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Biomedical subjects

F Ito

Publications and source records attributed to F Ito.

At least 163 records · Page 9Linked to original sources
PubMed1992

Specific immunofluorescent staining of pathogenic treponemes with a monoclonal antibody.

Two hybrid cell lines which produced mouse monoclonal antibody to the DAL-1 street strain of Treponema pallidum subsp. pallidum were established. These monoclonal antibodies strongly reacted with T. pallidum subsp. pallidum (Nichols strain, DAL-1, and two other street strains, strains MN-1 and MN-3) and T. pallidum subsp. pertenue by indirect microimmunofluorescent antibody and enzyme-linked immunosorbent assay techniques, but they did not react with normal rabbit testicular tissue. These monoclonal antibodies did not react with nonpathogenic treponemes, such as T. phagedenis Reiter, T. denticola MRB, T. refringens Noguchi, or other spirochetes, such as Borrelia burgdorferi and Leptospira interrogans serovar pomona in microimmunofluorescent antibody smear slides or in Western blots (immunoblots). While unlabeled antibodies are useful for investigating the antigenic structures of T. pallidum, we labeled these monoclonal antibodies with fluorescein isothiocyanate and used them for diagnosing syphilis by direct staining of lesion exudate or T. pallidum subsp. pallidum in formalin-fixed tissues from patients suspected of having syphilis. Both monoclonal antibodies were directed against antigens of T. pallidum subsp. pallidum with a molecular weight of 37,000 as determined by the Western blotting technique.

Animals↗
PubMed1992

Hepatocyte growth factor and transforming growth factor-beta stimulate both cell growth and migration of human gastric adenocarcinoma cells.

Hepatocyte growth factor (HGF) induced scattering and cell migration of human gastric adenocarcinoma MKN-74. HGF also significantly promoted the growth of MKN-74 cells in a dose-dependent manner, although HGF is reported to be antiproliferative for the growth of tumor cell lines. This result indicates that HGF stimulates cell proliferation of not only normal epithelial cells but also certain carcinoma cells. Furthermore, transforming growth factor-beta (TGF-beta), which is recognized to inhibit the growth of most epithelial cells, additively enhanced both the cell proliferation and migration induced by HGF. These additive effects of HGF and TGF-beta may be responsible for the tumor invasiveness and uncontrolled growth of certain types of carcinoma.

Adenocarcinoma↗
PubMed1992

[A patient with epilepsy presenting developmental regression after seizures--consideration of the mechanism from the findings of CT-scan and SPECT].

We report a 6-month-old female infant with frequent brief seizures who subsequently showed developmental regression. CT-scans right after her seizures revealed enlargement of bilateral subdural space more on the right side with an evidence to suggest destruction of the blood brain barrier in enhanced CT-scan, CT-scan, one month after the onset, showed diffuse brain atrophy. 123I-SPECT, which was performed 11 days after cessation of her seizures, still showed diffuse hypoperfusion predominantly in the right temporal area, and it returned to normal 3 months after the onset. We discussed the mechanisms of developmental regression in this case from the neuroradiological findings.

Child, Preschool↗
PubMed1992

[A case of frontal lobe epilepsy presenting with gelastic seizures].

We described a 9-year-old boy with frontal lobe epilepsy presenting with gelastic seizures. CT-scan showed mild widening of the left sylvian fissure. Abnormal findings in the left frontal operculum were detected by both MRI and SPECT. Attacks mainly consisted of gelastic seizures with comfortable feeling followed by screaming with fear. Administration of anticonvulsants resulted in reducing the frequency and severity of seizures. Finally the patient had brief laughter attacks only. In the present case, the clinical course suggests that the gelastic seizures does not occur by way of the spreading of epileptic discharges to the temporal or hypothalamic region; rather it might occur as a focal symptom of the frontal region.

Brain↗
PubMed1991

Structure of the bovine atrial natriuretic peptide receptor (type C) gene.

The bovine gene encoding the type C atrial natriuretic peptide (ANP) receptor was isolated and characterized. The gene appears to exist as a single copy in the haploid genome and is comprised of eight exons distributed over more than 85 kilobases. The transcription start site was identified by primer extension and ribonuclease protection assay. A "TATA" box-like sequence was found just upstream of the start site (at position -32); however, no CAAT box was apparent. Exon boundaries of the ANP receptor gene correlated well with the functional domain boundaries of the receptor protein; for example, exon 1 contains coding information for a large proportion of the ANP-binding domain and the transmembrane and cytoplasmic domains are encoded by separate exons, namely by exon 7 and exon 8, respectively. These structural features suggest that the organization of the ANP receptor gene reflects the domain structure of the receptor.

Amino Acid Sequence↗
PubMed1991

Desensitization of the epidermal adenylate cyclase system: agonists and phorbol esters desensitize by independent mechanisms.

Exposure of pig epidermis to adenylate cyclase stimulators results in receptor-specific desensitization. We investigated the nature of the agonist-induced desensitization, which was compared with the phorbol ester-induced, receptor-nonspecific desensitization. Both phorbol ester-induced desensitization and the agonist-induced desensitization were accompanied by an increase in forskolin- and cholera toxin-induced cyclic AMP accumulations. The magnitude of the increase in the agonist-induced desensitization was parallel to the degree of the initial cyclic AMP accumulation; histamine and adenosine, which increase more cyclic AMP than epinephrine, resulted in a more marked increase in forskolin- and cholera toxin-induced cyclic AMP accumulations. Similarly, epidermis desensitized to multiple receptors revealed more marked forskolin- and cholera toxin-induced cyclic AMP accumulations than epidermis desensitized to a single receptor. In contrast to the phorbol ester-induced desensitization, agonist-induced desensitization was not affected by the protein kinase C inhibitors H-7 and staurosporin. Further, agonist-induced desensitization was still inducible in phorbol ester-desensitized epidermis and vice versa. In contrast to the agonist-induced desensitization, which is accompanied by the preceding adenylate cyclase stimulation, no evidence for the stimulation of the adenylate cyclase during phorbol ester treatment was obtained. Neither agonist-induced desensitization nor phorbol ester-induced desensitization affected the content of inhibitory guanine nucleotide binding protein of the epidermis, which was monitored by the pertussis toxin (IAP)-catalyzed ADP ribosylation reaction. Our results indicate that agonist-induced desensitization and the phorbol ester-induced desensitization are independent of each other. Although both processes are characterized by increased forskolin- and toxin-induced cyclic AMP accumulations, the former is accompanied by initial cyclic AMP accumulation; the latter is not.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Solubilization of human placental tumor necrosis factor receptors as a complex with a guanine nucleotide-binding protein.

Human placental membranes exhibited high-affinity receptors for tumor necrosis factor (TNF) (Kd = 5.6 x 10(-10) M) with a density of 1.2-1.7 x 10(10) sites/mg protein. The receptors were solubilized from these membranes with 1% Nonidet P-40, and the solubilized receptor was adsorbed to Con A-Sepharose and wheat germ agglutinin agarose columns, indicating that the TNF receptor derived from human placenta contains carbohydrate chains recognized by these lectins. TNF binding activity was eluted from a column of Sephacryl S-300 as a single peak of Mr 300 kDa. The solubilized receptor was further purified by TNF-Sepharose prepared by coupling of TNF to tresyl-activated Sepharose 4B. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of the purified sample resolved five major bands of Mr 90, 78, 41, 35, and 11 kDa, suggesting that these polypeptides constitute a multimeric complex with a molecular mass of 300 kDa, as observed in gel filtration study. Furthermore, the TNF-Sepharose-bound fraction demonstrated GTP gamma S binding and GTPase activity. Immunoblot analysis showed that the 41- and 35-kDa polypeptides were recognized by antisera against alpha subunits and beta subunit of GTP-binding proteins, respectively. These results suggest that the native TNF receptor couples to a guanine nucleotide-binding protein to form a large complex structure in human placental membranes.

Binding, Competitive↗
PubMed1991

Prostaglandins antagonize fibroblast proliferation stimulated by tumor necrosis factor.

Tumor necrosis factor (TNF) is known to be a mitogen for human diploid FS-4 fibroblasts. We have shown in an earlier study (Hori et al. (1989) J. Cell. Physiol. 141, 275-280) that indomethacin further enhances the cell proliferation stimulated by TNF. Since indomethacin inhibits the activity of cyclooxygenase, the role of prostaglandins in TNF-stimulated cell growth was examined. Cell growth stimulated by TNF and indomethacin was inhibited by exogenously added prostaglandins (PGE2, PGF2 alpha, and PGD2), among which PGE2 caused the greatest inhibition of cell growth. Treatment of FS-4 cells with 10 ng/ml TNF resulted in the release of prostaglandins (PGE2, 6-keto-PGF1 alpha, PGA2, PGD2, and PGF2 alpha) 2 to 4 fold over that of untreated cells. The amount of all these prostaglandins increased in a time-dependent manner over 6 h after treatment. In both TNF-treated and control cells, PGE2 was released as the predominant prostaglandin. Furthermore, when PGE2 production and DNA synthesis were determined in FS-4 cells treated with increasing doses of indomethacin, these two cellular responses were inversely affected by indomethacin. These data show that prostaglandins induced by TNF antagonize growth stimulatory action of TNF.

Arachidonic Acids↗
PubMed1991

Distribution of fluoride in sound and periodontally diseased human cementum.

Fluoride distribution was investigated by an abrasive micro-sampling technique. The fluoride concentration increased with age in both sound and diseased cementum. In sound teeth, the fluoride profiles (distribution of fluoride from the surface to interior) of the middle and apical cementum were similar. In the diseased cementum the profile of the middle region tended to be more variable than that of the apical cementum, suggesting a possible effect of the oral environment on the fluoride profile at this site.

Adult↗
PubMed1991

Specific immunofluorescence staining of Treponema pallidum in smears and tissues.

To date, tissue sections prepared from Formalin-fixed tissues have not been successfully stained with Treponema pallidum subspecies-specific antibody in a direct fluorescent-antibody assay. While current methods stain T. pallidum, they do not distinguish T. pallidum from other spirochetes such as Borrelia burgdorferi (E. F. Hunter, P. W. Greer, B. L. Swisher, A. R. Simons, C. E. Farshy, J. A. Crawford, and K. R. Sulzer, Arch. Pathol. Lab. Med. 108:878-880, 1984). Because trypsin pretreatment of tissue sections has enhanced other immunofluorescent-antibody (IFA) applications, we compared the use of the trypsin digestion method with the current 1% ammonium hydroxide (NH4OH) method as a means to obtain specific staining of T. pallidum in tissues by both direct and indirect IFA techniques. Pretreated T. pallidum-infected tissues sections from rabbits, hamsters, and humans were quantitatively examined with the direct fluorescent-antibody-T. pallidum test conjugate absorbed with Treponema phagedenis, the Reiter treponeme. For indirect staining, a serum specimen from a patients with syphilis absorbed by affinity chromatography with T. phagedenis was used as the primary reagent, and a fluorescein isothiocyanate-labeled rabbit anti-human globulin was used as the secondary reagent. Serum specificity was established first by examining antigen smears of T. pallidum subsp. pallidum, T. pallidum subsp. pertenue, B. burgdorferi, T. phagedenis, and Treponema denticola MRB and then by examining tissues infected with these pathogens plus those infected with four Leptospira serovars. When we stained tissue using the direct IFA method that is currently a standard method for the examination of chancre smears, we found it to be unsuitable for use with tissue. Trypsin digestion did not offer an improvement over the NH4OH pretreatment method in the specific identification of T. pallidum by direct IFA. However, specific identification of T. pallidum in tissue sections was obtained by the indirect IFA technique after either trypsin or NH4OH pretreatment.

Animals↗
PubMed1991

Involvement of prostaglandin-producing pathway in the cytotoxic action of tumor necrosis factor.

To elucidate the cytotoxic mechanism of tumor necrosis factor (TNF), we isolated TNF-resistant sublines of L929 cells. As compared with L929 cells, TNF-resistant cells retained similar number and affinity of TNF-binding sites, and showed a similar growth rate. TNF stimulated arachidonate release from L929 cells, while no stimulation was observed at all in TNF-resistant cells tested. The cytotoxic action of TNF on L929 cells was inhibited by indomethacin, suggesting that prostaglandin may be involved in the action. Therefore, TNF-stimulated prostaglandin production was examined in L929 and TNF-resistant sublines. The amount of PGE2 produced by L929 cells was increased more than 5-fold after the addition of TNF, whereas the amount of PGE2 did not change in the resistant sublines following addition of the factor. TNF-stimulated arachidonate release and PGE2 production were reversed by islet-activating protein (IAP)-treatment of L929 cells. These results suggest that arachidonate release and subsequent prostaglandin production are important for the cytotoxic action of TNF and that these processes are mediated by GTP-binding protein (G protein) that is coupled to the TNF-receptor.

Animals↗
PubMed1991

[A family of von Hippel-Lindau disease with renal cell carcinoma--case report and review of the literature].

We report a 63-year-old woman with renal cell carcinoma associated with von Hippel-Lindau disease. The patient was referred to the department of neurosurgery at our hospital, complaining of gait disturbance. There was a history of retinal hemangioma. After further examination, von Hippel-Lindau disease was the conclusion with evidence of cerebellar hemangioblastoma. An abdominal CT-scan and arteriography revealed multiple hypervascular tumors in the right kidney, but not in the left. She underwent a right radical nephrectomy and lymphadenectomy 2 months after resection of a brain tumor. Von Hippel-Lindau disease is generally recognized as an autosomal-dominant inherited disorder. The patient had a positive family history, seen in both her younger brother and son. Both were diagnosed with renal cell carcinoma with central nervous system involvement before any sign of disease was found in the patient. Twenty one cases of von Hippel-Lindau disease associated with renal tumors have been reported in the Japanese literature. The clinical findings of these cases are discussed.

Adult↗
PubMed1990

Growth inhibition of human fibroblasts by epidermal growth factor in the presence of arachidonic acid.

The effect of epidermal growth factor on growth of human fibroblasts was investigated in serum-free medium supplemented with various fatty acids. When linoleic acid, arachidonic acid, or eicosapentaenoic acid was added, each inhibited epidermal growth factor-induced cell growth and showed cytotoxicity at high concentrations (greater than 10 microM). This cytotoxic effect was not observed in the presence of indomethacin, suggesting that prostaglandin production is important in mediation of the growth inhibition. Prostaglandin E2 was increased more than ten thousand times by epidermal growth factor in combination with arachidonic acid.

Arachidonic Acid↗
PubMed1990

Intramembrane particles and responses of sensory axon terminals during reinnervation of the frog muscle spindle.

Changes in the density of intramembrane particles (IMPs) of sensory nerve terminals in the bullfrog muscle spindle were correlated with recovery in the response of the spindle to stretch during postcrush reinnervation. A few IMPs on the protoplasmic (P) face in summer experiments (June to October) reappeared by the 3rd week after the nerve crush, then rapidly increased to 110% and 120% of control values 2 and 2.5 months after the crush. Afferent responses to stretch could be recorded after the mean IMP density on the P-face in terminal branches had recovered to more than 25% of the control value. The discharge rate showed a plateau pattern during the period of the excessive IMPs. This was supplanted by a normal pattern after a myelinated branch of the sensory axon was cut. The IMPs in winter experiments (November to April) reappeared by day 90 after nerve crush, and then slowly increased. The sustained responses to stretch reappeared after 5 months, when the mean IMP density on the P-face was restored to 25% or more of the control. Neither excessive density of the IMPs nor plateau pattern of the discharge rate were observed in winter experiments. The relation between the regenerated IMP densities and the functional recovery is discussed.

Action Potentials↗