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H Uchimura

Publications and source records attributed to H Uchimura.

At least 19 recordsLinked to original sources
PubMed1998

Protein kinase C modulates ischemia-induced amino acids release in the striatum of hypertensive rats.

The role of protein kinase C (PKC) in mediating the ischemia-induced release of amino acids in the striatum was studied using an in vivo brain dialysis technique in the striatum of spontaneously hypertensive rats (SHRs). Using HPLC combined with fluorescence detection methods, we investigated the concentrations of amino acids in the dialysates produced by 20 min of transient forebrain ischemia. We studied the effects of an inhibitor of PKC, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H7) and another isoquinoline analog (HA1004) with less inhibitory effect on the C kinase in ischemia-induced amino acids release. Bilateral carotid artery occlusion caused a marked reduction in the striatal blood flow by 91 +/- 6%. The extent of the cerebral blood flow (CBF) reduction were essentially the same among H7-, HA1004-, and the vehicle-treated groups. Forebrain ischemia produced a marked increase in glutamate (21-fold of the basal concentration), aspartate (19-fold) and taurine (16-fold). Pretreatment with H7 markedly attenuated the ischemia-in-duced release of these three amino acids to 3, 3 and 4-fold of the basal values, respectively. Increase of gamma-aminobutyric acid (GABA) was also attenuated by H7 (vehicle; 2.46 +/- 1.26 microM, H7; 0.62 +/- 0.75 mM). HA1004 did not affect the release of glutamate, aspartate or GABA during ischemia. The ischemia-induced release of taurine was significantly inhibited by HA1004 but the effect was much smaller than that of H7. These results thus indicate that PKC plays a major role in the ischemia-induced release of amino acids in the striatum of SHR.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1998

Involvement of gamma-aminobutyric acid neurotransmission in phencyclidine-induced dopamine release in the medial prefrontal cortex.

The present study was designed to examine the possible involvement of gamma-aminobutyric acid (GABA) neurotransmission in the mechanism of phencyclidine (1-(1-phenylcyclohexyl)piperidine; PCP)-induced dopamine release in the medial prefrontal cortex, using in vivo microdialysis in awake, freely moving rats. Local perfusion via the dialysis probe into the medial prefrontal cortex with PCP (100 and 500 microM) and dizocilpine ((+)-5-methyl-10,11-dihydroxy-5-H-dibenzo(a,d)cyclo-heptan-5,10-im ine; MK-801, 10 and 50 microM), a selective non-competitive NMDA receptor antagonist, was found to increase extracellular dopamine levels. Co-perfusion with NMDA (1 mM) or the GABAA receptor agonist muscimol (50 microM) attenuated the effects of PCP (500 microM) and MK-801 (50 microM) on extracellular dopamine levels. The dopamine reuptake inhibitor nomifensine (50 microM) also produced an increase in extracellular dopamine levels in the medial prefrontal cortex, but this effect was not affected by co-perfusion with muscimol (50 microM). On the other hand, local perfusion with PCP (100 and 500 microM) and MK-801 (10 and 50 microM), but not nomifensine (50 microM), reduced extracellular GABA levels in the medial prefrontal cortex. Co-perfusion with NMDA (1 mM) reduced the effects of PCP (500 microM) and MK-801 (50 microM) on extracellular GABA levels. These results suggest that PCP may facilitate dopamine release in the medial prefrontal cortex, at least in part, by the inhibition of GABA release via the antagonism of NMDA receptors.

Animals↗
PubMed1997

AMPA receptor antagonist, YM90K, reduces infarct volume in thrombotic distal middle cerebral artery occlusion in spontaneously hypertensive rats.

We examined the effects of a potent and selective antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) subtype of glutamate receptor, YM90K, on brain infarction using a newly developed stroke model of thrombotic distal middle cerebral artery occlusion. Male spontaneously hypertensive rats (5-7 months old) were subjected to photochemically-induced distal middle cerebral artery occlusion as previously described [Stroke 26 (1996) 333-336]. Intravenous infusion of YM90K (n = 8) (5 mg/kg per h for 1 h) or the same amount of vehicle (n = 8) (alkaline saline) was started 5 min after distal middle cerebral artery occlusion. Penumbral cerebral blood flow was determined with laser-Doppler flowmetry. Three days after the ischemic insult, brains were stained with 2,3,5-triphenyltetrazolium chloride and infarct volumes were determined. One hour infusion of YM90K significantly reduced infarct volume by 34% (93 +/- 23 mm3 in control group vs. 61 +/- 25 mm3 in YM90K-treated group, P = 0.017). There were no significant differences in the degrees of cerebral blood flow reduction after distal middle cerebral artery occlusion between the YM90K treated and control groups. YM90K reduces infarct volume in experimental ischemia produced by photothrombotic distal middle cerebral artery occlusion in rats. The present results demonstrated beneficial effects of AMPA receptor blockade on acute ischemic stroke.

Animals↗
PubMed1997

Differentiation and morphogenesis in pellet cultures of developing rat retinal cells.

We previously developed a reaggregate cell culture system (pellet cultures) in which retinal neuroepithelial cells proliferate and give rise to rod photoreceptor cells (rods) in vitro (Watanabe and Raff, 1990, Neuron 4:461-467). In the present study, we analyzed cell differentiation and morphogenesis in pellet cultures by using both cell-type-specific markers with immunofluorescence and electron microscopy. We demonstrated that, in addition to rods, the other major retinal cell types, including amacrine cells, bipolar cells, Müller cells, and ganglion cells were all present in the pellets, where most were able to develop from dividing precursor cells in vitro. The different cell types in the pellets became organized into two distinct structures: dark rosettes and pale rosettes. The cellular composition of these structures indicated that the dark rosettes correspond to the outer nuclear layer and the pale rosettes to the inner nuclear layer of the normal retina. Ultrastructural studies have indicated that the thin layer of neuronal processes surrounding the dark rosettes correspond to the outer plexiform layer, and the central region of the pale rosettes correspond to the inner plexiform layer of the normal retina. Other features of normal retinal development also occurred in the pellets, including programmed cell death and the formation of inner and outer rod cell segments and synapses. Thus, pellet cultures provide a convenient way to study different aspects of retinal development where one can control the size and the cellular composition of the initial reaggregate.

Animals↗
PubMed1997

Age-related changes in the DNA and RNA content of the brain in spontaneously hypertensive rats.

To elucidate the effects of aging accompanied with hypertension on brain nucleic acid, we measured both the DNA and RNA contents of six specific brain regions in adult (5-6 months old) and aged (18-22 months old) female spontaneously hypertensive rats (SHRs). Although no statistical difference was observed in the RNA content, the DNA content did tend to increase in the hippocampal CA1 of aged SHR (4.24 +/- 0.55 ng/microgram protein, mean +/- SD, n = 6) in comparison to that of adult SHR (3.21 +/- 0.71 ng/microgram protein, n = 4). Hence, aged SHRs showed a significant decrease in the RNA to DNA ratio in the CA1 subfield of the hippocampus (3.79 +/- 0.61) compared to adult SHR (5.27 +/- 0.81). On the other hand, no other regions, except for the dorsolateral region of the striatum, showed any difference in the RNA/DNA ratio between aged and adult SHR. We therefore conclude that subtle changes in the nucleic acid occur in vulnerable regions of the brain in aged SHRs.

Aging↗
PubMed1997

[Isolation frequency and biological characteristics of the multiple-antibiotic resistant Pseudomonas aeruginosa isolated from clinical specimens].

Isolation frequency of multiple-antibiotic resistant Pseudomonas aeruginosa (MARPA) was 11.9% (fifty six strains) of a total of four-hundred seventy-one strains of P. aeruginosa isolated from clinical specimens at the Kyorin University Hospital from October 1994 to December 1996. Eighteen strains of MARPA and thirteen strains of antibiotic sensitive P. aeruginosa (ASPA) isolated from clinical specimens in internal medicine ward A were determined O serotype, and characterized with production of pyocyanin, pyoverdin, hemolysin, elastase, and caseinase. Sixteen strains (88.9%) of MARPA were identified as serotype C. The ability to produce pyocyanin, hemolysin, elastase, and caseinase was not detected in all MARPA. One side, thirteen strains of ASPA showed various serotypes, i.e., B: 5 strains (38.4%), G: 4 strains (30.8%), C: 2 strains (15.4%), E: 1 strain (7.7%) and unknown type: 1 strain (7.7%), and the production of both hemolysin and pyoverdin was observed in 13 strains (100%), pyocyanin in 8 strains (61.5%), elastase and caseinase in 9 strains (69.2%) of ASPAs, which suggests that ASPAs do maintain the synthetic ability of pathogenic factors and pigments, but MARPAs do not. These results indicate that from epidemiological points of view the current strains of MARPA spread from one clone within the internal medicine ward A with nosocomial outbreak by serotype C.

Ampicillin Resistance↗
PubMed1997

[Properties of extracellular products produced by group A streptococci isolated from patients with streptococcal toxic shock syndrome].

Extracellular products of group A streptococci isolated from patients with streptococcal toxic shock syndrome (STSS) were examined. The outline of the discussion of the 3 products are as follows; streptolysin O (SLO), proteinase and erythrogenic toxin. SLO and proteinase showed a relatively large amount of products more than erythrogenic toxin. SLO produced by group A streptococci isolated from the patient with STSS had an isoelectric point (pI) of 6.0 and a molecular weight of 64,000 and showed hemolytic activity in the presence of 2-mercaptoethanol (2-ME). Furthermore, the hemolytic activities of all components were inhibited by gamma-globulin and cholesterol. Proteinase had pIs of 8.7 and 8.9, and a molecular weight of 21,000. These data suggest that STSS clinical criteria probably reflects a characteristic of a large amount of products of individual S. pyogenes isolates.

Bacterial Proteins↗
PubMed1997

[Serum soluble CD8 and soluble interleukin-2-receptor levels during interferon therapy in chronic hepatitis C].

We examined the relationship between the changes of serum soluble CD8 (sCD8) and soluble interleukin-2 receptor (sIL-2R) levels and effectiveness of interferon (IFN) in patients with chronic hepatitis (CH) C. Changes in sCD8 levels were parallel with fluctuations of alanine aminotransferase (ALT) in CH patients during IFN treatment but decreases of sCD8 levels were slower than those of ALT. In IFN effective and ALT decreased patients sCD8 levels is also decreased. sIL-2R levels was increased transiently during administration of IFN in most cases. It was suggested that decrease in sCD8 levels is indicative of the effectiveness of IFN therapy.

Adult↗
PubMed1996

Localization and ontogeny of GLUT3 expression in the rat retina.

This study investigates the presence, localization, and developmental expression of a neuron-specific facilitated-diffusion glucose transporter, GLUT3, in the rat retina so as to elucidate molecular mechanisms regulating glucose homeostasis in support of the visual function. Immunoblot analysis using anti-GLUT3 antibody (ALM3-C) revealed the presence of GLUT3 as a heterogeneously glycosylated protein with an average molecular weight of approximately 44 kDa. Although immunofluorescence staining showed it to be localized primarily in the inner and outer plexiform layers, some of the cell bodies in the inner nuclear layer also showed weak immunoreactivity. Immunoblot analysis of developing rat retinal tissues revealed the presence of the GLUT3 protein as early as embryonic day 15 (E15), and immunofluorescence staining revealed its expression in the inner plexiform layer near the time of birth and in the outer plexiform layer at postnatal day 14 (P14), i.e., when the eyes normally open and retinal activity commences. The protein's abundance remained at a relatively low level during the embryonic stages and up until the end of the first postnatal week (P7), though a transient increase was confirmed to occur at E18. From P13, however, the abundance steadily increased, rapidly reaching the adult level at P24. Based on these observations, we hypothesize that GLUT3 is expressed in some subsets of retinal neurons, being preferentially abundant in their neuronal processes, and that its ontogeny is closely associated with morphological and functional development of the retina. As such, this suggests that GLUT3 plays some important role(s) in the retina where glucose metabolism is essential.

Animals↗
PubMed1996

Angiotensin II increases norepinephrine turnover in the anteroventral third ventricle of spontaneously hypertensive rats.

We evaluated the effect of angiotensin II (Ang II) administered by intracerebroventricular injection on norepinephrine turnover in the anteroventral third ventricle in adult spontaneously hypertensive rats (SHR, n = 35) and age-matched Wistar-Kyoto rats (WKY, n = 38). Ang II (100 ng) or saline (vehicle control) was administered into the cerebral ventricle 30 minutes after injection of alpha-methyl-p-tyrosine (250 mg/kg IP). Norepinephrine turnover was assessed by evaluation of the norepinephrine concentration before and 1 hour after such administration. The pressor response to Ang II administration was significantly greater in SHR than in WKY (+43 +/- 3 versus +23 +/- 2 mm Hg, P < .01). Baseline norepinephrine turnover (response to saline) was reduced in the ventral median preoptic nucleus of SHR. Ang II significantly increased norepinephrine turnover in the organum vasculosum lamina terminalis and ventral median preoptic nucleus of SHR (organum vasculosum lamina terminalis: 40 +/- 5% by Ang II versus 18 +/- 6% by saline, P < .05; ventral median preoptic nucleus: 32 +/- 3% by Ang II versus 21 +/- 2% by saline, P < .05) but not of WKY (37 +/- 5% versus 29 +/- 5%, P = NS, and 30 +/- 2% versus 32 +/- 3%, P = NS, respectively). Thus, norepinephrine turnover in the anteroventral third ventricle region induced by intracerebroventricular administration of Ang II was increased in SHR. This effect may contribute to the enhanced pressor response to central Ang II seen in this model.

Angiotensin II↗
PubMed1995

Potentiation of phencyclidine-induced dopamine release in the rat striatum by the blockade of dopamine D2 receptor.

Local perfusion with phencyclidine (PCP) increased extracellular dopamine levels in the rat striatum in a dose-dependent manner, as measured by in vivo microdialysis. While pretreatment with SCH 23390, a selective dopamine D1 receptor antagonist, had no significant effect on PCP-induced increases in extracellular dopamine levels, pretreatment with YM-09151-2 (cis-N-(1- benzyl-2-methylpyrrolidin-3-yl)-5-chloro-2-methoxy-4-methylamin obenzamide), a selective dopamine D2 receptor antagonist, markedly potentiated the effect of PCP. These results suggest that the blockade of dopamine D2 presynaptic autoreceptors strongly potentiates the PCP-induced dopamine release in the striatum.

Animals↗
PubMed1995

The effect of phencyclidine on the basal and high potassium evoked extracellular GABA levels in the striatum of freely-moving rats: an in vivo microdialysis study.

The effect of phencyclidine (PCP) on the gamma-aminobutyric acid-ergic (GABAergic) transmission in the striatum of freely-moving rats was investigated using an in vivo microdialysis. The high potassium (100 mM) increased the extracellular GABA level to 4000% of the basal level. Although the basal GABA level in the striatal dialysate did not show either calcium dependency or tetrodotoxin (TTX) sensitivity, the high potassium evoked GABA level was reduced by 82% under calcium-free conditions (with 12.5 mM magnesium) and by 54% in the presence of 10 microM TTX. The systemic administration of PCP (7.5 mg/kg) or the local perfusion of PCP (100 microM and 1 mM) significantly inhibited the high potassium evoked GABA release in the rat striatum. The local perfusion of MK-801 (10 microM and 100 microM), a more potent and selective N-methyl-D-aspartate (NMDA) receptor antagonist, also inhibited the high potassium evoked striatal GABA release. These drugs did not show any significant effect on the basal extracellular GABA level. NMDA (1 mM) either partly or completely blocked the effect of PCP (1 mM) or MK-801 (100 microM) on the high potassium evoked striatal GABA release. On the other hand, nomifensine (100 microM), a dopamine uptake blocker, did not show any effect on the high potassium evoked GABA release. These results suggest that PCP inhibited the striatal GABAergic neuronal transmission through its antagonism of the NMDA receptor.

Animals↗
PubMed1995

Ischemia-induced release of amino acids in the hippocampus of aged hypertensive rats.

We have recently demonstrated the age-related vulnerability of hippocampal neurons to 20-min forebrain ischemia in spontaneously hypertensive rats (SHR). In the present study, we investigated the effect of aging on the release of amino acids in the hippocampus during transient cerebral ischemia for 20 min. Concentrations of extracellular amino acids and cerebral blood flow in the CA1 subfield were examined by an in vivo brain dialysis technique and a hydrogen clearance method, respectively, in adult (5-7 month) and aged (19-23 month) female SHR. During cerebral ischemia by bilateral carotid artery occlusion, cerebral blood flow to the hippocampus decreased to 20% of the resting values in both groups. After recirculation, both groups showed delayed hypoperfusion which was more prominent in the aged SHR. In the adult rats, concentrations of both aspartate and glutamate increased to approximately 8-fold of the resting values during ischemia. The elevation of these excitatory amino acids in the adult SHR was not significantly different from that in the aged rats. In contrast, the concentration of taurine increased 26-fold in the adult SHR but only 16-fold in the aged rats. Changes in other amino acids were not different between the two groups. These results indicate that an imbalance of excitatory and inhibitory amino acids, e.g., smaller release of taurine, during ischemia may, at least in part, contribute to the age-related vulnerability of hippocampal neurons to transient cerebral ischemia in SHR.

Aging↗
PubMed1995

Mortality in psychiatric patients, with a specific focus on cancer mortality associated with schizophrenia.

BACKGROUND: Higher mortality rates among psychiatric patients compared with the general population have been widely reported. On the other hand, lower cancer mortality for schizophrenics has been occasionally pointed out. Few studies from Japan have investigated mortality among psychiatric patients, and this study is the first large-scale follow-up in this country. METHODS: A total of 4980 patients admitted to a national mental hospital from 1948 through 1982 were followed up until 31 August 1985. The standardized mortality ratios (SMR) were calculated in comparison to the general population, using the person-years method. RESULTS: The SMR for total deaths and those for malignancy were as follows for males/females respectively: 2.55/3.02 and 0.84/1.37 for schizophrenia, 1.76/2.37 and 1.44/2.10 for depression, 2.45/3.04 and 1.18/1.82 for mania, 1.81/1.90 and 0.27/1.07 for neurosis, 5.55/4.33 and 1.85/3.34 for alcohol/drug abuse, and 3.65/3.57 and 1.01/0.72 for organic brain syndrome. CONCLUSIONS: The SMR for total deaths were significantly elevated in schizophrenia, depression, mania, neurosis, alcohol/drug abuse, and organic brain syndrome, respectively. The SMR for malignancy were not elevated nor lowered significantly in any of these disease categories. The SMR for stomach cancer in male schizophrenics was significantly lower (0.27; P < 0.05).

Cause of Death↗
PubMed1995

Involvement of dopamine D1 receptors in phencyclidine-induced behavioral stimulation in rats.

The effects of dopamine receptor antagonists on phencyclidine (PCP)-induced behaviors were examined in rats. Acute administration with PCP (7.5 mg/kg i.p.) produced various behavioral changes, such as increases of spontaneous activity, head-weaving, sniffing, rearing, back-pedaling, and ataxia. To determine which dopamine receptor subtypes were involved in mediating the PCP-induced behaviors, SCH 23390 (0.05 and 0.5 mg/kg), sulpiride (20 and 100 mg/kg), or haloperidol (0.05 and 0.5 mg/kg) were pretreated 30 min before PCP treatment (7.5 mg/kg). A higher dose of SCH 23390 significantly reduced the increase of spontaneous activity induced by PCP. Both doses of sulpiride did not affect the PCP-induced behaviors. A higher dose of haloperidol decreased the PCP-induced spontaneous activity, whereas a lower dose of haloperidol enhanced the activity. Ketanserin (0.5 and 5 mg/kg) did not alter any PCP-induced behaviors. These results suggest that the D1, but not D2, dopamine receptor subtype may be involved in the PCP-induced behavioral abnormality.

Animals↗
PubMed1995

[Present status and future of enzyme immunoassay--hormone].

Recently various non-radioisotopic immunoassays have been developed instead of radioisotopic assay and widely used in the laboratory. Enzyme immunoassay (EIA) is most popular in use including chemiluminescent enzyme immunoassay (CLEIA). At present few hormones (thyroid related and gonadotropic hormones) are measured by EIA with semi or full automatic analysers and satisfactory specificity and sensitivity were already obtained. However, most hormones are still measured by RIA or IRMA. EIA for these hormones should be developed. Standardization of reference interval and calibrators would also be needed for the compatibility between different assays.

Calibration↗
PubMed1994

Effect of phencyclidine on dopamine release in the rat prefrontal cortex; an in vivo microdialysis study.

The effect of phencyclidine (PCP) on the extracellular dopamine levels in the rat prefrontal cortex was investigated using an in vivo brain dialysis technique. PCP increased extracellular dopamine levels in the prefrontal cortex of freely-moving rats after the systemic (7.5 mg/kg i.p.) or the local injection (100 microM and 500 microM). The local injection of MK-801, which is a more selective and potent NMDA receptor antagonist than PCP also increased the extracellular dopamine levels (from 10 microM to 100 microM). These results suggest that part of the effect of PCP is attributable to its antagonist effect on the NMDA receptor.

3,4-Dihydroxyphenylacetic Acid↗