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Biomedical subjects

H Shintaku

Publications and source records attributed to H Shintaku.

At least 37 records · Page 2Linked to original sources
PubMed1995

[A sensitivity of CRP determination of cord blood and neonatal serum for neonatal infection].

CRP was determined for 110 cord bloods and peripheral blood of 36 newborns collected within 72 hours after delivery for the early diagnosis of newborn infection. The determination of CRP was done by a counting immunoassay method using PAMIA-30(Sysmex, Kobe, Japan). Sample volume needed was small and the time for determination was short. Within-run and between-run precisions were satisfactory, with CV values being approximately 6%. The CRP of healthy newborns was lower than that of cord blood, and the mean value was 33.4 +/- 4.2 ng/ml and the value was not significantly different from that obtained from the newborn babies with turbid amnionic fluid or early rupture of a sac. The CRP gradually increased after delivery had a peak at 24 to 48 hours after delivery. This tendency was observed both in healthy and infected newborns. The data were divided into 6 groups depending on the time collected after delivery (6, 12, 24, 48, and 72 hours). The CRP of blood from infected newborns tended to have higher CRP than that of healthy newborns in each group. Increased amount of CRP (ng/ml/hrs) was calculated as ((CRP of peripheral blood at time x)--(CRP of cord blood))/x, and this value was significantly higher (p < 0.05) in infected newborns than in healthy newborns 12hrs and more after delivery. Thus, CRP might be useful for monitoring the newborn infection.

Biomarkers↗
PubMed1992

Inhibitory effect of CCK-8 and ceruletide on glutamate-induced rises in intracellular free calcium concentrations in rat neuron cultures.

To study the mechanism by which cholecystokinin octapeptide (CCK-8) and its potent analogue, ceruletide, prevent glutamate-induced neuronal cell death in rat neuron cultures, we examined the effect of both peptides on glutamate-induced increases in the intracellular free calcium concentrations ([Ca2+]i), which are known to be a crucial trigger of the neurodegeneration induced by glutamate. CCK-8 itself did not alter [Ca2+]i in rat neuron cultures. Glutamate increased [Ca2+]i in neuron cultures rapidly and markedly. CCK-8 and ceruletide significantly suppressed the increases in [Ca2+]i induced by glutamate. The maximum inhibitory effects of CCK-8 and ceruletide at 10(-6) M reached 43 and 46% of the response to glutamate, respectively. Gastrin-I and CCK-4 also significantly attenuated the increases in [Ca2+]i induced by glutamate. The inhibitory effect of CCK-8 was completely blocked by the selective antagonist for CCK-B receptors, (+)L-365,260, but not by (-)L-364,718, which is a selective antagonist for CCK-A receptors. CCK-8 significantly suppressed [Ca2+]i response to kainate and high concentrations of extracellular K+, but not to N-methyl-D-aspartate. With cultured astrocytes, CCK-8 did not inhibit the increment of [Ca2+]i induced by glutamate. These findings clearly demonstrated that CCK-8 and ceruletide inhibit glutamate-induced increases in [Ca2+]i in neuron cultures through CCK-B receptors, suggesting that CCK-8 may participate in the central actions of glutamate.

Animals↗
PubMed1992

Systemic administration of a cholecystokinin analogue, ceruletide, protects against ischemia-induced neurodegeneration in gerbils.

The neuroprotective action of a cholecystokinin octapeptide analogue, ceruletide, was evaluated in models of cerebral ischemia using Mongolian gerbils. Ceruletide significantly suppressed the hyperactivity and amnesia induced by ischemia when injected s.c. 30 min before 5-min occlusion of the bilateral common carotid arteries at room temperature or immediately after their reperfusion. Ceruletide also reduced behavioral changes in ischemic gerbils whose body temperature was maintained at 37 degrees C during the 3-min occlusion. In these groups, delayed neuronal cell death in the hippocampal CA1 area following ischemia was markedly attenuated by s.c. administration of ceruletide. On the other hand, ceruletide could not inhibit the behavioral changes or the neurodegeneration induced in the hippocampal CA1 area by 5-min occlusion at 37 degrees C. These findings indicate that peripheral injection of ceruletide produces a neuroprotective action against moderate cerebral ischemia, which is the first evidence suggesting the efficacy of ceruletide in neurodegenerative diseases.

Amnesia↗
PubMed1992

Frequency and distribution of phenylketonuric mutations in Orientals.

The frequency and distribution of eight mutations (R111X, IVS4nt-1, Y204C, R243Q, IVS7nt-2, W326X, Y356X, and R413P) in the phenylalanine hydroxylase gene of Orientals in Japan and Korea were examined by allele-specific oligonucleotide hybridization. The mutant alleles comprised 54 and 55% of the phenylketonuria (PKU) chromosomes examined in 36 patients in Japan and 10 patients in Korea, respectively. The spectrum of PKU mutations in Japan was similar to that in China, particularly in northern China, but different from that in Korea. The IVS4nt-1 mutation had a high frequency in Korea and southern China, due to the result of the founder effect and genetic drift. The R413P mutation, which may have originated in the regions surrounding the Baikal, expanded to northern China and Japan. We did not find Caucasian mutations in the Japanese or Korean PKU chromosomes. Thus, PKU mutations occurred after racial divergence between Caucasians and Mongoloids, and there were different founding populations for PKU in the two populations.

Alleles↗
PubMed1992

Ferritin, creatine kinase, and neopterin in subacute sclerosing panencephalitis.

To study the disease process in the brain in subacute sclerosing panencephalitis (SSPE), sequential changes in ferritin, creatine kinase (CK), and neopterin in the cerebrospinal fluid (CSF) of two patients with SSPE were compared with the changes in the clinical signs and symptoms and the findings by magnetic resonance imaging (MRI). On the basis of changes in various substances in the CSF, especially ferritin, CK and neopterin, we concluded that the high-intensity area in MRI might be evidence of local inflammation and the resulting cell damage. Ferritin, CK and neopterin seemed to be biochemical markers in patients with SSPE for detection of the extent of lesions, and their measurement may provide information useful for evaluation of the therapeutic response.

Adolescent↗
PubMed1992

[The metabolic basis of the hyperphenylalaninemias and tyrosinemia].

The hyperphenylalaninemias are caused by the defect of either phenylalanine hydroxylase (PAH) or tetrahydrobiopterin (BH4) cofactor. The former is diagnosed as phenylketonuria (PKU) or benign hyperphenylalaninemia, based on the serum phenylalanine values. The latter, so called malignant hyperphenylalaninemia, includes three enzyme defects, dihydropteridine reductase (DHPR), 6-pyruvoyl tetrahydropterin synthase (PT PS) and guanosine triphosphate cyclohydrolase (GTP-CH). Excess phenylalanine and its metabolites cause brain damage before 6 years of age. Deficiency of BH4 impairs two other hydroxylases (tyrosine and tryptophan), and severe neurological symptoms develop because of the lack of neurotransmitters. Tyrosinemia I, II, and III are different enzyme defects, fumarylacetoacetate hydrolyase (FAH), hepatic tyrosine aminotransferase (TAT), and 4-hydroxyphenylpyruvate acid oxidase, respectively. Tyrosinemia I is associated with severe involvement of the liver, kidney and central nervous system. Tyrosinemia II has mental retardation, palmar hyperkeratosis and corneal ulcers. Tyrosinemia III has mild mental retardation but no eye or skin manifestations.

Amino Acid Metabolism, Inborn Errors↗
PubMed1991

Protective effect of CCK-8 and ceruletide on glutamate-induced neuronal cell death in rat neuron cultures: possible involvement of CCK-B receptors.

Cholecystokinin octapeptide (CCK-8), ceruletide (CLT) and gastrin-I, which were added simultaneously with glutamate to rat neuron cultures, significantly suppressed the neuronal cell death induced by glutamate which can be observed from the efflux of lactate dehydroxylase into the culture medium. However, gastrin-I (1-13) had no effect on the response to glutamate. The inhibitory effect of CLT on glutamate-induced neuronal cell death could be completely blocked by a selective antagonist for CCK-B receptors, (+)L-365,260. These findings clearly indicate that CCK-8, CLT and gastrin-I exhibit a protective effect against glutamate-induced neurotoxicity via the CCK-B receptor.

Animals↗
PubMed1988

Tetrahydrobiopterin deficiency: assay for 6-pyruvoyl-tetrahydropterin synthase activity in erythrocytes, and detection of patients and heterozygous carriers.

6-Pyruvoyl-tetrahydropterin synthase (PTS), a key enzyme in the synthesis of tetrahydrobiopterin in man, is defective in the most frequent variant of tetrahydrobiopterin-deficient hyperphenylalaninaemia (atypical phenylketonuria). An assay for PTS activity in erythrocytes was developed. It is based on the PTS-catalysed formation of tetrahydrobiopterin from dihydroneopterin triphosphate in the presence of magnesium, sepiapterin reductase, NADPH, dihydropteridine reductase, and NADH, and fluorimetric measurement of the product as biopterin by high performance liquid chromatography (HPLC) after oxidation with iodine. The PTS activity was higher in younger erythrocytes, including reticulocytes, than in older ones. Fetal erythrocytes showed approx. four times higher activities than those of adults. Using a more purified human liver sepiapterin reductase fraction which gave a lower yield than a crude preparation, adult controls (n = 8) showed a mean erythrocyte PTS activity of 17.6 (range 11.0-29.5) microU/g Hb. Nine of 11 patients with typical PTS deficiency showed activities between 0% and 8% of the mean of controls, and two of 11 showed 14% and 20%, respectively. The obligate heterozygotes (n = 16) had activities of 19% (range 8%-31%) of the mean of controls, i.e., significantly less than the expected 50%. Four patients with the "peripheral" type of the disease showed 7%-10% of the mean of controls. Thus, the assay did not distinguish between patients and heterozygotes in every family. The assay is well suited to the identification of heterozygotes of PTS deficiency in family studies.

Adult↗
PubMed1988

Thienylpyrazoloquinolines: potent agonists and inverse agonists to benzodiazepine receptors.

Synthesis and structure-activity relationships of a series of 2-(thien-3-yl)- and 2-(thien-2-yl)-2,5-dihydro-3H-pyrazolo[4,3-c]quinolin-3-ones are reported. A number of the compounds possessed 1 order of magnitude higher affinity for the receptors than diazepam. Planarity was one of the structural requirements for binding to benzodiazepine receptors. The activities of agonists and inverse agonists were assessed on the basis of inhibition or facilitation of the pentylenetetrazole-induced convulsions, respectively. Thien-3-yl compounds exhibited inverse agonist activity whereas thien-2-yl analogues with a 5'-alkyl group showed agonist activity. Substitution on the quinoline moiety did not enhance in vivo activity. The most potent compounds were the 5-methylthien-3-yl derivative 6a as an inverse agonist and the 5-methylthien-2-yl compound 13a as an agonist.

Animals↗