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Biomedical subjects

A Horii

Publications and source records attributed to A Horii.

At least 145 records · Page 8Linked to original sources
PubMed1995

Neuropharmacological mechanisms of emesis. I. Effects of antiemetic drugs on motion- and apomorphine-induced pica in rats.

The effects of diphenhydramine, domperidone, ondansetron, and diphenidol on motion- and apomorphine-induced pica (i.e., kaolin ingestion) in rats as the measure analogous to emesis in other species were examined. Diphenhydramine (10 and 20 mg/kg) and diphenidol (30 mg/kg) inhibited kaolin intake induced by 60-min double rotation, while domperidone and ondansetron did not. Kaolin intake induced by apomorphine (10 mg/kg) was inhibited by domperidone (2 mg/kg) and diphenidol (30 mg/kg), but not by diphenhydramine or ondansetron. These findings suggest that the emetic pathways through the inner ear (double rotation) and the chemoreceptor trigger zone (apomorphine) are pharmacologically independent and are mediated by histamine H1 receptors and dopamine D2 receptors, respectively. Diphenidol may inhibit a common locus of emesis.

Animals↗
PubMed1995

Neuropharmacological mechanisms of emesis. II. Effects of antiemetic drugs on cisplatin-induced pica in rats.

The effects of diphenhydramine, domperidone, ondansetron, and diphenidol on cisplatin-induced pica (i.e., kaolin ingestion) in rats as the measure analogous to emesis in other species were examined. Ondansetron (2 mg/kg) and diphenidol (30 mg/kg) inhibited kaolin intake induced by cisplatin (10 mg/kg), but diphenhydramine and domperidone did not. Diphenhydramine and diphenidol have been shown to inhibit kaolin intake induced by double rotation, while domperidone and ondansetron did not, and kaolin intake induced by apomorphine was inhibited by domperidone and diphenidol, but not by diphenhydramine or ondansetron. These observations, together with the present findings, suggest that the emetic pathways through the inner ear (double rotation), chemoreceptor trigger zone (apomorphine) and visceral afferent (cisplatin), are pharmacologically independent and are mediated by histamine H1 receptors, dopamine D2 receptors and serotonin 5-HT3 receptors, respectively. It is conceivable that diphenidol may inhibit the emetic center itself, although the receptor on which it acts is not known.

Animal Feed↗
PubMed1994

Cloning, characterization and chromosomal assignment of the human genes homologous to yeast PMS1, a member of mismatch repair genes.

Mutations in genes associated with the DNA mismatch repair system were considered to play important roles in predisposition to cancer, since hMSH2 and hMLH1, human homologues of yeast MSH2 and MLH1 as well as bacterial mutS and mutL genes, were found to be involved in hereditary nonpolyposis colorectal cancer (HNPCC). In addition, yeast PMS1 that is homologous to bacterial mutL and hexB, has also been proven to be related to the DNA mismatch repair system. As the first step to understand whether human homologue of the yeast PMS1 gene is associated with genetic predisposition to cancer, we have isolated and analyzed human counterpart of yeast PMS1 genes. DNA sequencing analyses indicated that human PMS genes constituted a multiple gene family and that some of the family members have been mapped to chromosomal bands 7q11.23 and 7q22 by fluorescent in situ hybridization.

Amino Acid Sequence↗
PubMed1994

Frequent replication errors at microsatellite loci in tumors of patients with multiple primary cancers.

Nearly 10% of cancer patients develop a second primary cancer within 10 years after surgical removal of the first tumor. Hence, detection of a genetic risk for developing multiple primary tumors would be of clinical importance. To investigate whether a genetic defect(s) involving the mismatch repair system constitutes an important risk factor in patients with multiple primary cancers, we examined replication errors (RER) at microsatellite loci in 79 primary cancers which had developed among 38 patients with multiple primary cancers. The RER(+) phenotype was observed at five microsatellite loci on chromosomes 2, 3, 11, or 17 in tumors from 34 (89%) of 38 patients with multiple primary cancers but only in 19 tumors from 174 patients (11%) with a single primary cancer. Our results suggested that: (a) genetic instability may play an important role in development of multiple primary cancers, and (b) testing for RER in a primary cancer may be an appropriate approach to detection of patients at high risk for developing multiple primary cancers.

DNA Repair↗
PubMed1994

Germ-line and somatic mutations of the APC gene in patients with Turcot syndrome and analysis of APC mutations in brain tumors.

The Turcot syndrome (TS) is a rare, probably autosomal recessive, disorder characterized by development of primary neuroepithelial tumors of the central nervous system (CNS) and numerous adenomatous colorectal polyps. To examine the possible involvement of mutations of the APC gene, which is responsible for familial adenomatous polyposis (FAP), in Turcot syndrome, we examined DNAs from TS patients for alterations in this gene by means of ribonuclease protection analysis. Germ-line APC mutations were detected in each of three unrelated cases of TS, and additional (somatic) mutations were observed in colonic adenomas that had developed in one of these patients. However, no somatic mutations in APC were found among 91 neuroepithelial tumors (medulloblastoma, glioblastoma, astrocytoma, and oligodendroglioma), whether sporadic or associated with TS. These results suggest that the APC gene is associated with pathogenesis of one feature of TS, but that at least one other gene is responsible for the genesis of neuroepithelial tumors in the CNS.

Adenomatous Polyposis Coli↗
PubMed1994

Histaminergic modulation of hippocampal acetylcholine release in vivo.

In order to elucidate the modulatory role of the histaminergic neural system in the cholinergic neural system, the acetylcholine release from the CA1-CA3 region in the hippocampus of anesthetized rats was studied by an in vivo microdialysis method coupled with HPLC-electrochemical detection. The mean value for the basal acetylcholine release was 0.98 +/- 0.04 pmol/20 min. The acetylcholine release was increased to 172% of the basal level when an electrical stimulation at 200 microA was applied to the tuberomammillary nucleus. An administration of alpha-fluoromethylhistidine (100 mg/kg i.p.) blocked the electrically evoked release of histamine both from the septal-diagonal band complex and the hippocampus, and abolished the electrically evoked release of acetylcholine from the hippocampus. Zolantidine (5 mg/kg i.p.) attenuated the increase in the electrically stimulated acetylcholine release, but pyrilamine (5 mg/kg i.p.) did not attenuate the increase in the acetylcholine release. These drugs showed no significant effect on the basal acetylcholine release. An administration of (R)-alpha-methylhistamine (5 mg/kg i.p.) caused a decrease in the acetylcholine release to 48.7% of the basal level, whereas thioperamide (5 mg/kg i.p.) caused an increase in the acetylcholine release 60 min after the injection. These results suggest that the histaminergic system may contribute to the modulation of the activity of the septohippocampal cholinergic system, mainly through H2 receptors.

Acetylcholine↗
PubMed1994

Effects of vestibular stimulation on acetylcholine release from rat hippocampus: an in vivo microdialysis study.

1. The effects of electrical stimulation to the round window of the inner ear and caloric vestibular stimulation on the in vivo release of acetylcholine (ACh) from rat hippocampus were investigated, using brain microdialysis coupled with high performance liquid chromatography-electrochemical detection. 2. Hippocampal ACh release was increased to 152% of the basal release by 1-Hz, 200-ms, and 500-microA electrical stimulation to the round window. This effect was dependent on current intensity. 3. Microinjection of 6,7-dinitroquinoxaline-2,3-dione (DNQX) (10 nmol/0.2 microliter), an antagonist of the non-N-methyl-D-aspartate (non-NMDA) type of glutamate receptor, into the medial vestibular nucleus blocked the increase of hippocampal ACh release by electrical stimulation to the round window. In contrast, microinjection of DNQX (10 nmol/0.2 microliter) into the ventral cochlear nucleus did not inhibit the increase of hippocampal ACh release by electrical stimulation to the round window. 4. Electrical stimulation of the round window increased histamine release from the medial septum, which is the origin of the hippocampal cholinergic terminals. However, the depletion of neuronal histamine by alpha-fluoromethylhistidine (100 mg/kg ip) did not suppress the vestibular-evoked release of hippocampal ACh. 5. Although caloric stimulation with water at 37 degrees C did not affect the hippocampal ACh release, the release was increased to 131% of the basal release by caloric stimulation with hot water at 45 degrees C and was also increased to 160% of the basal release by caloric stimulation with ice water, suggesting that the changes in activities of vestibular afferents increased the hippocampal ACh release.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1994

Structure, expression and chromosome assignment of the human catenin (cadherin-associated protein) alpha 1 gene (CTNNA1).

We have isolated the human alpha-catenin gene (CTNNA1), which encodes a cadherin-associated protein, and have determined its primary structure and chromosomal localization. The transcript of CTNNA1 is 3.4 kb long and consists of 16 coding exons encoding 906 amino acids and at least one 5' noncoding exon. The 102-kDa predicted protein is the same size as the murine homolog, and the amino acid sequences of the two proteins are 99.2% homologous. Analysis by reverse transcription-PCR revealed that this gene is expressed ubiquitously in normal tissues. It was mapped to chromosome band 5q31 by fluorescent in situ hybridization.

Amino Acid Sequence↗
PubMed1994

[Evaluation of the results of one session of extracorporeal shock-wave lithotripsy (ESWL) for a single urinary tract stone].

Fourteen hundred seventeen patients with a single stone under either general or epidural anesthesia were treated by one session of ESWL using the Dornier HM3 while 255 cases by one session of ESWL using the Dornier MPL9000 under no anesthesia but only with some analgesics, with 3 months' follow up available in all patients. The ratio of stone location in the kidney vs ureter was 7 to 3 in the Dornier HM3 and 5 vs 6 in the Dornier MPL9000. The overall success rate (stone free and residual stone fragments of less than 4 mm, 3 months after ESWL) was 58% (591 cases/1016 cases) for kidney stones with the Dornier HM3 and 35% (41/117) with the Dornier MPL9000. On the other hand, the overall success rate for ureter stones was 61% (245/401) with the Dornier HM3 and 70% (96/138) with the Dornier MPL9000. The overall success rate for stones of more than 10 mm, was poor when treated by the Dornier MPL9000 compared with the Dornier HM3.

Adolescent↗
PubMed1994

A case of Recklinghausen neurofibromatosis associated with membranous nephropathy.

A 68-year-old woman who had a history of Recklinghausen neurofibromatosis from 1964 showed nephrotic syndrome in 1989. Renal biopsy revealed membranous nephropathy. Various suspected causes of secondary membranous nephropathy were not found. Coexistence of Recklinghausen neurofibromatosis and membranous nephropathy has rarely been reported.

Aged↗
PubMed1993

Multiple forms of the APC gene transcripts and their tissue-specific expression.

We have detected multiple forms of RNA transcript from APC, the gene which is responsible for familial adenomatous polyposis (FAP). Transcriptional initiation occurs at three sites in two distinct non-translating exons at the 5' end of the gene. At least five different forms of 5' non-coding sequences, generated by alternative splicing, exist. The splicing mechanism seems to be regulated in a tissue-specific fashion, and one type of transcript contained an additional exon, which was transcribed specifically in brain. Analyses of mRNAs from two colorectal-tumor cell lines by reverse-transcriptase polymerase chain reaction (RT-PCR) revealed that one or another of the transcriptional forms was absent in both cell lines. This observation suggested the presence of mutations in the control region or the first exon of APC, or that mutation(s) could have affected the splicing efficiency or transcriptional initiation of the gene in these tumors. Furthermore, we found that the alternative splicing involving the 19 kDa protein of signal recognition particle (SRP19) gene, that is known to occur at exon 14 of APC, is also controlled in a tissue-specific manner, and one type of transcript lacked in some organs.

Adenomatous Polyposis Coli↗
PubMed1993

Somatic mutations of the APC gene in precancerous lesion of the stomach.

The adenomatous polyposis coli (APC) gene, responsible for familial adenomatous polyposis, is also associated with development of sporadic tumors in digestive system as colon, stomach, or pancreas. In order to investigate whether or not APC mutations occur as an early genetic event during gastric carcinogenesis, we examined somatic mutations of APC in flat adenomas of the stomach. DNAs isolated from flat adenomas were examined by means of an RNase protection analysis coupled with polymerase chain reaction (PCR) followed by DNA sequencing of the PCR products. By screening a mutation cluster region (MCR: codons between 1286 and 1513) of APC in which two-thirds of somatic mutations were detected in colorectal tumors, somatic mutations were found in four of ten flat adenomas: three of which caused truncation of the gene product due to a nonsense mutation or 4-bp deletion; one other was a point mutation that altered amino acid from alanine to threonine. Our results imply that APC plays a crucial role in an early step of gastric carcinogenesis, as was observed in colorectal carcinogenesis.

Adenoma↗
PubMed1993

Effect of unilateral vestibular stimulation on histamine release from the hypothalamus of rats in vivo.

1. We investigated the effect of unilateral vestibular stimulation on histamine release from the anterior hypothalamic area of urethan-anesthetized rats in vivo, using a brain microdialysis method coupled with high-performance liquid chromatography fluorometry. 2. The histamine release was increased to approximately 180% of the basal release by the electrical stimulation of the inner ear with 1 Hz, 500 microA, and 200 ms for 20 min. This effect was dependent on the current intensity. 3. Activation of the unilateral horizontal semicircular canal by middle ear irrigation for 15 min with 45 degrees C water increased the histamine release to approximately 200% of the basal release. 4. Irrigation of the middle ear with ice water for 15 min increased the histamine release to approximately 190% of the basal release. 5. The histamine release was not changed by the irrigation of the middle ear with 37 degrees C water and the irrigation of the auricle with ice water, which suggests that neither somatosensory stimulation to the middle ear nor nonspecific cold stress affects the histamine release. 6. All these findings suggest that the sensory mismatch signals induced by caloric stimulation and unilateral electrical vestibular stimulation activate the histaminergic neuron system in the brain.

Afferent Pathways↗
PubMed1993

Neuropharmacology of motion sickness and emesis. A review.

Histamine H1-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimulus, a signal for sensory conflict activates the histaminergic neuron system, and the histaminergic descending impulse stimulates H1-receptors in the emetic center of the brain stem. The histaminergic input to the emetic center through H1-receptors is independent of dopamine D2-receptors in the chemoreceptor trigger zone and serotonin 5HT3-receptors in the visceral afferent, which are also involved in the emetic reflex. Antihistamines block emetic H1-receptors to prevent motion sickness. Acetylcholine muscarinic receptors are involved in the generation of signals for sensory conflict. Anti-cholinergic drugs prevent motion sickness by modifying the neural store to facilitate the acquisition of habituation to provocative motion.

Animals↗
PubMed1993

Motion sickness induced by sinusoidal linear acceleration in rats.

The characteristics of linear acceleration to cause motion sickness of rats were examined using pica as a behavioral index of motion sickness. A vestibular sled was used to generate sinusoidal linear acceleration. At 0.4 Hz and with a peak acceleration of 0.15 G, the effectiveness of linear acceleration in inducing motion sickness was X-axis > Y-axis > Z-axis. At 0.4 Hz and along the X-axis, rats suffered from more severe motion sickness with a high peak G load (0.15 G) than with a low one (0.08 G). Along the X-axis and with a peak acceleration of 0.15 G, the severity of motion sickness was not related to frequency (0.4, 0.6 Hz).

Acceleration↗