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Biomedical subjects

A Nishiyori

Publications and source records attributed to A Nishiyori.

At least 19 recordsLinked to original sources
PubMed2003

Simultaneous genotyping of alcohol dehydrogenase 2 and aldehyde dehydrogenase 2 by single-strand conformation polymorphism analysis.

Alcohol dehydrogenase (ADH; EC 1.1.1.1) and aldehyde dehydrogenase (ALDH; EC 1.2.1.3) have important roles in the elimination of ingested ethanol. These enzymes have polymorphisms resulting from single-point mutations that cause kinetic differences in their respective enzyme activities. Simultaneous observation of these enzymes would be useful in investigating the association between these enzyme polymorphisms and alcohol-related problems. In this study amplified genomic DNA was amplified from nail clippings with two sets of primers for ADH2 and ALDH2 genes, respectively, in a micro test tube and the accuracy of the amplification was verified by direct sequencing. The PCR products were separated into four distinct bands by single-strand conformation polymorphism analysis. This genotyping method is fast, accurate. reliable and inexpensive, and requires the same amount of template DNA as non-simultaneous methods. In other words, the required amount of template DNA for this method is only half that required for the separate genotyping of ADH2 and ALDH2.

Alcohol Dehydrogenase↗
PubMed1999

Aldehyde dehydrogenase genotypes and male alcohol use disorders: a case-control study in Khon Kaen, north-east Thailand.

A genetic epidemiological case-control study on aldehyde dehydrogenase 2 (ALDH2) genotype and male probable alcohol use disorders (AUD) was performed in Khon Kaen province, northeast Thailand. One hundred and twenty-four of cases (probable AUD) were obtained from male villagers aged 18-65 years using the modified Michigan Alcoholism Screening Test-Thai version. The same number of controls were selected, being matched with the cases in terms of age (+/-4 years) within the same village. Marital status, education history and past or present histories of physical illnesses were essentially the same for the cases and the controls. All of the cases and 85.5% of the controls were current drinkers, and the cases tended to drink significantly more often than the controls. Genomic DNA was extracted from fingernails and ALDH2 genotypes were determined by polymerase chain reaction technique and digested by Ksp 632I. The ALDH2 genotypes of the cases and the controls were not significantly different: 90.3% versus 91.1% normal homozygote; 8.1% versus 8.9% heterozygote; and 1.6% versus 0.0% mutant homozygote, respectively. Among the normal homozygote, the daily amount of alcohol intakes of the cases were significantly larger than that of the controls (56.2+/-40.6g vs. 8.1+/-14.1 g), the same was found among the ALDH2 deficient (55.9+/-43.4 vs. 2.2+/-5.8 g). Multivariate analysis based on the conditional logistic regression model showed no significant association of AUD with ALDH2 genotype, marital status, education history, or past history of injury, however, occupation and daily amount of alcohol intake were found to be significantly associated with AUD (OR = 10.72, 95% CI = 1.15-99.99, P = 0.037, and OR = 1.12, 95% CI = 1.06-1.18, P = 0.000, respectively). Non-farmers showed 10.7 times larger risk of developing AUD compared to farmers, and the subjects had three times more chance of developing AUD for each increase of 10 g of the daily amount of alcohol intake.

Adult↗
PubMed1998

A hyperalgesic effect of intracerebroventricular cytokine-induced neutrophil chemoattractant-1 in the rat paw pressure test.

Cytokine-induced neutrophil chemoattractant-1 (CINC-1) is a member of the chemokine superfamily. The effect of intracerebroventricular (i.c.v) injection of CINC-1 on the mechanical nociceptive threshold in the rat was examined using the paw-pressure test. An i.c.v. injection of CINC-1 at doses of 1 and 10 pg/rat tended to decrease the nociceptive threshold for mechanical stimuli at 15 min after the injection, and significantly lowered the threshold at 30 min. The threshold stayed at these lowered level over 180 min after the injection. Lower (100 fg/rat) and higher (30 and 100 pg/rat, and 1 and 10 ng/rat) doses of CINC-1 had no effect on the mechanical nociceptive threshold. The present results suggest that CINC-1 facilitates mechanical nociception in the central nervous system (CNS).

Animals↗
PubMed1998

Expression of stromal cell-derived factor-1 and CXCR4 chemokine receptor mRNAs in cultured rat glial and neuronal cells.

The expression of the mRNAs for stromal cell-derived factor-1alpha and -1beta (SDF-1alpha and -1beta) and their receptor CXCR4 in cultured rat glial and neuronal cells was examined. SDF-1alpha mRNA was expressed intensely in astrocytes and weakly in neurons, but not in microglia. SDF-1beta mRNA was expressed weakly in these three types of cells. The expressions of SDF-1alpha and -1beta mRNAs in astrocytes were decreased by treatment with LPS (100 ng/ml) for 1-6 h but markedly increased by that for 24-72 h, whereas the expression of SDF-1beta mRNA in microglia was hardly changed by the treatment for 0.5-6 h, and was decreased by that for 24-48 h. The expression of CXCR4 mRNA was observed in astrocytes, microglia and neurons, and was not altered by LPS treatment.

Animals↗
PubMed1998

Localization of fractalkine and CX3CR1 mRNAs in rat brain: does fractalkine play a role in signaling from neuron to microglia?

Localization of the mRNAs for fractalkine, a CX3C chemokine, and for its receptor CX3CR1 was investigated in the rat brain. In situ hybridization study revealed that fractalkine mRNA was dominantly expressed in neuronal cells particularly in the olfactory bulb, cerebral cortex, hippocampus, caudate putamen and nucleus accumbens. In vitro study using enriched neuronal or glial culture supported the dominant expression of fractalkine mRNA in neurons. On the other hand, CX3CR1 mRNA was dominantly expressed in glial cells throughout the whole brain. The in vitro study suggested the cells expressing CX3CR1 mRNA are microglia, not astrocytes or neurons. Fractalkine appears to function as a signal molecule from neuron to microglia.

Amino Acid Sequence↗
PubMed1998

Diagnosis of the first Japanese patient with 3-oxo-delta4-steroid 5beta-reductase deficiency by use of immunoblot analysis.

UNLABELLED: A 3-oxo-delta4-steroid 5beta-reductase (5beta-reductase) deficiency is difficult to diagnose because severe liver damage can result in a similar pattern of metabolite excretion. We investigated the usefulness of immunoblot analysis for diagnosis of 5beta-reductase deficiency and quantitatively analysed urinary bile acids by gas chromatography-mass spectrometry in a 5-month-old Japanese boy with severe neonatal cholestasis associated with hypertyrosinaemia. A liver sample was examined by immunoblot analysis using monoclonal antibodies against 5beta-reductase. Urinary 3-oxo-delta4 bile acids accounted for 88.3% of total bile acids, 5alpha-bile acids for 0.9%, and primary bile acids for 9.1%. Immunoblot analysis of the liver tissue showed an indistinct band of 5beta-reductase. CONCLUSIONS: These findings suggest that this patient had a secondary 5beta-reductase deficiency due to severe liver damage, even though 3-oxo-delta4 bile acids constituted more than 70% of total urinary bile acids. However, the patient may possibly have had an inherited 5beta-reductase deficiency.

Amino Acid Metabolism, Inborn Errors↗
PubMed1998

A case-control study on male hepatocellular carcinoma based on hospital and community controls.

A case control study on male primary hepatocellular carcinoma(HCC) and hepatitis B or C virus and some potential risk factors, e.g. blood transfusion, aldehyde dehydrogenase 2(ALDH2) genotype and drinking habits, was performed using two controls, i.e. a hospital control(HC) and a community control(CC) in Fukuoka and Saga Prefectures. Cases were obtained from the Second Department of Internal Medicine, Kurume University Hospital. The HCs were obtained from inpatients of two general hospitals in Kurume and the CCs were randomly sampled from the Kurume citizens being matched with age and sex to each case. Based on the HCs, odds ratios(ORs) of developing male HCC were statistically significant due to HBsAg or anti-HCV antibody positive status. Some discrepancies were observed between the two controls, i.e. higher proportions of past histories of diabetes or hypertension, of ALDH2 typical homozygote(ALDH2(1)/ALDH2(1)), and of heavy drinkers among the HCs, suggesting slight deviation of the HCs from the CCs in alcohol related aspects. Although ORs regarding accumulated amount of alcohol intake by age 40 based on the HCs were insignificant, two of the three corresponding ORs based on the CCs were statistically significant. Judging from alcohol related aspects between the two controls, the ORs for alcohol based on the HCs seems to be underestimated.

Adult↗
PubMed1997

Type 2 interleukin-1 receptor mRNA is induced by kainic acid in the rat brain.

The in situ hybridization technique was used to examine the expression of type 2 interleukin-1 receptor (IL-1R2) mRNA in the rat brain following the systemic injection of kainic acid at a convulsive dose. The expression of IL-1R2 mRNA was not detected in any brain regions of the saline-injected control rats. 8 h after the systemic injection of kainic acid, weak expression of IL-1R2 mRNA was observed in the dentate gyrus and basolateral amygdaloid nucleus. At 12 and 24 h after the injection of kainic acid, IL-1R2 mRNA was markedly induced in various brain regions including the CA1 and CA3 fields of the hippocampus, dentate gyrus, basolateral amygdaloid nucleus, piniform cortex, claustrum, tenia tecta, arcuate hypothalamic nucleus, dorsomedial hypothalamic nucleus, suprachiasmatic nucleus, tuberal magnocellular nucleus and supramammillary nucleus. In these regions, the signals of IL-1R2 mRNA were observed on likely neuronal cells. Around the mediodorsal thalamic nucleus and the paraventricular thalamic nucleus, dispersed intense signals were observed on the non-neuronal cells. In addition, the expression of the mRNA on the venules was observed at 12 h. The strength of signals significantly decreased by 48 h after the injection. These findings revealed the spatiotemporal induction of IL-1R2 mRNA in the rat brain following the systemic administration of kainic acid, which has shown to cause neuronal degeneration, suggesting the pathological roles of IL-1R2 in the brain.

Animals↗
PubMed1997

Beta2-adrenoceptors on the glial cells mediate the induction of interleukin-1beta mRNA in the rat brain.

Interleukin-1beta mRNA was induced by i.c.v. injection of the beta-adrenoceptor agonist isoproterenol. Lower doses of procaterol, a beta2-adrenoceptor agonist showed stronger induction of the mRNA than isoproterenol. These inductions were primarily observed in the glial cells. On the other hand, the beta1-adrenoceptor agonist dobutamine induced expression of this mRNA only in the meninges. These results suggest the existence of a system for regulation of interleukin-1beta gene expression via beta2-adrenoceptors in the brain parenchyma.

Adrenergic beta-Agonists↗
PubMed1997

Intracerebroventricular injection of isoproterenol produces its analgesic effect through interleukin-1beta production.

The effects of isoproterenol, a beta-adrenoceptor agonist, on the production of interleukin-1beta in the brain and on mechanical nociception were examined in rats. Intracerebroventricular (i.c.v.) injection of isoproterenol at the dose of 3 microg/rat markedly induced interleukin-1beta mRNA in the molecular layer of the hippocampus, medial preoptic area, paraventricular thalamic nucleus, paraventricular hypothalamic nucleus, ventromedial hypothalamic nucleus, dorsomedial hypothalamic nucleus and central gray 1 h after injection. In these regions, interleukin-1beta mRNA was expressed mainly in the glial cells. The thresholds to the mechanical stimulation to the hind paw were elevated by i.c.v. administration of isoproterenol (1 to 10 microg/rat). When isoproterenol was given at the dose of 3 microg/rat, the analgesic effect showed two peaks. The first peak was observed at 60 min after injection and the second was observed at 180 min. The second phase of analgesia was antagonized by coadministration of interleukin-1 receptor antagonist. These results suggest that isoproterenol produces an analgesic effect, at least in part, through the induction of interleukin-1beta expression in the brain.

Analgesics↗
PubMed1997

Induction of macrophage inflammatory protein MIP-1alpha mRNA on glial cells after focal cerebral ischemia in the rat.

The distribution and cell source of macrophage inflammatory protein-1alpha (MIP-1alpha) mRNA induced by transient and permanent middle cerebral artery occlusion (MCAO) were investigated by a double in situ hybridization technique. The distribution and time course of the induction of MIP-1alpha mRNA were similar in the two MCAO models. MIP-1alpha mRNA was not detected in the sham-operated rat brain. MIP-1alpha mRNA was induced by MCAO with the peak of expression at 4-6 h after the onset of occlusion, and the signals of MIP-1alpha mRNA were observed in the ischemic core region at an earlier time point, and thereafter intensely in the penumbra of the ischemic area. The signals of MIP-1alpha mRNA were evident on Mac-1alpha mRNA-positive cells, but not on glial fibrillary acidic protein (GFAP) mRNA-positive cells, indicating that MIP-1alpha mRNA was induced in microglia/macrophages of the rat brain after focal cerebral ischemia.

Animals↗
PubMed1997

The R40H mutation in a late onset type of human ornithine transcarbamylase deficiency in male patients.

Ornithine transcarbamylase (OTC) deficiency is an X-linked trait and is one of the most frequent of the inherited urea cycle enzyme deficiencies. Most male patients with OTC deficiency develop a hyperammonemic crisis and die in the neonatal period or in early infancy. In contrast to those patients, in some male patients the disease first becomes overt in adolescence or during the reproductive age period. In the present report, we describe six such male patients who first developed clinical signs at ages ranging from 6 to 58 years, all of whom came from a limited area of the northern part of Kyushu Island in southern Japan. The mutation analysis disclosed a R40H mutation in exon 2 of the OTC gene in each of these patients. Transmission of this mutant gene through paternal lineage as well as through maternal lineage was documented in one family. The levels of mRNA of the mutant OTC gene expressed in transfected Cos 1 cells and in the liver tissue obtained by biopsy in one patient were both similar to those of the wild-type gene. The activity of the mutant OTC was, however, decreased to a level of 28% of the wild-type OTC, and the levels of the mutant OTC protein expressed in Cos 1 cells were decreased, as assessed by western blot analysis. Apparent Km values of the mutant enzyme for ornithine (1.1 mM) and carbamylophosphate (2.0 mM) were similar to those of the wild-type enzyme. Both enzymes gave similar pH-dependency profiles, giving a maximal activity at pH 7.8-7.9. Activity of wild-type OTC expressed in Cos 1 cells did not change after five cycles of freezing and thawing, whereas that of the mutant OTC decreased to 17% by this treatment. These results suggest that deficiency is due to inactivation of the mutant OTC under certain conditions.

Adolescent↗
PubMed1996

Biphasic effects of intracerebroventricular interleukin-1 beta on mechanical nociception in the rat.

The effects of interleukin-1 beta on the mechanical nociceptive threshold in rat were examined using the paw-pressure test. An intracerebroventricular (i.c.v.) injection of interleukin-1 beta at doses of 10 and 100 pg/rat caused hyperalgesia to mechanical stimuli. Higher doses of interleukin-1 beta (1 and 10 ng/rat) induced an analgesic effect. The coadministration of the interleukin-1 receptor antagonist completely antagonized the hyperalgesic and analgesic effects of interleukin-1 beta. An i.c.v. injection of alpha-helical-corticotropin-releasing factor [9-41] 15 min prior to interleukin-1 beta administration completely blocked the hyperalgesic and analgesic effects of interleukin-1 beta. An i.c.v. injection of sodium salicylate 15 min prior to interleukin-1 beta administration inhibited the hyperalgesic effect of interleukin-1 beta, but not the analgesic effect. These results suggest that interleukin-1 beta produces biphasic effects on the mechanical nociceptive threshold through the interleukin-1 receptor in the brain and that a corticotropin-releasing factor-mediated pathway is involved. Furthermore, the hyperalgesic effect of interleukin-1 beta may be mediated by prostaglandins.

Animals↗