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Biomedical subjects

S Tamura

Publications and source records attributed to S Tamura.

At least 649 records · Page 36Linked to original sources
PubMed1986

Thrombocytosis in patients with malignant pleural mesothelioma.

Thrombocytosis above 40.0 X 10(4)/mm3 occurred in five of six (83%) patients with malignant mesothelioma. In contrast, the incidence of thrombocytosis was 7.5% in patients with lung adenocarcinoma, 12.5% in squamous cell carcinoma, 5.1% in small cell carcinoma, and 41.7% in large cell carcinoma, respectively. The platelet count in large cell carcinoma was significantly higher than that in other cell types of lung cancer; however, the platelet count in malignant mesothelioma was much higher than that in large cell carcinoma. These results show that the incidence of thrombocytosis seems to be high in malignant mesothelioma, although the mechanism is thus far unknown.

Adenocarcinoma↗
PubMed1986

Identification and characterization of Mg2+-dependent phosphotyrosyl protein phosphatase from rat liver cytosol.

Although highly purified preparations of Mg2+-dependent phosphoseryl protein phosphatase (also designated phosphatase IA or phosphatase 2C) dephosphorylated phosphotyrosyl histone, the activity has been resolved from phosphatase IA by polyacrylamide gel electrophoresis at pH 9.5. This novel phosphotyrosyl-specific protein phosphatase absolutely requires Mg2+ or Mn2+ for activity, is inhibited by Zn2+, vanadate and fluoride, and has an optimal pH of 9.0 and Mr = 50,000. Certain properties of this phosphatase so closely resemble those of phosphatase IA that the two enzymes tend to be copurified through various separation procedures.

Animals↗
PubMed1986

The maitotoxin-evoked Ca2+ entry into synaptosomes is enhanced by cholera toxin.

Effects of the Gs protein-mediated adenylate cyclase facilitatory system on Ca2+ entry into synaptosomes were studied, using two specific toxins. A putative Ca2+-channel agonist, maitotoxin (MTX), increased the 45Ca2+ entry and [Ca2+]i, determined with Quin-II, into synaptosomes of the rat brainstem, which were not attenuated by nifedipine. However, another Ca2+-channel agonist, BAY K-8644 did not alter the 45Ca2+ entry nor [Ca2+]i. The MTX-induced increase of the 45Ca2+ entry was significantly enhanced by addition of dibutyryl cyclic adenosine monophosphate and by the pretreatment with cholera toxin. These findings support the view that stimulation of presynaptic receptors coupled to the Gs-adenylate cyclase system may lead to a facilitation of the release of neurotransmitters, through a cAMP dependent enhancement of the opening of the Ca2+ channels located on nerve terminals.

Adenylyl Cyclases↗
PubMed1986

Urinary excretion of pseudouridine in patients with hepatocellular carcinoma.

The urinary concentration of pseudouridine, primarily a degradation product of transfer ribonucleic acid, was determined by high-performance liquid chromatography in 23 patients with primary hepatocellular carcinoma, 13 patients with liver cirrhosis, and 24 healthy controls. The urinary concentration of pseudouridine in the patients with hepatocellular carcinoma was significantly higher than that in the patients with liver cirrhosis or the healthy controls. Sixteen (70%) of the 23 patients with hepatocellular carcinoma had urinary pseudouridine levels higher than the mean value for the healthy controls plus 2 standard deviations. Nine of the 13 patients (69%) who had a serum alpha-fetoprotein level below 400 ng/ml, had elevated urinary pseudouridine levels. Thus, the two markers, urinary pseudouridine and serum alpha-fetoprotein in combination, which were detected in a total of 19 of the 23 patients (83%) with hepatocellular carcinoma, are considered to serve as complementary markers for the diagnosis of this disease.

Aged↗
PubMed1986

Urinary pseudouridine as a tumor marker in patients with small cell lung cancer.

The urinary concentration of pseudouridine, primarily a degradation product of transfer ribonucleic acid, was determined by high-performance liquid chromatography in 22 patients with small cell lung cancer, 30 patients with non-small cell lung cancer, 13 patients with pulmonary infectious diseases and 24 healthy controls. The concentration of pseudouridine in both groups of patients with lung cancer was on the average significantly higher than that in the patients with pulmonary infectious diseases or in healthy controls. Thirteen (59%) of the patients with small cell lung cancer and 8 (27%) of those with non-small cell lung cancer had a urinary pseudouridine level above the mean value plus 2 for the healthy controls. In 11 patients followed up during chemotherapy, urinary pseudouridine levels changed almost in parallel with the changes in the clinical responses.

Aged↗
PubMed1986

Glycosaminoglycan in malignant pleural mesothelioma.

The quantitative analysis on glycosaminoglycan (GAG) in the tumor tissues of five patients with malignant pleural mesothelioma and in the pleural fluid of two patients was performed with the use of biochemical methods. In the tumor tissues, it was found that the average of the total amount of GAG was more than 7.9 times as high as that in adenocarcinoma of the lung, and that hyaluronic acid and chondroitin sulfate were main constituents of mesothelioma GAG. However, there was no significant difference in the content of dermatan sulfate and heparan sulfate between this neoplasm and adenocarcinoma. In the pleural fluid, the amount of hyaluronic acid was about 40 to 230 times higher than that in adenocarcinoma of the lung with the increment of chondroitin sulfate (11-87 times). These findings suggest that a marked increase in the total amount of GAG and the elevation of either the hyaluronic acid or the chondroitin sulfate level, or both, are characteristic abnormalities in malignant pleural mesothelioma.

Adult↗
PubMed1986

Radiological analysis of hemifacial spasm with special reference to angiographic manifestations.

Fifty-one patients with hemifacial spasm secondary to facial nerve compression by normal appearing, elongated, tortuous and/or dilated arteries, were treated by microsurgical neurovascular decompression. Post-operatively, 91% of 44 of these patients with one to six year postoperative follow-ups were satisfactory. The angiographic findings showed significant increase in the number of common trunk anomalies. Variations of the anterior and posterior inferior cerebellar and vertebral arteries are discussed in relation to nerve compression.

Adult↗
PubMed1986

Changes in the peripheral vasculature of various organs in patients with sarcoidosis--possible role of microangiopathy.

Vascular involvement in sarcoidosis is briefly reviewed with emphasis on the outcome of a 10-year project-study by the Sarcoidosis Research Committee of the Japanese Ministry of Health and Welfare. Examples of vascular disorder associated with sarcoidosis are presented, including basal lamina layering of the capillaries in the skeletal muscle, cardiac muscle, and lung, glomerulopathy in the kidney, vascular changes in the ocular fundus and bronchi, and impaired peripheral circulation that could be detected by thermography. According to our tentative definition, all of these disorders should be collectively called microangiopathy. The possible role of microangiopathy in the pathogenetic mechanism of sarcoidosis is also discussed. Although microangiopathy in sarcoidosis is a comprehensive term, it should be included, in addition to systemic granulomatous disease, as part of the clinicopathological entity of sarcoidosis.

Bronchi↗
PubMed1986

Mechanism by which pertussis toxin breaks unresponsiveness of delayed-type hypersensitivity to sheep red blood cells in mice.

The mechanism by which pertussis toxin (PT) breaks the unresponsiveness of delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) was examined in B10 mice. The unresponsiveness of DTH was induced in mice by iv injection of 10(9) SRBC and broken antigen-specifically by iv injection of 500 ng of PT into mice 1 or more days after SRBC injection. The restored DTH response in the SRBC-primed and PT-treated mice was accompanied by the appearance of Lyt-1-positive splenic T cells, capable of mediating DTH, fractionated in the low-density layers on a discontinuous bovine serum albumin density gradient. To examine the action of PT on the appearance of the DTH-effector cells, the splenic T cells from 10(9) SRBC-primed mice were treated with 100 ng/ml of PT for 60 min in vitro and then transferred into naive recipient mice. The PT-treated T cells acquired the ability to manifest DTH in the recipient mice several days after transfer. A large proportion of them were Lyt-1-positive small cells fractionated in the high-density layers before transfer and transformed into DTH-effector cells fractionated in the low-density layers in the recipient mice after transfer. Moreover, the ability of the PT-treated cells to manifest DTH on transfer was resistant to treatment with mitomycin C. These results suggest that PT acts on the sensitized, small Lyt-1-positive T cells from the unresponsive mice to differentiate them into large T-cell blasts, capable of mediating DTH, as one of the mechanisms by which PT breaks the unresponsiveness of DTH to SRBC.

Animals↗
PubMed1986

Interaction of famotidine with rat liver microsomes, a study showing less inhibition of drug metabolism than with cimetidine.

Interaction of famotidine with rat liver microsomes and its effect on drug metabolism in vitro were studied. Famotidine interacted with liver microsomes obtained from untreated, phenobarbital-pretreated and 3-methylcholanthrene-pretreated rats to produce characteristic type II spectral changes with peaks at 423-426 nm and troughs at 387-390 nm. The spectral dissociation constants were in the range of 0.84-0.94 mM. Famotidine inhibited aminopyrine N-demethylase activity to a much lesser extent than did cimetidine. The extent of inhibition at a concentration of 5 mM of famotidine was from 12 to 18% for the microsomes from the rats with different pretreatments. In contrast, 5 mM of cimetidine inhibited the activity 80, 59 and 80% in the microsomes from untreated, phenobarbital-pretreated and 3-methylcholanthrene-pretreated rats, respectively. Both famotidine and cimetidine inhibited aminopyrine N-demethylase in a mixed-type manner for the microsomes from phenobarbital-pretreated rats, with inhibition constants of 4.7 and 0.7 mM, respectively. These results demonstrate that famotidine is an in vitro inhibitor of microsomal drug metabolism in rats but is much less inhibitory than cimetidine.

Aminopyrine N-Demethylase↗
PubMed1986

Thymosin alpha 1 enhances haemopoietic colony formation by stimulating the production of interleukin 3 in nu/nu mice.

We have studied the action mechanism of thymosin alpha 1 in modulation of haemopoietic system. The present study demonstrated that thymosin alpha 1 enhanced the colony formation as determined by CFU-s, GM-CFU and T-CFU, as well as the production of IL-3, when administered twice a week for a total of six or twelve times into nu/nu mice. The incubation of bone marrow cells with thymosin alpha 1 in vitro did not cause an increase of CFU-s, in contrast to IL-3 which caused a marked increase of CFU-s during the incubation of 72 h. These experiments indicate that thymosin alpha 1 exerts its effect on colony formation of haemopoietic stem cells (CFU-s) indirectly through the enhancement of the IL-3 production. The present finding may support clinical applications of thymosin alpha 1 in a wide range, since IL-3 is known to be the growth factor for many kinds of haemopoietic precursor cells including not only CFU-s but also GM-CFU, BFU-E, Eos-CFU, Meg-CFU, Mast cells, Pre B-cells and Pre T-cells.

Animals↗
PubMed1986

Amino acid sequence of a prothoracicotropic hormone of the silkworm Bombyx mori.

We have determined the complete amino acid sequence of 4K-PTTH-II, one of three forms of the M(r) 4400 prothoracicotropic hormone of the silkworm Bombyx mori, active to brainless pupae of Samia cynthia ricini. Like vertebrate insulin, it consists of two nonidentical peptide chains (A and B chains). The A chain consists of 20 amino acid residues. The B chain is a mixture of four microheterogeneous peptides, two of which consist of 28 residues, and the other two, of 26 residues. 4K-PTTH-II has considerable sequence homology (40%) with human insulin, and it resembles porcine relaxin both in the carboxyl-terminal cysteine residue of the A chain and in the amino-terminal pyroglutamic acid residue of the B chain. The identical distribution of the six cysteine residues also indicates that 4K-PTTH-II belongs to the insulin family.

Journal Article↗
PubMed1986

Analysis of debromination of 1,2-dibromoethane by cytochrome P-450-linked hydroxylation systems as observed by bromide electrode.

Debromination of 1,2-dibromoethane (DBE) by a rabbit liver microsomal preparation and a reconstituted cytochrome P-450 enzyme system was investigated. The reaction was performed in our newly constructed reaction vessel, in which a bromide electrode was installed. During the reaction, the liberated bromide ion was continuously measured by the bromide electrode, and the amount was recorded. In the microsomal preparation, the DBE-debromination rate per nmol cytochrome P-450 was enhanced by phenobarbital-pretreatment of rabbits compared with the untreated microsomes, whereas it was diminished by 3-methylcholanthrene-pretreatment. The debromination reaction was reconstituted in a purified enzyme system containing phenobarbital-inducible rabbit liver microsomal cytochrome P-450 (P-450PB), NADPH-cytochrome P-450 reductase, and NADPH. The optimum conditions required the presence of dilauroylphosphatidylcholine and cytochrome b5. Cytochrome b5 was found not to be an obligatory component for the DBE-debromination in the reconstituted system, but it stimulated the activity about 3.4-fold. Preincubation of the reconstituted mixture with guinea pig anti-cytochrome P-450PB antiserum markedly inhibited the debromination reaction.

Animals↗
PubMed1986

IgE antibody responses against Japanese cedar pollen in the mouse.

IgE antibody responses against Japanese cedar pollen in the mouse were investigated to develop a mouse model of human allergy for combinations of factors including pollen administration routes, elicitation antigens and inbred mouse strains. Daily short term inhalation of native pollen or intratracheal administration of pollen suspended in saline induced IgE antibody responses in DBA/2, BDF1 and Balb/c mice, but failed to induce any detectable responses in C57BL/6 and C57BL/10 mice. Intraperitoneal injection of pollen suspension also induced IgE antibody responses in DBA/2, BDF1 and Balb/c mice but not in C57BL/6 mice. IgE antibody responses against pollen described above were detected by passive cutaneous anaphylaxis (PCA) reactions using crude extract of pollen as an elicitation antigen. On the other hand, IgE antibodies specific for antigen Sugi basic protein (AgSBP), which is a major allergen of pollen in humans (Yasueda, H., Yui, Shimizu, T., and Shida, T., 1983. Isolation and partial characterization of the major allergen from Japanese cedar (Cryptomeria japonica) pollen. J. Allergy Clin. Immunol. 71: 77-86), were also detected by PCA reactions using AgSBP in the sera from mice which received secondary or the tertiary stimulation by pollen. These results suggest that IgE antibody responses against Japanese cedar pollen in the mouse can be induced by airway sensitization and that the responses are genetically controlled by H-2-linked immune response genes. The results also suggest that not only IgE antibody responses specific for components other than AgSBP but also responses specific for AgSBP can be induced in the mouse by repeating appropriate sensitization by pollen.

Administration, Inhalation↗
PubMed1986

The antiallergic agent amoxanox suppresses SRS-A generation by inhibiting lipoxygenase.

Amoxanox has potent antiallergic activity because it inhibits the release of chemical mediators such as histamine and leukotrienes. We studied the in vitro effect of amoxanox on arachidonic acid metabolism, including the lipoxygenase and cyclooxygenase pathways. Amoxanox inhibited calcium ionophore A23187-induced formation of 5-HETE, LTB4, SRS-A (LTC4, LTD4 and LTE4), and 12-HETE in rat peritoneal resident monocytes. These results indicate that amoxanox inhibits 5- and 12-lipoxygenases. The compound, however, did not affect the formation of TXB2 or 6-keto-PGF1 alpha in guinea pig lung fragments and PGE2 or PGF2 alpha in bovine seminal vesicles, suggesting that it did not inhibit cyclooxygenase. These results show that the antiallergic action of amoxanox is associated, at least in part, with the reduction of leukotrienes due to the inhibition of lipoxygenases.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗