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Biomedical subjects

M Horiuchi

Publications and source records attributed to M Horiuchi.

At least 181 records · Page 10Linked to original sources
PubMed1995

Bovine herpesvirus meningoencephalitis association with infectious bovine rhinotracheitis (IBR) vaccine.

During 1992, on a farm in the Tokachi district of Hokkaido, Japan, approximately 20 Holstein-Friesian calves showed neuroparalysis and died within 7-10 days after routine vaccination. Six male calves, aged about 1.5 months, were submitted to our laboratory for pathological examination and diagnosed as acute or subacute necrotizing meningoencephalitis due to bovine herpes virus (BHV) infection. The main necropsy findings included a few hemorrhages or clots, and malacic lesions localized in the cortical to subcortical area of the cerebrum. Histopathological brain lesions were characterized by laminar or focal necrosis of neurons, accompanying macrophages, polymorphonuclear cell infiltration, severe astrogliosis, and perivascular cuffing in all six calves. Nuclear basophilic inclusion bodies, which showed positive reaction with immunocytochemical staining of BHV antigen, were observed in the necrotic neurons, astroglia and oligodendroglia in five affected calves. BHV antigens were also seen in the cell bodies and cell processes of the necrotic neurons, which was indicative of cell-to-cell propagation of infection. There was a general tendency for more severe lesions to be located at the cortex to subcortex of the cerebrum. Milder lesions were observed in the cerebellum and brain stem. These findings suggest that the infectious route to the cerebrum in the present cases was through the olfactory bulbs and/or along the meninges beginning from the ethmoid bone, rather than through the trigeminal ganglia route as had been emphasized in studies dealing with experimental infection.

Animals↗
PubMed1995

Characterization of a rat type 2 angiotensin II receptor stably expressed in 293 cells.

A cDNA clone for the rat type 2 (AT2) angiotensin II receptor was stably transfected into human embryonic kidney 293 cells. Binding characteristics of CGP42112A (Kd = 0.18 nM, Bmax = 10.8 pmol/mg protein) and ligand specificity were indistinguishable from those obtained with the whole rat fetus and with transiently transfected COS-7 cells. Non-hydrolyzable guanine nucleotide analogs did not affect the ligand binding curve; interestingly, the guanine nucleotide analog's effect was observed in the presence of sulfhydryl reducing agent, suggesting that a certain redox condition may affect G protein coupling to this receptor. Using the established cell line, several second messenger systems were assessed. None of cAMP levels, cGMP levels, arachidonic acid release, or phosphotyrosine phosphatase activity was affected by angiotensin II stimulation of this receptor. Furthermore, the AT2 receptor did not undergo agonist-stimulated internalization. These results using the cloned receptor suggest that the transfected AT2 receptor fails to effectively couple to the major G protein-mediated signaling mechanisms and ligand-activated internalization in transfected 293 cells.

Angiotensin II↗
PubMed1995

Amino acid polymorphisms of PrP with reference to onset of scrapie in Suffolk and Corriedale sheep in Japan.

We investigated the relationships between amino acid polymorphisms of the prion protein (PrP), restriction fragment length polymorphisms (RFLP) of the PrP gene and the incidence of natural scrapie in Japan. Six variant alleles of the PrP gene were found in healthy sheep. Based on the substitutions at codons 112, 136, 154 and 171, these allelic variants were designated PrPMARQ, PrPTARQ, PrPMVRQ, PrPMAHQ, PrPMARR and PrPMARH. Each RFLP haplotype (e1h2, e1h2 or e3h1) consisted bo multiple alleles including PrPMARQ. Three of these variant alleles were found in scrapie-affected Suffolk sheep. PrPMARQ was associated with high disease incidence, PrPTARQ and PrPMARR were associated with low disease incidence. We found that one scrapie-affected Suffolk was homozygous for PrPMARR and four PrPSc-positive Suffolks carried PrPMVRQ. Both of two scrapie-affected Corriedales and two out of three scrapie-affected cross-breeds between Suffolk and Corriedale carried PrPMARH, suggesting that this allele associates with high incidence of scrapie in Corriedale and its cross-breeds.

Alleles↗
PubMed1995

A cellular form of prion protein (PrPC) exists in many non-neuronal tissues of sheep.

A cellular form of the prion protein (PrPC) is thought to be a substrate for an abnormal isoform of th eprion protein (PrPSc) in scrapie. PrPC is abundant in tissues of the central nervous system, but little is known about the distribution of PrPC in non-neuronal tissues of sheep, the natural host of scrapie. This study investigated the tissue distribution of PrPC in sheep. Although PrPC was abundant in neuronal tissues, it was detected in non-neuronal tissues such as spleen, lymph node, lung, heart, kidney, skeletal muscle, uterus, adrenal gland, parotid gland, intestine, proventriculus, abomasum and mammary gland. Neither PrPC nor PrP mRNA was detected in the liver. The tissue distribution of PrPC appears to be inconsistent with the tissues which possess scrapie infectivity, suggesting that factor(s) specific to certain cell types may be required to support multiplication of the scrapie agent.

Amino Acid Sequence↗
PubMed1995

Influence of alterations in the oral environment on speech production.

We examined the influence on temporal aspects of three consonants, /k/, /c/ and /s/, of alterations in the oral environment produced by either palatal augmentation or by an increase in the vertical dimension of occlusion. Voice onset time (V.O.T.) for /k/ and /c/ was influenced more than aspiration time by the palatal augmentation. Consonant duration for /s/ was also influenced by palatal augmentation. Significant influence of an increase in vertical dimension on the timing was not recognized. Speech disorder caused by the malformation of palate seems to be more frequent than that caused by vertical dimension. Adaptation to prostheses would seem to be definitely concerned with orosensory feedback.

Adaptation, Physiological↗
PubMed1995

Effect of an angiotensin II receptor antagonist, TCV-116, on neointimal formation following balloon injury in the SHR carotid artery.

1. In the present study, we examined the effect of a novel angiotensin II type I receptor antagonist, TCV-116, on carotid neointimal formation after balloon injury in SHR and WKY rats. 2. Oral administration of TCV-116 at a dose of 10 mg/kg per day reduced not only systolic blood pressure but also neointimal formation after carotid balloon injury. TCV-116 also suppressed cardiac hypertrophy. An angiotensin-converting enzyme inhibitor, lisinopril (20 mg/kg per day), had a similar effect to that of TCV-116. 3. In the WKY experiment, both TCV-116 and lisinopril suppressed neointimal formation as well as systolic blood pressure, but did not suppress cardiac hypertrophy. 4. Although SHR showed markedly enhanced neointimal formation after balloon injury compared with age-matched WKY rat, both TCV-116 and lisinopril showed similar suppressive effects on neointimal formation in both SHR and WKY rats. 5. These results confirm the important role of angiotensin II in neointimal formation following balloon injury. Further studies are needed to clarify the mechanism of the difference between SHR and WKY rats in the response of vascular smooth muscle cells.

Angiotensin II↗
PubMed1995

Relations between deletion polymorphism of the angiotensin-converting enzyme gene and insulin resistance, glucose intolerance, hyperinsulinemia, and dyslipidemia.

Recent reports have shown that the frequency of the homozygous deletion genotype (DD) of the angiotensin-converting enzyme (ACE) gene is highly associated with myocardial infarction and cardiomyopathy, particularly in those considered to be at low risk for coronary heart disease (CHD) on the basis of their apoB or LDL cholesterol concentrations. The present study was initiated to extend this inquiry by exploring the possibility that the ACE/DD genotype might be associated with risk factors not evaluated in the initial reports. Consequently, we determined the ACE genotype in 181 subjects, 124 with normal glucose tolerance and 57 with noninsulin-dependent-diabetes mellitus (NIDDM), and compared various aspects of glucose, insulin, and lipoprotein metabolism in the three ACE genotypes. In general, normal subjects with the DD genotype had a lower body mass index, were more insulin sensitive (as assessed by the insulin suppression test), and had lower plasma glucose and insulin responses to oral glucose. In addition, plasma triglyceride and cholesterol concentrations were lowest and HDL cholesterol concentrations highest in the DD group. However, the only statistically significant differences were between the ID and DD groups; the latter had lower values for body mass index, was more insulin sensitive, and had a lower plasma insulin response to oral glucose. Similar but insignificant trends were noted in the patients with NIDDM. The present results show that subjects with the ACE/DD genotype are not at increased risk for CHD because of insulin resistance, relative hyperglycemia and hyperinsulinemia, or a dyslipidemia characterized by a high triglyceride and low HDL cholesterol concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗
PubMed1995

Investigation of the phenylethanolamine N-methyltransferase gene as a candidate gene for hypertension.

Genetic mapping studies have located a gene, Bp1, that accounts for approximately 30% of the genetic variation in the stroke-prone spontaneously hypertensive rat (SHRSP) to a region on chromosome 10 containing the angiotensin-converting enzyme gene. In humans, the gene encoding phenylethanolamine N-methyltransferase (PNMT) was localized near the angiotensin-converting enzyme gene on human chromosome 17. Since most of human chromosome 17 is known to be homologous to rat chromosome 10 and PNMT is known to play a role in blood pressure homeostasis, we reasoned (1) that the rat gene encoding PNMT (Pnmt) may reside on chromosome 10 within the confidence interval containing Bp1 and (2) that Pnmt is a good candidate gene for Bp1. With the use of a somatic cell hybrid panel and genetic mapping techniques, Pnmt mapped within the confidence interval that contains Bp1. To examine further this possibility of Pnmt as a candidate for Bp1, we cloned and characterized Pnmts of the original parental strains, the Wistar-Kyoto rat and SHRSP from the Heidelberg colony. We did not identify any sequence differences between the Wistar-Kyoto rats and SHRSP in the primary structure, in 1077 bp of the 5'-flanking region, or in the 256-bp 3'-end region, making Pnmt an unlikely gene for the genetic basis of salt-loaded hypertension.

Amino Acid Sequence↗
PubMed1995

Cloning, characterization, and genetic mapping of the rat type 2 angiotensin II receptor gene.

The renin-angiotensin system plays an important role in blood pressure homeostasis, but the contribution of the type 2 angiotensin II receptor (AT2R) is still unclear. The reports that the AT2R gene has been mapped to the X chromosome in human and rat and the previous report of a gene, Bp3, on the X chromosome responsible for an increase in blood pressure have suggested that the rat AT2R gene (Agtr2) could be this gene. To elucidate whether Agtr2 is Bp3, Agtr2 was cloned. A simple sequence repeat in the 3'-flanking region of this gene was identified and used as a genetic marker to map Agtr2 to the X chromosome at 18.1 cM distal to the androgen receptor locus. This map position is outside the confidence interval reported for Bp3, demonstrating that Agtr2 cannot be Bp3. However, these data will enhance the research into the AT2R biology as well as the study of the X chromosome.

Alleles↗
PubMed1995

In vivo identification of a negative regulatory element in the mouse renin gene using direct gene transfer.

DBA/2J mouse contains two renin gene loci (Ren1d and Ren2d). Ren2d but not Ren1d is expressed in submandibular gland (SMG) while both are expressed in the kidney. Based on vitro studies, we have postulated that a negative regulatory element (NRE) in the renin gene promoter is involved in its tissue-specific expression. In this study, we examined the molecular mechanism at the in vivo level using direct gene transfer. Fragments of the Ren1d or Ren2d promoter were fused to a chloramphenicol acetyltransferase (CAT) gene expression vector. These constructs complexed in fusogenic liposomes were injected directly into the mouse SMG or intraarterially into the mouse kidney via the renal artery. The vector containing the CAT exhibited readily detectable in vivo expressions in both SMG and kidney. In the SMG, Ren1d fragment containing the NRE abolished CAT expression while deletion of the NRE restored CAT expression. The homologous fragment from the Ren2d promoter did not inhibit CAT expression while deletion of the 150-bp insertion resulted in the inhibition. Cotransfection of Ren1d construct with Ren1d-NRE oligonucleotides as transcriptional factor decoy restored CAT expression. Contrary to the SMG, transfection with Ren1d fragment-CAT construct or Ren2d fragment-CAT construct into the kidney resulted in similar levels of CAT expression. Interestingly, human c-myc NRE oligonucleotides which share homology with Ren1d-NRE competed effectively with these oligonucleotides for the regulation of Ren1d gene expression in vivo. This NRE sequence is also homologous to silencer elements found in multiple mammalian genes, suggesting the presence of a family of NRE/NRE binding proteins regulating expression of diverse genes.

Animals↗
PubMed1995

Atrial natriuretic peptide and antihypertensive action due to beta-blockade in essential hypertensive patients.

The effects of beta-blocker treatment on hemodynamics were studied in relation to plasma atrial natriuretic peptide (ANP) levels in 17 outpatients with essential hypertension. Administration of propranolol for twelve weeks to untreated subjects resulted in a significant (P < 0.001) rise in plasma ANP levels (from 37.9 +/- 21.2 to 66.7 +/- 46.2 pg/mL, mean +/- SD). Systolic and diastolic blood pressures were significantly decreased (P < 0.05 and P < 0.01, respectively). Heart rate was also significantly decreased (P < 0.001). On the other hand, a significant reduction of cardiac index was detected (from 4.12 +/- 1.34 to 2.96 +/- 0.75 L/min/m2, P < 0.01) with chronic administration of propranolol, suggesting a reflection of decreased cardiac function. A significant negative correlation was observed between %changes in systolic blood pressure and %changes in plasma ANP (r = -0.594, P < 0.05). These results suggest that the increased plasma ANP levels may contribute to the antihypertensive effect with propranolol.

Adrenergic beta-Antagonists↗
PubMed1995

Restriction endonuclease analysis of bovine herpesvirus type 1 isolates from calves with fatal encephalitis: comparison with vaccine virus.

Meningo-encephalitis in feedlot cattle sporadically occurred in the Tokachi area in northern Japan. The calves had been vaccinated intranasally with a mixed live-vaccine (infectious bovine rhinotracheitis virus, bovine viral diarrhea-mucosal disease virus, and parainfluenza 3 virus) for which intramuscular inoculation was indicated. Two additional live vaccines, bovine adenovirus type 7 and bovine respiratory syncytical virus, had been inoculated simultaneously. Eleven isolates of bovine herpesvirus type 1 were plaque-purified from two brains with fatal encephalitis; their viral DNAs were examined by restriction endonuclease analysis (REA) using PstI and HindIII. The REA patterns of the virus clones were almost identical to those of the vaccine strains 758-43, suggesting that the isolates from this outbreak of fatal encephalitis originated in the abnormally administered vaccine.

Administration, Intranasal↗
PubMed1995

Pilot-hole preparation for proper implant positioning and the enhancement of bone formation.

We have demonstrated a new insertion technique, "pilot-hole preparation", for proper implant positioning. The purpose of this study was to investigate the histological and biomechanical efficacies of the technique. We analyzed the influence of implant position on the stress distribution to the bone by the two-dimensional finite element method (FEM). In addition, we studied the influence of the pre-operative pilot-hole preparation on the bone tissue in vivo using histological examination.

Adult↗
PubMed1994

A spontaneous internal deletion of the c-myb protooncogene enhances transcriptional activation in bovine T lymphoma cells.

Three double negative (BoCD4-, BoCD8-) bovine T cell lines, BTL-PC3, BLT2, and Pr2181, which have been established from bovine lymphosarcomas, were examined for expression and molecular function of bovine c-myb genes. BTL-PC3 expressed 4.0- and 3.6-kilobase c-myb transcripts, and BLT2 and Pr2181 expressed a 3.8-kilobase c-myb message. The c-Myb protein (75 kDa) was detected in Pr2181 but not as a clear band in BLT2, while BTL-PC3 exhibited a 65-kDa c-Myb band in immunoprecipitation tests with anti-Myb antiserum. Nucleotide sequences for c-myb cDNA clones from BTL-PC3 and BLT2 indicated that the predicted bovine wild-type c-Myb from BLT2 consists of 640 amino acids whereas that from BTL-PC3 consists of 555 amino acids lacking 85 internal amino acids. This deleted DNA region (255 base pairs consisting of 85 amino acids) corresponds to the human genomic exon 9 encoding a negative regulatory domain in the c-myb gene. Upon cotransfections with reporter plasmids containing myb binding sites, the internally deleted c-Myb exhibited a 3-fold higher transcriptional activity than the wild-type c-Myb in chloramphenicol acetyltransferase assays. These results indicate that internal DNA deletion in the c-myb gene is directly involved in the enhancement of transcriptional activation in bovine T lymphoma cells.

Amino Acid Sequence↗
PubMed1994

Human type 2 angiotensin II receptor gene: cloned, mapped to the X chromosome, and its mRNA is expressed in the human lung.

The human type 2 angiotensin II receptor (AT2R) gene was isolated from a human genomic DNA library of adult female leukocytes. The putative coding region of the human AT2R gene is intronless. The primary structure of the human AT2R deduced from the nucleotide sequence of this putative coding region contains 363 amino acid residues and is highly homologous to the sequences of the rat and mouse AT2R. The human AT2R gene was mapped to the X chromosome using chromosomal assignment analysis with a human/rodent somatic cell hybrid panel. Northern blot analysis demonstrated a 3.0 kb mRNA in the human fetal lung and kidney and the human adult lung. These data and probes should enhance research in human AT2R biology.

Adult↗
PubMed1994

Abnormal gene expression and regulation in the liver of jvs mice with systemic carnitine deficiency.

Carnitine-deficient jvs mice expressed reduced levels of a group of genes which are preferentially expressed in the liver, including urea cycle enzyme genes (Biochim. Biophys. Acta 1138, 167-171, 1992). The expression of alpha-fetoprotein and aldolase A was elevated, indicating that the liver of jvs mice is undifferentiated or dedifferentiated (FEBS Lett. 311, 63-66, 1992). Studies of the hormone signal transduction pathway showed that serum cortisol and plasma glucagon levels of jvs mice were 2 and 3 times higher, respectively, than those of normal mice, and that the hormone binding activity of glucocorticoid receptor (GR) in the cytosol of jvs liver was 50% of normal mice, which reflected the amount of receptor protein in the cytosol. On the other hand, GR protein accumulated in the nuclear fraction in jvs mice. Exogenously administrated dexamethasone induced carbamoyl phosphate synthetase (CPS) and tyrosine aminotransferase (TAT) mRNAs in jvs mice, indicating that CPS and TAT genes in jvs mice are responsive to induction by glucocorticoid and cAMP. Analysis of transacting factors by gel retardation assay revealed that HNF-1, COUP-TF and SP-1 were detected at almost the same level in the hepatic nuclear fraction of jvs mice as in normal littermates, and C/EBP and CREB were a little higher in jvs mice, suggesting that these factors are probably not targets of jvs mutation causing abnormal gene expression in the liver. On the other hand, AP-1 binding activity was much higher in jvs mice from an early age, preceding the abnormal expression of urea cycle enzyme, and carnitine administration normalized AP-1 binding activity. We suggest that elevated AP-1 binding induced by carnitine deficiency is closely connected with the abnormal gene expression in the liver.

Animals↗