Biomedical subjects

T Matsui

Publications and source records attributed to T Matsui.

At least 487 records · Page 27Linked 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

Nitric oxide synthase in cerebral ischemia. Possible contribution of nitric oxide synthase activation in brain microvessels to cerebral ischemic injury.

The results of our continuing studies on the role of nitric oxide (NO) in cellular mechanisms of ischemic brain damage as well as related reports from other laboratories are summarized in this paper. Repetitive ip administration of NG-nitro-L-arginine (L-NNA), a NO synthase (NOS) inhibitor, protected against neuronal necrosis in the gerbil hippocampal CA1 field after transient forebrain ischemia with a bell-shaped response curve, the optimal dose being 3 mg/kg. Repeated ip administration of L-NNA also mitigated rat brain edema or infarction following permanent and transient middle cerebral artery (MCA) occlusion with a U-shaped response. The significantly ameliorative dose-range and optimal dose were 0.01-1 mg/kg and 0.03 mg/kg, respectively. Studies using a NO-sensitive microelectrode revealed that NO concentration in the affected hemisphere was remarkably increased by 15-45 min and subsequently by 1.5-4 h after MCA occlusion. Restoration of blood flow after 2 h-MCA occlusion resulted in enhanced NO production by 1-2 h after reperfusion. Administration of L-NNA (1 mg/kg, ip) diminished the increments in NO production during ischemia and reperfusion, leading to a remarkable reduction in infarct volume. In brain microvessels obtained from the affected hemisphere, Ca(2+)-dependent constitutive NOS (cNOS) was activated significantly at 15 min, and Ca(2+)-independent inducible NOS (iNOS) was activated invariably at 4 h and 24 h after MCA occlusion. Two hour reperfusion following 2 h-MCA occlusion caused more than fivefold increases in cNOS activity with no apparent alterations in iNOS activity. Thus, we report here based on available evidence that there is good reason to think that NOS activation in brain microvessels may play a role in the cellular mechanisms underlying ischemic brain injury.

Animals↗

PubMed1995

Role of the kidney in the plasma clearance of angiotensinogen in the rat: plasma clearance and tissue distribution of 125I-angiotensinogen.

We studied the tissue distribution and plasma clearance of angiotensinogen (AGN) in rats following an i.v. injection of 125I-labeled AGN. The plasma clearance rate of [125I]AGN fits a two-compartment model with half-lives of 10.2 +/- 1.5 min and 4.1 +/- 0.5 h in non-treated rats, and the half-life of slower phase significantly increased to 10.2 +/- 1.1 h following bilateral nephrectomy. Radioactivity was predominantly distributed in the kidneys (4.9%), and to a lesser extent in the liver (1.8%), testis (1.2%), spleen (0.61%), heart (0.35%), lung (0.18%), thymus (0.03%) and brain (0.03%). The subcellular distribution of radioactivity in the kidney was 64% in the soluble fraction and 33% in the crude mitochondrial-lysosomal fraction. Sodium dodecylsulfate-polyacrylamide gel electrophoresis revealed that the radioactivity in the soluble fraction consisted of proteins corresponding to intact [125I]AGN, whereas the mitochondrial-lysosomal fraction contained additional radioactive proteins with molecular weights between 18,000 and 29,000. When isolated kidney cells were incubated with [125I]AGN at 0 degree C, the radioactive binding was saturable and specific with a Kd value of 4.8 x 10(-11)M, whereas incubation at 37 degrees C resulted in the appearance of degraded products of [125I]AGN in the medium. These results suggested that circulating AGN is cleared mainly by the kidneys via receptor-mediated endocytosis, which may play an important role in regulating plasma level of AGN.

Angiotensinogen↗

PubMed1995

Cloning of a retinoic acid-induced gene, GT1, in the embryonal carcinoma cell line P19: neuron-specific expression in the mouse brain.

Mouse P19 embryonal carcinoma cells can be reproducibly differentiated into neurons and glial cells upon treatment with high concentrations of retinoic acid (RA). To understand the molecular mechanisms that control early neural differentiation, we constructed P19 cell lines carrying an insertion of a gene-trap vector containing lacZ as the reporter gene and a G418 resistance gene. We tested expression of the lacZ gene during the RA-induced differentiation process of 300 clones selected with G418. Ten of these clones were stained with X-gal, and five of these ten clones showed up- or down-regulation of lacZ expression. We analyzed one clone, GT1, in which expression of the lacZ gene was markedly up-regulated. The 5'-flanking genomic DNA of the GT1 gene present at the site of integration was isolated by the plasmid rescue method, and we screened a cDNA library using this DNA gene as a probe. The GT1 cDNA is about 9000 bp long, with an open reading frame encoding 1840 amino acids. This amino acid sequence has a potential glycosaminoglycan attachment site (Ser-Gly-Gly-Gly) and three N-linked glycosylation sites, but no signal peptide. The sequence of GT1 does not show significant homology with any other known proteins, suggesting that GT1 may be a novel proteoglycan core protein. In situ hybridization revealed that GT1 mRNA was expressed ubiquitiously in the adult mouse brain. This expression was specifically localized in neurons but not in glial cells. Immunohistochemistry revealed that GT1 protein was also localized in neurons. These results suggest that this protein may play a fundamental role in neurons.

Amino Acid Sequence↗

PubMed1995

An orphan nuclear receptor, mROR alpha, and its spatial expression in adult mouse brain.

We have cloned cDNA encoding a mouse nuclear receptor mROR alpha which is a homolog of human retinoic acid receptor-related orphan receptor (hROR alpha). Cotransfection experiments revealed that mROR alpha activates transcription through a retinoic acid responsive element of the laminin B1 gene (lamRARE), but not through a RARE of RAR beta gene (beta RARE) or a synthetic palindromic thyroid hormone responsive element (TREpal). The most distal AGGTCA half-site among the three half-sites of lamRARE was sufficient for binding of mROR alpha and consequently for activation of transcription. Transactivation by mROR alpha was dependent on serum in culture medium after transfection, suggesting the presence of a possible ligand. Northern hybridization and in situ hybridization analyses revealed that mROR alpha is expressed in specific areas of the brain including thalamus and olfactory bulb as well as cerebellum where it is present at highest levels in Purkinje cells. In addition to regionally heterogeneous expression in brain, its expression was temporally regulated during differentiation of P19 cells into neural cells, but not into muscle cells. These observations suggest that mROR alpha plays important roles as a transcription factor not only in differentiation of neural cell lineages but also in the mature brain.

Amino Acid Sequence↗

PubMed1995

Zinc modulation of insulin-like growth factor's effect in osteoblastic MC3T3-E1 cells.

Whether the anabolic effect of insulin-like growth factor-I (IGF-I) in osteoblastic MC3T3-E1 cells is modulated by zinc, an activator of bone formation, was investigated in vitro. After subculture for 3 days, the cells were cultured for 72 h with IGF-I (10(-8) M). The peptide produced a significant increase of protein concentration, deoxyribonucleic acid (DNA) content, and cell number in the cells. These increases were markedly enhanced by the presence of zinc sulfate (10(-5) M), but not zinc-chelating dipeptide (beta-alanyl-L-histidinato zinc; 10(-5) M). Also, the cellular alkaline phosphatase activity was synergistically increased by the presence of both IGF-I and zinc sulfate. Thus, effect was not seen in the presence of both insulin (10(-8) M) and zinc sulfate (10(-5) M). The effect of zinc sulfate to enhance the IGF-I-increased alkaline phosphatase activity and protein concentration in the cells was clearly prevented by the presence of cycloheximide (10(-6) M), staurosporin (10(-8) M), or okadaic acid (10(-7) M) with an effective concentration. However, staurosporin had a partial inhibiting effect on the IGF-I or the IGF-I plus zinc-induced increases in cellular protein, although okadaic acid entirely blocked the IGF-I or the IGF-I plus zinc effect. The present study demonstrates that the anabolic effect of IGF-I in osteoblastic cells is enhanced by zinc ion. The enhancement by zinc may be mediated through the signaling pathway of protein kinase C and protein phosphatase in the cells.

3T3 Cells↗

PubMed1995

Binding of human IgM from a rheumatoid factor to IgG of 12 animal species.

The binding of IgM from a rheumatoid factor (RF-IgM) to IgG from 12 animal species was analyzed by an ELISA system. The RF-IgM bound various animal IgG with dissimilar affinities. The binding of RF-IgM to animal IgG was inhibited by addition of protein A, which binds some animal IgG by recognizing the junctional site on CH2-CH3 domains in the Fc region. As previously reported, no significant correlation was observed between the binding of RF-IgM to IgG and the content of galactose-free oligosaccharides, which is increased in IgG of rheumatoid arthritis patients or autoimmune mice. We suggest that the crucial epitope of IgG for RF-IgM binding is not the oligosaccharide structure generated specifically in IgG of autoimmune diseases but that RF-IgM may recognize a certain protein conformation of a region in IgG near the binding site of protein A.

Animals↗

PubMed1995

Characteristics of blood hemostatic markers in a patient with ovarian hyperstimulation syndrome who actually developed thromboembolism.

OBJECTIVE: To investigate whether a patient with ovarian hyperstimulation syndrome (OHSS) demonstrated characteristic changes in the blood hemostatic markers before she developed thromboembolism. DESIGN: Patients with OHSS had blood drawn to determine hemostatic markers and related factors. PATIENTS: Twenty-three OHSS patients, including a case complicated with thromboembolism. SETTING: The IVF-ET program of the Department of Obstetrics and Gynecology, The University of Akita, School of Medicine. MAIN OUTCOME MEASURES: Blood hemostatic markers and related factors. RESULTS: The patient with thromboembolism demonstrated marked leukocytosis and higher levels of activation in the blood markers related to fibrinolytic system, such as alpha 2 plasmin inhibitor, plasmin-alpha 2 antiplasmin complexes, and D-dimers, before the onset of this episode. CONCLUSION: Marked leukocytosis and higher levels of activation of the fibrinolytic system may be the signs of imminent thromboembolism in OHSS patients.

Adult↗

PubMed1995

Functional comparison of D-serine and glycine in rodents: the effect on cloned NMDA receptors and the extracellular concentration.

We compared the activity of free D-Ser on the potentiation of cloned NMDA receptors with that of Gly by using a Xenopus oocyte expression system. The extracellular concentration of free D-Ser and Gly was further studied by means of microdialysis. The ED50 values of D-Ser were three to four times lower than those of Gly in any combination of epsilon 1, epsilon 2, epsilon 3, or epsilon 4 and zeta 1. Site-directed mutagenesis of zeta 1 subunits revealed that some aromatic residues necessary for the action of Gly affected the ED50 value of D-Ser. This result showed that the residues play crucial roles in the action of D-Ser. In vivo microdialysis of rodent brain revealed that the extracellular concentration of free D-Ser in the frontal cortex (6.5 microM) was high enough to saturate the Gly site on the NMDA receptor, but that in the cerebellum was not. These findings suggest that D-Ser is a candidate of the endogenous potentiator of the NMDA receptor in the rodent frontal cortex.

Animals↗

PubMed1995

Tissue fibronectin is an endogenous ligand for galectin-1.

A 14K beta-galactoside-binding lectin (galectin-1) is present in many animal tissues. In a search for endogenous ligands, we surveyed galectin-1-binding proteins in human placenta. Extract of human placenta with 2 M urea was applied to a Sepharose 4B column conjugated with galectin-1 purified from frog (Rana catesbeiana) eggs. Two major proteins eluted with 100 mM lactose from the column-bound fraction showed apparent molecular masses of 220 and 180 kDa on SDS-PAGE under reducing conditions. Western blotting analysis using monoclonal antibodies indicated that these proteins were fibronectin and laminin, respectively. Most placental and amniotic fibronectins bound strongly to the column, whereas almost all plasma fibronectin passed through the column. The galectin-1, fibronectin and laminin were immunohistochemically shown to be co-localized in the extracellular matrix of placental tissue. In a cell attachment assay, rhabdosarcoma cells adhered to a plate coated with placental fibronectin, even in the presence of GRGDS peptide, if galectin-1 were also present. This adhesive effect of galectin-1 was inhibited by lactose. These results indicate that tissue fibronectin, as well as laminin, serve as endogenous ligands for galectin-1, suggesting that galectin-1 may play a role in assembly of the extracellular matrix, or in the control of cell adhesion based on lectin-extracellular matrix interaction.

Animals↗

PubMed1995

Prospective evaluation of simple morphological criteria for embryo selection in double embryo transfer cycles.

Preventing the occurrence of high-rank multiple pregnancies without reducing the pregnancy rate remains a high priority of in-vitro fertilization and embryo transfer programmes. Our previous study demonstrated that, if there is at least one embryo with a good morphological grade, then the transfer of two (a double embryo transfer) instead of three embryos does not result in a lower pregnancy rate, and that the influence of the number of embryos transferred becomes significant only when poor-quality embryos are transferred. This result allowed us to employ the simple policy of systematically selecting double embryo transfer cycles without affecting the pregnancy rate. Since January 1994, when patients < 37 years of age had more than two embryos available for transfer, only two instead of three embryos were transferred if at least one of the embryos demonstrated a good morphological grade. After a 1 year application of this policy, of the 147 cycles (group A) that fulfilled the above criteria, two embryos were transferred in 92 cycles, while three embryos were transferred in the other 55 cycles. The results of these cycles were compared to those of the control 144 cycles (group B) in which three embryos were transferred, prior to the application of this policy. The on-going pregnancy rates and the incidence of multiple and triplet pregnancies were 24% and 28%, 22% and 23%, and 2% and 9% in groups A and B respectively. The rates were not significantly different. In conclusion, although our prospective trial demonstrated a tendency of decreasing pregnancy rate and an invariable incidence of multiple pregnancies, the very low occurrence of triplets during this period indicated that this policy provided a practical compromise between achieving a high pregnancy rate and an acceptable incidence of triplet pregnancies.

Adult↗

PubMed1995

High incidence of embryo transfer cancellations in patients with polycystic ovarian syndrome.

This study was aimed at assessing the outcome of in-vitro fertilization (IVF) and embryo transfer in patients with polycystic ovarian syndrome (PCOS). The results of IVF and embryo transfer in PCOS patients (PCOS group, 78 cycles of 26 patients) were compared with those of a control group (423 cycles in 202 patients without male factor; age and ovarian stimulation protocol were matched). Although the pregnancy rate per transfer was not different in the two groups of patients (25 versus 34%, PCOS versus control group), the PCOS group had a significantly lower pregnancy rate per follicle aspiration (19 versus 31%, P < 0.05). A notable result was a significantly higher incidence of embryo transfer cancellations in the PCOS group (22 versus 8%, P < 0.01), which resulted from unpredictable failure of either oocyte recovery or fertilization. The incidence of unexplained complete failure of fertilization was significantly higher in the PCOS group (18 versus 5%, P < 0.01). These results may reflect a reduced quality of the oocytes in the PCOS group, and there was a subgroup of PCOS patients who repeatedly produced poor results of treatment. Although the ovarian stimulation regimen best suited to PCOS patients remains to be determined, special care should be taken during ovarian stimulation, especially when the PCOS patients had experienced unexplained failure of oocyte recovery or fertilization in the previous treatment cycle(s).

Adult↗

PubMed1995

Superoxide anions in the pathogenesis of talc-induced cerebral vasocontraction.

We have recently reported that sustained contraction of the canine basilar artery induced by the intrathecal injection of talc (crystallized hydrous magnesium silicate) mimicked delayed vasospasm following subarachnoid haemorrhage. The present study aims to examine the pathomechanism underlying talc-induced vasocontraction, from the viewpoint of free radical theory, which has been established as a cause of delayed vasospasm. We estimated the effects of a prolonged intrathecal infusion of human recombinant Cu/Zn superoxide dismutase (hr SOD) on the contraction of the basilar artery caused by the intrathecal injection of talc in beagle dogs, which were assigned to the three groups: G1, sham operation with saline treatment; G2, talc injection with saline treatment; and G3, talc injection with 2 ml of hr SOD (7 x 10(4) U/ml) treatment. Talc administration resulted in the reduction in the angiographic calibre of the basilar artery by 63 and 61% on days 3 and 7 (G2). The treatment with hr SOD (G3) led to a significant attenuation of talc-induced contraction of the basilar artery on days 3 (P < 0.05 vs. G2) and 7 (P < 0.05 vs. G2). In the basilar artery wall of days 3 and 7 in G2, pathological changes such as myonecrosis, cytoplasmic vacuolation and detached intercellular junctions were observed. However, these pathological changes almost disappeared in G3. The present findings suggest that superoxide anions may initiate and/or mediate talc-induced vasocontraction and subsequent structural damage of the basilar artery.

Animals↗

PubMed1995

ABO blood group genotype and plasma von Willebrand factor in normal individuals.

von Willebrand factor (vWF) is a multimeric plasma protein with ABO (H) blood group sugar chains. We investigated a total of 330 plasmas from normal individuals having various ABO genotypes, with special reference to vWF antigen and its platelet glycoprotein-Ib-related biological activities, termed ristocetin cofactor (RCof) and botrocetin cofactor (BCof). RCof reflects the biological activity of higher vWF multimers, while BCof reflects that of vWF of multimers of all sizes. Plasmas from normal individuals carrying one O gene (genotypes AO and BO) had slightly, but proportionally lower levels of vWF antigen, RCof, and BCof than those carrying no O gene (genotypes AA, AB, and BB). Normal plasmas from individuals carrying two O genes (genotype OO) showed much lower values for these parameters than the other plasmas, as previously reported. However, multimeric analysis of plasma vWF antigen revealed no differences among the different genotypes.

ABO Blood-Group System↗

PubMed1995

Tissue-specific distribution of a novel C-terminal truncation retinoic acid receptor mutant which acts as a negative repressor in a promoter- and cell-type-specific manner.

A cDNA clone which encodes a truncation form of the gamma subtype of the retinoic acid receptor (RAR gamma) has been isolated. The mutant RAR gamma (RAR gamma Bm382) has lost its 65 C-terminal amino acids, thus truncating a part of the dimerization and activation domains. By using a reverse transcription-coupled PCR technique, it was shown that RAR gamma Bm382 is expressed at different levels in various mouse tissues and that the level of its expression does not correlate with that of normal RAR gamma B. Cotransfection studies revealed that RAR gamma Bm382 acts as a repressor of normal RARs in a promoter- and cell-type-specific manner. Transcription of beta RARE and TREinv promoters was inhibited by RAR gamma Bm382 in both HeLa and F9 cells. Unlike these two promoters, however, RAR gamma Bm382 did not inhibit transcription of the TREpal promoter in HeLa cells but did so in F9 cells. Moreover, while transcription of the lamRARE promoter was inhibited by RAR gamma Bm382 in both HeLa and F9 cells, the inhibition was not observed when F9 cells were induced to differentiate with retinoic acid and dibutyryl cyclic AMP. DNA-binding analysis revealed that RAR gamma Bm382 is able to form a heterodimer with the retinoid X receptor and bind to the different types of retinoic acid response elements with almost the same efficiency as normal RAR. By comparison with effects of other truncation mutants created in vitro, it was suggested that the C-terminal end of the ligand binding domain of RAR is crucial for determining the specificity of transactivation by RAR. Given these observations, we discuss the possibility that protein factors which mediate retinoic acid response element- and cell-type-specific transactivation by RAR are present.

Amino Acid Sequence↗

PubMed1995

Activation of the renin-angiotensin system in anti-glomerular basement membrane antibody-induced glomerulonephritis.

Activity of the renin-angiotensin system in the nephrotic syndrome was investigated in rats with acute nephritis induced by anti-glomerular basement membrane (GBM) antibody. Injection of anti-GBM antibody resulted in a transient 2-fold elevation of both plasma renin and angiotensinogen with a peak at 12 h. Angiotensinogen mRNA levels in the liver also rapidly and transiently increased 4-fold at 3 h. The manifestation of acute nephritis, indicated by proteinuria, hypoalbuminemia, hypercholesterolemia and an increase in serum creatinine, following injection of anti-GBM antibody, was inhibited by a single administration of the selective angiotensin II type 1 receptor antagonist TCV-116 (1 mg/kg, p.o.) 2 h before an injection with the antibody, but not by successive administration of this drug for 1 week from 3 d after the injection of antibody. These results suggested that the enhanced generation of angiotensin II by elevated levels of both renin and its substrate in the early phase of anti-GBM nephritis promotes the evolution of acute nephritis via angiotensin II type 1 receptor.

Angiotensin Receptor Antagonists↗

PubMed1995

Antihypertensive effects of angiotensin fragments in SHR.

When angiotensin fragments, Val-Tyr and Angiotensin III (ANG III), with potent ACE inhibitory activity were intravenously administered to spontaneously hypertensive rat (SHR), a significant reduction of diastolic blood pressure was observed. After incubation of ANG III with SHR plasma, four fragments with ACE inhibitory activity, Val-Tyr (ANG (3-4)) (IC50 = 26.0 microM), Ile-His-Pro-Phe (ANG (5-8)) (11.6 microM), Tyr-Ile-His-Pro-Phe (ANG (4-8)) (457.5 microM), and Val-Tyr-Ile-His-Pro-Phe (ANG (3-8)) (6.55 microM), were confirmed to generate in SHR plasma. Compared the metabolic behavior of ANG II in SHR plasma with that in normotensive Wistar plasma, the initial degradation rate (3.07 nmol/ml/min) in Wistar plasma was about 2-fold higher than that in the SHR one (1.75 nmol/ml/min).

Amino Acid Sequence↗

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↗