Search PubMed⌕ Search

Biomedical subjects

T Tsuda

Publications and source records attributed to T Tsuda.

At least 523 records · Page 29Linked to original sources
PubMed1988

Biological characteristics of N-myc amplified neuroblastoma in patients over one year of age.

1. A genomic amplification of N-myc of neuroblastoma was frequently observed in patients in the advanced stage of the disease, in those with the tumor originating from the suprarenal region, and in those with a histologically undifferentiated neuroblastoma. Thus, N-myc may be one of the most pertinent prognostic factors of neuroblastoma in patients over one year of age. 2. The neuroblastoma patient with 1-10 copies of N-myc responded to aggressive multidisciplinary therapy, even those over one year of age. 3. Rapid invasion and progression of the tumor was evident in children with more than 10 copies of N-myc. 4. N-myc amplification may correlate with immaturity of catecholamine metabolism of neuroblastoma.

Age Factors↗
PubMed1988

Ectopic bone induction on and in porous hydroxyapatite combined with collagen and bone morphogenetic protein.

Porous hydroxyapatite (HA-P) discs (5 mm in diameter; 1.5 mm thick; porosity, 80%; mean pore size, 200 micron) were impregnated with purified bovine skin collagen (1 mg/disc) and a small amount of semipurified bone morphogenetic protein (BMP) of sarcoma origin (100 micrograms/disc) and implanted into dorsal muscles of ddY mice. Within one week new ectopic cartilagenous tissue was consistently formed on the surface of the discs adjacent to the host tissue. The cartilage was resorbed and replaced by normal bone containing hematopoietic bone marrow four weeks after implantation and the discs became encased in the newly formed bone. HA-P discs impregnated with only collagen (HA-P/collagen) or only BMP (100 micrograms/disc; HA-P/BMP) did not evoke formation of new cartilage or bone. These results indicate that collagen is effective as a carrier of BMP for expression of the biologic activity of the latter in vivo and that it may be of practical use as a carrier of BMP with synthetic biomaterials.

Animals↗
PubMed1987

Genetic analysis of the cell binding domain region of the chicken fibronectin gene.

We have determined the nucleotide sequence of the cell binding domain region of the chicken fibronectin gene and analyzed it evolutionaly. We present here the complete nucleotide sequence of 4.3 kb HindIII/EcoRI segment from the clone lambda FC23 of the chicken fibronectin gene. There were five exons in this segment. When we lined up the amino acid of exons 28, 29 and 31, three alignments, known as the Type III repeat, appeared. Tetrapeptide, -RGDS-, called the cell binding domain, existed in the second repeat, coding exon 30. It was presumed that the Type III repeats were composed of two exons in the chicken gene, the same as in the rat and humans. We found repeatedly appearing amino-acid sequences such as -TIT- (three arrays in these Type III repeats) but also found one of the amino acids substituted in the tripeptide in these Type III repeats (seven arrays). We analyzed these repeats from the point of view of evolution. We used three of the nucleotide sequences (12-18 bp) coding such -TIT- repeats as a unit length for comparing the various homologies after dividing the coding region into 56 segments. The mutual homology of the divided segments to each one of three showed 53% on average. On the other hand, the mutual nucleotide homology of the Type III repeat was 44%. This suggested that the Type III repeat may have been developed by frequent duplication of small gene units.

Amino Acid Sequence↗
PubMed1987

Hodgkin's disease in hairy cell leukemia. Phenotypic characterization of neoplastic cells.

A case of Hodgkin's disease (HD) in a patient with long-standing hairy cell leukemia (HCL) is reported. The diagnosis of HCL was confirmed by clinical features (chronic illness with marked splenomegaly) and hematopathologic findings (increase of characteristic hairy cells with tartrate-resistant acid phosphatase activity in peripheral blood and bone marrow). Cervical lymphadenopathy first appeared 6 years after the diagnosis of HCL, and histologic features of the node were characteristic of HD. As it was possible that the neoplastic cells of both lesions might have originated from a single clone, their phenotypic features were defined. The hairy cells were found to bear surface immunoglobulin, receptors for complement components, leukocyte common antigen, and antigen defined by LN-1 monoclonal antibody, whereas lymph node lesion was characterized as HD because the Reed-Sternberg-like cells were positive for Leu M1 antigen, lysozyme, alpha-1-antitrypsin, and nonspecific cross-reacting antigen. Since there was no evidence indicating a common clonal origin, it is more likely to consider that both lesions are derived from different clones.

Antigens, Neoplasm↗
PubMed1987

Analysis of N-myc amplification in relation to disease stage and histologic types in human neuroblastomas.

Both untreated and treated primary neuroblastomas from 52 patients were analyzed to determine the correlation between the amplification of N-myc oncogene and various prognostic factors. Amplification of N-myc was observed in eight of 28 untreated cases and in 12 of 24 treated cases. As a whole, 12 of 18 tumors (67%) in Stage IV had N-myc amplification, but there were fewer cases in the unadvanced disease stage, as reported previously by others. Furthermore, the authors detected N-myc amplification in three of nine tumors in Stage IV-S, although the amplification was less than 50 copies. Analysis of progression-free survival at 24 months revealed that amplification of N-myc was associated with the worst prognosis (P less than 0.001). In the untreated group, no amplification of N-myc was detected in any of two ganglioneuromas and four ganglioneuroblastomas, whereas amplification of N-myc was observed in all two round-cell and six of 20 rosette fibrillary neuroblastomas. On the other hand, the authors detected amplification of N-myc in three of eight less differentiated ganglioneuroblastomas in the treated group and observed the worst prognosis in these three patients. The total percentage of the cases from both untreated and treated groups suggest that amplification of N-myc may occur more frequently in undifferentiated types of neuroblastomas than in less malignant types. In conclusion, the amplification of N-myc in neuroblastomas was closely associated with the worst prognosis, which was suggested by both disease stage and histologic characteristics.

Child↗
PubMed1987

Role of the thymus and T-cells in slow growth of B16 melanoma in old mice.

Clinical observations suggest that tumors grow more slowly in aged subjects. To investigate the influence of age on tumor growth, we injected the same number of cultured B16 melanoma cells into C57BL/6 mice of various ages. B16 melanoma cells, inoculated s.c., grew more slowly in old (18-20-month-old) as compared to young (6-8-week-old) mice. In young tumor-bearing mice there was a significant increase in the number and the proliferative response to phytohemagglutinin and concanavalin A of splenic T-cells as compared to old tumor-bearing animals. There was no difference in the response of B-lymphocytes from old and young tumor-bearing mice to lipopolysaccharide. The positive association between T-cells and the rate of tumor growth was also suggested by the slower growth of melanoma cells in thymectomized or thymectomized and anti-theta antiserum-treated young mice. Finally, the age-associated difference in tumor growth could be transferred by spleen cells from old or young mice to thymectomized and lethally irradiated syngeneic young animals. Young mice with rapidly growing B16 melanoma tumors have increased numbers and proliferative responses of thymic-derived lymphocytes. It is likely that T-cells or their products facilitate the growth of B16 tumor cells.

Aging↗
PubMed1987

Inhibition of DNA synthesis by phorbol esters through protein kinase C in cultured rabbit aortic smooth muscle cells.

In cultured rabbit aortic smooth muscle cells (SMC), 12-O-tetradecanoylphorbol-13-acetate (TPA) induced DNA synthesis in the presence of plasma-derived serum to a small extent, but inhibited markedly the rabbit whole blood serum (WBS)-, platelet-derived growth factor (PDGF)- and epidermal growth factor-induced DNA synthesis. Phorbol-12,13-dibutyrate (PDBu) mimicked this antiproliferative action of TPA, but 4 alpha-phorbol-12,13-didecanoate was inactive in this capacity. Prolonged treatment of the cells with PDBu caused the partial down-regulation of protein kinase C. In these protein kinase C-reduced cells, WBS still induced DNA synthesis, but TPA did not inhibit the WBS-induced DNA synthesis. We have previously shown that protein kinase C is involved at least partially in the PDGF-induced DNA synthesis in rabbit aortic SMC. The present results together with this earlier observation suggest that protein kinase C has not only a proliferative but also an antiproliferative action in rabbit aortic SMC.

Animals↗
PubMed1987

Determination of butyltin and phenyltin compounds in biological and sediment samples by electron-capture gas chromatography.

A method is described for the gas chromatographic determination of nanogram amounts of mono-, di- and tributyltin compounds and mono-, di- and triphenyltin compounds in biological and sediment samples. These compounds are converted into the corresponding chlorides with hydrochloric acid, extracted with ethyl acetate and hydrogenated with sodium tetrahydroborate. The corresponding hydrides, mono-n-butyltin hydride, di-n-butyltin hydride, tri-n-butyltin hydride, monophenyltin hydride, diphenyltin hydride triphenyltin hydride, are detected by electron-capture gas chromatography after clean-up by silica gel column chromatography. The detection limits are 10-20 ng/g for mono-n-butyltin chloride, 0.5-1 ng/g for di-n-butyltin chloride, 1-2 ng/g for tri-n-butyltin chloride and diphenyltin chloride and 2.5-5 ng/g for monophenyltin chloride and triphenyltin chloride, in biological and sediment samples.

Animals↗
PubMed1987

Antiproliferative action of protein kinase C in cultured rabbit aortic smooth muscle cells.

In rabbit aortic smooth muscle cells (SMC), protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited the whole blood serum (WBS)-induced DNA synthesis. The inhibitory action of TPA was mimicked by another protein kinase C-activating phorbol ester, phorbol-12,13-dibutyrate (PDBu), but not by 4 alpha-phorbol-12,13- didecanoate known to be inactive for this enzyme. Prolonged treatment of the cells with PDBu caused the down-regulation of protein kinase C. In these cells, WBS still induced DNA synthesis but the inhibitory action of TPA was abolished. DNA synthesis started at 18 h and reached a maximal level 24 h after the addition of WBS. TPA inhibited the WBS-induced DNA synthesis even when added 12 h after the addition of WBS. These results suggest that protein kinase C has an antiproliferative action in rabbit aortic SMC and that this action is attributed to the inhibition of the progression from the late G1 into S phase of the cell cycle. TPA also inhibited the phospholipase C-mediated hydrolysis of phosphoinositides which was induced by WBS within several minutes, but the relevance of this effect on the antiproliferative action of TPA is uncertain.

Animals↗
PubMed1987

Possible involvement of protein kinase C in platelet-derived growth factor-stimulated DNA synthesis in vascular smooth muscle cells.

In cultured rabbit aortic vascular smooth muscle cells (VSMC), protein kinase C-activating phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and phorbol-12,13-dibutyrate (PDBu) stimulated DNA synthesis in the presence of 10% cell-free plasma-derived serum. This stimulation was half that shown by PDGF. 4 alpha-Phorbol-12,13-didecanoate, known to be inactive for protein kinase C, was without effect in stimulating DNA synthesis. Prolonged treatment of the cells with PDBu led to a marked decrease in protein kinase C. In the pDBu-treated cells, the TPA-stimulated DNA synthesis was completely abolished whereas the PDGF-stimulated DNA synthesis was decreased to about half that in the control cells. These results suggest that protein kinase C is involved in PDGF-stimulated proliferation of VSMC.

Animals↗
PubMed1987

Effects of intravenous injection of butyrate on the exocrine pancreatic secretion in guinea pigs.

1. The stimulus-secretion coupling in the pancreatic exocrine responses to i.v. injection of sodium butyrate was investigated in guinea pigs in vivo and in vitro. 2. Intravenous single injection of sodium butyrate (12.5-100 mumol/100 g body wt) caused an increase in fluid and amylase secretion in a dose-dependent manner. The responses evoked by sodium butyrate (100 mumol/100 g body wt) were not affected by prior injection of atropine (0.14 mumol/100 g body wt) or hexamethonium (4 mumol/100 g body wt). 3. The chloride concentration in secreted fluid increased slightly with an increase in flow rate in response to sodium butyrate, but decreased in response to secretin. 4. The amylase release from the pancreatic segments evoked by sodium butyrate (10(-6)-10(-2) M) increased dose-dependently. The responses were potentiated in the presence of secretin (1 C.H.R.u./ml), but were suppressed in the presence of acetylcholine (10(-6) M) or in a Ca-free solution containing EGTA (10(-4) M). 5. These results suggest that the secretory effects in response to i.v. injection of sodium butyrate probably arise from direct action on the acinar cells, and that an increase in cellular calcium concentration might be an important step in the secretion process, in guinea pig exocrine pancreas.

Acetylcholine↗
PubMed1987

Correlative studies on changes in lipid composition of gills and uptake of chemicals of willow shiner fish (Gnathopogon caerulescens) by exposure to detergent.

One group of willow shiner (Gnathopogon caerulescens) was exposed to 0.1 mg/l dodecylbenzenesulfonate (DBS) for analysis of lipid composition of gill extracts. Another group of fish was exposed to 0.0003 mg/l 2,4,6-trichlorophenyl-4'-nitrophenyl-ether (CNP) after regular intervals of pre-exposure to 0.1 mg/l DBS for analysis of uptake of CNP. The whole body residues of CNP were characterized by a 60% drop in DBS pre-exposure for 14 and 21 days. The cholesterol/total phospholipid ratio increased to 0.22 and 0.28 after 14 and 21 days from the normal of 0.18. These biochemical results might be correlated with the changes observed by the uptake of CNP.

Animals↗
PubMed1987

Comparative studies on additive effects of sodium dodecylbenzensulfonate and sodium stearate on uptake of chemicals by willow shiner (Gnathopogon caerulescens).

Comparative studies between sodium dodecylbenzensulfonate (DBS) and sodium stearate (SNa) were performed on the additive effects of the uptake of chemicals in a fresh water fish, the willow shiner (Gnathopogon caerulescens), by the use of a continuous flow water system. The chemicals selected were 2,4,6-trichlorophenyl-4'-nitrophenyl ether (CNP) as a non-polar lipophilic substance and cadmium salt (Cd) as polar hydrophilic substance. DBS had no promotive and depressive effects on the uptake of Cd. SNa had no promotive and depressed effects on the uptake of CNP and Cd.

Animals↗
PubMed1987

Amplification of N-myc oncogene in stage II and IVS neuroblastomas may be a prognostic indicator.

The amplification of N-myc oncogene is frequently observed in tumors of patients with advanced, poor prognostic stages of neuroblastoma (unfavorable stage group). However, there has been little documentation of the N-myc amplification in tumors of patients with stages II and IVS neuroblastoma (favorable stage group). In this communication, we present data on one patient in stage II and two in stage IVS. In these children, the primary tumors had an amplified N-myc and the clinical course was poor. In addition, from an analysis of the N-myc oncogene of 26 neuroblastomas, genomic amplification of more than three copies was observed in 4 of 11 (36%) in the favorable stage group, and in 9 of 15 (60%) in the unfavorable stage group. Death occurred only in those with an amplified N-myc, in both groups. The smaller copy number of N-myc amplification of stage IVS tumors as compared with those of stages III and IV, appeared to be characteristic. These findings suggest that N-myc amplification may be a reliable prognostic indicator even in the favorable stage group of neuroblastomas, and may be clinically useful as a guide for treating those with a poor prognosis in stages II and IVS.

Adrenal Gland Neoplasms↗
PubMed1987

N-myc oncogene amplification and prognostic factors of neuroblastoma in children.

The N-myc oncogene of 28 neuroblastic tumors obtained from 16 untreated and 12 pretreated children was clinically evaluated and compared with known prognostic factors. Significant amplification of the N-myc (more than ten copies) was observed in 0 of 2 tumors in stage I, 1 of 5 in stage II, 2 of 6 in stage III, 6 of 9 in stage IV, and 2 of 6 in stage IVS. In stages II, III, IV, and IVS, all 15 patients with low N-myc amplification (under ten copies) are alive without disease, while among 11 patients with the amplification, seven died with progressive disease and two have a recurrence (P less than .01). All tumors with N-myc amplification originated from the suprarenal region and the amplification appeared in 55% of those from that origin. The amplification also correlated with the age factor. These results suggest that the genomic amplification of N-myc seems to be correlated with known prognostic factors of neuroblastoma, and may be a reliable factor even in the case of preoperatively treated tumors.

Age Factors↗
PubMed1987

Involvement of two intracellular messenger systems, protein kinase C and cyclic AMP, in the regulation of c-fos gene expression in human promyelocytic leukemia (HL-60) cells.

Incubation of human promyelocytic leukemia (HL-60) cells with 12-O-tetradecanoyl-phorbol-13-acetate (TPA), a protein kinase C-activating phorbol ester, caused a marked increase in c-fos mRNA in a dose-dependent manner. Phorbol-12,13-dibutyrate and 1-oleoyl-2-acetyl-glycerol, other protein kinase C-activating agents, were also active in this capacity. 4 alpha-Phorbol-12,13-didecanoate, known to be inactive for protein kinase C, was ineffective. 8-Bromo-cyclic AMP (8-Br-cAMP) also increased c-fos mRNA in a dose-dependent manner. This action of 8-Br-cAMP was mimicked by prostaglandin E2, which is known to raise the cyclic AMP level in HL-60 cells. c-fos mRNA increased within 15 min and reached a maximal level 45 min after the stimulation of the cells by TPA or 8-Br-cAMP. The simultaneous stimulation of the cells by TPA and 8-Br-cAMP at the respective doses giving maximal elevation of c-fos mRNA increased this mRNA in an additive manner. These results suggest that in HL-60 cells expression of the c-fos gene is regulated independently by two different intracellular messenger systems, protein kinase C and cyclic AMP.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1987

Pathochemistry, pathogenesis and enzyme replacement in multiple-sulfatase deficiency.

Multiple-sulfatase deficiency (MSD) is now considered to be heterogeneous and could be classified into three or four clinical phenotypes according to the onset of the disease: neonatal, late infantile, juvenile and possibly adult type. Neonatal-type MSD shows severe clinical involvement and practically no arylsulfatase A, B and C activities in cultured skin fibroblasts. Furthermore, arylsulfatase A activity in neonatal-type MSD was not enhanced by the addition of thiosulfate. Therefore, it is distinct from late infantile-type MSD. The degradation of 14C-sulfatide can occur in MSD-cultured skin fibroblasts and was much higher than in late infantile-type MLD. The addition of thiol protease such as leupeptin to cultured MSD skin fibroblasts enhanced arylsulfatase A activity as well as the degradation of 14C-sulfatide. This suggests that the decreased activities of arylsulfatase A is due to an acceleration of the enzyme degradation. Enzyme replacement by the addition of arylsulfatases of different sources (human liver, brain, fungus) was carried out in cultured MSD skin fibroblasts. Human enzymes of arylsulfatase A and B were mostly taken up by MSD cells rather than those of fungus origin. By the exposure to leukocytes to cultured skin fibroblasts, MSD cells corrected arylsulfatase A and B activities.

Adolescent↗