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Biomedical subjects

M Ishihara

Publications and source records attributed to M Ishihara.

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

[Transcranial magnetic stimulation of the accesory nerve--investigation of the site and mechanism of excitation in the cat].

The site where transcranial magnetic stimulation excites the accessory nerve was studied in 5 cats. Transcranial magnetic stimulation of the accessory nerve was recorded from the right trapezius. The accessory nerve was stimulated electrically at the C1 level, jugular tubercle and jugular foramen. The latencies of the compound muscle action potentials (CMAPs) for each portion were measured and compared with the magnetic response, which was coincidental with that of the jugular tubercle. The accessory nerve was then transected in steps distally from the C1 level, and CMAPs following magnetic stimulation were recorded at each step. The CMAPs disappeared following the nerve transection at the jugular tubercle. The results of both approaches in this study conclude that transcranial magnetic stimulation excites the accessory nerve at jugular tubercle. This stimulation site was anatomically coincidental with that of the facial nerve and trigeminal nerve in being right before the point where the nerve bends. Following the accessory nerve transection at the C1 level, the amputation stump was moved cranially, and CMAPs disappeared. CMAPs recorded after the accessory nerve was returned to its original position. These examinations suggested that sudden alteration of the traveling lie of the nerve participates in the mechanism of transcranial magnetic stimulation.

Accessory Nerve↗
PubMed1995

[Cooperative multicentric study on posttraumatic epilepsy].

A multicenter cooperative study was conducted to investigate factors influencing posttraumatic epilepsy (PTE) and to evaluate the prophylactic effect of anticonvulsants. A retrospective study of 102 PTE patients revealed the following typical clinical features: occurrence in young males, traffic accidents, contusion and/or cerebral hematoma. The latent period after the injury was longer in children. The percentage of EEG paroxysmal activity gradually increased as the generalized abnormality diminished. A retrospective-prospective study of 1998 patients who suffered a head injury between 1984 and 1988 was conducted till 1994. During the follow-up period, 62 patients (3.1%) developed PTE. The drop-out cases were excluded, and the 154 cases followed at least two years were analyzed. Statistical analysis of differences between patients with and without PTE suggested following factors: young, immediate early epilepsy (within 24 hours after injury; IMEE) and early epilepsy (within one week after injury). The risk with the highest relative risk rate was early epilepsy. Multiple regression analysis revealed that three factors, IMEE, early epilepsy and young age, contributed to the prediction of PTE. There was no significant difference in the percentage of patients having PTE in the group treated with anticonvulsants and the untreated group. Anticonvulsant treatment after head injury was unlikely to have a prophylactic effect on the development of PTE.

Adolescent↗
PubMed1994

Suppression of c-myc or fosB-induced cell transformation by the transcription factor IRF-1.

The transcriptional activator IRF-1 and its antagonistic repressor IRF-2 are regulators of the interferon (IFN) system and of cell growth. Overexpression of IRF-2 leads to transformation of NIH3T3 cells, and the concomitant overexpression of IRF-1 reverts this transformed phenotype. Here we report that c-myc- or fosB-transformed rat embryonic fibroblast cells can be reverted by the introduction of the IRF-1 gene. Thus, the anti-oncogenic function of IRF-1 is not limited to only IRF-2 overexpressing cells, suggesting the broad role of IRF-1 as a tumor suppressor.

Animals↗
PubMed1994

Cellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1.

The transcriptional activator interferon regulatory factor 1 (IRF-1) and its antagonistic repressor IRF-2 are regulators of the interferon (IFN) system and of cell growth. Here we report that embryonic fibroblasts (EFs) from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice) can be transformed by expression of an activated c-Ha-ras oncogene. This property is not observed in EFs from wild-type or IRF-2-/- mice but is still observed in EFs from mice deficient in both genes. The transformed phenotype of ras-expressing IRF-1-/- EFs could be suppressed by the expression of the IRF-1 cDNA. Thus, IRF-1 functions as a tumor suppressor. Furthermore, expression of the c-Ha-ras oncogene causes wild-type but not IRF-1-/- EFs to undergo apoptosis when combined with a block to cell proliferation or treated by anticancer drugs or ionizing radiation. Hence, IRF-1 may be a critical determinant of oncogene-induced cell transformation or apoptosis.

Animals↗
PubMed1994

A monomeric protein in the Golgi membrane catalyzes both N-deacetylation and N-sulfation of heparan sulfate.

Recent studies have shown that the rat liver heparan sulfate N-deacetylase/N-sulfotransferase is a glycoprotein encoded by a single polypeptide chain of 882 amino acids. Using radiation inactivation analyses, we have now determined that in rat liver Golgi vesicles the target size for the N-deacetylase is 88 +/- 14 kDa, whereas that of the N-sulfotransferase is 92 +/- 8 kDa. These results, together with previous biochemical and molecular cloning approaches, demonstrate that 1) in rat liver Golgi membranes there exists only on population of molecules expressing both activities, 2) the active protein in the Golgi membrane functions as a monomer, and 3) there is no evidence that a large independent protein acts as a regulator of either activity.

Amidohydrolases↗
PubMed1994

[Fat suppression failure artifacts at the susceptibility interface on frequency selective fat suppression MR imaging in the head and neck].

Fat suppression MR imaging is a valuable technique mainly used for the orbit, head and neck, and spine, where the high signal from fat can often obscure adjacent pathology. Fat suppression failure artifact manifested as a high signal area without geographic distortion. The purpose of this study was to investigate the frequency and common location of these artifacts in clinical MR imaging and to caution against their misinterpretation. Fat suppression MR imaging of the head and neck was performed in 30 consecutive patients. The artifact was found in the orbital floor (57%), the skull base (10%), and subcutaneous fat (10%), where the air-fat interface is parallel to the static magnetic field direction. The fat signal in the air-fat interface perpendicular to the static magnetic field was well suppressed. This artifact was independent of the duration of TE, frequency/phase encoding direction, and the strength of gradient amplitude, and appeared to be related to the amount of surrounding air. This may simulate pathology if fat suppression is only performed following Gd-DTPA administration. The radiologist should be aware of the presence of artifact by considering the geographic relation to the static magnetic field.

Adipose Tissue↗
PubMed1994

Molecular cloning and expression of a glycosaminoglycan N-acetylglucosaminyl N-deacetylase/N-sulfotransferase from a heparin-producing cell line.

Heparin has a higher content of N-sulfated glucosamine and L-iduronic acid than heparan sulfate. Deacetylation of N-acetylglucosamine followed by N-sulfation may be important steps differentiating the biosynthesis of these glycosaminoglycans. We have cloned, by cross-hybridization with the cDNA from rat liver heparan sulfate N-deacetylase/N-sulfotransferase, a protein from a heparin synthesizing mastocytoma derived cell line called MST. This protein, which has both N-deacetylase/N-sulfotransferase activities, has a predicted amino acid sequence homology of 70% with the above rat liver enzyme and is unique for the following reasons. 1) It was found to be encoded by a 3.8-kilobase mRNA that was unique to heparin-producing cells; an 8.5-kilobase mRNA encoding the rat liver enzymes has been found to occur in all mammalian cells tested on the basis of nucleic acid cross-hybridization; 2) the protein overexpressed in COS cells in its full-length transmembrane form or as a soluble secreted protein A chimera displayed ratios of N-deacetylase to N-sulfotransferase activities that were 4-8-fold higher than that observed for the enzyme found in liver that is involved in the biosynthesis of heparan sulfate. These results suggest that the MST-derived enzyme is probably unique to the production of heparin in mast cells.

Amidohydrolases↗
PubMed1994

KP-10, a novel protein kinase C substrate in intact mouse epidermal cells, is phosphorylated by novel protein kinase C eta and/or zeta.

Recently this group found an endogenous substrate protein for Ca(2+)-independent novel protein kinase C (nPKC), i.e. KP-10 (pI 4.7/25,500 M(r)), in primary cultured mouse epidermal cells [Nishikawa, K. et al. (1992) Cell. Signal. 4, 757-776]. In the present study, the nPKC isozymes which phosphorylate KP-10 in these cells were determined. Western blot analysis revealed that PKC alpha, eta and zeta were present in epidermal cell 105,000 g supernatants and that the content of PKC zeta was much higher than those of PKC alpha and eta. Neither PKC beta, delta nor epsilon was detected in the 105,000 g supernatants. Phosphatidylserine and phorbol 12-myristate 13-acetate (PMA)-dependent KP-10 phosphorylating activity was immunoprecipitated by anti-PKC eta and zeta antibodies, but not by antiPKC alpha antibody. These results suggest that PKC eta and/or zeta phosphorylate KP-10 and play pivotal roles in intracellular signal pathways in intact epidermal cells.

Amino Acid Sequence↗
PubMed1994

Discrimination by means of pulsed-field gel electrophoresis between strains of Campylobacter jejuni Lior type 4 derived from sporadic cases and from outbreaks of infection.

The cleavage patterns of the genomic DNA in 42 strains of Campylobacter jejuni Lior type 4, obtained from sporadic cases and from outbreaks of infection were analysed by means of pulsed-field gel electrophoresis (PFGE). The cleavage of DNA with SmaI and SalI restriction enzymes showed 16 distinct fragment patterns in 20 sporadic isolates, indicating that they were heterogeneous. On the other hand, the patterns of 22 isolates derived from two outbreaks showed the same unique restriction patterns, respectively. PFGE may therefore prove useful for subclassifying strains of C. jejuni Lior type 4 and for discriminating between strains derived from sporadic cases and those derived from outbreaks of infection.

Bacterial Typing Techniques↗
PubMed1994

Seasonal variations of nasal resistance in allergic rhinitis and environmental pollen counts. III: Efficacy of antiallergic agents.

We previously reported that, in a patient with Japanese cedar pollinosis, preseasonal increase in total nasal airway resistance (NAR) possibly caused from circannual endogenous rhythm was suppressed by preseasonal systemic administration of antiallergic agent. In this study, in order to determine the influence of preseasonal use of a topical antiallergic agent and seasonal administration of a peroral antiallergic agent, we made measurement of nasal airway resistance and pollen counts under the previous respective conditions in separated years. Preseasonal high mean values of total NAR for a couple of weeks was not suppressed by the preseasonal topical administration of ketotifen nasal spray in 1992 which was a low pollen season (974/cm2). However, the patient did not complained of severe episodes of hay fever at all throughout the season. Preseasonal increases in mean values of total NAR were observed in 1993 which was a high Japanese cedar pollen season (4,875/cm2) with NAR the same as untreated seasons. This may have been because the patient was not treated with preseasonal use of peroral azelastine. On extremely high Japanese cedar pollen count days further increased NAR occurred in the patient. The patient experienced relatively severe hay fever episodes, but used no other anti-histamine nor topical steroid during the season.

Administration, Topical↗
PubMed1994

Structural features in heparin which modulate specific biological activities mediated by basic fibroblast growth factor.

The biological activity of basic fibroblast growth factor (bFGF) is influenced greatly by direct binding to heparin and heparan sulphate (HS). Heparin-derived oligosaccharides have been utilized to determine the structural requirements present in the polymer that account for binding to bFGF. We had previously demonstrated that fragments > 6 mer can inhibit the interaction between cell surface heparan sulphate proteoglycan (HSPG) and bFGF, and bFGF-induced proliferation of adrenocortical endothelial (ACE) cells. In contrast, oligosaccharides > 10 mer can enhance the binding of bFGF to its high-affinity receptor or support bFGF-induced mitogenesis in ACE cells (Ishihara et al., J. Biol. Chem., 268, 4675-4683, 1993). We have extended these studies to size- and structure-defined oligosaccharides from heparin, 2-O-desulphated (2-O-DS-) heparin, 6-O-desulphated (6-O-DS-) heparin, carboxy-reduced (CR-) heparin and carboxy-amidomethylsulphonated (AMS-) heparin. Oligosaccharides from these polymers were fractionated on a bFGF-affinity column and were assessed as inhibitors or enhancers of specific bFGF-derived biological activities. The results of these studies indicate that both 2-O-sulphate and the negative charge of the carboxy group [L-iduronic acid (IdoA) residues] are required for specific interactions of heparin-derived oligosaccharides with bFGF and for modulation of bFGF mitogenic activity. In addition, the charge of the carboxy groups in uronic acids can be replaced by other functional groups with a negative charge, such as the amidomethyl sulphonate moiety described here.

Animals↗
PubMed1994

Structural requirements in heparin for binding and activation of FGF-1 and FGF-4 are different from that for FGF-2.

Size- and structure-defined oligosaccharides from heparin, 2-O-desulphated (2-O-DS-) heparin, 6-O-desulphated (6-O-DS-) heparin, carboxy-reduced (CR-) heparin, and carboxyamidomethylsulphonated (AMS-) heparin were utilized in characterizing the structural properties of heparin to specifically bind to basic fibroblast growth factor (FGF-2) and to modulate the mitogenic activity of FGF-2 (Ishihara, M. et al., Glycobiology, 4, 451-458, 1994). The previous results showed that both 2-O-sulphate groups and the negative charge of the carboxy group in iduronate residues are required for specific interaction with FGF-2, but the 6-O-sulphate groups in N-sulphated glucosamine (GlcNS) residues do not influence the interaction with FGF-2. In the present study, the same oligosaccharides were fractionated on a FGF-1- or FGF-4-affinity column, and were assessed as promoters of FGF-1- or FGF-4-induced proliferation of adrenocortical endothelial (ACE) cells and chlorate-treated ACE cells. The present results suggest that the smallest heparin-derived oligosaccharide binding to these growth factors with the highest affinity and promoting their mitogenic activities is a fully N-sulphated decasaccharide enriched in 2-O- and 6-O-sulphated disaccharide units. In contrast to our results with FGF-2, a high content of 6-O-sulphate groups in GlcNS residues is required for specific interaction with FGF-1 and FGF-4.

Binding Sites↗
PubMed1994

Amino acid sequence and inhibitory activity of rhesus monkey tissue factor pathway inhibitor (TFPI): comparison with human TFPI.

Rhesus monkey cDNA for tissue factor pathway inhibitor (TFPI) was cloned by means of the reverse transcriptase-polymerase chain reaction, using liver mRNA, and its nucleotide sequence was determined by sequencing five independent clones. Monkey TFPI was found to have a signal peptide of 28 amino acid residues and to be a mature protein of 276 amino acid residues, in which three and seventeen amino acid residue substitutions compared to human TFPI were found, respectively. All the cysteine residues, three putative carbohydrate-linked asparagine residues, and the P1 amino acid residues of each of the three Kunitz inhibitor domains were conserved in the two species. Recombinant monkey TFPI (rTFPI) was isolated from the culture medium of transformed Chinese hamster ovary cells. Amino acid sequence analysis and immunoblotting analysis, using polyclonal and monoclonal antibodies, showed that the carboxyl-terminal basic part of Rhesus monkey rTFPI had been truncated. The inhibitory activity of monkey rTFPI was compared with that of human rTFPI without the carboxyl-terminal basic part. The prothrombin time of human plasma was slightly more prolonged by the addition of monkey rTFPI than by that of human rTFPI. However, no significant differences were found between the potencies of human and monkey rTFPI as to the inhibition of factor Xa and tissue factor-factor VIIa complex.

Amino Acid Sequence↗
PubMed1994

Molecular genetic studies of HLA class II alleles in sarcoidosis.

Previous HLA serological studies showed positive associations of the DR52 antigen, the DR52-associated antigens (DR3, DR5 and DR6) and the DR8 antigen with sarcoidosis. To investigate the HLA alleles that may contribute to the genetic susceptibility to sarcoidosis at the DNA level, HLA-DRB1, -DRB3, -DQA1 and DQB1 genotyping using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was performed in 63 Japanese patients with sarcoidosis. The frequencies of the DR52-associated DRB1 alleles (DRB1*11, DRB1*12 and DRB1*14 except DRB1*1302), DRB1*08, DRB3*0101, DQA1*0501 and DQB1*0301 were significantly increased in patients compared with healthy controls. The significant increase of DRB3*0101, DQA1*0501 and DQB1*0301 could be explained by linkage disequilibrium with the DR52-associated DRB1 alleles. It must be noted that the DR8 haplotype, which does not possess the DRB3 gene, also showed a significant increase in sarcoidosis. These results suggest that the HLA-alleles responsible for the susceptibility to sarcoidosis are located at the HLA-DRB1 locus rather than the HLA-DRB3, -DQA1 and -DQB1 loci. In contrast, DRB1*1302 may confer resistance to the disease.

HLA-DQ Antigens↗