Search PubMed⌕ Search

Biomedical subjects

K Nose

Publications and source records attributed to K Nose.

At least 109 records · Page 6Linked to original sources
PubMed1989

[Late complications after successful Kasai's operation for biliary atresia].

The late complications in 25 patients more than 3 years after successful Kasai's operation for biliary atresia were presented. Nine (36%) of these 25 patients had episodes of variceal hemorrhage with portal hypertension, and biliary reobstruction in 3 (12%), bleeding from duodenal ulcer in 2, bleeding from gastric erosion in one, and diffuse pulmonary arterio-venous shunt in one were observed. Recently esophageal varices have been well controlled by endoscopic sclerotherapy, and the surgical treatment may be indicated in older children complicated with severe hypersplenism and marked splenomegaly, which are resistant for sclerotherapy. As a surgical procedure, splenectomy with periesophago-gastric devascularization (Hassab's operation) seems to be very useful for portal hypertension by biliary cirrhosis. The reoperation, hepaticoenterostomy, was performed in 3 patients with biliary reobstruction. All three patients are alive and well, and two of them are at 19 years (university student) and 24 years (married life) of age. Hepatic Rehepaticoenterostomy is well indicated rather than liver transplantation, if biliary reobstruction is incurable with conservative therapy. Many of the patients with complications were able to carry on an almost normal life, if suitable treatments for complications were taken.

Adolescent↗
PubMed1988

Enhancement of inositol phospholipid metabolism and activation of protein kinase C in ras-transformed rat fibroblasts.

The inositol phospholipid metabolism is one of the main pathways of signal transduction in cells. We measured the activities of its key enzymes in v-Ha-ras-transformed 208F rat fibroblasts. In the ras-transformed clones, incorporation of [32P]Pi into intermediates of the inositol phospholipid metabolism was stimulated. The activities of phosphatidylinositol and phosphatidylinositol-4-phosphate kinases in the transformed clones were about 35-50% more than in untransformed cells, indicating increased inositol phospholipid metabolism. However, the activity of diacylglycerol kinase in their membrane fraction was 25-35% less than that of untransformed cells, although the total diacylglycerol kinase activity did not change. The imbalance of these kinases could constitute one of the main reasons leading to the increased level of inositol phosphates and the accumulation of diacylglycerol to 2-2.2 times that in control 208F cells. Phosphatidylinositol-4,5-bisphosphate-phospholipase C activity did not change on the transformation when assayed under various conditions. The increased level of diacylglycerol caused intracellular translocation, activation, and down-regulation of protein kinase C changes which may be one of the essential events in transformation by the v-Ha-ras gene.

Animals↗
PubMed1988

Superoxide as a signal for increase in intracellular pH.

We examined the role of superoxide in the increase in intracellular pH (pHi) of human histiocytic leukemia U937 cells treated with 4 beta-phorbol-12,13-didecanoate (4 beta-PDD) or serum. 4 beta-PDD or serum induced a rapid increase in pHi, and antioxidants such as superoxide dismutase (SOD), vitamin E, and butylated hydroxyanisole (BHA) were found to inhibit the amiloride-sensitive increase in pHi induced by 4 beta-PDD. SOD inhibited the increase in pHi caused by serum, and essentially the same was found in concanavalin A-stimulated mouse thymocytes. Also, a superoxide-generating system, xanthine-xanthine oxidase (X-XOD), increased pHi of U937 cells as much as 4 beta-PDD or serum. From these findings, it appears that superoxide is the basis for the modulation of pHi.

Amiloride↗
PubMed1988

Modified responsiveness of v-Ha-ras-transfected rat fibroblasts to growth factors and a tumor promoter.

The correlation of the phenotypic changes of v-Ha-ras transfected cells with the expression of p21ras and the modified responses to growth factors and a tumor promoter were examined. Transfection of the v-Ha-ras gene together with the neomycin-resistance gene into 208F rat fibroblasts yielded transformed clones characterized by morphological changes, anchorage-independent growth, and tumorigenicity in nude mice. The degrees of these biological alterations were parallel with the expression of mRNA and protein of the ras gene. In ras-transformed cells, anchorage-independent growth was stimulated by epidermal growth factor (EGF), insulin, bombesin, and fibroblast growth factor, whereas in the parental 208F cells, anchorage-independent growth was observed only in the presence of EGF, and there were many fewer EGF-induced colonies than those in the ras-transformed clones. A tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) also augmented anchorage-independent growth of ras-transformed cells and induced morphological changes in monolayer cultures without altering the expression of the ras gene or phosphorylation of the p21ras protein. Retinoic acid inhibited the TPA-induced anchorage-independent growth. These results showed a good correlation of the expression of p21ras with the phenotypic changes and the increased sensitivity of the p21ras-expressing cells to the stimulation of growth factors and tumor promoter.

Animals↗
PubMed1987

Induction of c-fos proto-oncogene by a chemotactic peptide in human peripheral granulocytes.

The chemotactic peptide, fMet-Leu-Phe (fMLP), induced proto-oncogene c-fos mRNA in purified human peripheral granulocytes. The induction was transient, and was inhibited by pertussis toxin or by an inhibitor of protein kinase C. These results suggest that activation of a guanine nucleotide-binding protein and of protein kinase C is involved in c-fos induction in granulocytes.

Enzyme Activation↗
PubMed1987

Effects of the protein kinase C inhibitor H-7 and calmodulin antagonist W-7 on superoxide production in growing and resting human histiocytic leukemia cells (U937).

Serum, phorbol 12,13-didecanoate (PDD) and 1-oleoyl-2-acetoy-sn-glycerol (OAG) stimulated O2- release in human histiocytic leukemia U937 cells. The kinetics of O2- release caused by PDD but not by serum or OAG in growing cells differed from those in resting cells. Both the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl) 2-methylpiperidine (H-7) and calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) reduced the superoxide generation induced by these stimuli. H-7 inhibited the O2- release either from growing or resting cells but the effect of W-7 varied according to the growth phase. From these results, it is suggested that activation of protein kinase C and calmodulin-dependent process has an important role in O2(-)-release induced by serum, OAG and PDD, and that the mechanism for PDD-induced O2(-)-release is different in growing and resting cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Inhibition of proto-oncogene c-fos transcription by inhibitors of protein kinase C and ion transport.

Both 4 beta-phorbol 12,13-didecanoate (PDD) and calcium ionophore A23187 induced c-fos mRNA accumulation with similar kinetics in human monocyte-like cells (U937). Their effects were additive. Cells pretreated with PDD were not induced to accumulate c-fos mRNA by PDD but remained responsive to the induction by A23187. Similarly cells pretreated with A23187 responded to PDD but not to A23187. Nuclear run-off transcription assay indicated that increase in the c-fos mRNA level after the second inducer treatment corresponded to transcriptional activation of the c-fos gene. The accumulation of c-fos mRNA and the transcriptional activation of c-fos induced by PDD or A23187 were inhibited by the protein kinase inhibitor H-7 and by quinidine and amiloride. The induction by A23187, but not that by PDD, was also inhibited by 4-aminopyridine, or tetraethylammonium. From these results, it is proposed that activation of protein kinase C and Na+ or K+ transport are required for c-fos induction caused by PDD and A23187.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Regulation of metallothionein gene expression by 1 alpha,25-dihydroxyvitamin D3 in cultured cells and in mice.

1 alpha,25-Dihydroxyvitamin D3 [1 alpha,25(OH)2D3], a hormonally active form of vitamin D3, has been shown to modulate cell differentiation and tumor promotion. This report demonstrates that mRNA of the metallothionein (MT) gene was induced by 1 alpha,25(OH)2D3 in cultured epidermal keratinocytes and also in liver, kidney, and skin tissues when 1 alpha-hydroxyvitamin D3, a synthetic precursor of 1 alpha,25(OH)2D3, was applied in vivo. Exposure of FRSK cells, a cell line derived from fetal rat skin keratinocytes, to 1 alpha,25(OH)2D3 at 5 ng/ml (12 nM) increased MT mRNA to almost the same extent as that induced by 10 microM dexamethasone or 1 microM CdCl2. This increase in the level of MT mRNA was evident within 2 hr and was maximal 12-24 hr after the addition of 1 alpha,25(OH)2D3. The induction was dose-dependent with concentrations of 1 alpha,25(OH)2D3 from 0.05 to 5.0 ng/ml. Amounts of MT increased with the increase of MT mRNA induced by 1 alpha,25(OH)2D3. Of the derivatives of vitamin D3 tested, only 1 alpha,25(OH)2D3 caused marked induction. Treatment with cycloheximide did not inhibit MT mRNA induction by 1 alpha,25(OH)2D3. 1 alpha,25(OH)2D3 induced MT mRNA in primary cultures of mouse epidermal keratinocytes but not in IAR-20, a liver cell line. 1 alpha,25(OH)2D3 had a similar effect in vivo: oral administration of 1 alpha-hydroxyvitamin D3 to mice resulted in increased levels of MT mRNA in the liver, kidney, and skin 24 hr later. Increase in the level of MT mRNA may be relevant to some biological actions of 1 alpha,25(OH)2D3.

Administration, Oral↗
PubMed1987

1 alpha,25-Dihydroxyvitamin D3 induces anchorage-independent growth and c-Ki-ras expression of BALB/3T3 and NIH/3T3 cells.

1 alpha,25-Dihydroxyvitamin D3, a hormonally active form of vitamin D, induces anchorage-independent growth of BALB/3T3 A31-1-1 and NIH/3T3 cells with concomitant increase of their mRNA level of c-Ki-ras but not of c-Ha-ras or c-myc, through a receptor-mediated mechanism. Under the same conditions, 12-O-tetradecanoylphorbol-13-acetate did not induce anchorage-independent growth in these cell lines.

Calcitriol↗
PubMed1986

Multistep process of neoplastic transformation of normal human fibroblasts by 60Co gamma rays and Harvey sarcoma viruses.

As reported previously (Namba et al., 1985), normal human fibroblasts were transformed by 60Co gamma-ray irradiation into immortal cells with abnormal karyotypes. These transformed cells (KMST-6), however, showed a low cloning efficiency in soft agar and no transplantability. However, upon treatment with Harvey murine sarcoma virus (Ha-MSV), the cells acquired elevated clonability in soft agar and transplantability in nude mice. Ha-MSV alone, however, did not convert normal human fibroblasts into either immortal or tumorigenic cells. The Ha-MSV-transformed KMST-6 cells showed an enhanced expression of the ras oncogene, but normal and 60Co gamma-ray-transformed cells did not. Our current data suggest that gamma rays worked against normal human cells as an initiator, giving rise to chromosome aberrations and immortality, and that Ha-MSV, probably through its ras oncogene, played a role in the progression of the malignant cell population to a more malignant one showing enhanced colony formation in soft agar and tumorigenicity in nude mice.

Animals↗
PubMed1986

Intranuclear appearance of the phosphorylated form of cytoskeleton-associated 350-kDa proteins in U1-ribonucleoprotein regions after growth stimulation of fibroblasts.

Cytoskeleton-associated 350-kDa and 80-kDa polypeptides, which were immunoprecipitated with polyclonal antibody against microtubule-associated protein 1 (MAP-1), were rapidly phosphorylated on mitogenic stimulation of quiescent fibroblasts with serum or growth factors. The enhanced phosphorylation was evident within 5 min and reached a maximum 2 hr after the stimulation. Phosphorylated MAP-1 analogues were first detected in the cytoplasm around the microtubule-organizing center and then in the nucleus by immunofluorescent staining with a monoclonal antibody that recognized the phosphorylated form of MAP-1. The monoclonal antibody reacted with the 350-kDa protein in immunoblot analysis and immunostained intranuclear speckles; both immunoreactions were abolished by treatment with alkaline or acid phosphatase. The nuclear speckles stained by the monoclonal antibody were also stained by anti-U1 small nuclear ribonucleoprotein antibodies on double immunofluorescence, suggesting that the stained regions are sites of maturation of messenger RNA. These results support the idea that part of the cytoskeleton-associated 350-kDa protein is phosphorylated and transferred to the nuclear region of mRNA modification as a common early process after growth stimulation.

Animals↗
PubMed1986

Characterization of nuclear matrix from cultured normal human fibroblasts.

Nuclear matrix was isolated from cultured human fibroblasts by extraction of nuclei with 2 M NaCl. Electron microscopic observation on the isolated nuclear matrix revealed a fine network structure. The matrix fraction contained approximately 15% of total nuclear DNA and the matrix DNA was about 3- to 4-fold enriched in transcriptionally active collagen I (alpha 2) gene sequences, whereas transcriptionally inactive beta-globin gene sequences were not enriched. The nuclear matrix contained two major proteins of 65,000 and 45,000 daltons (pI 5.9 and 5.6, respectively). The DNA-binding activity of these nuclear matrix proteins was examined by Western blotting or by nitrocellulose filter-binding assay using cloned specific gene probes. The results suggest that there is no base sequence specificity in the binding, and that protein species of 60,000 to 200,000 daltons showed DNA-binding activity. These results indicate that association of transcribing genes with the nuclear matrix may reflect the functional state of the genes and may not be determined solely by the base sequence specificity of DNA binding. The nuclear matrix protein of 65,000 daltons was phosphorylated in vivo, and was the main substrate for protein kinase(s) associated with the nuclear matrix.

Cell Nucleus↗
PubMed1985

Amplification of c-Ki-ras gene and aberrant expression of c-myc in WI-38 cells transformed in vitro by gamma-irradiation.

The expression of c-oncogenes was examined with normal human fibroblasts (WI-38) and the cells transformed in vitro by gamma-irradiation (CT-1). The amount of Ki-ras-specific mRNA in CT-1 cells was found to be approximately twice that in WI-38 cells. By Southern blot hybridization, the c-Ki-ras 2 gene of CT-1 cells was found to be amplified about two-fold. CT-1 cells have higher levels of c-myc mRNA than normal cells, although the gene dosage and the restriction nuclease pattern of the c-myc gene was the same. The content of c-myc mRNA in CT-1 cells was found to be constitutively high, whereas that in normal cells was increased by serum addition.

Cell Line↗
PubMed1985

Measurement of cutaneous blood flow by clearance of hydrogen gas generated by electrolysis.

In an attempt to assess the reliability of a method for measurement of local blood flow-namely, the clearance of electrochemically generated hydrogen gas-a series of experiments were conducted using the skin and skin flap in rats and rabbits. The results showed high accuracy in obtained values, good reproducibility in the repeated measurements, and consistency with the values obtained by the hydrogen gas inhalation method. Histological examination revealed only minimal damage to the tissue resulting from the measurement. Using this method, blood flow was measured at different sites on the flap in rats. The critical point of blood flow as measured by this method was thoroughly consistent with the dye distance as well as with the survival length. No injurious effects of the measurement procedure on flap survival were noticed. The present study suggests a wide potential application of this method in plastic surgery because of its high reliability and because no radioactivity is involved.

Animals↗
PubMed1984

Inhibition by flavonoids of RNA synthesis in permeable WI-38 cells and of transcription by RNA polymerase II.

The effects of various flayonoids on RNA synthesis in permeable human fibroblasts or on transcription with mouse RNA polymerase II were studied. Quercetin or kaempferol inhibited transcription in permeable cells but flavone did so only slightly. In the transcription of naked DNA with purified RNA polymerase II, mutagenic quercetin, kaempferol or fisetin strongly inhibited the reaction but non-mutagenic or weakly mutagenic flavone and chrysin inhibited it only weakly. Quercetin seems to inhibit the transcription by interaction with the enzyme.

Animals↗
PubMed1984

Transcriptionally active and inactive genes are similarly modified by chemical carcinogens or X-ray in normal human fibroblasts.

Chemical carcinogens and ionizing radiation induce DNA modifications and strand breaks in cells. This damage is reported to be affected by chromatin proteins or chromatin of a higher structure order. To compare the sensitivity of transcriptionally active and inactive genes on chromatin toward DNA-damaging agents, we treated normal human fibroblasts (WI-38) cells in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), X-ray, 4-hydroxyaminoquinoline 1-oxide or N-acetoxy-2-acetylaminofluorene, and high molecular weight DNA was isolated. After digestion with EcoRI to completion, the DNA was electrophoresed on an alkaline agarose gel, blotted on a nitrocellulose filter and hybridized with a transcriptionally active gene probe (human type I(alpha 2) procollagen gene) or an inactive gene probe (human beta-globin gene). The results show that both genes are similarly modified by these agents. Repair of DNA damage caused by MNNG also occurred similarly in collagen and beta-globin genes after removal of MNNG.

Carcinogens↗