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Biomedical subjects

J Yamada

Publications and source records attributed to J Yamada.

At least 19 recordsLinked to original sources
PubMed1992

Antiepileptic effects of CNK-602A, a novel thyrotropin-releasing hormone analog, on absence-like and tonic seizures of spontaneously epileptic rats.

The effects of CNK-602A (N-[(6-methyl-5-oxo-3-thiomorpholinyl) carbonyl]-L-histidyl-L-prolinamide), a novel thyrotropin-releasing hormone related analog, were investigated on absence-like seizure and tonic convulsion in the spontaneously epileptic rat (SER), which is a genetically defined double-mutant. When CNK-602A of 0.2-1 mg/kg was given intravenously to the animal, there were no changes in the background EEG except for an increase in low-voltage fast waves concomitant with behavioral alertness. However, CNK-602A suppressed absence-like seizure and tonic convulsion in a dose-dependent manner for over 1 h. These antiepileptic effects of CNK-602A on both seizures were antagonized by pretreatment with haloperidol (1 mg/kg, i.p.). It was found, using a brain in vivo microdialysis method, that CNK-602A at a dose of 1 mg/kg, which inhibits the seizures, increased the release of dopamine in the caudate nucleus. These results suggest that CNK-602A inhibits the seizures of SER in a similar manner to thyrotropin-releasing hormone (TRH), probably by increasing the release of dopamine in the central nervous system. In addition, the antiepileptic effects of CNK-602A were more potent and lasted longer than those of TRH.

Animals↗
PubMed1992

Induction of peroxisomal beta-oxidation enzymes by dehydroepiandrosterone and its sulfate in primary cultures of rat hepatocytes.

Treatment of cultured rat-hepatocytes with 50 microM dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) for up to 5 days resulted in a progressive increase in peroxisomal beta-oxidation and carnitine acetyltransferase activity. After 5 days, the increases in activity were 2.6- and 4.8-fold for peroxisomal beta-oxidation and 11.7- and 17.1-fold for carnitine acetyltransferase over the initial activity, in DHEA- and DHEAS-treated cells, respectively. The stimulation of the activity of these enzymes by the respective agents was dose-related; it was maximum with 50 to 100 microM DHEA and 50 to 250 microM DHEAS, although DHEAS was more effective for stimulation than DHEA. Western blot analyses revealed the induction of acyl-CoA oxidase, enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme and carnitine acetyltransferase in the treated cells. Moreover, induction of fatty acid omega-hydroxylase proteins (P-450IVAS) was also revealed. These results indicate that DHEA and DHEAS act directly on hepatocytes. The induction of hepatic peroxisomal beta-oxidation enzymes and several other enzymes in rats administered with DHEA could be accounted for, at least in part, by the direct action of DHEA and its sulfate-conjugate (DHEAS) on liver cells.

Animals↗
PubMed1992

Hyperglucagonemia induced in mice by tryptamine: involvement of the peripheral 5-HT2 receptors.

The effects of an indoleamine, tryptamine, on plasma glucagon levels were investigated in mice. Tryptamine induced dose-related increases in plasma glucagon levels. The hyperglucagonemia effects of tryptamine were completely antagonized by methysergide and ketanserin which have a high affinity to 5-HT2 receptors. In addition, the peripheral 5-HT2 receptor antagonist, xylamidine, also strongly inhibited tryptamine-induced hyperglucagonemia. Our results indicate that the peripheral 5-HT2 receptors mediate the increase in plasma glucagon levels induced by tryptamine and that these receptors may have a role in the control of glucagon secretion.

Animals↗
PubMed1992

A specific method for determination of peroxisomal beta-oxidation activity in cultured human skin fibroblasts using a specific substrate, C9: a possible application for screening of peroxisomal disorders.

We developed a specific method for direct determination of peroxisomal beta-oxidation activity in cultured human skin fibroblasts. When control fibroblasts were incubated with N-(alpha-methylbenzyl)azelaamic acid (C9), a specific peroxisomal substrate, C5 and C7, the chain-shortened products, were detected with cell concentration and incubation time dependencies and no other products including C3 were detected. In glutaric aciduria type I and type II fibroblasts, the formation rates of C2 units liberated from C9 were almost similar to that in control cells. In contrast to these cell types, the fibroblasts from patient of Zellweger syndrome, in which peroxisomal beta-oxidation was impaired, showed no conversion of C9 to C5 and C7. The lack of the C2 units liberation in Zellweger fibroblasts was not due to an impairment of mitochondrial beta-oxidation and/or activation of C9 to C9-CoA derivative for subsequent beta-oxidation reaction, but rather, appeared to be due to the specific defect of peroxisomal beta-oxidation system. These results indicate that C9 is a useful substrate for the estimation of peroxisomal beta-oxidation activity in cultured human skin fibroblasts.

Cells, Cultured↗
PubMed1992

Comparison of the inducing effect of dehydroepiandrosterone on hepatic peroxisome proliferation-associated enzymes in several rodent species. A short-term administration study.

The in-vivo effect of dehydroepiandrosterone (DHEA) on hepatic enzyme activities of rats, mice, hamsters and guinea pigs was investigated. After DHEA treatment (300 mg/kg body weight, per os, 14 days), the activities of peroxisomal beta-oxidation, catalase, carnitine acetyltransferase, carnitine palmitoyltransferase, lauric acid omega-hydroxylation, 1-acylglycerophosphocholine acyltransferase, malic enzyme and cytosolic palmitoyl-CoA hydrolase were increased in rats and in mice although to a smaller extent in the latter. These enzyme activities, however, were unchanged in hamsters with the exception of omega-hydroxylation (2.5-fold increase) and 1-acylglycerophosphocholine acyltransferase (2.0-fold increase). No significant changes were observed in any of these enzyme activities in guinea pigs. Immunoblot analysis confirmed the induction of peroxisomal acyl-CoA oxidase and enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme in rats and mice. These results indicate that there are species differences in the inducing effect of DHEA on hepatic peroxisome proliferation-associated enzymes, which correlates well with the enzyme induction observed with other peroxisome proliferators.

Animals↗
PubMed1992

Effects of growth hormones on bone formation and resorption in rainbow trout (Oncorhynchus mykiss), as examined by histomorphometry of the pharyngeal bone.

Effects of salmon and eel growth hormones (GHs) on bone metabolism in rainbow trout (Oncorhynchus mykiss) were studied using histomorphometry of their pharyngeal bones. When salmon GH (sGH) was injected intraperitoneally at a dose of 0.01 or 0.1 microgram/g/week for 10 times into fed trout, body growth in both length and weight was accelerated. Formation and resorption of bone were enhanced only by the higher dose of sGH. When a cholesterol pellet containing recombinant eel GH (reGH-pellet) was implanted subcutaneously into starved trout for 1 week (37 micrograms reGH/18 g fish), formation and resorption of bone increased, although activity of bone formation was low. The results indicate that the GHs increased both formation and resorption of bone, regardless of the nutritional status of the fish.

Animals↗
PubMed1992

Why are kana words named faster than kanji words?

Feldman and Turvey (1980) found that colors conventionally written in kanji (a logo-graphic script) are named slower than are the unconventional kana (a syllabic script) transcriptions of the kanji color words. This surprising finding was attributed to the closer relation of kana to phonology, which is consonant with the general dual-route theory. However, the present study has shown that kanji numerals are named faster than are the corresponding kana numerals. A hypothesis involving selection difficulty inherent in most kanji is presented to explain those apparently conflicting results. Some implications for further research on the kanji versus kana issue are also discussed.

Adult↗
PubMed1992

Spinal cord cells innervating the bilateral parabrachial nuclei in the rat. A retrograde fluorescent double-labeling study.

The internal lateral nucleus (IL) of the parabrachial nucleus receives information from the spinal cord. The IL perhaps relays nociceptive signals to the intralaminar nuclei of the thalamus, apparently being implicated in the motivational-affective component of pain reactions. However, cells of origin of spinal fibers to the IL have not been investigated enough. We intended to clarify these cells, as well as their shapes, by retrograde double-labeling techniques. Fast blue and diamidino yellow dyes were injected, respectively, into the left and right ILs. The distribution of double-labeled cells was almost the same as that of single-labeled cells on both sides of the spinal cord. The total number of bilateral double-labeled cells was highest in the dorsolateral part of the lateral funiculus (DL), followed, in order, by lamina I, the dorsomedial part of the lateral funiculus (DM), lamina V and lamina VII. A few double-labeled cells were seen in laminae II-IV, VI, VIII and X. The ratio of the total number of bilateral double-labeled cells to the total number of bilateral single-labeled cells through the spinal cord was 43% in the DL, 37% in the DM, 28% in lamina V and 24% in lamina I. The ratio was 10% or less in the other remaining laminae. No marked differences were observed between the shapes of double- and single-labeled cells.

Amidines↗
PubMed1992

A single serine:pyruvate aminotransferase gene on rat chromosome 9q34-q36.

It was found in our previous study (Oda et al., 1990. J. Biol. Chem. 265: 7513-7519) that in the rat two mRNAs encoding mitochondrial and peroxisomal serine:pyruvate aminotransferase (SPT/AGT) are formed from a single SPT/AGT gene through alternative transcription initiation in exon 1. In an attempt to analyze the mechanisms underlying this unique phenomenon, we have isolated genomic clones harboring the entire rat SPT/AGT gene. In the present study, the location of the rat SPT/AGT gene was determined to be in the q34-q36 region of chromosome 9 by fluorescence in situ hybridization. Southern blot analysis of rat genomic DNA revealed an allelic BamHI restriction fragment length polymorphism among three different inbred rat strains. These results indicated that a single copy SPT/AGT gene is located on chromosome 9q34-q36 in the rat genome. This locus has been assigned the gene symbol Spat.

Animals↗
PubMed1992

Chromosomal assignments of 17 structural genes and 11 related DNA fragments in rats (Rattus norvegicus) by Southern blot analysis of rat x mouse somatic cell hybrid clones.

DNA from 18 rat x mouse somatic cell hybrid clones, which segregated individual rat chromosomes, was analyzed by Southern blot for chromosomal gene assignments. Through the use of 17 DNA probes cloned from 7 rat genes, A2M, ATP1A1, ATP1A2, ATP1A3, B2M, GSTP, and SMST; 5 mouse genes, Ncam, Ngfg, Pim-1, Tcp-1, and Trp53; and 5 human genes, MBP, MYB, NEFM, SCN2A, and TCRGC1, 17 structural genes including 15 newly assigned genes and 11 related DNA fragments were assigned to particular rat chromosomes. Syntenic conservation of the genes among rats, mice, and humans is discussed.

Animals↗
PubMed1992

Loss of peroxisomal enzyme expression in preneoplastic and neoplastic lesions induced by peroxisome proliferators in rat livers.

Immunohistochemical staining of enoyl CoA hydratase (ECH), a key peroxisomal enzyme, revealed that the putative preneoplastic lesions induced in livers by administration of the peroxisome proliferator (PP) clofibrate (0.3% in diet) to rats for 60 weeks or more, lacked this enzyme so that they could be detected as ECH-negative foci. ECH and other peroxisomal enzymes such as acyl CoA oxidase, catalase and carnitine-dependent acetyltransferase were also either not or only weakly expressed in most hepatic hyperplastic nodules and hepatomas induced by ciprofibrate (0.025% in diet), Wy-14,643 (0.1%) or BR-931 (0.2%), while being strongly induced in surrounding hepatocytes. These results indicate that the expression of ECH and other peroxisomal enzymes is repressed in putative preneoplastic and neoplastic lesions induced by PPs in rat livers and that these peroxisomal enzymes might therefore be used as negative markers.

Animals↗
PubMed1992

Rat gene mapping using PCR-analyzed microsatellites.

One hundred and seventy-four rat loci which contain short tandem repeat sequences were extracted from the GenBank or EMBL data bases and used to define primers for amplification by the polymerase chain reaction (PCR) of the microsatellite regions, creating PCR-formatted sequence-tagged microsatellite sites (STMSs). One hundred and thirty-four STMSs for 118 loci, including 6 randomly cloned STMSs, were characterized: (i) PCR-analyzed loci were assigned to specific chromosomes using a panel of rat x mouse somatic cell hybrid clones. (ii) Length variation of the STMSs among 8 inbred rat strains could be visualized at 85 of 107 loci examined (79.4%). (iii) A genetic map, integrating biochemical, coat color, mutant and restriction fragment length polymorphism loci, was constructed based on the segregation of 125 polymorphic markers in seven rat backcrosses and in two F2 crosses. Twenty four linkage groups were identified, all of which were assigned to a defined chromosome. As a reflection of the bias for coding sequences in the public data bases, the STMSs described herein are often associated with genes. Hence, the genetic map we report coincides with a gene map. The corresponding map locations of the homologous mouse and human genes are also listed for comparative mapping purposes.

Animals↗
PubMed1992

Alterations of benzodiazepine receptor binding in tremor rats with absence-like seizures.

Tremor rats begin to exhibit clinical or electrical absence-like seizures after 6 weeks of age, and by 14 weeks of age, all have seizures. Central-type benzodiazepine receptor binding was investigated in tremor rats and control rats, aged 4 weeks and 16 weeks. Significantly lower benzodiazepine receptor density and no differences in affinity were found in the hippocampus of the tremor rats in comparison with that of control rats at both ages. This abnormality is considered to be due to a tremor gene and may be the cause of absence-like seizures in tremor rats. A significantly lower receptor density was found in the cerebellum at 4 weeks of age in the tremor rats than in the control rats. These changes may be related to tremorous movements in the tremor rats. Receptor density was significantly lower in the brainstems of tremor rats and control rats at 16 weeks of age than at 4 weeks of age, and the decrease was more marked in control rats. These facts may reflect a reduced decrease in the response to the dysfunction of gamma-aminobutyric acidergic neurons, or the function of the gamma-aminobutyric acid/benzodiazepine receptor system may be secondarily increased to suppress seizures in 16-week-old tremor rats.

Animals↗