Search PubMed⌕ Search

Biomedical subjects

K Mizoguchi

Publications and source records attributed to K Mizoguchi.

At least 37 records · Page 2Linked to original sources
PubMed1999

Identification of an amino acid transporter associated with the cystinuria-related type II membrane glycoprotein.

We identified an amino acid transporter that is associated with the cystinuria-related type II membrane glycoprotein, rBAT (related to b(0,+) amino acid transporter). The transporter designated BAT1 (b(0, +)-type amino acid transporter 1) from rat kidney was found to be structurally related to recently identified amino acid transporters for system L, system y(+)L, and system x(-)C, which are linked, via a disulfide bond, to the other type II membrane glycoprotein, 4F2hc (4F2 heavy chain). In the nonreducing condition, a 125-kDa band, which seems to correspond to the heterodimeric complex of BAT1 and rBAT, was detected in rat kidney with anti-BAT1 antibody. The band was shifted to 41 kDa in the reducing condition, confirming that BAT1 and rBAT are linked via a disulfide bond. The BAT1 and rBAT proteins were shown to be colocalized in the apical membrane of the renal proximal tubules where massive cystine transport had been proposed. When expressed in COS-7 cells with rBAT, but not with 4F2hc, BAT1 exhibited a Na(+)-independent transport of cystine as well as basic and neutral amino acids with the properties of system b(0,+). The results from the present investigation were used to establish a family of amino acid transporters associated with type II membrane glycoproteins.

ATP-Binding Cassette Transporters↗
PubMed1999

Clinicopathological study of an autopsy case with sensory-dominant polyradiculoneuropathy with antiganglioside antibodies.

A previously reported patient presenting sensory-dominant neuropathy with antiganglioside antibodies, bound preferentially to polysialogangliosides including GD1b, was autopsied. While axonal degeneration was predominant in the sural nerve, many demyelinated fibers were present in the spinal roots. Dorsal roots had undergone significant damage. These pathological findings were well correlated with the electrophysiological results showing decreased F-wave conduction velocities and conduction blocks in motor nerves and decreased or absent sensory action potentials in sensory nerves, with distribution of GD1b in nerve tissues such as dorsal root ganglia and paranodal myelin in the ventral and dorsal roots.

Aged↗
PubMed1999

Reaction of neuronal nitric oxide synthase with the nitric oxide spin-trapping agent, iron complexed with N-dithiocarboxysarcosine.

A water-soluble iron complex with N-dithiocarboxysarcosine (Fe-DTCS) has been developed as an ESR spin-trapping agent for NO and successfully applied to ESR imaging of endogenous NO production in mice. We attempted to measure NO produced by purified neuronal NO synthase (nNOS) by this method, but could not detect NO. We speculated that Fe-DTCS inhibits NOS activity. In fact, it markedly inhibited NOS activity with an IC50 value of 9.7 +/- 0.7 microM in the citrulline-formation assay. DTCS alone did not inhibit the activity. An iron complex with N-methyl-D-glucamine dithiocarbamate, a similar spin-trapping agent for NO, also inhibited the activity, with an IC50 value of 25.1 +/- 2.9 microM. Fe-DTCS suppressed cytochrome c and ferricyanide reductase activities of nNOS, and markedly increased nNOS-mediated NADPH oxidation. Concomitantly, it accelerated oxygen consumption caused by activated nNOS. These results suggest that the ESR spin-trapping agent Fe-DTCS inhibits NO synthesis by interfering with the physiological electron flow from NADPH to nNOS heme iron.

Animals↗
PubMed1999

Mechanically elicited nerve root discharge: mechanical irritation and waveform.

OBJECTIVE: Intraoperative monitoring is very important for protecting nerve roots during lumbar surgery for spinal degeneration. Our objective was to evaluate the correlation between the type of mechanical irritation and waveform by mechanically elicited EMGs during the surgery. METHOD: Mechanically elicited EMGs were recorded bilaterally on muscle groups innervated by the lumbar nerve roots in the area of surgery in 24 consecutive patients with lumbar spinal degenerative disease. RESULTS: It was confirmed that surgical irritation produced 3 types of waveforms as discharges from nerve roots; short, waning and continuous discharges. Each waveform was easily elicited mechanically and was sensitively related to the type and strength of mechanical stimulation. CONCLUSION: It was indicated that the mechanical irritation on the root could elicit the nerve root discharge with no post-operative nerve root deficit. It may be useful to monitor the mechanically elicited EMGs during the surgery for spinal degeneration.

Adult↗
PubMed1998

NMDA- and MK801-induced changes in dopamine release are attenuated in kainic acid-lesioned nucleus accumbens of conscious rats: an in vivo microdialysis study.

Local application of N-methyl-d-aspartate (NMDA) and a NMDA receptor antagonist, MK801 through the dialysis membrane into the nucleus accumbens (NAC) caused a significant decrease and increase in extracellular dopamine (DA) in the NAC of conscious rats, respectively. These neurochemical changes were significantly smaller in the kainic acid (KA)-lesioned NAC than in the intact NAC. These findings show that locally applied NMDA and MK801 into the NAC modulate DA release mainly through indirect mechanism involving putative GABA neuron of the NAC.

Animals↗
PubMed1998

[A case of active infective endocarditis in the remission phase of virus-associated hemophagocytic syndrome].

We successfully treated a case of active infective endocarditis in the remission phase of virus-associated hemophagocytic syndrome (VAHS). A 21-year-old man was admitted to our hospital for fever, arthralgia, and general fatigue. His blood cultures revealed staphylococcus epidermidis. He underwent urgent aortic valve replacement and closure of the abscess cavity because of an ineffective antibiotic therapy and a progressive left heart failure. Operative findings showed about 100 ml bloody pericardial effusion, fresh vegetation on the aortic left coronary and non-coronary leaflets, and aortic root abscess just below the left coronary ostium. The aortic root abscess extended to the left ventricular wall between the base of left atrial appendage and the base of main pulmonary artery and was in the state of impending rupture. The left main coronary artery was fully exposed after debridement in the abscess cavity. It was thought that left atrial appendage as a pedicle was useful for filling up the abscess cavity to protect infection.

Adult↗
PubMed1998

Anti-GQ1b IgG antibody activities related to the severity of Miller Fisher syndrome.

The correlation between the activities of anti-GQ1b IgG antibodies in sera of patients with Miller Fisher syndrome and their clinical manifestations was investigated. The clinical severity was analyzed for 16 patients by scoring their symptoms during the peak of the clinical course and 4 weeks after onset. Serum samples were obtained from all the patients within the first 2 weeks of onset and from 12 of them 4 weeks after onset. Samples were immunostained by TLC after which antibody activities were measured by the ELISA. Anti-GQ1b IgG antibody activities reflect the severity of the patients' symptoms, especially ophthalmoplegia. Lessening of symptoms, expressed by the difference in MFS severity scores of the two tests, occurred with the marked decrease in antibodies. Results of cerebrospinal fluid and nerve conduction studies, performed during the first 2 weeks, showed no fluctuation with changes in the clinical symptoms or antibody activities.

Adult↗
PubMed1997

Stimulation of cell-surface urokinase-type plasminogen activator activity and cell migration in vascular endothelial cells by a novel hexapeptide analogue of neurotensin.

To investigate if neurotensin (NT) could induce activation of urokinase-type plasminogen activator (uPA) in vascular endothelial cells, we utilized the acetyl-NT (8-13) analogue, TJN-950, in which the C-terminal leucine is reduced to leucinol. TJN-950 inhibited the binding of 125I-NT to membranes of newborn rat brains and of COS-7 cells transfected with rat NT receptor cDNA, but at 10(4) higher doses than NT (8-13). However, TJN-950 was as effective as NT in inducing the fibrinolytic activity in bovine vascular aortic and human umbilical vein endothelial cells, and enhanced the migration of vascular endothelial cells. Moreover, administration of TJN-950 induced neovascularization in the rat cornea in vivo. TJN-950 had no effect on expression of uPA, plasminogen activator inhibitor-1 or uPA receptor mRNA. The binding of 125I-TJN-950 to cell membranes was blocked by unlabeled uPA and TJN-950, but not the amino-terminal or 12-32 fragment of uPA. TJN-950 may enhance uPA activity in vascular endothelial cells by interacting with the uPA receptor, resulting in induction of angiogenesis.

Animals↗
PubMed1997

The regulatory effect of fermentable sugar levels on the production of leukotoxin by Actinobacillus actinomycetemcomitans.

The relationship between sugar availability and RTX (repeats in toxin) cytotoxin (leukotoxin) production in the periodontopathic bacterium, Actinobacillus actinomycetemcomitans, was investigated using a chemostat. A actinomycetemcomitans 301-b produced significant amounts of leukotoxin in anaerobic fructose-limited chemostat cultures at a dilution rate of 0.15 h-1 and at pH 7.0. When the growth limitation was relieved by pulsing the cultures with 50 or 150 mM fructose (final concentrations), leukotoxin production immediately stopped and the amount of cellular leukotoxin decreased until the culture was returned to fructose-limited conditions. Leukotoxin synthesis was also repressed in the chemostat cultures by pulsing with glucose but not with the non-fermentable sugar analog, alpha-methyl-D-glucoside. Leukotoxin production was also repressed by fructose in chemostat cultures of ATCC 33384, which is generally recognized as a non-leukotoxin-producing or minimally leukotoxic strain.

Aggregatibacter actinomycetemcomitans↗
PubMed1997

Nonfatal suicidal intoxication by clozapine.

CASE REPORT: A rare case of clozapine intoxication of a 23-year-old woman, who intended suicide by its overdose, but recovered under medical treatments, is presented. METHOD: Gas chromatography/mass spectrometry and gas chromatography with nitrogen phosphorus detection were employed for its identification and quantitation, respectively. RESULTS: Clozapine serum concentration reached 3.62 micrograms/mL 3 h after ingestion. The urine concentration 32 h after ingestion was 4.28 micrograms/mL.

Adult↗
PubMed1997

A modified form of a vitamin B12 compound extracted from whey fermented by Lactobacillus helveticus.

The content of vitamin B12 in whey was reduced considerably during lactic acid fermentation, which was analogous to the lactic acid fermentation of milk. This apparent B12 decrease in whey was caused by B12 compounds that were unextractable by conventional extraction with potassium cyanide but that could be extracted by sonication and treatment by proteases such as pepsin and papain. Forms of the extracted B12 compounds were examined by bioautographies with Escherichia coli 215, coupled with cellulose acetate membrane electrophoresis or HPLC, and were identified as adenosylcobalamin, cyanocobalamin, and hydoroxocobalamin. A considerable amount of unidentified B12 was also detected, and this unidentified B12 compound seems to be the principal B12 compound that was unextractable from the cells.

Chromatography, High Pressure Liquid↗
PubMed1996

Oligomeric regulation of gastric H+,K+-ATPase.

The H+,K+-ATPase of intact gastric vesicles has two Km values for ATP hydrolysis, 7 and 80 microM. Irradiation of vesicles with ultraviolet light in the presence of 1 mM ATP resulted in K+-ATPase activity that shows only the low affinity ATP binding. The irradiation stimulated or inhibited proton uptake rate compared with control vesicles at high or low ATP concentrations, respectively. The relation between proton uptake rate and K+-ATPase activity at different ATP concentrations was linear with irradiated vesicles and nonlinear with control vesicles. These results indicate that hydrolysis at the high affinity ATP binding site regulates the energy-transport coupling in negative and positive manners at high and low ATP concentrations, respectively. The complete inhibition of K+-ATPase by a specific proton pump inhibitor E3810 (rabeprazole) (2-([4-(3-methoxypropoxy)-3-methylpyridin-2-yl]methylsulf i nyl)-1H-benzimidazole sodium salt) occurred when E3810 bound to half of the alpha-subunit of H+,K+-ATPase in unirradiated vesicles at both 200 and 10 microM ATP, whereas the complete inhibition of proton uptake occurred when E3810 bound to half or a quarter of the alpha-subunit at 200 or 10 microM ATP, respectively. These results suggest that dimeric interaction between the alpha-subunits is necessary for the enzyme activity at all ATP concentrations and that dimeric or tetrameric interaction is necessary for proton transport at high or low ATP concentrations, respectively.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

ATP-sensitive K+ channel openers block sulpiride-induced dopamine release in the rat striatum.

In vivo brain microdialysis was used to investigate the role of ATP-sensitive K+ (KATP) channel openers in dopamine release regulated by dopamine autoreceptors in the rat striatum. Local infusion of two KATP channel openers, nicorandil (10(-5)-10(-3) M) and cromakalim (10(-5)-10(-3) M), into the striatum thorough the dialysis membrane produced dose-dependent decreases in extracellular concentrations of dopamine. Local application of the dopamine D2 receptor antagonist, (-)-sulpiride (10(-5) M), produced significant increases in extracellular concentrations of dopamine. Both nicrorandil (10(-5) M) and cromakalim (10(-4) M) blocked significantly (-)-sulpiride (10(-5) M)-induced increases in dopamine levels in the striatum. These results suggest that activation of KATP channels in the striatum causes decreases in endogenous dopamine release in vivo. Furthermore, the sulpiride-induced increases in dopamine levels caused by blocking the tonic activation of dopamine autoreceptors were inhibited by activation of KATP channel. These data indicate that KATP channels may be present in nigrostriatal dopaminergic terminals and that striatal dopamine autoreceptors inhibit dopamine release tonically by activation of KATP channels.

Adenosine Triphosphate↗
PubMed1996

Blue light induced ADP ribosylation of 38 and 56 kDa proteins in the soluble fraction of mycelia of Neurospora crassa.

Soluble fractions prepared from the mycelia of wild type (74-OR23-1A) and band (bd) exhibited an increase in the rate of the ADP ribosylation of a 38 kDa protein from nicotinamide adenine [32P]dinucleotide ([32P]NAD) in the presence of 10(-7) M riboflavin caused by blue light irradiation in vitro. The soluble fraction was mixed with a reaction mixture containing 5 microCi [32P]NAD at 0 degree C for 20 s and then it was irradiated with blue light (420 nm, 42 mumol m-2 s-1) for 12.5, 25, 50, 100, 200 or 400 s at 0 degree C or for 100 s with photon irradiance of 0.42, 4.2, 6.4 or 42 mumol m-2 s-1. Immediately after irradiation, the reaction was stopped and analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. An increase in the ADP ribosylation of the 38 kDa protein could be detected within 100 s of irradiation, and the enhancement in the rate of ADP ribosylation of the 38 kDa protein was proportional to the increase in the photon irradiance. By the irradiation with blue light for 200 or 400 s, the ADP ribosylation of a 56 kDa protein could also be detected. Analysis by two-dimensional gel electrophoresis of proteins after ADP ribosylation of them revealed that the 38 kDa proteins displayed at least four radioactive protein spots and the 56 kDa protein a single radioactive protein spot. Soluble fractions of mycelia prepared from blind mutants wc-1, wc-2, delta ps15-1, lis-1, lis-2 and lis-3 exhibited also the enhancement of the ADP ribosylation of the 38 kDa protein by blue light irradiation, and at least wc-1, delta ps15-1, lis-1 and lis-2 displayed a similar blue light response in the 56 kDa protein.

Adenosine Diphosphate Ribose↗
PubMed1996

Point mutation in the alpha-galactosidase A gene of atypical Fabry disease with only nephropathy.

A point mutation in exon 6 of the alpha-galactosidase A gene (alpha-GAL A) was found in a Japanese hemizygous male without typical manifestations of Fabry disease other than renal involvement. This 45-year-old man developed moderate proteinuria and was diagnosed with Fabry disease on the basis of renal histologic findings and prominent decreases in alpha-GAL A activity in his plasma, urine, leukocytes, and skin fibroblasts. Determination of the cDNA sequence of his alpha-GAL A gene revealed substitution of a G to A in codon 301, resulting in a glutamine rather than an arginine residue. Our case is unique in that this patient only demonstrated renal manifestations while all other reported patients with atypical Fabry disease, including a case with the identical point mutation, present with a cardiomyopathy. Direct DNA sequencing of exon 6 and measurement of alpha-GAL A activity among the patient's family confirmed that the mutation was transmitted from his mother.

Biopsy↗
PubMed1996

[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm].

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.

Aged↗