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Biomedical subjects

M Nishimura

Publications and source records attributed to M Nishimura.

At least 1,135 records · Page 63Linked to original sources
PubMed1988

Arterial H+ as a determinant for interindividual variability of respiratory chemosensitivity to hypoxia in man.

Ventilatory response to normocapnic progressive hypoxia (A/BSA) was measured in 76 healthy males to examine how arterial blood gases and acid base status are involved in interindividual variability of hypoxic chemosensitivity. A/BSA and HCO3- were significantly higher in Group 1 (26 subjects, mean age = 15.8 +/- S.D. 0.9 years) than those in Group III (26 subjects, mean age = 46 +/- 7.1 years). A/BSA and HCO3- in Group II (24 subjects, mean age = 29.8 +/- 6 years) were in the middle of Groups I and III. Arterial blood gases and H+ were similar among the 3 groups. Arterial H+ correlated inversely with A/BSA (subjects with lower arterial H+ on air had higher hypoxic response) in Group I, while the correlation was positive (subjects with higher H+ on air had higher hypoxic response) in Group III. The correlation was not seen in Group II. PaCO2 and H+ correlated positively in the 3 groups. Intrasubject stability was equivalent among H+, PaCO2, and HCO3- (mean coefficients of variation = 1.81, 1.83, and 1.65, respectively), but smaller than that in PaO2 (3.28%). These results indicate that interindividual variability in hypoxic ventilatory response is related to arterial H+ in adolescent and middle age groups but the relation is opposite between the 2 groups.

Acid-Base Equilibrium↗
PubMed1988

[Cholangiocarcinoma associated with Caroli's disease].

We report on an autopsy case of cholangiocarcinoma associated with Caroli's disease. A 38-year-old woman was admitted to our hospital suffering from epigastralgia. A diagnosis of Caroli's disease was made after CT, US, and ERCP testing. Because of diffuse intrahepatic bile duct dilatation, the patient was treated with antibioticus. In August 1985, her CA 19-9 level was 3,800 U/ml. This data suggested the development of a carcinoma secondary to Caroli's disease, but no tumor in the liver had been detected in the US and CT examinations. The patient died on February 1, 1986, of hepatorenal failure, approximately seven years after her first admission. An autopsy revealed diffuse dilatation of the intrahepatic bile duct (Caroli's disease) with a cholangiocarcinoma.

Adenoma, Bile Duct↗
PubMed1988

[Xanthogranulomatous pyelonephritis: clinical experience of 8 cases].

Xanthogranulomatous pyelonephritis (XGP) is an uncommon form of granulomatous inflammation characterized by destruction of the renal parenchyma and replacement by solid sheets of lipid-laden macrophages. The first report was made by Schlagenhaufer in 1916. Due to diagnostic difficulties, relatively few cases have been reported. However, within the past 20 years, XGP has been recognized with increasing frequency. At present, over 400 cases have been reported. Recently, the computed tomographic (CT) findings of XGP have been described in a few sporadic case reports (1-4). Our clinical experience consists of 8 cases of XGP. The sonographic and computed tomographic findings in our cases are presented along with the correlation with the pathological specimens. We stress the importance of sonography and CT in preoperative planning. Moreover, in our cases we could obtain typical findings on sonography and CT, which enabled us to make a correct preoperative diagnosis. In this report we describe some specific features.

Adult↗
PubMed1988

[Aorto-caval fistula due to a ruptured abdominal aortic aneurysm--an emergency operation following echoic diagnosis].

A successful emergency operation for a 75-year-old man with aorto-caval fistula secondary to rupture of the abdominal aortic aneurysm is reported. A definite diagnosis of aorto-caval fistula was made by echography with characteristic engorgement of the caval vein. Clinical signs and symptoms characterized by lung edema, sudden onset, and circulatory collapse were also noticeable. In the operation, the fistula was closed via inside of the aneurysm with several mattress sutures following control of aortic flow and opening of the aneurysm. Back-flow of the blood through the fistula was readily controlled by finger tip. The aneurysm was replaced conventionally by a vascular prosthesis. There might be several suitable surgical selection available properly to individual case. No delay in surgical treatment depending on definite diagnosis by echography in such urgent condition should be stressed.

Aged↗
PubMed1988

Membrane actions of quinidine sulfate in the rabbit atrioventricular node studied by voltage clamp method.

The effects of quinidine (0.01-20 micrograms/ml) on spontaneous action potentials and membrane current systems of the rabbit atrioventricular node were studied. At therapeutic concentrations, this drug decreased the action potential amplitude, the maximal diastolic potential, the threshold potential as well as the maximal rate of depolarization and showed a negative chronotropic action. Quinidine, at 5 micrograms/ml, decreased the peak slow inward current by 30.2%, increased its time constant of inactivation by 27.3%, shifted the steady-state inactivation curve toward more negative membrane potentials by 2.8 mV and decreased its fully activated current. Quinidine exerted not only resting but also use-dependent blocking actions on the slow inward current. The depression of the action potential upstroke can thus be explained by the reduction in this current. The outward K+ tail current was decreased by 65.4% and its deactivation time constant was increased by 19.0%. These effects may have contributed to the prolongation of the action potential duration, the reduction in the maximal diastolic potential and the slowing of diastolic depolarization. Quinidine shifted the steady-state activation curve for this K+ current toward hyperpolarization by as much as 7.8 mV. It decreased the hyperpolarization-activated inward current by 16.3% and increased its activation time constant by 10.1%, but this current appeared to play a small role in reducing the rate of diastolic depolarization. These observations indicate that, depending upon dose, quinidine has the potential to decrease all of the time- and voltage-dependent ionic currents in atrioventricular nodal cells.

Action Potentials↗
PubMed1987

Electrophysiologic effects of nicorandil, a new antianginal agent, on action potentials and membrane currents of rabbit atrioventricular node.

Electrophysiologic effects of nicorandil, a newly developed coronary vasodilator, on the atrioventricular (AV) node were studied using space-clamped small preparations of the rabbit AV node. At the concentrations of 10(-6), 10(-5) and 10(-4) mol/l, this drug did not cause significant changes in the action potential characteristics including the spontaneous firing frequency, overshoot, maximum diastolic potential, maximum rate of depolarization and action potential duration. When the resting membrane potential of the AV node was obtained by a superfusion with verapamil and then nicorandil was added to the perfusate, no hyperpolarization was observed. This was in sharp contrast to the reported hyperpolarizing action of this drug on the atrial muscle, Purkinje fibres and vascular smooth muscle where the resting potential is much more negative. On the other hand, voltage clamp experiments using double microelectrode techniques revealed that 10(-5) to 10(-4) mol/l nicorandil increased the steady-state outward current at potentials positive to -40 mV and the steady-state inward current at potentials negative to -40 mV. Such a nicorandil-sensitive component of the steady-state current had an average reversal potential of -41.8 mV (n = 5). This component was considered to reflect changes in the time-independent background current, although, at more negative potential levels, it may partially reflect an increase in the hyperpolarization activated inward current (ih). Nicorandil, at the concentrations of 10(-5) and 10(-4) mol/l, increased the slow inward current (isi) by 10.8% (n = 5, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Zinc competitively inhibits calcium-dependent release of transmitter at the mouse neuromuscular junction.

The effect of zinc on the release of transmitter was investigated in preparations of mouse diaphragm by conventional microelectrode techniques. The frequency (F) of miniature end-plate potentials (MEPPs), elevated by Ca2+ in high K+ medium, was reduced by zinc in a concentration-dependent fashion. When the extracellular concentration of Ca2+ ([Ca2+]o) was varied in the absence of zinc, a linear relationship between log(F) and log([Ca2+]o) was obtained. When the effect of zinc was depicted graphically, it was found that zinc shifted the relationship between log(F) and log([Ca2+]o) to the right, with respect to the control in the absence of zinc, without altering the slope. Zinc also reduced the quantal content (m) of end-plate potentials (EPPs). As [Ca2+]o was varied in the absence of zinc, a linear relationship between ln(m) and ln([Ca2+]o) was observed. Zinc shifted this linear relationship between ln(m) and ln([Ca2+]o) to the right, with respect to the control, without altering the slope. Thus, zinc reduced both the asynchronous and the phasic release of transmitter. These results suggest that zinc competes with Ca2+, and this conclusion is confirmed by examination of a modified Lineweaver-Burk plot of the data. Zinc probably inhibits the entry of Ca2+ into the nerve terminals, thereby inhibiting transmitter release.

Action Potentials↗
PubMed1987

Golgi study on brain of macular mutant mouse as a model of Menkes kinky hair disease.

This study was undertaken to elucidate, using the Golgi method, the neuropathological change in the brain of the macular mutant mouse, whose hemizygote (Ml/y) is considered to be a model of Menkes kinky hair disease (MKHD). The hemizygote mice gradually lost weight after 10 days of age and died with emaciation and seizure around day 15. The normal littermate (+/y) was well developed. In the cerebrum, the arborization of pyramidal neurons in the layer V of the Ml/y was the same as that in the +/y on day 10. However, development of arborization in the Ml/y was delayed in comparison with that in the +/y on days 12 and 14. Purkinje cells with several somal sprouts were observed in the cerebellum in both the Ml/y and +/y on day 7. The somal sprouts in the +/y had regressed gradually by day 12, while they were still in the anterior and middle lobes of the Ml/y on day 14. Additionally, the trunks of Ml/y stem dendrites became thicker and a cactus formation was recognized on the branching portion of the dendrites on day 14. Arborization of these abnormal Purkinje cells was distinctly poor compared with that in the +/y. These results suggest that the growth of the neurons is delayed in the Ml/y and simultaneously their cytoskeletal developments are disturbed, especially in the Purkinje cells. There is a close similarity in many respects to the neuropathological change in MKHD.

Animals↗
PubMed1987

Clinico-pathological study on macular mutant mouse.

The macular mutant mouse was clinically and pathologically examined. The hemizygotes began to show white fur color and curly whiskers around postnatal day 3, then seizures and ataxia around day 8, while the normal littermates did not. The hemizygotes also increased weight gradually from birth to day 9, but then showed weight loss and died around day 15 with severe emaciation. These clinical features resembled those in Menkes kinky hair disease. There were no pathological changes in the cerebral cortex in the hemizygotes on day 7. On day 10, two to three clear vacuoles began to appear in a few neurons in the cerebrum. These neurons with vacuoles increased gradually in number and degenerative neurons were also observed by day 14. Ultrastructurally, they corresponded to giant abnormal mitochondria with an electron-lucent matrix and short peripherally located cristae. Other abnormal mitochondria, which were characterized by an electron-dense matrix with tubular or vesicular cristae, were also observed in the cerebral cortical neurons.

Age Factors↗
PubMed1987

Myotonic dystrophy: ambulatory electrocardiogram, electrophysiologic study, and echocardiographic evaluation.

Myotonic dystrophy is frequently associated with functional and anatomic derangements in the myocardium. Ten myotonic dystrophy patients (seven men and three women, ages ranging from 35 to 58 years) were evaluated with a 12-lead ECG, 24-hour Holter monitor recording, invasive electrophysiologic studies, and echocardiographic examination. Nine patients displayed abnormalities in the conduction system. ECG and Holter monitor abnormalities were first-degree atrioventricular block (n = 8), second-degree atrioventricular block (n = 1) (Wenckebach type), complete left bundle branch block (n = 2), left anterior fascicular block (n = 5), left posterior fascicular block (n = 1), sinus bradycardia (n = 6), sick sinus syndrome (n = 2), frequent premature ventricular complexes (n = 4), and ventricular tachycardia (n = 2). Electrophysiologic study abnormalities included AH interval less than or equal to 140 msec (n = 7), AH interval greater than 140 msec (n = 3), HV interval greater than 60 msec (n = 9), and ventricular tachycardia induction (n = 1). Echocardiographic examination revealed mitral valve prolapse (n = 6). We conclude that diffuse conduction abnormalities were seen in a majority of our patients with myotonic dystrophy. Ventricular arrhythmias, including ventricular tachycardia, were seen in some of these patients, and mitral valve prolapse was a frequent finding.

Adult↗
PubMed1987

Subcortical vascular encephalopathy in a normotensive, young adult with premature baldness and spondylitis deformans. A clinicopathological study and review of the literature.

Progressive subcortical vascular encephalopathy (PSVE) usually occurs in elderly individuals, suffering from hypertension. We here describe a male, born of consanguineous parents, who first showed signs of PSVE at the age of 30. Despite the absence of hypertension or known metabolic causes, the degenerative cerebral vascular disease developed progressively. Several cases, surprisingly identical to the one reported here, were traced using Japanese medical records. They are clinically characterized by: early onset of PSVE (at age 25-30), absence of persistent hypertension, diffuse alopecia since youth, spondylitis deformans with early onset, often so severe as to necessitate surgery, and the possible existence of an autosomal recessive transmission. Cases with these features appear to constitute a distinct clinical entity, possibly a new form of premature aging syndrome.

Adult↗
PubMed1987

Light and electron microscopic study on cerebellar cortex of macular mutant mouse as a model of Menkes kinky hair disease.

The macular mouse is a mutant mouse, the hemizygotes of which show clinical and biochemical abnormalities similar to those in Menkes kinky hair disease (MKHD) in humans. The cerebellar cortex of this mutant suckling mouse was examined by light and electron microscopy. In hemizygotes, the Purkinje cells showed a delay in the maturation of dendrites and somatic spines. Somal sprouts, abnormal mitochondria, and filamentous cytoplasmic inclusions were observed on these cells on day 13. Axonal swellings, containing abnormal mitochondrias were also seen in the inner granular layer. These findings correspond with those of MKHD in humans and those of the brindled mouse, another model mouse of MKHD.

Animals↗
PubMed1987

Multiple system atrophy with retinal degeneration in a young child.

A 4-year-old girl with multiple system degeneration and retinal degeneration was presented. There was onset of an ataxic gait at two years and rapid progression of retinal degeneration, myoclonus and cranial nerve palsy. Neuropathological examination revealed severe degeneration of the cerebellar cortex and the pathways of auditory and deep sensation, as well as degeneration of the cerebellar efferent fibers, the striatonigral system, the cerebellar afferent fiber system and lower motor neurons. Cases of young children with spinocerebellar degeneration have been reported in several families of olivopontocerebellar atrophy (OPCA), but degenerative changes in our case were more widespread than those in OPCA cases. The multiple system lesions in the central nervous system and retina of this child are different from those of any other previously reported cases.

Brain Stem↗
PubMed1987

Flash-induced proton release in Rhodopseudomonas sphaeroides spheroplasts.

Proton release by flash excitations was measured with right-side-out vesicles prepared from Rhodopseudomonas sphaeroides by lysozyme-EDTA treatment followed by hypotonic treatment. Absorbance change at 586 nm in the presence of bromcresol purple was measured to monitor the pH change. In the presence of horse heart cytochrome c, which catalyzes the electron transfer from the cytochrome b-c1 complex to the primary electron donor, the single-turnover flash elicited release of about two protons per primary electron donor, which was rereduced rapidly by the added cytochrome c. The halftime of the proton release was about 70 ms at pH 6.3 and at a redox potential of about 150 mV. The rate was considerably lower than that of the electron transfer from the cytochrome b-c1 complex to cytochrome c. However, multiple flashes with intervals of 60 ms caused release of the same amount of protons as that by flashes with longer intervals. This indicated that the proton release itself was rapid, but delocalization was slower. Antimycin A inhibited the proton release, and myxothiazol almost completely abolished it.

Biological Transport↗
PubMed1987

Complete amino acid sequence of cytochrome c551 from Erythrobacter species strain OCh 114.

The complete amino acid sequence of cytochrome c551 isolated from an aerobic photosynthetic bacterium, Erythrobacter sp. strain OCh 114, was determined. The cytochrome molecule was composed of a total of 119 amino acid residues and its molecular weight including heme was calculated to be 13,235. The sequence was (Sequence: see text). Its molecular weight indicates that this cytochrome is of the L-type. Sequence alignment with other bacterial cytochromes c shows that this cytochrome is similar to cytochromes c of Rhodobacter capsulatus, Rhodobacter sphaeroides, and Paracoccus denitrificans, which were grouped into the alpha-3 subcluster from the 16S rRNA sequence analysis.

Amino Acid Sequence↗