidylcholine, but not in the adenoma or hyperplasia tissues. None of those tissues showed any enhancement in alkaline CEase activity when phosphatidylcholine was added to the substrates. It is therefore suggested that the mechanism of regulation of CEase among three different kinds of human adrenals may be different from the data for the effect of phosphatidylcholine. Basal activity of acid CEase in adenoma and hyperplasia was significantly higher than that in normal tissue, and also that of alkaline CEase in hyperplasia tissue was significantly higher than that in normal tissue. Thus it is suggested that such an adrenocortical disorder as Cushing's syndrome due to adenoma and diffuse hyperplasia of the adrenal cortex may possess the nature and characteristics of autonomy of steroidogenesis which seems to be induced by the active metabolism of cholesterol, when compared with normal tissue.

Adenoma↗