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T Tsuda

Publications and source records attributed to T Tsuda.

At least 487 records · Page 27Linked to original sources
PubMed1989

Periosteal bone formation elicited by partially purified bone morphogenetic protein.

A small amount of partially purified, water-soluble murine osteosarcoma-derived bone morphogenetic protein (BMP) was implanted into the dorsal muscles of mice in combination with calf skin gelatin or collagen as carriers. Changes in the ribs adjacent to the implants were then chronologically observed. On implantation of BMP with gelatin, the gelatin was rapidly absorbed and no ectopic bone formation was observed, but periosteal cellular proliferation with subsequent formation of periosteal cartilage and bone was seen in ribs adjacent to the implant. Implantation of the same amount of BMP fraction or gelatin alone as controls did not result in either any ectopic bone formation in situ or any periosteal bone formation in adjacent ribs. Implantation of BMP with collagen resulted consistently in both ectopic bone formation in situ and periosteal bone formation in adjacent ribs. These results suggest that BMP is diffusible in vivo and is capable of eliciting a response from periosteum to stimulate periosteal bone formation.

Animals↗
PubMed1989

HST1 and INT2 gene coamplification in a squamous cell carcinoma of the gallbladder.

The HST1 gene has previously been found to be amplified in over 40% of squamous cell carcinomas of the esophagus. We performed Southern blot analyses on squamous cell carcinomas of the lung, nasal cavity, uterine cervix and gallbladder, using HST1, INT2 and five other oncogenes as probes. The HST1 and INT2 genes, both of which were mapped to chromosome 11 at band q13, were coamplified in a squamous cell carcinoma of the gallbladder. The degree of amplification exceeded eight fold.

Blotting, Southern↗
PubMed1988

Angiotensin II stimulates vimentin phosphorylation via a Ca2+-dependent, protein kinase C-independent mechanism in cultured vascular smooth muscle cells.

Intermediate filaments have been proposed, via phosphorylation by protein kinase C, to be involved in sustained contraction of smooth muscle. We examined the effect of angiotensin II on the phosphorylation of the intermediate filament protein, vimentin, in cultured rat aortic vascular smooth muscle cells. Angiotensin II induced phosphorylation of a Triton X-100- and high salt-insoluble protein with a molecular weight of 58,000. This protein was identified as vimentin based on its specific interaction with anti-vimentin antibody as detected by immunoblot analysis. Angiotensin II-induced phosphorylation of vimentin was time- and dose-dependent. Phosphorylation was detectable at 15 s, peaked at 2 min after angiotensin II stimulation, and gradually declined to a new plateau which was sustained for at least 30 min. The threshold, half-maximal and maximal concentrations of angiotensin II that stimulated vimentin phosphorylation were 0.01, 0.1, and 10 nM, respectively. The Ca2+ ionophore, ionomycin, stimulated vimentin phosphorylation to the same extent as angiotensin II, whereas the protein kinase C-activating phorbol ester, phorbol 12-myristate 13-acetate, had only marginal effects on this reaction. Pretreatment of the cells with [ethylene-bis(oxyethylenenitrilo)]tetraacetic acid attenuated angiotensin II- and ionomycin-induced vimentin phosphorylation to the same extent. Down-regulation of protein kinase C induced by prolonged treatment of the cells with phorbol 12,13-dibutyrate did not inhibit angiotensin II-induced vimentin phosphorylation. These results indicate that angiotensin II stimulates vimentin phosphorylation via a Ca2+-dependent, protein kinase C-independent mechanism in vascular smooth muscle cells and suggest that cytoskeletal proteins are major targets for angiotensin II-induced phosphorylation events.

Angiotensin II↗
PubMed1988

The production of anorexigenic substances by intestinal flora.

The role of intestinal flora in the production of anorexigenic substance was investigated. Proteus mirabilis (P. mirabilis) and Escherichia coli (E. coli) were found to produce an anorexigenic substance, while Enterococcus faecalis (E. faecalis, type 1 and 2) and Staphylococcus intermedius (S. intermedius) did not. The anorexigenic substance was purified and was detected as, a single though broad band by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The specific activity of the final form of the purified substance was 120 units/mg carbohydrate. The substance contained no protein residue and appeared to be a lipopolysaccharide. The evidence that intestinal flora produces an anorexigenic substance leads to an interesting assumption that the intestinal flora may be responsible for regulating food intake.

Animals↗
PubMed1988

Angiotensin II induces expression of the c-fos gene through protein kinase C activation and calcium ion mobilization in cultured vascular smooth muscle cells.

Incubation of the serum-deprived cultures of rat vascular smooth muscle cells with angiotensin II, a potent vasoconstrictor, caused a rapid and transient increase in the c-fos mRNA level. The doses of this agonist necessary for the increase in the c-fos mRNA level coincided with those for the phospholipase C-mediated hydrolysis of phosphoinositides. Moreover, protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate and Ca2+-ionophore A23187 increased the c-fos mRNA level in an additive manner. These results suggest that angiotensin II induces expression of the c-fos gene through the activation of protein kinase C and Ca2+ mobilization in cultured vascular smooth muscle cells.

Angiotensin II↗
PubMed1988

Clinical and biochemical studies of Japanese neuronal ceroid-lipofuscinosis.

We studied clinical manifestations of Japanese patients with neuronal ceroid-lipofuscinosis (NCL). The onset of the disease and initial symptoms were almost identical to those reported previously in Caucasians. Japanese patients with NCL were not significantly clinically different from Caucasian cases. An atypical case NCL associated with a deficiency of diaminobenzidine peroxidase activity was also presented. Pathogenesis of NCL was studied on the basis of urine dolichol excretion, autofluorescent compounds in urine, thiol protease activities and protein analysis in tissues of NCL patients. Possible biochemical abnormalities in NCL are discussed.

Adolescent↗
PubMed1988

Old mice recover the ability to produce IgG and high-avidity antibody following irradiation with partial bone marrow shielding.

The splenic plaque-forming-cell (PFC) response to trinitrophenylated bovine gamma globulin of 18- to 20-month-old mice is markedly depressed, with a preferential loss of indirect (IgG) PFC and high-avidity-antibody-secreting cells compared to 6- to 8-week-old animals. The anti-trinitrophenyl response of old mice, whose peripheral lymphoid system has been reconstituted from their own bone marrow after irradiation while their bone marrow was partially shielded, includes high-avidity and IgG PFCs relatively comparable to those of normal young mice. If young mice are irradiated while their bone marrow is partially shielded and given purified splenic T cells from either old or young donors during recovery from irradiation, then the avidity distribution and the ratio of IgG/IgM PFCs they produce in response to trinitrophenylated bovine gamma globulin reflects the characteristic immune response of the T-cell donor. These results are consistent with the hypothesis that the bone marrows of old and young mice are similar with regard to the spectrum of B-cell clones that they can generate and that it is peripheral regulatory effectors that are responsible for much of the age-related change in the immune response. In addition, if one calculates the PFC avidity distribution taking into account those cells whose secretion of antibody was inhibited by anti-idiotype autoantibodies, then it is clear that there are more high-avidity B cells present in old mice than are detected by the conventional plaque-inhibition assay. Thus, the reduced avidity of the PFC response of old mice appears to be, at least in part, due to down regulation by anti-idiotype autoantibodies.

Aging↗
PubMed1988

Passage of indigestible particles of various specific gravities in sheep and goats.

1. Eight kinds of indigestible particles with specific gravities (SG) ranging from 0.92 to 1.87 (2 mm diameter and 4 mm length) were injected into the reticulo-rumen of sheep and goats in order to investigate the relation between SG and passage through the gastrointestinal tract, and the difference in passage time in the two species of animals. 2. The percentage of excreted particles significantly increased, while the percentage of ruminated particles in the excreted particles significantly decreased, as the SG increased. 3. The daily and cumulative recovery rates of particles of SG 1.38 were slower in sheep than in goats, while those with SG 0.92 were not different between species. 4. It is concluded that particles with SG higher than 1.27 would pass through the gastrointestinal tract of sheep and goats more quickly than those with SG lower than 1.21.

Animals↗
PubMed1988

Inhibition of DNA synthesis by protein kinase C-activating phorbol esters in NIH/3T3 cells.

Fibroblast growth factor (FGF) plus insulin induced DNA synthesis in and proliferation of NIH/3T3 cells. The protein kinase C-activating phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), inhibited both the DNA synthesis and cell proliferation induced by FGF plus insulin. The concentration of TPA required for 50% inhibition of the DNA synthesis was about 5 nM. Phorbol-12,13-dibutyrate, another protein kinase C-activating phorbol ester, also inhibited the DNA synthesis but 4 alpha-phorbol-12,13-didecanoate, known to be inactive for this enzyme, was ineffective. DNA synthesis started at about 12 h after the addition of FGF plus insulin. The inhibitory action of TPA on the DNA synthesis was observed when it was added within 12 h after the addition of FGF plus insulin. These results suggest that phorbol esters exhibit an antiproliferative action through protein kinase C activation in NIH/3T3 cells, and that this action of phorbol esters is due to inhibition of the progression from the late G1 to the S phase of the cell cycle.

Animals↗
PubMed1988

Amplification of the hst-1 gene in human esophageal carcinomas.

The hst-1 gene, previously designated as the hst gene, and seven other oncogenes were examined for possible structural changes in esophageal, gastric and colorectal carcinomas by Southern blot hybridization. The hst-1 gene was amplified in eight (42.1%) of the nineteen esophageal squamous cell carcinomas and in all four metastatic tumors of lymph nodes. The degree of amplification ranged from two to eight times. Coamplification of the hst-1 and c-erbB-1 gene was found in one case of esophageal carcinoma. However, no amplification of the hst-1 gene was detected in gastric and colorectal carcinomas.

Adult↗
PubMed1988

Amplified allele of the human N-myc oncogene in neuroblastomas.

The N-myc amplification unit was investigated using two restriction fragment length polymorphisms for SphI and PvuII which we previously found to occur in the 2nd intron and in the 3' region of the human N-myc oncogene, respectively. All the three haplotypes which are dominant in the Japanese population were observed in the amplified DNA after analyses of a total of 22 DNA samples of fresh neuroblastomas with N-myc amplification. We conclude that only one of the alleles was amplified and that either allele could be amplified with respect to both the SphI and PvuII polymorphisms.

Alleles↗
PubMed1988

Secondary signalling mechanisms in angiotensin II-stimulated vascular smooth muscle cells.

1. Activation of vascular smooth muscle by angiotensin II results in the generation of two second messengers, inositol trisphosphate (IP3) and diacylglycerol (DG). 2. IP3 is responsible for mobilizing calcium from endoplasmic reticulum. This signal is transient, most likely serving to initiate calcium events leading to contraction, and is attenuated by activation of protein kinase C. 3. DG stimulates protein kinase C and ultimately Na+/H+ exchange, leading to intracellular alkalinization. Accumulation of DG/activation of protein kinase C is sustained, and may be enhanced by concurrent intracellular alkalinization. The delay in induction of the sustained response appears to be related to cellular processing of the angiotensin II-receptor complex. 4. Angiotensin II-stimulated, phospholipase C-mediated IP3 formation is also modulated by a pertussis toxin-insensitive guanine nucleotide regulatory protein. 5. The GTP binding protein, movement of the receptor-ligand complex, and the signals generated by the two second messengers, IP3 and DG, interact in a complex manner to cause an integrated response of vascular smooth muscle cells to angiotensin II stimulation.

Angiotensin II↗
PubMed1988

Adrenergic modulation of pancreatic glucagon and insulin secretion in sheep.

The effect of intravenous infusion of epinephrine, either alone or together with various doses of phentolamine or propranolol, on the secretion of both glucagon and insulin was determined in six sheep. Intravenous infusion of epinephrine alone caused increases in plasma glucagon and glucose concentrations and produced a slight but significant decrease in plasma insulin concentration. The concomitant infusion of propranolol and epinephrine augmented glucagon release and inhibited insulin secretion. Combined propranolol plus epinephrine infusion also caused a marked hyperglycemia. The concomitant infusion of phentolamine and epinephrine produced slight inhibition of glucagon secretion and markedly promoted insulin secretion. Epinephrine-induced hyperglycemia was eliminated by phentolamine infusion. The effects of isoproterenol infusion on plasma glucagon, insulin, and glucose concentrations were similar to that caused by the concomitant infusion of phentolamine and epinephrine. The effects of isoproterenol were abolished by the infusion of propranolol. It is concluded that an alpha-receptor mechanism is the most important component of adrenergic modulation of pancreatic glucagon secretion, whereas beta-receptor activation stimulates and alpha-receptor activation inhibits insulin secretion in sheep.

Adrenergic alpha-Antagonists↗
PubMed1988

Stimulation of phospholipase C-mediated hydrolysis of phosphoinositides by adenosine 5'-triphosphate via P2-purinoceptors in cultured rat aortic vascular smooth muscle cells.

Incubation of [3H] inositol-labeled cultured rat aortic vascular smooth muscle cells with angiotensin II caused the dose- and time-dependent formation of inositol mono-, bis- and trisphosphates. Under these conditions, adenosine triphosphate (ATP) stimulated the formation of these inositol phosphates. The maximal reaction velocities obtained by ATP and angiotensin II were roughly the same. The doses of ATP giving half maximal and maximal reaction velocities were about 100 microM and 1 mM, respectively. This action of ATP was mimicked by other nucleotides such as adenosine diphosphate (ADP) and guanosine triphosphate (GTP), but these nucleotides were far less effective than ATP. Adenosine monophosphate (AMP), adenosine, guanosine diphosphate (GDP), guanosine monophosphate (GMP), deoxythymidine trisphosphate (dTTP), and cytosine triphosphate (CTP) were almost ineffective. The formation of inositol phosphates induced by ATP was inhibited partially by pretreatment of the cells with pertussis toxin. This toxin ADP-ribosylated a protein with a molecular mass of about 40,000. These results indicate that ATP induced the phospholipase C-mediated hydrolysis of phosphoinositides probably via P2-purinoceptors in rat aortic vascular smooth muscle cells, and suggest that a pertussis toxin-sensitive GTP-binding protein is involved at least partially in the coupling of this receptor to the phospholipase C in this cell type.

Adenosine Triphosphate↗
PubMed1988

Morphological assessment of left ventricular wall and ventricular aneurysm by thallium-201 myocardial emission computed tomography.

To evaluate the influence of left ventricular (LV) aneurysm on non-infarcted ventricular wall, the shape of the left ventricular wall was assessed by thallium-201 single photon emission computed tomography (SPECT). From the morphology of the ventricular wall close to the apex, the rest images along the transaxis, horizontal long axis and vertical long axis were classified into 4 types: convergent, parallel, divergent and completely defective. LV aneurysm was detected by 2-dimensional echocardiography and/or contrast left ventriculography in 39 of 80 patients with previous myocardial infarction. Although convergence in the normal configuration of ventricular walls close to the apex, 4 of 39 patients with LV aneurysm showed this pattern. The divergent type was very specific (100%) and the most sensitive (56.4%) of the 4 for identifying LV aneurysm. Moreover, the parallel configuration indicated aneurysm in cases of inferoposterior infarction and all the completely defective cases exhibited this abnormality. Thus, thallium-201 SPECT is suitable for observing the morphology of the ventricular wall and can provide highly reliable information for detecting postinfarction ventricular aneurysm with a sensitivity of 89.7%, a specificity of 87.8% and a diagnostic accuracy of 88.8%.

Adult↗
PubMed1988

Mode of potentiating action of cocaine in morphine analgesia.

The mechanism of antinociceptive interactions among morphine, cocaine and alcohol was studied in mice, guinea pigs and rabbits. In the tail-pressure test in mice, cocaine and alcohol alone showed almost no antinociceptive effects at doses up to 8 mg/kg, s.c., and 4 g/kg, respectively. Alcohol at 2 g/kg, i.g., also did not influence the effect of morphine, while cocaine at 4 mg/kg, s.c., significantly potentiated the antinociceptive effects of not only morphine but also pentazocine. In an analysis of serum and brain concentration levels of morphine in mice, when morphine and cocaine were simultaneously administered at 2 mg/kg, s.c., and 4 mg/kg, s.c., respectively, both serum and brain levels of morphine showed neither increase nor decrease in comparison with the levels in mice administered morphine alone. In myenteric plexus-longitudinal muscle preparations of isolated guinea pig ileum, 1 microM cocaine enhanced the agonistic effects of both pentazocine and ethylketocyclazocine. Furthermore, cocaine as well as ethylketocyclazocine showed naloxone-reversible agonistic effects in isolated rabbit vas deferens. These results indicate that cocaine may potentiate the antinociceptive effects of morphine and pentazocine by acting on the kappa-opioid receptors as an agonist.

Analgesia↗