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Biomedical subjects

M Imoto

Publications and source records attributed to M Imoto.

At least 73 records · Page 4Linked to original sources
PubMed1993

Involvement of tyrosine kinase in growth factor-induced phospholipase C activation in NIH3T3 cells.

Tyrosine kinase inhibitors such as erbstatin and lavendustin derivative inhibited platelet-derived growth factor (PDGF)- and bombesin-induced inositol phosphate formation and phospholipase C (PLC) activation in quiescent NIH3T3 cells. However, bombesin-induced PLC activation was only partially inhibited by tyrosine kinase inhibitors, whereas PDGF-induced activation was completely. Moreover, although bombesin-induced PLC activation was partially inhibited by pertussis toxin alone, this toxin inhibited almost completely in the presence of tyrosine kinase inhibitors. Thus, tyrosine kinase was suggested to be involved in PDGF- and bombesin-induced PLC activation in a different manner.

3T3 Cells↗
PubMed1993

Dephostatin, a novel protein tyrosine phosphatase inhibitor produced by Streptomyces. I. Taxonomy, isolation, and characterization.

A novel inhibitor of protein tyrosine phosphatase, dephostatin, was isolated from the culture broth of a strain of Streptomyces. The active principle was extracted from the broth filtrate with ethyl acetate and purified by silica gel chromatography and by HPLC. Dephostatin inhibited protein tyrosine phosphatase prepared from a human neoplastic T-cell line with an IC50 at 7.7 microM. The inhibitory pattern of dephostatin was competitive against the substrate. Dephostatin inhibited the growth of Jurkat cells.

Cell Division↗
PubMed1993

Effects of macrophage colony-stimulating factor on the proliferation and the function of Kupffer cells.

Using flow cytometric methods, the influence of recombinant human macrophage colony-stimulating factor (rhM-CSF) on DNA synthesis, the phagocytosis of microspheres and the uptake of lipopolysaccharide (LPS) in cultured rat Kupffer cells was investigated. Incubation with 10(3) U/ml of rhM-CSF did not increase the S-phase population of Kupffer cells, however, 10(5) U/ml of M-CSF significantly increased that population from 6.26 +/- 0.68% to 8.31 +/- 0.99%. Significantly increased rate of cells phagocytosing microspheres was provoked by rhM-CSF at concentration higher than 10(3) U/ml. Uptake indexes at concentrations of 10(3), 10(4), 10(5), and 10(6) U/ml of rhM-CSF were 114.2 +/- 7.7, 116.5 +/- 8.7, 117.5 +/- 9.1, and 120.0 +/- 11.5, respectively. Significantly increased rate of cells stained with fluorescent LPS was provoked by rhM-CSF at concentrations higher than 10(5) U/ml. Uptake indexes at concentrations of 10(5) and 10(6) U/ml were 115.2 +/- 6.4 and 118.0 +/- 4.3, respectively. These results indicate that M-CSF has a potency to stimulate DNA synthesis, phagocytic activity, and LPS uptake of mature Kupffer cells in vitro. This potency may be helpful to the enhancement or the recovery of the role of Kupffer cells, which is a part of the host defense mechanism, in diseased states.

Animals↗
PubMed1993

[Utilization of Lotus 1-2-3 for on-line data logging system from clinical monitors].

We contrived to obtain digital output data from clinical monitors using "Lotus 1-2-3" and its on-line data logging add-in software "1-2-3 DataLogger". Easy macroprogramming of Lotus 1-2-3 enabled us to obtain digital data automatically into the worksheet of Lotus 1-2-3 from the monitors. Data taken up into the worksheet could be analysed readily using graphic function or calculation of Lotus 1-2-3.

Anesthesiology↗
PubMed1993

[Disease-free survival in a patient with squamous cell lung carcinoma following complete response with the combination chemotherapy of cisplatin and etoposide].

Disease-free survival is reported in a patient with non-small cell lung carcinoma successfully treated with the combination chemotherapy of cisplatin and etoposide (CDDP-ETOP). An 80-year-old woman was diagnosed as having squamous cell carcinoma of the lung with bone metastasis. Chest X-ray showed a tumor (64 x 68 mm in size) in the S1/4 segment of the right lobe, and CT scan revealed no apparent metastasis of hilar lymphnode. In March 1989, the patient achieved a complete response (CR) after two courses of CDDP-ETOP therapy, followed by ETOP(100mg) every two weeks and daily UFT (400 mg) for 10 months. Subsequently, a single course of CDDP-ETOP was administered as a consolidation therapy. The patient is alive with no evidence of recurrent disease for 3 years and half after achieving CR.

Aged↗
PubMed1992

Correlation between detection of anti-viral antibody and histopathological disease activity in an epidemic of hepatitis C.

There was an epidemic of non-A non-B hepatitis in a small area of a town in the central part of Japan, which began with an outbreak of several patients in 1981 and then spread extensively with the result that about one third of the inhabitants showed abnormality in serum liver function tests at the health check performed in 1985. We determined histological diagnoses on that occasion for 167 individuals of the abnormal population and recently assayed antibodies against hepatitis C virus (HCV) for most of their sera left available. Histologically, chronic active hepatitis (CAH) was the major pattern, accounting for 59.3% (99 cases) of the total. Others were chronic persistent hepatitis (CPH) (13.2%), chronic lobular hepatitis (CLH) (16.2%), liver cirrhosis (LC) (6.6%) and fatty liver (4.8%). In the serological studies, the newly developed system to detect antibodies against the viral core protein p 22 was found to be much more sensitive than the conventional system to detect anti C 100-3 antibodies. By using these two methods in combination, we found that 82% were antibody-positive, indicating strong implication of HCV in this epidemic. This was further supported by direct detection of the viral genome in patients' sera by polymerase chain reaction following reverse transcription. We further found a strong correlation between the histological inflammatory activity and the antibody prevalence, since nearly all (97.6%) of the CAH cases were antibody-positive by at least either of the antibody assays, while only about 50% were positive in the less active cases such as CPH and CLH.

Base Sequence↗
PubMed1992

Inhibition of CDP-DG: inositol transferase by inostamycin.

Inostamycin, a novel microbial secondary metabolite, inhibited [3H]inositol and 32P1 incorporation into phosphatidylinositol (PtdIns) induced by epidermal growth factor (EGF) in cultured A431 cells, the IC50 being 0.5 micrograms/ml, without inhibiting macromolecular synthesis. The drug inhibited cellular inositol phosphate formation only when it was added at the same time as labeled inositol. It was found to inhibit in vitro CDP-DG:inositol transferase activity of the A431 cell membrane, the IC50 being about 0.02 micrograms/ml. It did not inhibit tyrosine kinase, PtdIns phospholipase C, or PtdIns kinase. Therefore, inhibition of PtdIns turnover by inostamycin must be due to the inhibition of CDP-DG:inositol transferase. Thus, inostamycin is a novel inhibitor of CDP-DG:inositol transferase.

Anti-Bacterial Agents↗
PubMed1991

Induction of morphological change by tyrosine kinase inhibitors in Rous sarcoma virus-transformed rat kidney cells.

Erbstatin and methyl 2,5-dihydroxycinnamate, related tyrosine kinase inhibitors, induced a morphological change in temperature-sensitive Rous sarcoma virus-transformed rat kidney (RSVts-NRK) that brought the cells close to the morphology of their normal counterpart. Erbstatin did not change the morphology of normal or Kirsten sarcoma virus-transformed rat kidney cells. Erbstatin also inhibited morphological transformation of RSVts-NRK cells induced by a shifting in temperature. Actin stress fibres were observed only in normal cells and not in transformed cells. Erbstatin induced stress fibre organization in transformed cells. Erbstatin and methyl 2,5-dihydroxycinnamate increased fibronectin gene expression in RSV-transformed cells. Thus, tyrosine kinase inhibitors induced normal phenotypes specifically in v-src-expressing cells.

Actins↗
PubMed1991

Immunohistochemical study on tissue inhibitors of metalloproteinases in normal and pathological human livers.

The localization of tissue inhibitor of metalloproteinases (TIMP) in normal and pathological livers was examined by immunohistochemistry using monoclonal antibodies at the light microscopic level. In normal liver, immunoreactive TIMP was detected in smooth muscle cells and endothelial cells of blood vessels, fibroblasts, bile duct cells and Kupffer cells, indicating that TIMP is likely to be a general element of the liver. Immunoreactivity was observed in newly-formed blood vessels, proliferating bile ductules, and fibroblasts in the expanded portal area and fibrous septa of chronic active hepatitis and cirrhosis. TIMP was strongly stained in the capsule of hepatocellular carcinoma. The intensity of the immunoreaction in the capsule was generally greater than that in cirrhotic liver apart from the tumor mass. In three of five cases with hepatocellular carcinoma, endothelial walls in contact with tumor cells were positive.

Antibodies, Monoclonal↗
PubMed1991

Histochemical properties of vascular and sinusoidal endothelial cells in liver diseases.

Liver biopsy specimens with or without liver diseases were examined immunohistochemically to determine the distribution of endothelial cell markers, factor VIII-related antigen (FVIII-RAg). Ulex europaeus agglutinin I (UEA-I) lectin and PAL-E. We also investigated the localization of laminin, a component of the basement membrane. In normal livers, FVIII-RAg, UEA-I and laminin were negative in sinusoidal endothelial cells, but positive in blood vascular endothelia of the portal area. The antigen detected by PAL-E was distributed in venous endothelial cells. PAL-E did not label endothelial cells of the artery. In the lobule, immunoreactivity with PAL-E was weakly detected only in some sinusoids of the periportal area. In chronic active hepatitis and liver cirrhosis, FVIII-RAg and UEA-I stained endothelial cells of neovasculatures in the enlarged portal areas of the fibrous septum surrounding pseudolobules. Some sinusoidal endothelial cells in cirrhotic livers were reactive to UEA-I and FVIII-RAg, whereas PAL-E-positive cells were found rarely in the pseudolobules. In carcinomatous sinusoidal endothelial cells, FVIII-RAg, UEA-I and PAL-E were strongly stained. Laminin underlay these carcinomatous sinusoids. These suggest capillarization of sinusoids in hepatocellular carcinoma. The histochemical approach using endothelial cell markers could be a practical tool in the diagnosis of hepatocellular carcinoma.

Antibodies, Monoclonal↗
PubMed1990

Inhibition of EGF-induced phospholipase C activation in A431 cells by erbstatin, a tyrosine kinase inhibitor.

Erbstatin, a tyrosine kinase inhibitor, inhibited epidermal growth factor (EGF)-induced inositol phosphate production in cultured A431 cells. However, it did not inhibit ATP-induced inositol phosphate production. Cytosolic but not membrane-associated phospholipase C was activated by EGF, and erbstatin inhibited enhancement of the phospholipase C activity in EGF-treated cells. Thus, tyrosine kinase of A431 cells is suggested to be functionally involved in phospholipase C activation.

Cell Line↗
PubMed1990

Inhibition of epidermal growth factor-induced DNA synthesis by tyrosine kinase inhibitors.

We prepared methyl 2,5-dihydroxycinnamate as a stable analogue of erbstatin, a tyrosine kinase inhibitor. This analogue was about 4 times more stable than erbstatin in calf serum. It inhibited epidermal growth factor receptor-associated tyrosine kinase in vitro with an IC50 of 0.15 micrograms/ml. It also inhibited in situ autophosphorylation of epidermal growth factor receptor in A431 cells. Methyl 2,5-dihydroxycinnamate was shown to delay the S-phase induction by epidermal growth factor in quiescent normal rat kidney cells, without affecting the total amount of DNA synthesis. The effect of erbstatin on S-phase induction was smaller, possibly because of its shorter life time.

Animals↗