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Biomedical subjects

S Kaneko

Publications and source records attributed to S Kaneko.

At least 307 records · Page 17Linked to original sources
PubMed1998

[Protective effect of neurotrophin against glutamate neurotoxicity in cortical cultures].

This study was performed to investigate the effects of neurotrophins on glutamate cytotoxicity by using cultured cortical neurons. Primary cultures obtained from the cerebral cortex of fetal rats (17-19 days gestation) were used for experiments. NGF did not elicit tyrosine phosphorylation of Trks whereas BDNF induced Trk tyrosine phosphorylation within 10 min, followed by time-dependent decrease. Brief glutamate exposure to the cell induced delayed cytotoxicity. Similar cytotoxicity was observed with the brief application of a calcium ionophore, ionomycin, and nitric oxide (NO) generating agents, S-nitrosocysteine (SNOC) and SIN-1. Exposure of the cultures to NGF and BDNF for 1 or 24 hr prior to glutamate exposure reduced glutamate-induced cytotoxicity. In contrast, simultaneous addition of NGF and BDNF with glutamate did not affect glutamate-induced cytotoxicity. Ionomycin-induced cytotoxicity was prevented by exposing cultures to NGF and BDNF for 24-hr. Moreover, NGF and BDNF ameliorated cytotoxicity induced by SNOC and SIN-1. These results suggest that neurotrophins prevent NO mediated glutamate cytotoxicity.

Animals↗
PubMed1998

Protective effect of MKC-231, a novel high affinity choline uptake enhancer, on glutamate cytotoxicity in cultured cortical neurons.

This study was performed to examine the neuroprotective action of 2-(2-oxopyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofuro [2,3-b]quinolin-4-yl)acetoamide (MKC-231), which enhances choline uptake and acetylcholine release in the central nervous system. Glutamate neurotoxicity was assessed with cortical cultures obtained from fetal rats. Exposure of cultures to MKC-231 for 12-24 hr ameliorated glutamate cytotoxicity. MKC-231 reduced cytotoxicity induced by ionomycin, a calcium ionophore, but did not affect the cytotoxicity induced by S-nitrosocysteine, a nitric oxide (NO) donor. These findings suggest that MKC-231 protects against glutamate neurotoxicity by suppressing the NO formation triggered by Ca2+-influx.

Animals↗
PubMed1998

Bifemelane protects cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.

This study was performed to examine the neuroprotective action of bifemelane against glutamate cytotoxicity in cultured cortical neurons obtained from fetal rats. Cell viability was markedly reduced by a brief exposure to glutamate. Glutamate cytotoxicity was reduced by exposing cultures to bifemelane at concentrations of 1-10 microM for 24 hr prior to glutamate exposure. In contrast, glutamate cytotoxicity was not affected by adding bifemelane to the glutamate-containing-medium without pretreatment. Bifemelane did not affect N-methyl-D-aspartate (NMDA)-induced currents, although the higher concentration (100 microM) of the drug reduced them. These findings suggest that bifemelane protects against glutamate neurotoxicity without affecting NMDA receptors.

Animals↗
PubMed1998

Inhibition by [Arg8]-vasopressin of long term potentiation in guinea pig hippocampal slice.

We examined the effects of [Arg8]-vasopressin (AVP) on long term potentiation (LTP) of the field excitatory postsynaptic potentials at CA1 and CA3 synapses in adult guinea pig hippocampal slices. AVP (10 nM) depressed the magnitude of LTP without any effects on basal responses at both synaptic pathways. The depressive effect by AVP at CA1 synapses appears to be receptor-mediated since it was inhibited by an AVP V1-receptor antagonist, [Pmp1,Tyr(Me)2]-AVP. From these results, AVP may play an inhibitory role on the induction of LTP via V1 receptors in the guinea pig hippocampus.

Animals↗
PubMed1998

Inhibitory effects of bifemelane on brain Ca2+ channel subtypes expressed in Xenopus oocytes.

Effects of the cerebroprotective agent bifemelane on voltage-dependent Ca2+ channel currents were evaluated in Xenopus oocytes expressing specific Ca2+-channel subtypes. Extracellular perfusion of bifemelane showed a dose-dependent blocking action on both N-type and Q-type Ca2+ channels, but not on cardiac L-type Ca2+ channels expressed in the oocytes, and the inhibitory action on Q-type current was stronger than that on N-type current. The time course of inhibition by bifemelane was comparatively slow; a 20-min perfusion with 1 microM bifemelane was required to reduce the amplitude of the Q-type current to 80% of the control level. When bifemelane was applied intracellularly, the potency and time-course of inhibition was equivalent to that caused by the perfusion of bifemelane. The bifemelane-induced inhibition was voltage-dependent but not use-dependent in Q-type channels since it was apparent at more depolarized potentials but not influenced by the interval of depolarization. These results suggest that bifemelane inhibits the opening of the specific Ca2+ channels located at nerve terminals to suppress excessive neurotransmitter release from neurons in some pathophysiological conditions such as ischemia.

Animals↗
PubMed1998

Substrate specificity of the alpha-L-arabinofuranosidase from Trichoderma reesei.

The precise substrate specificities of an alpha-L-arabinofuranosidase from Trichoderma reesei were investigated. The enzyme released arabinose at appreciable rates from p-nitrophenyl-alpha-L-arabinofuranoside, O-alpha-L-arabinofuranosyl-(1-->3)-O-beta-D-xylopyranosyl-(1-->4) -D-xylopyranose (A1X2), arabinan, arabinoxylan, arabinogalactan, debranched-arabinan and gum arabic, but not from O-beta-D-xylopyranosyl-(1-->4)-[O-alpha-L-arabinofuranosyl-(1-->3)] -O-beta-D-xylopyranosyl-(1-->4)-D-xylopyranose (A1X3) or O-beta-D-xylopyranosyl-(1-->2)-O-alpha-L-arabinofuranosyl -(1-->3)-O-beta-D-xylopyranosyl-(1-->4)-O-beta-D-xylopyranosyl-(-->4) -D-xylopyranose (A1X4). The enzyme hydrolyzed methyl 2-O-, methyl 3-O- and methyl 5-O-alpha-L-arabinofuranosyl-alpha-L-arabinofuranosides to arabinose and methyl alpha-L-arabinofuranoside with the order of hydrolysis being: (1-->5)- > (1-->2)- > or = (1-->3)-linkages. The enzyme hydrolyzed the (1-->3)-linkage faster than the (1-->5)-linkage of methyl 3,5-di-O-alpha-L-arabinofuranosyl-alpha-L-arabinofuranoside. The degree of conversion of arabinan and debranched-arabinan to monosaccharides by the enzyme was 33.0% and 9.1%, respectively. The alpha-L-arabinofuranosidase preferentially cleaved the arabinosyl side-chain from the arabinan rather than the terminal arabinosyl residue of the arabinan backbone.

Carbohydrate Conformation↗
PubMed1998

Substrate specificities of alpha-L-arabinofuranosidases produced by two species of Aspergillus niger.

Precise substrate specificities of alpha-L-arabinofuranosidases from Aspergillus niger 5-16 and Aspergillus niger (Megazyme) were investigated. Both enzymes hydrolyzed arabinan and debranched-arabinan at almost the same rate. The alpha-L-Arabinofuranosidase from A. niger (Megazyme) preferentially released arabinosyl side-chains of arabinan. The enzyme tore off both arabinoses attached to O-alpha-L-arabinofuranosyl-(1-->3)-O-beta-D-xylopyranosyl-(1--> 4)-D-xylopyranose and O-beta-D-xylopyranosyl-(1-->4)-[O-alpha-L- arabinofuranosyl-(1-->3)]-O-beta-D-xylopyranosyl-(1-->4)-D-xylopyranose, but did not tear off xylosyl-arabinose from O-beta-D-xylopyranosyl-(1-->2)-O-alpha-L-arabinofuranosyl-(1-->3) -O-beta-D-xylopyranosyl-(1-->4)-O-beta-D-xylopyranosyl-(1-->4)-D- xylopyranose. The enzyme from A. niger (Megazyme) hydrolyzed methyl 2-O-, methyl 3-O- and methyl 5-O-alpha-L-arabinofuranosyl-alpha-L-arabinofuranosides to arabinose and methyl alpha-L-arabinofuranoside in the order of (1-->5)->(1-->2)->(1-->3)-linkages. On the other hand, alpha-L-arabinofuranosidase from A. niger 5-16 successively liberated the arabinose of arabinan from non-reducing terminals. The enzyme hydrolyzed in the order of (1-->2- > (1-->3)- > (1-->5)-linkages. Both of the enzymes hydrolyzed the (1-->3)-linkage more than the (1-->5)-linkage of methyl 3,5-di-O-alpha-L-arabinofuranosyl-alpha-L-arabinofuranoside.

Arabinonucleosides↗
PubMed1998

[Inflammatory pseudotumor of the ureter: a case report].

A 57-year-old male was admitted because of the right flank pain. The image examinations, retrogradeurography, abdominal CT and MRI, showed a mass located at the upper right ureter. Although the tumor was not typical as ureteral cancer, we could not make a diagnosis of a benign tumor by image examinations. Therefore nephroureterectomy that was surgical method for ureteral cancer was performed. The tumor was diagnosed as inflammatory pseudotumor of the ureter by histological findings. Inflammatory pseudotumor is extremely rare for ulogeital organs. And this lesion is difficult to distinguish from malignancy only by image examinations. Therefore, the surgical resection and pathological studies are necessary.

Diagnosis, Differential↗
PubMed1998

Safety management of a patient undergoing thoracic aortic surgery by spinal evoked potential monitoring.

We have presented a patient (48 year-old male) in whom the evoked spinal potential monitor detected impending spinal ischemia after aortic cross-clamping, which allowed surgical intervention to be modified so as to restore the decaying evoked spinal potential. The patient received replacement of the dissecting aneurysm in the thoracic descending aorta with clamping of the aorta at the sites immediately proximal and distal to the aneurysm and initiation of femoro-femoral venoarterial bypass under normothermia. The evoked spinal potential was recorded via the T12/L1 epidural electrode in response to transdural electric stimulation of the spinal cord at the C7/T1 level. As the evoked spinal potential gradually decreased in amplitude without latency prolongation after aortic cross-clamping, the distal clamp was moved from the T6 vertebral level to the T4. The reduced spinal potential then returned to the baseline amplitude. This episode was repeated twice from surgical necessity. The patient was free from any neurological disorders postoperatively.

Aortic Dissection↗
PubMed1998

Floating density of hepatitis C virus particles and response to interferon treatment.

Hepatitis C virus (HCV) particles can be classified into two major fractions according to their floating density in serum. However, the genomic heterogeneity of each fraction and the relationship between this viral characteristic and interferon (IFN) response in patients with chronic hepatitis are not known. In this study, floating density and single strand conformation polymorphism (SSCP) of the hypervariable region 1 (HVR1) of HCV were examined in 16 patients with chronic hepatitis prior to IFN treatment. The ratio of HCV RNA titers in the top (T) and bottom (B) fractions, or T:B ratio, was 10:1 in 4 patients, 1:1 in 7, and 1:10 in 5. Three of the 4 patients with a 10:1 ratio showed a sustained response to IFN, while none of the 5 patients with a 1:10 ratio demonstrated a sustained response (P < 0.05). All 4 patients with a 10:1 ratio had 1 or 2 SSCP bands, and 4 of the 5 patients with a 1:10 ratio had 4 or 5 bands (P < 0.01). Furthermore, the number of SSCP bands in the top fraction from 6 sustained responders (1.8 +/- 0.3) was significantly smaller than from 10 non sustained responders (4.1 +/- 0.8) (P < 0.05). Thus, patients with a high T:B ratio and low heterogeneity in HVR1 demonstrated sustained responses to IFN, while those with low T:B ratios and high heterogeneity did not.

Adult↗
PubMed1998

[Comparison of the vascular effects of propofol and those of thiopental in patients under cardiopulmonary bypass].

The effects of propofol (1 mg.kg-1) and thiopental (2.5 mg.kg-1) on the vascular smooth muscle were investigated in 10 cardiac patients on cardiopulmonary total bypass using a constant perfusion flow. Radial mean arterial blood pressure (mAP) decreased to 85 +/- 5% (P < 0.01, vs preinjection) in the post-injection late phase (2-3 min) after propofol, and to 90 +/- 6% (P < 0.01) after thiopental. MAP after thiopental showed a transient initial increase to 115 +/- 8% (P < 0.01) in the post-injection early phase (-1 min). Skin blood flow (SBF) in the middle finger-tip increased to a peak of 450 +/- 120% (P < 0.01) in the post-injection late phase after propofol, and to 240 +/- 60% (P < 0.05) after thiopental. The increase in SBF after propofol was greater than that after thiopental (P < 0.05). The decrease in mAP and the increase in SBF under the constant perfusion flow are considered mainly due to a direct drug action of dilating peripheral vessels. In conclusion, this in vivo human study suggests that propofol (1 mg.kg-1) causes more potent vasodilatation in the peripheral vessels than thiopental (2.5 mg.kg-1).

Aged↗
PubMed1998

[A case of accessory spleen presenting as retroperitoneal tumor].

We report the 13th case of accessory spleen in the retroperitoneum in the world literature. A 53-year-old man visited our hospital complaining of lassitude. Laboratory studies revealed significant anemia. Several imaging studies revealed a large retroperitoneal tumor (70 x 63 x 48 mm) in the medial aspect of the lower pole of the left kidney. The tumor was supplied arterially from the first and second lumbar arteries. Since the tumor adhered tightly to the left kidney, the kidney was resected as well as the tumor. The tumor was very hemorrhagic. On histological examination, the tumor exhibited a structure typical of splenic tissue. The retroperitoneal accessory spleen is very rare, and the literature on it is reviewed here.

Choristoma↗
PubMed1998

Pharmacological interactions between magnesium ion and adenosine on monoaminergic system in the central nervous system.

The effects of magnesium ion (Mg2+), adenosine A1 and A2 receptor ligands on basal extracellular levels of striatal dopamine, hippocampal dopamine and serotonin were investigated by using in vivo microdialysis in freely moving rats. An increase in extracellular levels of Mg2+ ([Mg2+]o) reduced extracellular striatal and hippocampal monoamine levels, in a concentration dependent manner. The extracellular monoamine level was increased by perfusion with a non-selective adenosine receptor antagonist, caffeine, a selective adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT), and an antiepileptic drug, carbamazepine, whereas adenosine, a selective adenosine A1 receptor agonist, 2-chloro-N6-cyclopentyladenosine (CCPA) reduced extracellular monoamine levels. The former and latter were reduced and enhanced by an increase in [Mg2+]o, respectively. Neither a selective adenosine A2 agonist, N6-[2-(3,5-dimethoxyphenyl)-2-(methylphenyl) ethyl]adenosine (PD125944), nor an antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX), affected extracellular monoamine levels. Under the conditions of adenosine A1 receptor blockade by CPT, adenosine, PD125944 and carbamazepine increased extracellular monoamine levels, whereas caffeine and DMPX decreased them. These stimulatory effects of adenosine, PD125944 and carbamazepine were enhanced by an increase in [Mg2+], whereas the inhibitory effects of caffeine and DMPX were reduced by Mg2+, in a concentration dependent manner. It is concluded that an activation of adenosine A1 and A2 receptors decrease and increase extracellular levels of striatal dopamine, hippocampal dopamine and serotonin, respectively. These whereas the stimulatory effects of adenosine A2 receptor on extracellular levels of monoamine are masked by the inhibitory effects of adenosine A1 receptor. In addition, an increase in [Mg2+]o enhances and reduces the effects of adenosine receptor agonists and antagonists on extracellular monoamine levels, respectively.

Adenosine↗
PubMed1997

L-DOPA neurotoxicity is mediated by glutamate release in cultured rat striatal neurons.

The exposure of cultured rat striatal neurons to L-DOPA caused marked cell death. The L-DOPA cytotoxicity was inhibited by the addition of Mg2+ to and by the removal of Ca2+ from the culture medium, and also by the application of tetrodotoxin. Moreover, prolonged application of L-DOPA increased the glutamate content in the culture medium. These results indicate that L-DOPA produces neurotoxicity by facilitating glutamate release.

Animals↗
PubMed1997

Induction of minisatellite mutation in NIH 3T3 cells by treatment with the tumor promoter okadaic acid.

Okadaic acid (OA) is a strong tumor promoter of mouse skin carcinogenesis and also a potent inhibitor of serine/threonine protein phosphatases. OA induces various genetic alterations in cultured cells, such as diphtheria-toxin-resistance mutations, sister chromatid exchange, exclusion of exogenous transforming oncogenes, and gene amplification. The present study revealed that it caused minisatellite mutation (MSM) at a high frequency in NIH 3T3 cells, although no microsatellite mutation was found. Nine of 31 clones (29%) exhibited MSM after 6 days of OA treatment, as opposed to only 1 of 30 clones (3%) without OA exposure. Moreover, NIH 3T3 cells treated with OA acquired tumorigenicity in nude mice, giving rise to 7 tumors within 25 weeks in 20 sites where 3 x 10(6) cells were injected. In contrast, the same numbers of untreated cells gave rise to only one tumor, and the tumor grew much slower. All of three OA-induced tumors examined manifested the MSM. The findings thus point to a molecular mechanism by which OA could function as a tumor promoter, and also the biological relevance of the induction of MSM in the tumorigenic process by OA.

3T3 Cells↗
PubMed1997

Nicotine protects cultured cortical neurons against glutamate-induced cytotoxicity via alpha7-neuronal receptors and neuronal CNS receptors.

We examined the effects of nicotine on glutamate-induced cytotoxicity using primary cultures of rat cortical neurons. The cell viability decreased significantly when cultures were exposed to glutamate for 10 min and then incubated with glutamate-free medium for 1 h. The exposure of cultures to nicotine (10 microM) for 8-24 h prior to glutamate application ameliorated the glutamate-induced cytotoxicity, with no significant effect of nicotine alone on the cell viability. Neuroprotection by nicotine was dependent on the incubation period. alpha-bungarotoxin (alpha-BTX) and methyllycaconitine (MLA), both of which are alpha7-neuronal receptor antagonists, and dihydro-beta-erythroidine (DHbetaE), a neuronal central nervous system (CNS) receptor antagonist, each significantly antagonized the protection by nicotine against glutamate-induced cytotoxicity. Ionomycin, a calcium ionophore, and S-nitrosocysteine (SNOC), a nitric oxide (NO) donor, also induced cytotoxicity in a manner similar to glutamate. Nicotine protected cultures against ionomycin-induced cytotoxicity, but not against SNOC-induced cytotoxicity. These results suggest that nicotine protects cultured cortical neurons against glutamate-induced cytotoxicity via alpha7-neuronal receptors and neuronal CNS receptors by reducing NO-formation triggered by Ca2+ influx.

Aconitine↗
PubMed1997

Metabolic inactivation of retinoic acid by a novel P450 differentially expressed in developing mouse embryos.

Retinoic acid (RA) is a physiological agent that has a wide range of biological activity and appears to regulate developmental programs of vertebrates. However, little is known about the molecular basis of its metabolism. Here we have identified a novel cytochrome P450 (P450RA) that specifically metabolizes RA. In vitro, P450RA converts all-trans RA into 5,8-epoxy all-trans RA. P450RA metabolizes other biologically active RAs such as 9-cis RA and 13-cis RA, but fails to metabolize their precursors, retinol and retinal. Overexpression of P450RA in cell culture renders the cells hyposensitive to all-trans RA. These functional tests in vitro and in vivo indicate that P450RA inactivates RA. The P450RA gene is not expressed uniformly but in a stage- and region-specific fashion during mouse development. The major expression domains in developing embryos include the posterior neural plate and neural crest cells for cranial ganglia. The expression of P450RA, however, is not necessarily inducible by excess RA. These results suggest that P450RA regulates the intracellular level of RA and may be involved in setting up the uneven distribution of active RA in mammalian embryos.

Amino Acid Sequence↗