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Biomedical subjects

T Hosoi

Publications and source records attributed to T Hosoi.

At least 145 records · Page 8Linked to original sources
PubMed1988

Effect of fibroblast-derived differentiation inducing factor on the differentiation of human monocytoid and myeloid leukemia cell lines.

A fibroblast-derived differentiation inducing factor (F-DIF) purified from medium conditioned by a human fibroblast cell line (WI-26VA4) induced differentiation of human monocytic leukemia cell lines (U-937, THP-1) into cells with macrophage characteristics. F-DIF alone induced the differentiation of ML-1 cells only marginally, but it synergistically increased the differentiation when combined with TNF. Interferon-gamma, tumor necrosis factor, GM-CSF, interleukin-1 and interlukin-4 synergistically enhanced the differentiation of U-937 cells when combined with F-DIF.

Cell Differentiation↗
PubMed1988

Primary coronary artery dissection: its incidence, mode of the onset and prognostic evaluation.

The incidence, mode of the onset and prognosis of primary coronary artery dissection in 1,445 consecutive patients with myocardial infarction undergoing coronary angiography were elucidated in the present study. Primary coronary artery dissection was observed in four patients (0.28%). The first case was a 28-year-old man, who developed angina at rest, followed by inferior myocardial infarction. His coronary angiogram showed dual lumina in the proximal to distal segments of the right coronary artery, which were separated by a flap. A left ventriculogram showed severe impairment of contraction (akinesis) in its inferior segment. Six years later, he was classified as New York Heart Association (NYHA) functional class I. The second case, a 54-year-old man, developed vasospastic angina followed by inferior myocardial infarction. His coronary angiogram showed a similar dissection from the proximal to distal segments of the right coronary artery. A left ventriculogram showed akinesis of the inferior segment and a coronary angiogram five years later showed marked resolution of the dissection. Twelve years after the infarction, he was classified as NYHA functional class I. The third case, a 46-year-old woman, experienced sudden onset of inferior myocardial infarction. Her coronary angiogram showed dissection from the middle to distal segments, and the posterior descending branch of the right coronary artery. A left ventriculogram showed akinesis of the inferior segment, and three years later, she was asymptomatic. The fourth case, a 28-year-old woman, developed anterior myocardial infarction following delivery. Her coronary angiogram revealed dissection from the proximal to middle segments of the left anterior descending artery. A left ventriculogram showed akinesis in the anteroseptal segment and dyskinesis in the apical segment. She died suddenly four years after her myocardial infarction. Thus, primary coronary artery dissection is not extremely rare and it may have been associated with coronary vasospasm in at least two of these four cases.

Adult↗
PubMed1987

Effects of recombinant human tumor necrosis factor (rhTNF) on normal human and mouse hemopoietic progenitor cells.

We examined the effects of recombinant human tumor necrosis factor (rhTNF) on normal human and murine granulocyte-macrophage (CFU-gm) and erythroid (CFU-e, BFU-e) progenitor cells. We suppressed in vitro colony formation by human marrow CFU-gm, CFU-e and BFU-e or peripheral blood BFU-e by adding rhTNF to the culture in a dose-related manner. A half-maximal inhibition was observed with 1-10 ng/ml. Leukemic cell line K562 cells were found to be sensitive to rhTNF in the clonogenic colony assay. However, the clonal growth of murine marrow CFU-e and BFU-e colonies was less than 50% inhibited and CFU-gm growth was unaffected even at a concentration of 1,000 ng/ml. We observed slight to moderate inhibition after 24 h pulse exposure of both human and murine-committed progenitors to rhTNF prior to the culture. Intravenous injection of 1 mg/kg of rhTNF caused a marked decrease in marrow erythroid progenitors and consequently caused anemia in the mice. Our data indicate that rhTNF has a suppressive effect on normal human and murine hemopoietic colony formation in vitro and murine erythropoiesis in vivo.

Animals↗
PubMed1987

Protoplast-mediated gene transfer into human leukemia (K562) cells.

We have examined the usefulness of a protoplast fusion technique as a tool to transfer cloned genes into hematopoietic cells. Protoplasts carrying cloned plasmids, which would express specific markers when successfully transfected into human cells, were prepared and fused with human leukemic cell line K562 cells using polyethylene glycol as a fusogenic factor. As a result, K562 cells fused with protoplasts containing a plasmid pSV2-cat constructed to code for chloramphenicol acetyltransferase (CAT) expressed CAT activity efficiently. K562 cells were also readily transformed to geneticin-(G418) resistant cells following fusion with protoplasts carrying a plasmid pSV2-neo-SV-gpt, which confers the resistance of mammalian cells to G418 and mycophenolic acid. It was also demonstrated that the plasmid genome was stably integrated into the chromosomal DNA of G418-resistant K562 cells. Our results proved that protoplast fusion could be used to study the specific expression and the biologic activities of cloned genes in human hematopoietic cells.

Acetyltransferases↗
PubMed1987

[Detection and prognosis of alimentary tract cancers--mass screening].

The limitation of detectability and curability in terms of current techniques (screening and details) were sought in otherwise healthy examinees. Not a few cancers were present in the alimentary tract, except for the stomach, in these otherwise healthy examinees who voluntarily underwent gastric cancer mass screening. The prognosis of alimentary tract cancers deteriorates in the descending, following order: colon cancer, stomach cancer, and esophageal cancer. The survival rate of primary liver cancer, cholecyst cancer, and pancreas cancer is extremely low. Unless new techniques are developed in these diagnoses, no improvement in the survival rate can be anticipated.

Digestive System Neoplasms↗
PubMed1986

In-vitro effects of antineoplastic prostaglandins on human leukemic cell growth and normal myelopoiesis.

The effects of prostaglandin (PG)E1, PGD2 and 9-deoxy-delta 9-PGD2 (PGJ2) on the clonogenic growth of six kinds of human leukemic cell lines (K562, KG1, HL60, U937, THP1 and Molt4) and normal human myeloid progenitor cells (CFU-GM) were studied using semisolid agar cultures. While the degree of suppression of leukemic growth by PGE1 varied from cell line to cell line, PGD2 and PGJ2 equally suppressed the growth of all leukemic cell lines. The potency of growth inhibition was as follows: PGJ2 greater than PGD2 greater than PGE1. The increase of cellular cAMP level induced by prostaglandin treatment did not parallel their cytotoxic potency. Normal myeloid colony formation was also suppressed by PGE1, PGD2 or PGJ2. In contrast to the preferential inhibition of macrophage colony formation by PGE1, such lineage-selective suppression was not observed for PGD2 or PGJ2. These findings suggest that PGD2 and PGJ2 potently inhibit the leukemic growth by a different mechanism from that of PGE1 and by a cAMP-independent mechanism. These prostaglandins seem to be promising chemotherapeutic agents for acute leukemia.

Adenylyl Cyclase Inhibitors↗
PubMed1985

Microinjection of macromolecules into leukemic cells by cell fusion technique: search for intracellular growth-suppressive factors.

To investigate the intracellular molecular events during leukemic cell proliferation, we have examined the method of ghost-mediated microinjection of macromolecules into leukemic cell line cells (HL-60). Samples were packed into red cell ghosts. Microinjection was performed by the fusion of ghosts and HL-60 cells using the hemagglutinating virus of Japan (HVJ). Fusion rate was about 80-90%, when determined by the injection of FITC-labeled globulins (IgG) or diphtheria toxin fragment A into HL-60 cells. When the nuclear protein extract from normal granulocytes was injected into HL-60 cells, their growth was significantly suppressed. The injection of the nuclear protein extract from HL-60 itself into HL-60 cells did not inhibit their growth. This finding suggests that leukemic cells may be deficient in intracellular regulatory factors which have suppressive activity on cell growth.

Animals↗
PubMed1985

Introduction of macromolecules into hemopoietic stem cells with an erythrocyte-ghost-mediated system.

We have developed a method of introduction of macromolecules into normal human hemopoietic stem cells. The erythrocyte ghosts were loaded with diphtheria toxin fragment A (molecular weight = 22,000 daltons), which exerts cytotoxicity only in the intracellular space. Granulocyte-macrophage colonies of human bone marrow cells incubated with the above ghosts in the presence of Sendai virus decreased in number to about 10% of the control. This means that the cell fusion and the subsequent introduction of the fragment A into granulocyte-macrophage progenitors occurred at a high incidence (about 90%). This method will be useful to study intracellular events during the proliferation and differentiation of hemopoietic stem cells.

Cell Fusion↗
PubMed1985

Effects of recombinant interferons on the clonogenic growth of leukemic cells and normal hemopoietic progenitors.

We have examined the effects of recombinant immune and leukocyte interferons (rIFN-gamma and rIFN-alpha) on the clonogenic growth of leukemic cells and normal hemopoietic progenitors using in vitro colony assays. Both interferons suppressed the colony formation by granulocyte-macrophage progenitors (CFU-gm) and erythroid progenitors (CFU-e and BFU-e) in a dose-dependent manner. Six myeloid leukemic cell lines were less sensitive to rIFN-gamma than CFU-gm. The colony formation of some myeloid leukemic cell lines was suppressed more potently by rIFN-alpha than by CFU-gm. Four lymphoid leukemic cell lines of the T-cell type were very resistant to both recombinant interferons. Reduced sensitivity of leukemic cells to rIFN-gamma, a possible hemopoietic regulator, may explain partially the unregulated proliferation of leukemic cells in vivo.

Cell Division↗
PubMed1985

Recombinant immune interferon inhibits leukemic cell growth by a monocyte-macrophage-mediated mechanism.

We have investigated direct and monocyte-macrophage (Mono/M phi)-mediated indirect effects of recombinant immune interferon (IFN-gamma) on the growth of established leukemic cell lines (K562, KG1, ML1, HL60, U937, and THP1). The direct antiproliferative effects of IFN-gamma on these leukemic cells were mild or negligible, when estimated by 3H-thymidine incorporation. Indirect effects were assessed by the growth pattern of leukemic cells cocultured with Mono/M phi that were pretreated with INF-gamma. While the leukemic cell growth was slightly suppressed by untreated Mono/M phi, this suppression was significantly augmented by the treatment of Mono/M phi with IFN-gamma (10-10,000 U/ml). In addition, the indirect effects of IFN-gamma on leukemic cell growth were examined at different stages of maturation of Mono/M phi. The augmentation of cytotoxicity was detected only when mature Mono/M phi were treated with INF-gamma. This suggests that IFN-gamma acts on tissue macrophages and augments their cytotoxicity against leukemic cells.

Cell Division↗