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Biomedical subjects

T Mizutani

Publications and source records attributed to T Mizutani.

At least 127 records · Page 7Linked to original sources
PubMed2000

Arterial dissections of penetrating cerebral arteries causing hypertension-induced cerebral hemorrhage.

OBJECT: For the past 130 years, it has been believed that hypertension-induced cerebral hemorrhages are the result of ruptures of microaneurysms or ruptures of arteries that have degenerative changes. The majority of previous investigations have focused on autopsied brain. In this study, the authors attempted to verify the cause of hypertension-induced cerebral hemorrhage by using surgical specimens of the penetrating arteries responsible for the hemorrhages. METHODS: Between 1997 and 1999, the authors performed pathological studies in surgical specimens of lenticulostriate arteries that had been confirmed during microsurgery to be the cause of hypertension-induced hemorrhage of the putamen. Nineteen lenticulostriate arteries were collected from 12 patients. Fifteen of these arteries were verified as the pathological causes of hemorrhage. They included six arterial dissections, six arterial ruptures with substantial degenerative changes, and three arterial ruptures with few degenerative changes. The pathological findings in the lenticulostriate artery dissections were similar to those of typical arterial dissections in major cerebral arteries. CONCLUSIONS: To the best of the authors' knowledge, arterial dissections of lenticulostriate arteries have not been identified as a cause of hypertension-induced cerebral hemorrhages. When penetrating arteries are included as causative vessels, cerebral arterial dissections may be much more common than previously thought.

Aged↗
PubMed2000

[Intracellular calcium kinetics after odorant stimulus in olfactory receptor cells isolated from mice].

cAMP and IP3 act as secondary messengers in olfactory signal transduction and when activated, stimulate calcium levels in olfactory receptor cells. Little is known however, about the causal mechanism. We studied calcium kinetics in mouse olfactory receptor cells after odorant stimuli. Olfactory receptor cells were isolated from female BALB/c mice, treted with trypsin, and stained with Fura-2/AM. Changes in intracellular Ca2+ concentrations in stained cells were measured with a fluorescent microscopic image-processing device (ARGUS-50; Hamamatsu Photonix, Japan). We found that intracellular Ca2+ concentrations rose after exposure to a set of odorants, including 3-ethoxy-4-hydroxy-benzaldehyde, caprylic acid, heptanoic acid, nonanoic acid, eugenol, phenethyl alcohol, and n-amyl acetate. Adding 2', 5'-dideoxyadenosine, a cAMP inhibitor, beforehand suppressed olfactory receptor cell response to odorants. Intracellular Ca2+ concentrations increased substantially in response to stimulation by odorants in calcium-free Ringer's solution, but only a slight increase was seen in intracellular calcium concentration in response stimulation by a high concentration of K+ (145.6 mM) in calcium-free Ringer's solution. The increase in intracellular Ca2+ concentration after odorant stimuli was suppressed when olfactory receptor cells were pretreated with ryanodine, which releases Ca2+ from intracellular stores. These findings suggest that elevated Ca2+ concentrations may be involved in releasing Ca2+ from intracellular calcium stores in mouse olfactory receptor cells, in which cAMP functions as a secondary messenger in olfactory signal transduction.

Animals↗
PubMed2000

Acetazolamide reactivity in atherothrombotic, cardioembolic and lacunar infarctions.

Ten cases of atherothrombotic brain infarction, 10 cases of cardioembolic brain infarction, 10 cases of lacunar brain infarction, 10 cases of transient ischemic attack (TIA) and 10 age-matched controls were studied. The cerebral blood flows in the cerebral cortex and cerebral white matter were significantly lower in the atherothrombotic, cardioembolic and lacunar infarction groups than in the TIA and control groups. The acetazolamide reactivity in the cerebral cortex was significantly lower in the atherothrombotic and lacunar infarction groups than in the cardioembolic, TIA and control groups. The rate of association of hypertension was significantly higher in the atherothrombotic, lacunar and TIA groups than in the cardioembolic and control groups. Plasma fibrinopeptide A, platelet factor 4 and beta-thromboglobulin concentrations were higher in the atherothrombotic, cardioembolic and lacunar groups than in the TIA and control groups. The present study suggests that the degree of thrombolysis and platelet activation is less in TIA than in cerebral infarction and that underlying cerebral arteriosclerosis is more severe in atherothrombotic and lacunar infarction than in cardioembolic infarction.

Acetazolamide↗
PubMed2000

Cerebral blood flows in the acute and chronic stages of cerebral infarction.

Regional cerebral blood flows (rCBFs) were studied in the acute and the chronic stages of 8 patients with supratentorial cerebral infarction. In 2 patients with cardioembolic infarction, the rCBF increased in one patient and decreased in the other during the chronic stage. This decrease was explained by the risk factors of the latter patient because the patient had more risk factors than the former patient with increased rCBF. In 6 patients with lacunar infarction, the rCBF increased in 2 patients and decreased in 4 during the chronic stage. In all the patients with decreased rCBF, the number of lacunar infarction and/or the degree of leuko-araiosis on MRI increased during the chronic stage. Therefore, the decrease in rCBF during the chronic stage in lacunar infarction is considered to be due to the increase in the number of lacunar infarction, the increased degree of leuko-araiosis or both.

Acute Disease↗
PubMed2000

Diaschisis and acetazolamide reactivity in brainstem infarction.

Regional cerebral blood flows (rCBF) were studied in 6 patients with lateral medullary infarction and 4 patients with pontine infarction, using stable xenon computed tomography method. In lateral medullary infarction, the rCBF and acetazolamide reactivity were decreased in the ipsilateral cerebellum and the rCBF was decreased with normal acetazolamide reactivity in the contralateral frontal lobe in one patient accompanying ipsilateral cerebellar infarction. rCBF was decreased with normal acetazolamide reactivity in the cerebellum in 3 patients, and both rCBF and acetazolamide reactivity were decreased in the whole brain in 2 patients. In pontine infarction, rCBF was decreased in ipsilateral frontal lobe and contralateral cerebellum in one patient, rCBF was decreased in the cerebellum with normal acetazolamide reactivity in the other patients. The hypoperfusion with normal acetazolamide reactivity was considered to be due to diaschisis. The rCBF decrease in the remote areas in patients with brainstem infarction was considered to be due to diaschisis or underlying arteriosclerosis.

Acetazolamide↗
PubMed2000

[Diffuse left ventricular hypokinesis mimicking dilated cardiomyopathy with multi-vessel coronary vasospasm].

We investigated 7 patients with multi-vessel coronary vasospasm (> or = 75%) and diffuse left ventricular hypokinesis by coronary angiography and echocardiography. Four patients were male and 3 were female and mean +/- SD age was 63.0 +/- 11.2 years. Chief complaints were dyspnea in 3 patients, and chest pain, appetite loss, palpitation and general fatigue in one each. New York Heart Association functional classification was I in one patient, II in 5 and III in one. Mean heart rate was 73.9 +/- 11.6 beats/min. Initial echocardiography showed left ventricular end-diastolic diameter (LVDd) 54.4 +/- 5.5 mm, left ventricular end-systolic diameter (LVDs) 43.7 +/- 4.8 mm and percentage fractional shortening (%FS) 19.7 +/- 2.6%. The left ventricle was not remarkably enlarged despite poor contraction. Coronary vasospasm was induced after acetylcholine injection into the right coronary artery in 6 patients, left anterior descending artery in 7 and circumflex artery in 5. Four patients developed three-vessel coronary vasospasm. Three patients underwent endomyocardial biopsy which showed non-specific mild fibrosis. They were treated with nitrates and/or Ca-antagonists to prevent coronary vasospasm. Follow-up echocardiography was performed in 6 patients after 8.5 +/- 6.6 months. Echocardiography revealed marked improvement in left ventricular contraction (LVDd 49.7 +/- 4.6 mm, LVDs 35.8 +/- 4.4 mm, p < 0.05; %FS 27.9 +/- 4.5%, p < 0.05). These data suggested that left ventricular dilation was not prominent despite the poor contractility in patients with multi-vessel coronary vasospasm and diffuse left ventricular hypokinesis. The left ventricular dysfunction might be hibernating myocardium produced by multiple episodes of coronary vasospasm. Anti-vasospastic agents were effective in these patients.

Acetylcholine↗
PubMed2000

[Diagnostic criteria of diffuse Lewy body disease].

DLBD is also called Dementia with Lewy bodies(DLB) which was proposed by the consortium on DLB international workshop(CDLB) in 1995. CDLB criteria of clinical diagnosis contain progressive cognitive decline as a mandatory feature, and fluctuating cognition, recurrent visual hallucinations and parkinsonism as 3 core features. Supportive features include repeated falls, syncope, transient loss of consciousness, neuroleptic sensitivity, and systematized delusions. CDLB pathologic criteria include the presence of Lewy bodies as the only essential feature, and associated features included Lewy-related neurites, senile plaques, neurofibrillary tangles, and regional neuronal loss in the areas vulnerable to Parkinson's disease. Lewy bodies are counted and scored from 0 to 2 in 5 designated cortical areas. Total Lewy body score of 7-10 indicates DLBD.

Brain↗
PubMed2000

[A case report of central respiratory failure due to hemimedullary syndrome].

A hemimedullary infarction, in which both medial and lateral medullary infarctions occur simultaneously, is a rare cerebrovascular disease. Pontomedullary lesions often cause central respiratory failure, and the majority of central respiratory failures are due to bilateral pontomedullary lesions. We report a 66-year-old man with central respiratory failure due to a hemimedullary infarction detected by magnetic resonance imaging. He was admitted to our hospital on March 7, 1998, because of a sudden onset of dysarthria, and both numbness and weakness on his left side. Soon after arriving at the hospital, his spontaneous respiration ceased. Therefore, he was intubated and artificial ventilation was started. Pertinent neurological abnormalities on admission consisted of dysarthria, dysphagia, right Horner's sign, right gaze evoked horizontal nystagmus, right soft palate palsy, and tongue deviation to the right. In addition, left hemiparesis, left Babinski's sign, sensory impairment on the left side including the face, and central respiratory failure were noted. Although voluntary respiration recovered in 12 days, sleep apnea continued for 5 months, which was considered to be due to the automatic respiratory failure. An important feature of this patient was that the hemimedullary infarction caused the central respiratory failure. To our knowledge, this is the third patient whose central respiratory failure occurred because of a hemimedullary infarction.

Aged↗
PubMed1999

Control of the expression of luteinizing hormone receptor by local factors in rat granulosa cells.

To identify the mechanisms underlying the hormone-dependent induction and maintenance of luteinizing hormone receptor (LH-R) in rat granulosa cells, the effect of follicle-stimulating hormone (FSH) and local factors on the LH-R mRNA levels were studied. LH-R mRNA levels of the cells incubated with FSH decreased rapidly after medium removal, and readdition of FSH with the fresh medium did not restore these levels. On the other hand, 8-bromoadenosine 3,5-cyclic monophosphate significantly enhanced the expression of LH-R mRNA after medium removal, while the level of LH-R mRNA was lower than that of the cells replaced by original medium including FSH. In addition, the incubation with 8-Br-cAMP produced dose-dependent responses for LH-R mRNAs and enhanced the activity of 1379 bp of the LH-R 5'-flanking region, while the level of LH-R mRNA decreased 3 days after medium removal. Further studies were undertaken to assess the role of factors in maintaining the LH receptor once induced by FSH. Since FSH and cAMP increase follistatin production in granulosa cells, we examined the effect of follistatin on LH-R induction in the presence of activin and FSH. Activin induced LH-R in the presence of FSH significantly, and follistatin antagonized this effect in a dose-dependent manner. However, insulinlike growth factor-I (IGF-I) induced LH-R mRNA in the presence of FSH even after medium change. IGF-I might be one of the important factors that act in the medium to maintain LH-R levels in granulosa cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1999

Regulation of cAMP responsive element binding modulator isoforms in cultured rat ovarian granulosa cells.

A pituitary glycoprotein hormone FSH stimulates ovarian granulosa cells to induce ovarian follicular development. In this study we identified rat ovarian genes that were rapidly induced by FSH in the cultured rat granulosa cells by means of subtraction cloning. Complementary DNA clones encoding cAMP responsive element binding modulator (CREM) were identified as one of the FSH inducible genes. Northern blotting and reverse transcription and polymerase chain reaction (RT-PCR) analyses revealed that only the repressor type of CREM gene products, ICER (inducible cAMP early repressor) isoforms, were induced by FSH treatment in cultured rat granulosa cells. The induction of ICER by FSH was mimicked by reagents known to increase intracellular cAMP levels, indicating that the induction is through cAMP and protein kinase A signal transduction system. Induction of ICER was also confirmed as the protein levels. Electrophoretic mobility shift assay of granulosa cell extracts with a radiolabeled double stranded oligonucleotide corresponding to somatostatin cAMP responsive element also revealed that only the ICER proteins were induced by FSH treatment, whereas levels of CREM proteins were nearly constant regardless of the FSH treatment. Our present study demonstrates that FSH-induced and cAMP-mediated induction and attenuation of transcriptional responses by CREM gene products may be a key mechanistic component for the granulosa cell differentiation and proliferation.

Animals↗
PubMed1999

Protection against tick-borne encephalitis virus isolated in Japan by active and passive immunization.

In order to establish a firm preventive measure for tick-borne encephalitis (TBE) in Japan, we evaluated the immune response of European vaccine against Japanese TBE virus strain (Oshima 5-10) for man and mouse. Furthermore, the efficacy of pre- and post-exposure protection by a polyclonal rabbit anti-TBE virus serum was examined in the mouse model. 80% of vaccinees seroconverted against Oshima 5-10 strain after the 2nd immunization of vaccine and the remaining 20% seroconverted after the 3rd immunization. Two persons with pre-existing anti-Japanese encephalitis virus (JEV) antibodies showed low immune responses against TBE virus. In mouse vaccination and challenge tests, efficient protection was observed in mice challenged with lethal doses of Oshima 5-10 strain as well as those observed in mice with the Western subtype and the Far Eastern subtype of TBE strains. Pre-exposure treatment with rabbit anti-TBE virus serum provided complete protection against lethal challenge with Oshima 5-10 strain. For post-exposure treatment with the antibody, significant protection was observed when mice were treated 24 h after virus challenge, whereas it was not observed 48 h after virus challenge. reserved.

Animals↗
PubMed1999

Modulation of halobenzene-induced hepatotoxicity by DT-diaphorase modulators, butylated hydroxyanisole and dicoumarol: evidence for possible involvement of quinone metabolites in the toxicity of halobenzenes.

Recent metabolic studies have demonstrated the importance of reactive intermediates like quinones or semiquinone radicals in the covalent binding of halobenzenes to liver protein. The current studies were designed to examine if quinone intermediates are involved in the toxicity of hepatotoxic halobenzenes, bromobenzene (BB) and 1,2,4-trichlorobenzene (1,2,4-TCB). Two-electron reduction of the quinone intermediates by DT-diaphorase is considered to be a detoxication pathway since the resulting hydroquinone may be readily conjugated and excreted. Mice were pretreated with butylated hydroxyanisole (BHA; 0.5% in the diet, for 3 days), an inducer of DT-diaphorase, or dicoumarol (0.3 mmol/kg, p.o.), an inhibitor of this enzyme. The mice were then given BB (2.5 or 3.5 mmol/kg, i.p.) or 1,2,4-TCB (0.75 or 1.5 mmol/kg, i.p.). Dietary BHA markedly suppressed the hepatotoxicity caused by both BB and 1,2,4-TCB while dicoumarol significantly enhanced it, as judged by serum alanine aminotransferase activity. When mice were treated with BB at different times after the end of dietary BHA exposure, the degree of the protection against the hepatotoxicity appears to correlate to the extent of the induction of DT-diaphorase activity by BHA pretreatment. BHA pretreatment failed to protect against carbon tetrachloride-induced hepatotoxicity. These results seem to provide evidence for the involvement of the quinone metabolites in BB- and 1,2,4-TCB-induced hepatotoxicity and for the protective role of DT-diaphorase against the toxicity.

Alanine Transaminase↗
PubMed1999

Pathogenicity of tick-borne encephalitis virus isolated in Hokkaido, Japan in mouse model.

The pathogenic characteristics of tick-borne encephalitis (TBE) virus strain (Oshima 5-10) isolated from a sentinel dog in Hokkaido, Japan, was compared by use of a mouse model with several inoculation routes to other strains of TBE virus (the Far Eastern subtype; Sofjin strain and the Western subtype; Hochosterwitz strain) and TBE complex virus (Langat virus; TP-21 strain). The degree of neuroinvasiveness of the strains in mice subcutaneously (s.c.) inoculated was Sofjin equaled Hochosterwitz which was greater than Oshima and TP-21, respectively. Neurovirulence, as determined after intracerebral inoculation was Sofjin > Oshima = Hochosterwitz > TP-21. Virus replication in the brains of mice s.c. or intracerebrally inoculated with Oshima strain was slower and of lower titer than that of Sofjin strain. Histopathological findings indicated that subarachnoid infiltration of mononuclear cells prior to necrosis of the cerebrum was characteristic in Oshima strain. These findings indicated that the Oshima strain possessed a pathogenic potential common to TBE viruses and is less virulent for mice as compared with the two other TBE strains examined.

Animals↗
PubMed1999

Purification and some properties of two enzymes from rat liver cytosol that catalyze carbonyl reduction of 6-tert-butyl-2, 3-epoxy-5-cyclohexene-1,4-dione, a metabolite of 3-tert-butyl-4-hydroxyanisole.

6-tert-Butyl-2,3-epoxy-5-cyclohexene-1,4-dione (TBE), a metabolite of 3-tert-butyl-4-hydroxyanisole, was converted to 6-tert-butyl-2, 3-epoxy-4(R)-hydroxy-5-cyclohexen-1-one ((4R)-TBEH) and 6-tert-butyl-2,3-epoxy-4(S)-hydroxy-5-cyclohexen-1-one ((4S)-TBEH) by TBE-reducing enzymes in rat liver cytosol. Two TBE-reducing enzymes (TBE-R1 and TBE-R2) were purified 18- and 117-fold, respectively, to apparent homogeneity from rat liver cytosol using DEAE-Sephacel, Blue Sepharose CL-6B, hydroxylapatite, and Sephadex G-100 column chromatography. Gel filtration and sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated that both enzymes were monomeric. The purified TBE-R1 and TBE-R2 had molecular weights of 37 and 35 kDa and isoelectric points of 6.5 and 5.8, respectively. Both enzymes had an optimum pH of about 5.5 with TBE as substrate. TBE-R1 utilized NADH or NADPH equally as cofactor, and the Km values of NADH and NADPH for TBE with TBE-R1 were estimated to be 15 and 29 microM, respectively. On the other hand, TBE-R2 specifically utilized NADPH and the Km value for TBE was estimated to be 92 microM in the presence of NADPH. Both enzymes reduced aromatic aldehydes, ketones, and quinones at higher rates. In addition, TBE-R2 reduced and oxidized 3-ketosteroids at a higher rate in the presence of NAD(H) and/or NADP(H). Both enzyme activities were inhibited by quercitrin or p-chloromercuribenzoic acid, but little inhibition was observed with phenobarbital or pyrazole. Dicoumarol inhibited significantly TBE-R1 activity but not TBE-R2 activity. In the conversion of TBE to TBEH, TBE-R1 preferentially reduced TBE to (4R)-TBEH, whereas TBE-R2 preferred the reduction of TBE to (4S)-TBEH.

Alcohol Oxidoreductases↗
PubMed1999

Selenophosphate as a substrate for mammalian selenocysteine synthase, its stability and toxicity.

The mechanism of selenocysteine synthesis on tRNASec in mammals was previously studied by means of HSe- as a Se donor to synthesize selenocysteine. It has been recently established that HSe- in E. coli is activated by ATP to become selenophosphate (SeP). In this study, we provide evidence that [75Se]selenocysteine is produced by bovine selenocysteine synthase from Ser-tRNASec and [75Se]Sep, synthesized from elemental 75Se and Tris(trimethylsilyl)phosphite. We also studied the stability of SeP by NMR measurement. SeP was stable during storage under nitrogen at -80 degrees C for 3 months in 0.2 M Hepes buffer at pH 6.8. However, SeP decomposed at 0 degree C in air (half life 32 hrs) or at 22 degrees C under nitrogen (half life 30 hrs) at pH 6.8. The half lives of SeP at -19 degrees C in air and at 0 degree C under nitrogen at pH 6.8 were 740 and 840 hrs, respectively. At pH 4 under nitrogen at 22 degrees C, the half life was 240 hrs. The half life was only 9.2 hrs at pH 9 under nitrogen at 0 degree C. Thus, SeP was proved to be stable at low temperature, under acidic and anaerobic conditions, but labile under neutral and alkaline conditions. The LD50 of SeP administered i.p. to mice was 37.5 mg/kg body weight.

Air↗