Search PubMed⌕ Search

Biomedical subjects

A Tsukamoto

Publications and source records attributed to A Tsukamoto.

At least 55 records · Page 3Linked to original sources
PubMed1993

Chronic neutropenia associated with C2 and C9 deficiency.

A Japanese male with a deficiency of the second and ninth components of complement associated with chronic idiopathic neutropenia is presented. In this case the second component of complement is totally deficient while the ninth component is approximately half that of normal control. Neutrophil granulocytes are constantly few, but this case shows no evidence of susceptibility to either viral or bacterial infections. His HLA type is different from that of Caucasians, suggesting that the genetic abnormality responsible for the complement deficiency of this Japanese case is different from that seen in Caucasian patients.

Adult↗
PubMed1993

Thy-1-expressing CD34+ human cells express multiple hematopoietic potentialities in vitro and in SCID-hu mice.

We have detected a minor subset of fetal liver and bone marrow CD34+ cells that coexpress the Thy-1 antigen at their surface. In immune-deficient SCID mice engrafted with human fetal hematopoietic tissues, CD34+ Thy-1+ reconstitute the full range of thymic lymphocytes and yield a progeny of myeloid and B cells in the human bone marrow. The frequency of cells initiating long-term human myeloid and B lymphocytes in vitro cultures at the contact of the Sys-1 stromal cell line was also found to be 10-15 times higher among CD34+ Thy-1+ cells than in the Thy-1- counterpart population. We propose that CD34+ Thy-1+ cells include candidate human hematopoietic stem cells.

Animals↗
PubMed1993

[Natural type interferon-alpha (Namalwa) therapy for multiple myeloma complicated by hemolytic anemia].

A 45-year-old woman with Bence-Jones type multiple myeloma was treated with natural type alpha-interferon (Namalwa interferon), 3 million IU every other day subcutaneously. After about 5 months, she developed hemolytic anemia. However, screening tests for autoantibodies, including direct and indirect antiglobulin (Coombs' tests), were negative. This report is the first case in which hemolytic anemia appeared to be caused by natural type alpha-interferon. It is likely that interferons will be used in treating increasing numbers of patients and that more patients will develop this complication.

Anemia, Hemolytic↗
PubMed1992

Co-ordinate expression of c-fos, p53 and cytokeratin genes during the alteration of growth of human hepatoma cells. mRNA levels measured by reverse transcription and polymerase chain reaction.

Teleocidin, a tumor promoter, inhibited the proliferation, enhanced cytokeratin assembly and increased the type III procollagen production of PLC/PRF/5 hepatoma cells. Teleocidin transiently increased the levels of c-fos and p53 mRNAs measured by reverse transcription and polymerase chain reaction. This was followed by a reduction of c-myc mRNA and an increase of cytokeratin mRNA. The level of p120 mRNA was not remarkably altered. Sequential alterations of the expression of c-fos, p53, c-myc and cytokeratin genes induced by teleocidin may be responsible for the morphological and functional changes of hepatoma cells induced by this tumor promoter.

Base Sequence↗
PubMed1992

Increased assembly of cytoskeletal proteins associated with the transformation of human liver cells into fibroblast-like cells.

A topoisomerase II inhibitor, novobiocin, and a deacetylase inhibitor, butyrate, synergistically transformed human liver cells into fibroblast-like cells. This morphological change was associated with an increased production of procollagen type III peptide and a simultaneous assembly of actin, tubulin, vimentin and cytokeratin. Novobiocin and butyrate had no marked effect on the phosphorylation state of cytokeratin proteins, but synergistically enhanced [3H]acetate uptake. From these results, it can be speculated that protein acetylation plays an important role in inducing the assembly of cytoskeletal proteins and the morphological transformation of human liver cells.

Acetylation↗
PubMed1992

Transgenes expressing the Wnt-1 and int-2 proto-oncogenes cooperate during mammary carcinogenesis in doubly transgenic mice.

The Wnt-1 and int-2 proto-oncogenes are transcriptionally activated by mouse mammary tumor virus insertion mutations in virus-induced tumors and encode secretory glycoproteins. To determine whether these two genes can cooperate during carcinogenesis, we have crossed two previously characterized lines of transgenic mice to obtain bitransgenic animals carrying both Wnt-1 and int-2 transgenes under the control of the mouse mammary tumor virus long terminal repeat. Mammary carcinomas appear earlier and with higher frequency in the bitransgenic animals, especially the males, than in either parental line. Nearly all bitransgenic males develop mammary neoplasms within 8 months of birth, whereas only 15% of Wnt-1 transgenic males and none of the int-2 transgenic males have tumors. In virgin bitransgenic females, tumors occur approximately 2 months earlier than in their Wnt-1 transgenic siblings; int-2 transgenic females rarely exhibit tumors. Preneoplastic glands from the bitransgenic animals of either sex demonstrate pronounced epithelial hyperplasia similar to that seen in Wnt-1 transgenic virgin females and males, and both transgenes are expressed in the hyperplastic glands and mammary tumors. RNA from the int-2 transgene is more abundant in mammary glands from bitransgenic animals than from int-2 transgenic animals; the increase is associated with high levels of RNA specific for keratin genes 14 and 18, suggesting that Wnt-1-induced epithelial hyperplasia is responsible for the observed increase in expression of the int-2 transgene.

Animals↗
PubMed1992

[Isospora belli infection in a patient with adult T-cell leukemia].

An adult T cell leukemia (ATL) accompanied with Isospora belli infection was described. A 65-year-old male was admitted to our hospital because of a two month history of watery diarrhea. On admission, physical examination showed slight pallor but no detectable superficial lymphadenopathies. Hepatosplenomegaly was not observed. Laboratory examination revealed a leukocyte count 5,500/microliters with 10% abnormal lymphoid cells. A majority of the abnormal lymphoid cells expressed both CD 4 and CD 8 antigens. The patient was diagnosed as chronic ATL, since anti-HTLV-1 antibody in his serum and monoclonal integration of HTLV-1 proviral DNA in his peripheral mononuclear cells were detected. Isospora belli was found in his feces thereafter, and trimethoprim/sulfamethoxazole was effective for diarrhea. In Japan, there have been only 9 reported cases of lymphoproliferative disorders (including five ATL patients) accompanied with Isospora belli infection. From the descriptions in those reports, these 9 cases might all be ATL patients.

Aged↗
PubMed1991

Lymphoid reconstitution of the human fetal thymus in SCID mice with CD34+ precursor cells.

The search for human hematopoietic stem cells has been hampered by the lack of appropriate assay systems. Demonstration of the ability of precursor cell candidates to give rise to T cells is of significant difficulty since dissociated in vitro cultured thymus stroma cells lose their ability to sustain thymocyte maturation. To define further the differentiative capacities of the rare human fetal liver and bone marrow cells that express the CD34 surface antigen and exhibit in vitro myeloid and pre-B cell activities, we have microinjected them into HLA-mismatched fetal thymus fragments, partially depleted of hematopoietic cells by low temperature culture. In vitro colonized thymuses have then been allowed to develop upon engraftment into immunodeficient SCID mice. Using this modification of the SCID-hu system, we show that low numbers of fetal CD34+ progenitor cells can repopulate the lymphoid compartment in the human thymus.

Animals↗
PubMed1991

Vacuole formation and cytokeratin rearrangement of hepatoma cells induced by teleocidin are not associated with down-regulation of protein kinase C.

PLC/PRF/5 human hepatoma cells cultured with teleocidin reduced the rate of cell proliferation and were transformed into large cells with many vacuole-like subcellular structures. In these vacuolated cells, the protein content per cell increased without changing the total cellular protein synthesis. Cytokeratin was one of the proteins which increased quantitatively. This intermediate filament formed fibrous network structures throughout the enlarged cytoplasm. The assembly of other cytoskeletal proteins such as actin, tubulin, and vimentin was not altered remarkably, suggesting that teleocidin morphologically transformed the hepatoma cells by changing the assembly of cytokeratin protein selectively. On the other hand, the alterations of cell proliferation, cell morphology, and cytokeratin assembly induced by teleocidin were not associated with either down-regulation of protein kinase C or reduced number of epidermal growth factor receptors. In addition, these teleocidin effects were not mimicked by the protein kinase C agonist 1-oleoyl-2-acetylglycerol or inhibited by the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine. From these results it can be speculated that the morphological transformation and reduced cell proliferation induced by teleocidin may be mediated by still unknown mechanisms unrelated to protein kinase C.

Carcinoma, Hepatocellular↗
PubMed1991

Novobiocin modulates cytokeratin assembly and differentiation of human hepatoma cells induced by butyrate and teleocidin.

A differentiation inducer butyrate and a tumor promoter teleocidin had inhibitory effects on the proliferation of PLC/PRF/5 hepatoma. Both of these reagents stimulated the production of procollagen type III peptide, enhanced the cytokeratin assembly and altered the morphological appearance. Novobiocin, a topoisomerase II inhibitor, enhanced the cytokeratin assembly induced by butyrate but antagonized that induced by teleocidin without changing the expression and the phosphorylation state of cytokeratin proteins. In addition, novobiocin acted synergistically with butyrate but not with teleocidin in stimulating the procollagen production and the acetate uptake. These results suggest that butyrate and teleocidin induce cell differentiation via distinct signaling pathway and that novobiocin and butyrate can be used as subsidiary drugs in preventing the growth of hepatoma.

Acetylation↗