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Biomedical subjects

Y Kamata

Publications and source records attributed to Y Kamata.

At least 55 records · Page 3Linked to original sources
PubMed1999

Spontaneous recurrence of methampetamine psychosis: increased sensitivity to stress associated with noradrenergic hyperactivity and dopaminergic change.

We studied the factors precipitating spontaneous recurrences of methamphetamine (MAP)-induced paranoid-hallucinatory states (referred to as "flashbacks") in 28 flashbackers, along with 18 non-flashbackers with a history of MAP psychosis. Plasma levels of catecholamines and their metabolites were assayed in the 28 flashbackers, the 18 non-flashbackers, 8 subjects with persistent MAP psychosis, and 33 normal controls (22 MAP users and 11 non-users). The flashbackers had been exposed to significantly higher numbers of stressful events, and/or MAP-induced frightening paranoid-hallucinatory states during previous MAP use, than the non-flashbackers. Factors triggering the flashbacks met the DSM-III-R criteria for a mild psychosocial stressor. During flashbacks, plasma norepinephrine levels increased and plasma levels of 3-methoxytyramine, which is an indicator of dopamine release, showed a smaller increase. It follows that stressful experiences together with MAP use may induce sensitization to mild psychosocial stressors. Noradrenergic hyperactivity and some degree of increased dopamine release may be involved in this process. Stress sensitization may elicit memories of MAP psychosis associated with stressful experiences in response to mild psychosocial stressors, leading to the occurrence of flashbacks. Sensitization to stress associated with noradrenergic hyperactivity, involving increased dopamine release may be central to spontaneous recurrences of MAP psychosis.

Adaptation, Psychological↗
PubMed1999

[Intra-aortic balloon occlusion of the descending thoracic aorta for intra-abdominal hemorrhage].

Intra-aortic balloon occlusion (IABO) of the descending aorta is beneficial to rescue patients in shock following traumatic intra-abdominal hemorrhage. The authors experienced four such patients who had received IABO of the descending thoracic aorta to maintain hemodynamics prior to operation. After hemostasis, the balloon was deflated gradually. Releasing the balloon in the operating room was, however, abandoned in two patients because of severe deoxygenation and life threatening arrhythmia. In the other two patients, the balloon was successfully deflated during the operations; one of them died a week later from multiple organ failure. We conclude that shortening the aortic occlusion time as well as the treatments for adverse effects of balloon release are important in the anesthetic management of patients receiving IABO.

Abdomen↗
PubMed1998

Solid phase synthesis of oligomannopeptoids that mimic the concanavalin A-binding trimannoside.

Oligomannopeptoids from the dimer to the hexamer were produced by solid phase synthesis and their abilities to bind to concanavalin A (ConA) were assessed. The assessment indicated similarity between the oligomannopeptoids and the naturally occurring oligomannosides in the enthalpy of the binding and the valence number vs binding strength relationship, encouraging the use of the oligomannopeptoids as oligomannoside mimics.

Binding, Competitive↗
PubMed1998

Ganglioside GT1b as a complementary receptor component for Clostridium botulinum neurotoxins.

Clostridium botulinum type B neurotoxin (BoNT/B) recognizes a complex of synaptotagmin II and ganglioside GT1b or GD1a as the high-affinity toxin binding site. Recombinant deletion mutants of synaptotagmin II allowed us to demonstrate that the N-terminal domain including the transmembrane region retains BoNT/B binding activity while the C-terminal domain is not involved in constituting the BoNT/B receptor. BoNT/B binding to reconstituted lipid vesicles containing synaptotagmin II and gangliosides showed that GT1b and GD1a confer the difference in the maximum binding capacity but not in the dissociation constant. The direct binding of GT1b to the deletion mutants revealed that the transmembrane region is required to bind GT1b, suggesting that synaptotagmin II binds to the ceramide portion of gangliosides within the plasma membrane. A monoclonal antibody against GT1b effectively inhibited not only BoNT/B binding to the reconstituted lipid vesicles and brain synaptosomes but also type A BoNT (BoNT/A) binding to brain synaptosomes. In addition, the monoclonal antibody antagonized the action of both BoNT/A and BoNT/B on synaptic transmission of rat superior cervical ganglion neurons. These results suggest that GT1b functions as a component of the receptor complex.

Animals↗
PubMed1998

Inhibition by diazepam of ketamine-induced hyperlocomotion and dopamine turnover in mice.

PURPOSE: To investigate the effects of the benzodiazepine diazepam on ketamine-induced hyperlocomotion and dopamine turnover. METHODS: Adult male ddY mice were used (n = 218). Locomotor activity was measured with four circular activity cages equipped with three photocell sensor units. Interruptions by a mover of the infrared light Peams were recorded on electromechanical counters, and automatically printed every 10 min for three hours after the ketamine injection. All drugs were administered intraperitoneally (i.p.). The concentrations of dopamine and its metabolites in discrete brain regions were measured by high performance liquid chromatography with electrochemical detection. RESULTS: Ketamine (30 mg.kg-1) increased total locomotor activity counts for three hours to 442% of control in mice (P = 0.0001). Diazepam, 3 and 10 mg.kg-1, inhibited, in a dose-dependent fashion, this ketamine-induced hyperlocomotion by 26% (P = 0.0111) and 59% (P = 0.0001), respectively. Regional brain dopamine assays revealed that ketamine (30 mg.kg-1) increased the homovanillic acid:dopamine ratio (one indicator of dopamine turnover) to 121% of control in the nucleus accumbens (P = 0.0065) and to 111% in the striatum (P = 0.0135) at peak locomotion. Diazepam, 3 and 10 mg.kg-1, returned this increase in dopamine turnover produced by ketamine to control levels both in the nucleus accumbens (P = 0.0061 and P = 0.0117, respectively) and in the striatum (P = 0.0004 and P = 0.0047, respectively). CONCLUSION: These results suggest that the inhibition by diazepam of ketamine-induced hyperlocomotion may be related to its ability to suppress the activation of dopamine neurons in the nucleus accumbens and striatum.

Anesthetics, Intravenous↗
PubMed1998

Characterization of Clostridium botulinum type B neurotoxin associated with infant botulism in japan.

The neurotoxin of strain 111 (111/NT) associated with type B infant botulism showed antigenic and biological properties different from that (Okra/NT) produced by a food-borne botulism-related strain, Okra. The specific toxicity of 111/NT was found to be about 10 times lower than that of Okra/NT. The monoclonal antibodies recognizing the light chain cross-reacted with both neurotoxins, whereas most of the antibodies recognizing the carboxyl-terminal half of the heavy chain of Okra/NT did not react to 111/NT. Binding experiments with rat brain synaptosomes revealed that 125I-labeled 111/NT bound to a single binding site with a dissociation constant (Kd) of 2.5 nM; the value was rather lower than that (0.42 nM) of 125I-Okra/NT for the high-affinity binding site. In the lipid vesicles reconstituted with ganglioside GT1b, 125I-Okra/NT interacted with the amino-terminal domain of synaptotagmin 1 (Stg1N) or synaptotagmin 2 (Stg2N), fused with the maltose-binding protein, in the same manner as the respective full-length synaptotagmins, and the Kd values accorded with those of the low- and high-affinity binding sites in synaptosomes. However, 125I-111/NT only exhibited a low capacity for binding to the lipid vesicles containing Stg2N, but not Stg1N, in the presence of ganglioside GT1b. Moreover, synaptobrevin-2, an intracellular target protein, was digested to the same extent by the light chains of both neurotoxins in a concentration-dependent manner. These findings indicate that the 111/NT molecule possesses the receptor-recognition site structurally different from Okra/NT, probably causing a decreased specific toxicity.

Animals↗
PubMed1998

Quantitative analysis of lipid deposits from Schnyder's corneal dystrophy.

AIM: To report the quantitation of the lipid composition of a corneal button from a Japanese woman in her 60s with clinically and histopathologically proved Schnyder's corneal dystrophy. METHODS: Total lipids extracted from the corneal button of the patient were analysed by the method of thin layer chromatography flame ionisation detection. Two different solvent systems were used for neutral lipid analysis and phospholipid analysis. Results were compared with three age matched corneal buttons obtained from cadaveric eyes. RESULTS: The lipids that accumulated in the cornea in Schnyder's dystrophy consisted mainly of unesterified cholesterol and phospholipids. The analysis of phospholipids showed sphingomyelin to be the predominant phospholipid in the patient's cornea. CONCLUSION: Findings suggest that this disorder involves a disturbance of the metabolism of cholesterol and/or sphingomyelin metabolism that is limited to the cornea.

Cholesterol↗
PubMed1998

Whole-blood flow-cytometric analysis of eosinophil EG2 expression as a marker of the pathological conditions of asthma.

UNLABELLED: Using a simple technique detecting the eosinophil fraction in whole-blood flow cytometry, we measured intracellular antigen EG2 (a monoclonal antibody to eosinophil cationic protein) in 56 asthmatic patients (26 during an attack and 30 during an asymptomatic period) and 22 healthy subjects to determine whether EG2 reflects the pathological stages of allergy. METHODS: In brief, preparations of the sample included the following procedures: (1) hemolyzation of heparinized or EDTA-mixed whole blood; (2) fixation of white blood cells with 0.4% parabenzoquinone (PBQ) or paraformaldehyde (PFA); (3) permeabilizing the cell membrane with n-octyl-beta-D-glucopyranoside, and (4) staining of intracellular EG2 antigen with monoclonal EG2 antibody and FITC-labeled secondary antibody. RESULTS: In PBQ-fixed samples, there was a clearer boundary of the eosinophil fraction with a higher yield and purity than in those fixed with PFA. The number of EG2-positive eosinophils was significantly greater in subjects during attacks than in asymptomatic patients. In addition, when compared with normal controls, asthmatic subjects had significantly greater numbers of EG2-positive eosinophils regardless of their current condition. CONCLUSION: Eosinophil intracellular EG2 may indicate the pathological stage of asthma. This simple technique for analysing the properties of eosinophils using whole-blood flow cytometry would save time and labor in laboratories.

Adult↗
PubMed1998

Patient with Kearns-Sayre syndrome exhibiting abnormal magnetic resonance image of the brain.

A 33-year-old Japanese man had Kearns-Sayre syndrome (KSS), which consists of the triad of external ophthalmoplegia, heart block, and "salt-and-pepper" retinopathy. The other systemic manifestations included sensorineural hearing loss, slight generalized muscle weakness, cerebellar ataxia, and elevated levels of cerebrospinal fluid protein. He exhibited a heteroplasmic mitochondrial DNA deletion of approximately 9 kb between the cytochrome c oxidase subunit 1 and cytochrome b genes. In the authors' experience, this deletion is one of the longest to be observed in such patients. His fundi were characterized bilaterally by white flecks in the inner layers of retina at the midperiphery. Visual evoked potentials showed delayed latency in the P100 component. The tibial somatosensory evoked potential revealed a marked prolongation of interpeak latency between the N20 and P40 components. Brain magnetic resonance images revealed high-intensity foci in several regions on T2-weighted images. Electrophysiological and magnetic resonance imaging findings suggested an involvement of the white matter of the central nervous system in this patient that was not reflected in the clinical findings.

Adult↗
PubMed1997

Effects of ketamine on dopamine metabolism during anesthesia in discrete brain regions in mice: comparison with the effects during the recovery and subanesthetic phases.

The effects of ketamine on the levels of dopamine (DA), norepinephrine (NE), 5-hydroxytryptamine (5-HT, serotonin) and their metabolites were examined in discrete brain regions in mice. A high dose of ketamine (150 mg/kg, i.p.) did not change DA metabolism in the frontal cortex, nucleus accumbens, striatum and hippocampus, but did decrease it in the brainstem during anesthesia. In contrast, during recovery from the ketamine anesthesia, the high dose increased the level of homovanillic acid (HVA) in all brain regions. A low subanesthetic dose of ketamine (30 mg/kg, i.p.) increased the concentrations of both 3,4-dihydroxyphenylacetic acid (DOPAC) and HVA only in the nucleus accumbens. The DA level was not affected by any ketamine treatment. During ketamine anesthesia, the content of 3-methoxy-4-hydroxy-phenylglycol (MHPG) was decreased in the brainstem, whereas during recovery from anesthesia, the MHPG level was increased in the frontal cortex, nucleus accumbens and brainstem. The NE content was not altered in any region by ketamine treatment. The concentration of 5-hydroxyindoleacetic acid (5-HIAA) was reduced in the frontal cortex, striatum, hippocampus and brainstem during ketamine anesthesia. The 5-HT level was unaltered in all regions except the brainstem where it was reduced. In contrast, after anesthesia, the concentrations of both 5-HT and 5-HIAA were increased in the striatum. During the subanesthetic phase, however, the levels of NE, 5-HT and their metabolites were unchanged. These neurochemical results are consistent with the electrophysiological findings that a high dose of ketamine does not change the basal firing rates of nigrostriatal DA neurons during anesthesia, while low subanesthetic doses significantly increase those of ventral tegmental DA neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1997

rho, a small GTP-binding protein, is essential for Shigella invasion of epithelial cells.

Shigella, the causative agents of bacillary dysentery, are capable of invading mammalian cells that are not normally phagocytic. Uptake of bacteria by the mammalian cells is directed by bacterial factors named IpaB, IpaC, and IpaD invasins, in which Ipa invasins secreted into the bacterial environment can interact with alpha5beta1 integrin. We report here that Shigella invasion of epithelial cells requires rho activity, a ras-related GTP-binding protein. The invasive capacity of Shigella flexneri for Chinese hamister ovary (CHO) cells and other epithelial cells were greatly reduced when treated with Clostridium botulinum exoenzyme C3 transferase. Conversely, uptake of bacteria by CHO cells was promoted upon microinjection of an activated rho variant, Val14RhoA. Attachment of S. flexneri to CHO cells can elicit tyrosine phosphorylation of pp125FAK and paxillin, localized accumulation of F-actin, vinculin, and talin, and activation of protein kinase C, which were all blocked by the treatment with C3 transferase. Our results indicate that cellular signal transduction regulated by rho is essential for Shigella invasion of epithelial cells.

ADP Ribose Transferases↗
PubMed1997

Interaction between botulinum neurotoxin type A and ganglioside: ganglioside inactivates the neurotoxin and quenches its tryptophan fluorescence.

This study found that ganglioside quenched the tryptophan fluorescence of botulinum neurotoxin type A (BoNT A), accompanied by the inactivation of the toxin under low ionic strength conditions. This finding suggests that the ganglioside-binding site of BoNT A contains tryptophan residues. The quantum yield (a conformation parameter) in BoNT A under high ionic strength conditions differed from that under low ionic strength. This observation indicates that high ionic strength may alter the conformation of BoNT A, resulting in failure of the interaction between BoNT A and ganglioside.

Botulinum Toxins, Type A↗
PubMed1997

Immunohistochemical assessment of proliferative activity in mammary adenomyoepithelioma.

AIMS: Two cases of adenomyoepithelioma of the breast were examined by immunohistochemistry to evaluate proliferative activity of epithelial and myoepithelial components. METHODS AND RESULTS: The tumours showed a bicellular pattern of gland-forming epithelial cells and proliferative myoepithelial cells with clear cytoplasm. They showed foci of monotonous growth of myoepithelial cells devoid of glands with low mitotic rate (1-2/10 high-power fields) and mild cytological atypia. Immunohistochemically, the glandular cells were positive for epithelial membrane antigen, cytokeratin (KL-1 and CAM5.2) and carcinoembryonic antigen, whereas tumour cells with clear cytoplasm were reactive with muscle-specific actin (MSA), alpha smooth muscle actin, vimentin, and S100 protein but negative for desmin. Proliferative activities assessed by MIB-1 (Ki-67)/MSA positive cell index were greater in myoepithelial cells in both cases (19.2% and 17.7%) as compared to those in epithelial cells (MIB-1/CAM5.2 index: 10.2% and 9.5%). CONCLUSIONS: These results might account for the previous findings that myoepithelial components predominate over the epithelial ones in an advanced stage of this tumour as well as in recurrent or metastatic lesions.

Aged↗
PubMed1997

Probable participation of phospholipase A2 reaction in the process of fertilization-induced activation of sea urchin eggs.

In sea urchin eggs activated by sperm, A23187 or melittin, BPB (4-bromophenacyl bromide, a phospholipase A2 inhibitor) blocked fertilization envelope formation and transient CN(-)-insensitive respiration in a concentration-dependent manner. BPB had virtually no effect on the increase in [Ca2+]i (cytosolic Ca2+ level), the activity of phosphorylase a and the rate of protein synthesis, as well as acid production and augmentation of CN(-)-sensitive respiration. BPB also inhibited fertilization envelope formation and augmentation of CN(-)-insensitive respiration induced by melittin. Melittin, known to be an activator of phospholipase A2, induced the envelope formation, acid production, augmentation of CN(-)-insensitive and sensitive respiration, but did not cause any increase in [Ca2+]i, the phosphorylase a activity and the rate of protein synthesis. An activation of phospholipase A2 induced by Ca2+ or melittin seems to result in cortical vesicle discharge and production of fatty acids, which are to be utilized in CN(-)-insensitive lipid peroxidase reactions. Activation of other examined cell functions in eggs activated by sperm or A23187, probably results from Ca(2+)-triggered sequential reactions other than Ca(2+)-caused activation of phospholipase A2.

Acetophenones↗
PubMed1997

Inhibitory effect of several nitric oxide-generating compounds on purified Na+,K(+)-ATPase activity from porcine cerebral cortex.

Nitric oxide (NO)-generating compounds (NO donors) such as sodium nitroprusside, S-nitroso-N-acetylpenicillamine, S-nitroso-L-glutathione, 3-morpholino-sydnonimine (SIN-1), (DL)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-5-3-hexenamide, and 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene inhibited the Na+,K(+)-ATPase activity purified from porcine cerebral cortex. NO-reducing or -scavenging agents, such as superoxide dismutase or N-(dithiocarbamate)-N-methyl-D-glucamine sodium salt, L-ascorbic acid; and sulfhydryl (SH) compounds, such as dithiothreitol or the reduced form of glutathione, but not alpha-tocopherol, prevented the inhibition of the enzyme activity by all NO donors except sodium nitroprusside. Enzyme inhibition could also be reversed by these SH compounds, but not by superoxide dismutase, L-ascorbic acid, and alpha-tocopherol. 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazolin-1-oxyl 3-oxide (PTIO), which is able to scavenge NO radicals and generate nitrogen dioxide radicals (.NO2), potentiated the inhibition of this enzyme activity induced by all NO donors (except SIN-1). PTIO did not potentiate, but rather attenuated, the SIN-1-induced inhibition. SIN-1 has been reported to release both NO and superoxide and thereby to rapidly form peroxynitrite (ONOO-). These potentiated and attenuated inhibitions of the enzyme activity induced by PTIO plus all of the NO donors except sodium nitroprusside were prevented by SH compounds, but not by superoxide dismutase, L-ascorbic acid, and alpha-tocopherol. These results suggest that NO donors may release NO or NO-derived products, presumably .NO2 and ONOO-, and may inhibit the Na+,K(+)-ATPase activity by interacting with a SH group at the active site of the enzyme.

Animals↗
PubMed1997

Expression of botulinum toxin binding sites in Xenopus oocytes.

The binding of iodinated botulinum toxin type B to nerve membranes was studied by using rat and mouse preparations. The toxin was examined both in the single-chain and in the proteolytically processed dichain form, and binding sites both in the spinal cord and in various brain regions were assayed. Rat and mouse brains possessed specific binding sites for botulinum toxin type B. The average Kd values for the various rat and mouse membrane preparations examined were 4.2 +/- 0.7 nM and 3.7 +/- 0.9 nM, respectively. The average Bmax values for the same tissue preparations were 7.3 +/- 0.7 pmol/mg of protein and 7.5 +/- 1.9 pmol/mg protein, respectively. The binding of botulinum toxin type B to rat brain membranes was not antagonized by a polyclonal antibody against the cytosolic domain of synaptotagmin 1 or by a monoclonal antibody directed against the luminal domain of synaptotagmin 1. In addition, these antibodies did not protect the mouse phrenic nerve-hemidiaphragm from toxin-induced neuromuscular blockade. Extraction of whole-brain mRNA and injection into Xenopus oocytes led to expression of binding sites for botulinum toxin. Extraction and injection of cerebellar mRNA led to expression of a higher density of binding sites. The number of binding sites was not diminished when oocytes were pretreated with antibodies against the cytosolic and luminal domains of synaptotagmin 1. These findings are likely to aid in the isolation, characterization, and reconstitution of toxin binding sites.

Animals↗
PubMed1996

Dissociation of SNAP-25 and VAMP-2 by MgATP in permeabilized adrenal chromaffin cells.

In digitonin-permeabilized adrenal chromaffin cells, Ca(2+)-induced catecholamine release can be resolved into at least two sequential steps: a MgATP-dependent priming step and a MgATP-independent Ca(2+)-triggered step. Botulinum neurotoxins types A and E cleaved SNAP-25, and blocked MgATP-independent Ca(2+)-induced catecholamine release from the permeabilized chromaffin cells. When the permeabilized cells were primed by pretreatment with MgATP, the amount of SNAP-25 associated with VAMP-2 decreased, and the fraction of SNAP-25 proteolyzed by the neurotoxins increased. These results suggest that dissociation of SNAP-25 and VAMP-2 occurs during the MgATP-dependent priming step, and SNAP-25 plays some important roles in the subsequent MgATP-independent step.

Adenosine Triphosphate↗