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Biomedical subjects

Y Hamamoto

Publications and source records attributed to Y Hamamoto.

At least 73 records · Page 4Linked to original sources
PubMed1991

Immunocytochemical localization of laminin in the epithelial rests of Malassez of immature rat molars.

Immediately after disruption of Hertwig's root sheath, epithelial cells were found near the root apex, singly or in groups of two or three cells. They were irregular in shape with only a partial lining of basal lamina. Immunoreactivity for laminin was intense in the basal lamina and weak between projections of the epithelial cells. In 5-week-old rats, the epithelial rests consisted of about five cells and still had an incomplete basal lamina with collagen fibrils in the intercellular spaces. Immunoreaction products were seen in the basal lamina and diffusely in the intercellular spaces. The epithelial rests of 9-week-old rats had more cells, an almost complete lining of basal lamina, and narrowed intercellular spaces. Immunoreaction products were seen in the basal lamina but not in the intercellular spaces. These findings indicate the basal lamina is involved in the formation of the epithelial rests.

Animals↗
PubMed1991

[Virological evaluation of mumps meningitis following vaccination against mumps].

1) We report 5 cases of aseptic meningitis following vaccination against mumps. Of the 5 cases, 4 cases were diagnosed as mumps meningitis. 2 cases received monovalent mumps vaccine and the other 2 MMR vaccine. They consisted of 2 boys and 2 girls, aged 2 years and 2 months to 4 years and 5 months. The period between vaccination and symptoms ranged from 15 days to 20 days (mean 18 days). Cerebrospinal fluid of the cases contained 507 to 2688 cells/mm3. Eruption was observed in the 2 cases who received MMR vaccine, while parotid swelling was not seen in any case. 2) In all 4 cases, IgM antibody to mumps virus in the cerebrospinal fluid was detected by the ELISA or EIA methods. Causative organism of the fifth case was obscure. 3) PCR (Polymerase Chain Reaction) tests revealed that mumps virus isolated from 2 cases were of vaccine strain origin. 4) To evaluate the frequency of mumps meningitis following vaccination, it seems important to investigate carefully the number of children who received the vaccine and to exclude the cases of aseptic meningitis caused by other agents. On the other hand, cases of young infants tend to be overlooked because of atypical signs.

Child, Preschool↗
PubMed1990

Augmentation of cytotoxic effect of tumor necrosis factor on human immunodeficiency virus-infected cells by staurosporine, a potent protein kinase C inhibitor.

We have examined the effect of the protein kinase C (PKC) inhibitor, staurosporine, on tumor necrosis factor (TNF)-induced cytotoxic action and augmentation of human immunodeficiency virus (HIV) expression on the chronically HIV-infected T-cell line, MOLT-4/HIV (HTLV-IIIB strain). Staurosporine enhanced the decrease in the number of viable cells caused by TNF treatment for 3 days (1 ng/ml of TNF, 43% decrease; 1 ng/ml of TNF + 20 nM staurosporine, 94%), whereas the cytotoxic action on that cell line induced by 10 ng/ml of 12-O-tetradecanoylphorbol-13-acetate (TPA), which was known to be an activator of PKC, was partially inhibited by staurosporine. In addition, staurosporine augmented the TNF cytotoxic activity against other cell lines including HIV-uninfected U937 cells(100 ng/ml of TNF, 53% decrease in the number of viable cells; 100 ng/ml of TNF + 5 nM staurosporine, 86%). However, staurosporine did not change the sensitivity of cells to TNF; thus, those insensitive to TNF were not changed to TNF sensitive by staurosporine. Furthermore, staurosporine did not affect the augmentative effect of TNF on HIV expression evaluated by levels of p24 antigen. Moreover, HIV long terminal repeat (LTR)-directed chloramphenicol acetyltransferase assay showed that staurosporine strongly inhibited the TPA-induced activation of HIV LTR, while that caused by TNF was little affected (10 ng/ml of TPA, 98.4% conversion; 10 ng/ml of TPA + 40 nM staurosporine, 22.2%, 1 ng/ml of TNF, 98.5%; 10 ng/ml of TNF + 40 nM staurosporine, 93.9%). These results suggest that TPA and TNF facilitate HIV replication by different pathways and that staurosporine augments TNF cytotoxicity by possible suppression of PKC activity in both HIV-infected and uninfected cells.

Alkaloids↗
PubMed1990

Production of tumor necrosis factors by human T cell lines infected with HTLV-1 may cause their high susceptibility to human immunodeficiency virus infection.

The production of tumor necrosis factor (TNF)-alpha and TNF-beta by various human hematopoietic cell lines was quantitatively examined using a highly sensitive radioimmunoassay specific to TNF-alpha, or a cytolytic assay performed with mouse L929 cells. It was found that the HTLV-1-infected T cell lines examined produced large amounts of both TNF-alpha and TNF-beta. In particular, interleukin-2 (IL-2)-dependent cell lines produced large amounts of TNF-alpha. In contrast, human cell lines not infected with HTLV-1 essentially did not produce either of the TNFs. It was also found that the high production of TNF-alpha by HTLV-1-infected cells partially correlated to their high sensitivity to human immunodeficiency virus (HIV) infection. Treatment of MT-4 cells, one of the most HIV-sensitive HTLV-1-infected cell lines, with antibody specific to TNF-alpha reduced their sensitivity to HIV infection.

Animals↗
PubMed1990

The phorbol ester TPA strongly inhibits HIV-1-induced syncytia formation but enhances virus production: possible involvement of protein kinase C pathway.

Cocultivation of MOLT-4 and MOLT-4/HIVHTLV-IIIB cells with more than 0.01 ng/ml of 12-O-tetradecanoylphorbol-13-acetate (TPA) for 20 hr strikingly inhibited HIV-induced syncytia formation resulting from cell to cell infection. Interestingly, the production of HIV-specific p24 antigen in the culture fluid was significantly enhanced by TPA. TPA down-modulated the expression of CD4. CD4 is essential for syncytia formation through interaction with viral envelope protein gp120 on the surface of MOLT-4 cells. The effects of TPA on syncytia formation and on CD4 expression were specifically interfered with by nontoxic doses of blockers of protein kinase C (PKC) such as staurosporine and H7. These data suggest that (1) TPA inhibits HIV-induced syncytia formation through down-modulation of CD4 molecules on the surface of MOLT-4 cells and (2) PKC may play an important role in cell to cell as well as in cell-free infection of HIV.

Alkaloids↗
PubMed1990

Anti-Fas monoclonal antibody is cytocidal to human immunodeficiency virus-infected cells without augmenting viral replication.

A cytotoxic monoclonal antibody (anti-Fas mAb) against the 200-kDa cell surface Fas antigen, which is associated with the tumor necrosis factor (TNF) receptor, was examined for its in vitro activity on human immunodeficiency virus (HIV)-infected cells. It was found that both TNF and anti-Fas mAb selectively killed the chronically HIV-infected cells. Uninfected cells were less sensitive to the antibody than those infected with HIV. When the cells were cultured in the presence of anti-Fas mAb immediately after the HIV infection, the spread of HIV-infected cells was suppressed by the antibody. TNF augmented both the synthesis of HIV-specific mRNA in HIV-infected cells and formation of multinucleated giant cells. In contrast, the anti-Fas mAb did not augment HIV replication or enhance the HIV-induced formation of syncytia. The results indicated that anti-Fas mAb mimicks the cytocidal action of TNF but does not augment HIV replication.

Antibodies, Monoclonal↗
PubMed1990

[A case of tracheal calculus in the pathogenesis of which fungal infection was probably involved].

A 63-year-old woman with a past history of bronchial asthma was admitted to our hospital with a diagnosis of status asthmaticus. Examination revealed a ring-shaped, calcified stone within the trachea immediately below the vocal cords. As the patient complained of increasing difficulty in breathing, emergency tracheotomy was performed in an attempt to save her life, with success. Bronchial calculus (broncholithiasis) has been occasionally reported, and it is hypothesized that the calculus is mostly caused by intra-bronchial perforation of calcified lymph nodes around the bronchus. Tracheal calculus is a rare disease, and our case is only the third ever reported in Japan. However, perforation of calcified lymph nodes was probably not responsible for this case, which probably resulted from repeated chronic inflammation and fungal infection.

Calculi↗
PubMed1989

Effect of interleukin-1 on the augmentation of human immunodeficiency virus gene expression.

Among the cytokines tested here (IL-2, IL-3, IL-4, IL-5, IL-6, granulocyte colony stimulating factor (G-CSF), granulocyte/macrophage colony stimulating factor (GM-CSF), interferon-alpha (IFN-alpha), interferon-beta (IFN-beta) and interferon-gamma (IFN-gamma] only interleukin 1(IL-1) augmented HIV-long terminal repeat(LTR) directed chloramphenicol acetyl transferase(CAT) activity in protein kinase C(PKC)-independent manner. However, a stimulation by IL-1 was not as efficient as that due to tumor necrosis factor and the HIV production was not significant. IL-1 was not cytotoxic to MOLT-4/HIV cells.

Alkaloids↗
PubMed1989

Comparison of effects of protein kinase C inhibitors on phorbol ester-induced CD4 down-regulation and augmentation of human immunodeficiency virus replication in human T cell lines.

The potent protein kinase C inhibitors staurosporine, H-7, and UCN-01 were investigated for their effects on 12-0-tetradecanoylphorbol-13-acetate (TPA)--mediated CD4 down-regulation and on the augmentation of human immunodeficiency virus (HIV) expression. Staurosporine was the most effective TPA inhibitor for both of these actions. Because of its high cytotoxicity, the effect of H-7 on augmentation of HIV expression could not be determined. UCN-01 had no cytotoxic effect, but caused only little inhibition of the augmentation of HIV expression.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Characterization of human T-cell lines harboring defective human immunodeficiency virus type 1.

Defective HIV-producing T-cell lines were subcloned from MT-4/HIVHTLV-IIIB' MOLT-4/HIVHTLV-IIIB, and H9/HIVHTLV-IIIB cell lines chronically infected with HIV. The NY-M10 cell line derived from MOLT-4/HIVHTLV-IIIB and the NY-H6 cell line derived from H9/HIVHTLV-IIIB produce defective HIV, which lacks the ability to infect human T-cell lines. NY-M10 cells retain the capacity to form multinucleated giant cells in cocultivation with HIV-uninfected CD4-positive cells. However, NY-H6 cells failed to fuse with CD4-positive cells. Electron microscopic analysis indicated that the defective HIV produced from NY-M10, like those reported previously, lacked the structure of the nucleocapsid, and the virion released from NY-H6 was indistinguishable from those of authentic HIV particles. Southern and Northern blotting analyses of NY-M10 and NY-H6 cleared that the genome of those defective viruses was not significantly deleted, suggesting minor mutation(s) should take place on the viral genome.

Cell Line↗
PubMed1989

Ultrastructure of epithelial rests of Malassez in human periodontal ligament.

The cell rests in healthy periodontal ligament were studied by transmission electron microscopy. They consisted of clusters of cells surrounded by a basal lamina. These cells were characterized by an irregular nucleus with condensed heterochromatin, tonofilaments, relatively abundant mitochondria and poorly developed rough endoplasmic reticulum. They were connected to each other by desmosomes and gap junctions. Coated pits and vesicles were also seen at the periphery. In addition, a primary cilium accompanied by a centriole was often observed in association with the Golgi complex and rootlet-like structures. The findings suggest that the epithelial rests are more than a vestigial structure.

Adolescent↗
PubMed1989

Augmentation of human immunodeficiency virus type 1 gene expression by tumor necrosis factor alpha.

It is now well established that cytokines are involved in the regulation of gene expression from HIV-1 LTR. The present study provides evidence that TNF-alpha stimulates HIV-1 gene expression and that the enhancer sequence within the HIV-1 LTR is involved in the stimulation. These results support the idea that immunologic stimulation and infection may trigger the development of clinical AIDS in individuals latently infected with HIV-1.

Animals↗
PubMed1989

Enhancement of HIV replication and giant cell formation by tumor necrosis factor.

Human T cell lines Molt-4, Jurkat, and TLOm-1 were infected by HIV-1 in the presence of various concentrations of r-TNF. The infectivity of HIV-1 was monitored by an indirect immunofluorescence method using anti-HIV-1-positive human serum. We found that r-TNF enhanced the replication of HIV-1. HIV-1-induced giant cell formation between HIV-1 chronically infected Molt-4 cells and HIV-1-uninfected Molt-4 cells was accelerated by r-TNF. The median tissue culture infectious doses (TCID50) of HIV-1 determined in the presence of TNF revealed that TNF apparently accelerated the time of the appearance of CPE but did not affect final titer of HIV-1.

Cells, Cultured↗
PubMed1989

A novel method for removal of human immunodeficiency virus: filtration with porous polymeric membranes.

We propose a new method to rid solutions of a virus by using a novel regenerated multilayered structured cellulose membrane (BMM). When the filtrate of human immunodeficiency virus (HIV) preparation was obtained through BMM it showed no infectivity. Electron microscopic observation revealed that HIV was completely caught by the multilayers of the BMM. Conveniently, BMM was seldomly found to adsorb protein molecules and also to have a high filtration rate. These characteristics may have a use in the removal of other variously sized pathogenic agents from plasma.

Cells, Cultured↗
PubMed1989

Cytocidal effect of tumor necrosis factor on cells chronically infected with human immunodeficiency virus (HIV): enhancement of HIV replication.

Tumor necrosis factor (TNF), a monokine initially described as a tumoricidal agent, facilitated the replication of human immunodeficiency virus (HIV) in vitro. The viability of human T-cell line MOLT-4/HIV, chronically infected with HIV, was affected by the addition of a low dose (10 ng/ml) of recombinant TNF-alpha (rTNF-alpha), while uninfected MOLT-4 cells were resistant to treatment with rTNF-alpha at concentrations up to 1,000 ng/ml. A marked increase in the level of HIV-specific RNA was detected in MOLT-4/HIV cells as early as 1 h after exposure to rTNF-alpha and reached almost maximum level within 6 h. Production of HIV particles from MOLT-4/HIV was also increased at 6 h after treatment with rTNF-alpha. Nearly identical phenomena were observed in CCRF-CEM/HIV, Jurkat/HIV, and H9/HIV cells, although the sensitivity of these cell lines to rTNF-alpha varied. A human T-lymphotropic virus type 1-infected cell line, MT-4, was insensitive to treatment with rTNF-alpha.

Antibodies, Monoclonal↗
PubMed1989

Ultrastructural and histochemical study on the morphogenesis of epithelial rests of Malassez.

The morphogenesis of the epithelial rests of Malassez in rat molars was studied by light and electron microscopy. The epithelial islands immediately after disintegration of the Hertwig's root sheath consisted of a few irregularly shaped cells with scanty rough endoplasmic reticulum, which were surrounded in portions by disrupted basal lamina. Close topographic relationships between the epithelial cells and mesenchymal cells of the dental sac were often observed in this period. After thirty days of age, the epithelial cells started to form ovally shaped epithelial islands consisting of four or five cells, but collagen fibrils still remained in the intercellular spaces. Vacuoles containing collagen fibrils were occasionally observed in the cytoplasm of the epithelial cells during this period in association with an acid phosphatase positive reaction. In more mature rat molars, the epithelial islands were characterized by an increased number of epithelial cells, only rarely observed collagen fibrils in the cytoplasm and the intercellular spaces, and an almost complete lining of basal lamina. The results indicate that the phagocytosis of collagen fibrils by the epithelial cells is a crucial step in the formation of the epithelial rests. The possibility is suggested that interactions with mesenchymal cells of the dental sac and regeneration of the basal lamina may also contribute to the epithelial rest formation.

Animals↗