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F Yamaguchi

Publications and source records attributed to F Yamaguchi.

At least 55 records · Page 3Linked to original sources
PubMed1996

Molecular cloning of two cannabinoid type 1-like receptor genes from the puffer fish Fugu rubripes.

The puffer fish, Fugu rubripes (Fugu), has been proposed as a model vertebrate genome. We have characterized two putative G-protein-coupled receptor encoding genes, FCB1A and FCB1B, obtained by degenerate PCR and low-stringency hybridization of a Fugu genomic library. These two genes show high homology to the human cannabinoid receptor type 1 (HCB1), but very low homology to the type 2 receptor. The amino acid sequences of the FCB1A and FCB1B genes are 66.2% identical, and the homology of each gene to HCB1 is 72.2 and 59.0%, respectively. The transcripts of both the FCB1A and the FCB1B receptors are abundant in the brain. No type 2 receptor could be cloned from Fugu. These data suggest that although two cannabinoid receptor-like genes are found in the puffer fish, both show similarity to the type 1 receptor found in human.

Amino Acid Sequence↗
PubMed1995

Purification and properties of endo-beta-1,4-D-galactanase from Aspergillus niger.

An endo-beta-1,4-D-galactanase was purified 1735-fold from a commercial enzyme preparation of Aspergillus niger. The endogalactanase was homogeneous by SDS-PAGE, having an apparent molecular weight of 32,000. It specifically hydrolyzed beta-1,4-D-galactan, and is shown to be capable of releasing galactosyl oligomers and galactose from the soybean pectic polysaccharides.

Aspergillus niger↗
PubMed1995

Relationship between molecular weights of pectin and hypocholesterolemic effects in rats.

Hypocholesterolemic activities and other properties of three different molecular weight pectin were examined. The low-molecular-weight pectin (M(r) not equal to 66,000) obtained by decomposition of original pectin (M(r) not equal to 750,000) had the properties of low viscosity and high solubility, but it lost hypocholesterolemic activities in rats. On the other hand, the medium-molecular-weight pectin (M(r) not equal to 185,000) had characteristics of both low viscosity and hypocholesterolemic activities.

Animals↗
PubMed1995

[Antigenicity study of iodixanol, a new non-ionic contrast medium].

Antigenic potential of iodixanol, a new non-ionic contrast agent, was evaluated by systemic anaphylaxis (SA) test and homologous passive cutaneous anaphylaxis (Homo-PCA) test using guinea pigs and IgE mediated heterologous PCA (Hetero-PCA) test using rats passively sensitized with mouse sera. SA test was conducted in guinea pigs sensitized with iodixanol at dose levels of 32 or 320 mgI/kg emulsified with Freund's complete adjuvant, followed by challenge with iodixanol (320 mgI/kg). Four- or 24-hr Homo-PCA test was performed with sera from the sensitized animals. Neither positive SA nor Homo-PCA reaction was observed. Hetero-PCA test was performed with the sera from the mice which were sensitized with iodixanol (32 or 320 mgI/kg) with aluminum hydroxide gel. No positive Hetero-PCA reaction was detected in the sera, followed by challenge with iodixanol (320 mgI/kg). Thus, it is concluded that iodixanol possesses no antigenic potential under the present experimental conditions.

Anaphylaxis↗
PubMed1994

Fibroblast growth factor receptor gene expression and immunoreactivity are elevated in human glioblastoma multiforme.

Glioblastomas were examined for abnormalities in fibroblast growth factor receptor (FGFR) expression by polymerase chain reaction and immunocytochemical analysis. Polymerase chain reaction analysis demonstrated that FGFR1 mRNA levels were significantly higher in glioblastomas than in normal brain adjacent to the tumor or in untransformed human brain. These results were consistent with immunocytochemical localization of FGFR1 protein in glioblastomas: glioblastoma cells exhibited intense FGFR1 immunoreactivity in frozen sections of tumor and low to undetectable FGFR1 immunoreactivity in adjacent normal brain or in normal white matter obtained from patients without neoplastic disease. Endothelial cells of capillaries and larger vessels within the tumor were devoid of FGFR1 immunoreactivity. All glioblastomas evaluated in the present study expressed FGFR1 mRNA and FGFR1 immunoreactivity. Examination of the FGFR1 gene by Southern blot analysis indicated that overexpression of FGFR1 mRNA in glioblastomas did not result from gene amplification. These results indicate that glioblastoma cells, in contrast to endothelial cells within the tumor, display increased levels of FGFR1. Therefore, FGFR1 signal transduction may be associated with increased autocrine growth activity of tumor cells and is probably not related to the increased endothelial cell proliferation associated with these tumors.

Base Sequence↗
PubMed1994

Differential expression of two fibroblast growth factor-receptor genes is associated with malignant progression in human astrocytomas.

Malignant astrocytomas, which are highly invasive, vascular neoplasms, compose the majority of nervous system tumors in humans. Elevated expression of fibroblast growth factors (FGFs) in astrocytomas has implicated the FGF family of mitogens in the initiation and progression of astrocyte-derived tumors. In this study, we demonstrated that human astrocytomas undergo parallel changes in FGF-receptor (FGFR) expression during their progression from a benign to a malignant phenotype. FGFR type 2 (BEK) expression was abundant in normal white matter and in all low-grade astrocytomas but was not seen in malignant astrocytomas. Conversely, FGFR type 1 (FLG) expression was absent or barely detectable in normal white matter but was significantly elevated in malignant astrocytomas. Malignant astrocytomas also expressed an alternatively spliced form of FGFR-1 (FGFR-1 beta) containing two immunoglobulin-like disulfide loops, whereas normal human adult and fetal brains expressed a receptor form (FGFR-1 alpha) containing three immunoglobulin-like disulfide loops. Intermediate grades of astrocytic tumors exhibited a gradual loss of FGFR-2 and a shift in expression from FGFR-1 alpha to FGFR-1 beta as they progressed from benign to malignant phenotype. These results suggest that differential expression and alternative splicing of FGFRs may be critical in the malignant progression of astrocytic tumors.

Alternative Splicing↗
PubMed1994

Basic fibroblast growth factor and fibroblast growth factor receptor I are implicated in the growth of human astrocytomas.

Malignant astrocytomas are highly invasive, vascular neoplasms that comprise the majority of nervous system tumors in humans. A strong association has previously been made between malignancy in human astrocytic tumors and increased expression of certain fibroblast growth factor (FGF) family members, including basic and acidic FGF. The influence of endogenous basic FGF on glioblastoma cell growth in vitro was evaluated using basic FGF-specific antisense oligonucleotides. These studies indicated that human glioblastoma cell growth in vitro, can be inhibited by suppressing basic FGF expression. Human astrocytomas also exhibited changes in FGF receptor (FGFR) expression during the course of their progression from a benign to a malignant phenotype. FGFR2 (bek) expression was abundant in normal white matter and in all low grade astrocytomas, but was not observed in glioblastomas. Conversely, FGFR1 (flg) expression was absent or barely detectable in normal white matter, but was significantly elevated in glioblastomas. Glioblastomas also expressed an alternatively spliced form of FGFR1 containing two immunoglobulin-like disulfide loops (FGFR1 beta), whereas normal human adult and fetal brain expressed a form of the receptor containing three immunoglobulin-like disulfide loops (FGFR1 alpha). Intermediate grades of astrocytic tumors exhibited a gradual loss of FGFR2 and a shift in expression from FGFR1 alpha to FGFR1 beta as they progressed from a benign to a malignant phenotype. The underlying cytogenetic changes that contribute to these alterations are not entirely understood, but abnormalities in the p53 tumor suppressor gene may influence expression of bFGF as well as the FGFR. These results suggest that alterations in FGFR signal transduction pathways may play a critical role in the malignant progression of astrocytic tumors.

Astrocytes↗
PubMed1994

Inositolhexakisphosphate (InsP6): an antagonist of fibroblast growth factor receptor binding and activity.

Fibroblast growth factors (FGF), which have been implicated in tumor cell growth and angiogenesis, have biological activities that appear to be mediated by both heparinlike extracellular matrix sites and transmembrane tyrosine kinase receptor sites. In the present study, we demonstrated that inositolhexakisphosphate (InsP6) inhibits basic FGF (bFGF) binding to heparin. Our spectrofluorometric analyses demonstrated that InsP6 not only bound to bFGF, presumably within the bFGF heparin-binding domain, but also protected bFGF from degradation by trypsin. Also, InsP6 inhibited the cellular binding of bFGF and other fibroblast growth factor family members such as acidic FGF (aFGF) and K-FGF in a saturable and dose-dependent manner. Furthermore, concentrations as low as 100 microM InsP6 inhibited bFGF-induced DNA synthesis in AKR-2B fibroblasts, as well as the growth of bFGF- and K-FGF-transfected NIH/3T3 cells. Together, these results indicate that InsP6 may serve as a useful antagonist of FGF activity.

Animals↗
PubMed1994

Application of hematopoietic progenitor assays for the estimation of hematotoxicity in rats.

In a study to employ progenitor-derived clonogenic assays of granulocyte-macrophage colony-forming units (CFU-GM) and erythroid colony-forming units (CFU-E) for the assessment of chemically induced hematotoxicity in rats, we sought the appropriate culture medium for each assay. Then, the effect of cyclophosphamide or phenylhydrazine on bone marrow cells was examined in vivo and in vitro. Oral treatment of rats with 25 mg/kg of cyclophosphamide significantly decreased the number of CFU-GM, which was an earlier and more sensitive index than were other hematological parameters tested. Direct exposure of the culture to cyclophosphamide had little effect on CFU-GM production, but addition of sera from rats pretreated with cyclophosphamide strongly depressed their formation, which suggested that the active metabolites of cyclophosphamide produced in the body may play an important role in toxicity. Subcutaneous injection of rats with 40 mg/kg of phenylhydrazine produced a marked increase in CFU-E 6-24 hr after injection. Direct exposure of the culture to phenylhydrazine had severe cytotoxic effects, but addition of sera from rats receiving phenylhydrazine resulted in increased numbers of CFU-E, probably indicative of increases in endogenous erythropoietin in donor rats. These results demonstrate that the proper use of progenitor assays in the in vivo and in vitro studies may be a valuable tool for approaching the mechanism underlying hematotoxicity.

Animals↗
PubMed1994

The rash of measles is caused by a viral infection in the cells of the skin: a case report.

Measles skin rash was immunohistochemically examined in an effort to detect virus antigen in skin samples taken from a 15-year-old girl with measles. A sectioned specimen obtained by punch biopsy from a 2nd-day skin lesion showed localized parakeratosis and acanthosis with multinucleated giant cells in the epidermis, thickening and cellular edema of epithelia in the hair follicles, and vascular dilation in the papillary plexus. Measles virus antigen was detected by ABC immunoperoxidase in the epidermis, follicular epithelia, and lympho-histiocytic cell infiltrates in the upper of the dermis. This rash deemed to be caused in part by direct viral infection of the epidermal cells.

Adolescent↗
PubMed1994

Antigenicity study of the new cognition-enhancing agent nefiracetam.

The potential antigenicity of the new cognition-enhancing agent nefiracetam (N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl)acetamide, DM-9384, CAS 77191-36-7) was investigated by tests for passive cutaneous anaphylaxis (PCA), systemic anaphylaxis (SA) and skin reaction in mice and guinea pigs. Mice were sensitized with nefiracetam (10-100 micrograms/animal) or nefiracetam-egg albumin (OA) mixture (10 micrograms/animal). No IgE antibodies to nefiracetam were detected in plasmas obtained from nefiracetam and nefiracetam-OA sensitized mice, indicating that nefiracetam has no immunogenicity or antigenicity eliciting potential. Guinea pigs were sensitized with nefiracetam (20-100 or 20 mg/kg) or nefiracetam-OA (2 mg/kg). No antibodies to nefiracetam were detected in the sera obtained from sensitized guinea pigs by PCA. Neither SA nor skin reaction was observed in the sensitized guinea pigs after the injection of challenge. These results suggest that nefiracetam possesses no antigenicity in mice and guinea pigs.

Anaphylaxis↗
PubMed1993

Basic fibroblast growth factor expression is required for clonogenic growth of human glioma cells.

Basic fibroblast growth factor (bFGF) is a heparin-binding protein, expressing potent mitogenic and angiogenic properties. Elevated levels of bFGF have been identified in human gliomas and glioma cell lines, suggesting that bFGF expression is involved in the aberrant growth patterns associated with these tumors. In the present study, the influence of bFGF on additional parameters of glioma cell malignancy was evaluated utilizing three distinct methods to suppress bFGF expression or activity including antisense oligonucleotide primers, a neutralizing monoclonal antibody or an inhibitor of the agonist action of bFGF: (1) The addition of 30 microM bFGF-specific antisense oligonucleotide primer to the human glioma cell line SNB-19 resulted in a 55% inhibition in colony formation in soft agar. This effect was dose-dependent and specific, as sense strand primer was ineffective in suppressing growth. In addition to exhibiting fewer colonies, antisense treatment significantly altered colony morphology. (2) SNB-19 cell growth in culture was suppressed in the presence of a neutralizing bFGF-specific monoclonal antibody. (3) Inositolhexakisphosphate, a newly identified antagonist of FGF binding and activity, suppressed SNB-19 cell growth in soft agar culture. These results demonstrate that bFGF may regulate glioma growth and progression independent of its role in tumor angiogenesis and that bFGF release or secretion may be required for these actions.

Astrocytes↗
PubMed1993

Evaluation of delayed type hypersensitivity to beta-lactam antibiotics in mice.

This study was designed to determine whether delayed type hypersensitivity could be evoked by protein-unconjugated beta-lactam antibiotics emulsified with Freund's complete adjuvant (FCA) in mice. The method providing the strongest sensitization was assessed by measuring footpad swelling induced by several biweekly intervals of subcutaneous injections of 0.8 mg/mouse cephalothin with FCA, followed by intradermal challenge with 1.0 mg/site cephalothin into the footpad in four different strains of female mice. A total of three and four injections, once every two weeks, in BDF1 and DBA/2 mice, respectively, produced the greatest potential for swelling. This swelling could be reinduced by the local passive transfer of cephalothin-primed splenocytes into the footpad of naive recipient mice. Moreover, the reaction was diminished by the addition of anti-Thy-1.2 monoclonal antibody with low-toxicity rabbit complement to cephalothin-primed splenocytes. Swelling in the footpad was therefore induced via the delayed type hypersensitivity reaction, indicating T-lymphocyte dependence. When the potential for beta-lactam antibiotics to elicit delayed type hypersensitivity was investigated in BDF1 mice, eight of the nine agents employed showed a 10-90% positive incidence. This result had a significant correlation (r = 0.76) with the data for skin reaction in guinea pigs, the method generally used for estimating allergenicity. These results suggest that this procedure may be a useful tool for evaluating delayed type hypersensitivity induction during the early development of novel antibiotics, since not only can sensitization be induced with protein-unconjugated antibiotic, but also because assessment can be made using a small amount of sample.

Animals↗
PubMed1993

Comparison of the IgG subclass distribution of anti-thyroid peroxidase antibodies in healthy subjects with that in patients with chronic thyroiditis.

The IgG subclass distribution of anti-thyroid peroxidase (TPO) antibodies in patients with chronic thyroiditis and in healthy subjects has been investigated. Anti-TPO antibodies in sera of patients with chronic thyroiditis were predominantly associated with IgG1, with a lesser contribution by IgG4 and IgG3. In contrast, anti-TPO antibodies of healthy subjects were exclusively associated with IgG4. Since structural differences in IgG subclasses reflect differences in their biological roles, these findings suggest that the role of anti-TPO antibodies in patients may differ from that in healthy subjects.

Adolescent↗
PubMed1992

Effects of inorganic iodide, epidermal growth factor and phorbol ester on hormone synthesis by porcine thyroid follicles cultured in suspension.

Porcine thyroid follicles cultured in suspension for 96 h synthesized and secreted thyroid hormones in the presence of thyrotropin (TSH). The secretion of newly synthesized hormones was assessed by determining the contents of thyroxine (T4) and triiodothyronine (T3) in the media and by paperchromatographic analysis of 125I-labelled hormones in the media where the follicles were cultured in the presence and absence of inhibitors of hormone synthesis. The hormone synthesis and secretion was modified by exogenously added NaI (0.1-100 microM). The maximal response was obtained at 1 microM. Thyroid peroxidase (TPO) activity in the cultured follicles with TSH for 96 h was dose-dependently inhibited by NaI. One hundred microM of NaI completely inhibited TSH-induced TPO activity. Moreover, both epidermal growth factor (EGF: 10(-9) and 10(-8) M) and phorbol 12-myristate 13-acetate (PMA: 10(-8) and 10(-7) M) inhibited de novo hormone synthesis. An induction of TPO activity by TSH was also inhibited by either agent. These data provide direct evidences that thyroid hormone synthesis is regulated by NaI as well as TSH at least in part via regulation of TPO activity and also that both EGF and PMA are inhibitory on thyroid hormone formation.

Animals↗
PubMed1992

Antigenicity of the new quinolone antibacterial agent levofloxacin.

An antigenicity study of a new quinolone antibacterial agent, (-)-(S)-9-fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo- 7H-pyrido[1,2,3-de][1,4]benzoxazine-6-carboxylic acid hemihydrate (lefovloxacin, DR-3355, CAS 100986-85-4), was carried out in mice, guinea pigs and rabbits with passive cutaneous anaphylaxis (PCA), systemic anaphylaxis (SA) and enzyme linked immunosorbent assay (ELISA). Mice were sensitized with DR-3355 (1-100 mg/kg) or DR-3355-ovalbumin (OA) conjugate (DR-3355-OA; 500 micrograms/kg). No IgE antibodies to DR-3355 were detected in the sera obtained from the DR-3355-sensitized mice, indicating that DR-3355 has no immunogenicity in mice. By using DR-3355-OA as a sensitizing antigen, DR-3355-specific IgE was produced successfully in 7 out of 10 sera, and 4 sera showed positive responses in 24-h PCA on intravenous injection of DR-3355 (40 mg/kg). These responses disappeared on challenge with a dose of 2.5 mg/kg. Guinea pigs or rabbits were sensitized with DR-3355 (2-100 or 2-20 mg/kg) or DR-3355-OA (2 mg/kg). No SA was observed in the sensitized guinea pigs after the intravenous injection of DR-3355 (40 mg/kg). No antibodies to DR-3355 were detected in the sera obtained from the sensitized guinea pigs and rabbits by PCA or ELISA. These results suggest that DR-3355 may not possess antigenicity in guinea pigs and rabbits. On the other hand, the results of PCA in mice suggest that DR-3355 may have eliciting antigenicity potential.

Anaphylaxis↗
PubMed1991

Increase of extracellular insulin-like growth factor I (IGF-I) concentration following electrolytical lesion in rat hippocampus.

The change of extracellular insulin-like growth factor I (IGF-I) level following electrolytical lesion in rat hippocampus was studied by intracerebral microdialysis technique. The microdialysis probes were inserted into the lesioned and normal side of hippocampus on the day and each week after making the lesion for a period of four weeks. The content of IGF-I in the dialysis perfusate was measured by a radioimmunoassay. One week after surgery, IGF-I level (mean +/- S.E.M.) increased from 235.6 +/- 25.4 pg/100 microliters perfusate (day 0) to 305.5 +/- 15.6 pg/100 microliters perfusate (day 7), and then decreased gradually. This suggests that there is accumulation or increase in secretion of IGF-I at the lesioned site, and that IGF-I might have an important role in vivo in the brain tissue recovery from damage.

Animals↗