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Biomedical subjects

T Taniguchi

Publications and source records attributed to T Taniguchi.

At least 847 records · Page 47Linked to original sources

[Total cystectomy for bladder tumor: eight-year experience].

Between 1975 and 1982, 39 patients underwent total cystectomy and urinary diversion at our hospitals. The type of urinary diversions were ileal conduit (32 cases) and ureterocutaneostomy (7 cases). Preoperative irradiation was used in 10 patients. The postoperative mortality rate was 2.6%. Early complications occurred in 38.5% and included wound infection, acute pyelonephritis, intestinal obstruction, pelvic infection, intestinal leakage and/or medical complications. Ureteroileal stricture was most frequent in late complications. Over-all relative 1-, 3-, and 5-year survival rates were 92.4, 56.6, 41.7%, respectively. Survival was dependent on the stage and the grade of the tumor. No significant difference was found between the older (greater than or equal to 65 years old) and the younger (less than 65 years old) groups.

Acute Disease↗

Distribution of chicken anemia agent (CAA) and detection of neutralizing antibody in chicks experimentally inoculated with CAA.

When chicks were inoculated experimentally with chicken anemia agent (CAA) at 1 day of age, CAA was consistently recovered from all the organs, including the brain, up to 28 days postinoculation (PI). It was recovered from the brain and rectal contents even 49 days PI, when the experiment was finished. In chicks inoculated with CAA at 28 or 42 days of age, CAA was also proved to multiply in all the organs, except the brain. It disappeared from these chicks earlier than from the chicks inoculated at 1 day of age. Neutralizing antibody against CAA began to be detected 21 days PI in the chicks inoculated at 1 day of age, and 7 days PI in the chicks inoculated at 28 or 42 days of age.

Anemia↗

Chronological observations on hemato-pathological changes in chicks inoculated with chicken anemia agent.

Chicks were inoculated with the Gifu-1 strain of the chicken anemia agent (CAA) on the day of hatching. They manifested distinct anemia accompanied with pancytopenia 8--20 days after inoculation. Discoloration of the bone marrow and atrophy of the thymus began to be seen 6 days after inoculation. Histologically, hematopoietic cells began to decrease and large blastic cells to appear in the bone marrow 4--6 days after inoculation. Hypoplasia and subsequently aplasia occurred to all over the bone marrow 8 days after inoculation. In the bone marrow erythrocytopoiesis was noticed first 16--18 days after inoculation, granulocytopoiesis later, and transient hyperplasia finally. At last, the bone marrow returned to a normal condition 32 days after inoculation or later. In the thymus the depletion of cortical lymphocytes became distinct 4--6 days after inoculation, and lobular atrophy 8 days after inoculation or later. The depletion of lymphocytes in the other lymphatic tissues and hemorrhage in the lamina propria of the proventriculus were observed only in the anemic phase. The results mentioned above indicated that the anemia induced by CAA was caused by the disorder of hematopoietic cell formation in the bone marrow. It was also noteworthy that cortical lymphocytes in the thymus began to decrease remarkably soon after inoculation.

Anemia↗

Alterations in muscarinic cholinergic receptors after preganglionic denervation of the superior cervical ganglion in cats.

For identification and characterization of muscarinic cholinergic receptors, a radioligand binding assay using [3H]quinuclidinyl benzilate (QNB) was carried out using normal and preganglionically denervated cat superior cervical ganglion (SCG). Specific [3H]QNB binding to the cat SCG homogenates was saturable, reversible and of high affinity (KD = 13.9 +/- 4.0 pM) with a Bmax of 54.1 +/- 5.8 fmol/mg of protein. From a kinetic analysis of the data, we calculated the association and dissociation rate constants of 1.47 X 10(9) M-1 min-1 and 0.025 min-1, respectively. The dissociation constant calculated from the rate constants (KD = K-1/K+1 = 17.0 pM) was similar to the value determined from Scatchard analysis. Values of K1 for muscarinic cholinergic drugs that inhibited specific binding were: QNB, 0.10 pM; atropine, 0.57 nM; acetylcholine, 145 nM; and oxotremorine, 100 nM. Nicotinic cholinergic agents such as alpha-bungarotoxin, nicotine and hexamethonium were ineffective in displacing [3H]QNB binding, at a concentration of 10 microM. After preganglionic denervation, the specific [3H]QNB binding to the SCG significantly increased, compared to the nonoperated side of SCG. The Bmax value was significantly increased at 2 weeks without a change in the KD, thereby suggesting an increase in the density of muscarinic cholinergic receptors. The present study suggests that the existence of muscarinic cholinergic receptors in the cat SCG and preganglionic denervation may lead to an increase in the density of muscarinic cholinergic receptors.

Animals↗

In vivo and in vitro effects of Nocardia rubra cell wall skeleton on natural killer activity in mice.

The in vivo and in vitro effects of Nocardia rubra cell wall skeleton (N-CWS) on natural killer (NK) activity of spleen and peritoneal lymphocytes of C57BL/6 mice were studied. The NK activity of spleen and peritoneal lymphocytes against YAC-1 lymphoma cells and cultured B-16 melanoma cells peaked at 3 days after intraperitoneal or intravenous administration of N-CWS, and returned to the normal value 7 days later. The NK activity of spleen lymphocytes was augmented by in vitro incubation with N-CWS. The appropriate concentration of N-CWS for the in vitro stimulation of NK activity in spleen lymphocytes was 2-5 micrograms/ml.

Animals↗

Structures of the asparagine-linked sugar chains of subcomponent C1q of the first component of bovine complement.

Bovine C1q, a subcomponent of the first component of complement, contains six asparagine-linked sugar chains in 1 molecule. The sugar chains are exclusively distributed in the noncollagenous regions. The sugar chains were liberated as radioactive oligosaccharides from the polypeptide portion by hydrazinolysis followed by N-acetylation and NaB[3H]4 reduction, and their structures were studied by sequential exoglycosidase digestion in combination with methylation analysis. Bovine C1q was shown to contain equal amounts of neutral and acidic oligosaccharides with the following structures: (formula, see text) where NeuG1 is N-glycolylneuraminic acid.

Animals↗

Poly(ADP-ribose) synthetase. The DNA binding domain and the automodification domain.

Poly(ADP-ribose) synthetase is known to require double-stranded DNA for activity and to be susceptible to automodification with poly(ADP-ribose). This enzyme is cleaved into two fragments by limited proteolysis with papain. Their molecular weights are 74,000 and 46,000, respectively, as judged by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The fragment of Mr 46,000 binds to a nicked DNA-cellulose column with the same affinity as that of native enzyme, while the fragment of Mr 74,000 has little affinity for the DNA ligand. When the enzyme previously automodified with [adenine-U-14C]NAD (2 ADP-ribose units incorporated per molecule of enzyme) is digested with papain, the label is detected only in the fragment of Mr 74,000. These results indicate that poly(ADP-ribose) synthetase contains two domains, one acting as the site for binding of DNA and the other acting as the site(s) for accepting poly(ADP-ribose).

Animals↗

Participation of poly(ADP-ribosyl)ation in the depression of RNA synthesis caused by treatment of mouse lymphoma cells with methylnitrosourea.

When mouse lymphoma cells (L-1210) are treated with methylnitrosourea, a DNA-damaging agent, polyadenosine diphosphoribose (poly(ADP-ribose)) synthetase activity increases 5-8-fold in 2-3 h, while RNA polymerase activity remains constant for an initial 2 h and then gradually decreases to 25-30% of the control level in 5 h. Both alpha-amanitin-sensitive and -resistant RNA polymerase activities are depressed to the same degree by the treatment with methylnitrosourea. The depression in RNA synthesis is virtually prevented when the treated cells are cultured in the presence of 3-aminobenzamide, a specific inhibitor of poly(ADP-ribose) synthetase. Analyses of the RNA extracted from the cells labeled with [3H]uridine by agarose gel electrophoresis and by poly(U)-Sepharose column chromatography show that the contents of ribosomal precursor RNA and poly(A)-containing RNA are both low in the methylnitrosourea-treated cells as compared with those in the untreated cells and that the reduction in the contents of these kinds of RNA is almost completely prevented by the addition of 3-aminobenzamide to the culture medium. These results suggest that the enhancement of poly(ADP-ribosyl)ation causes the decrease in both synthesis of ribosomal RNA and messenger RNA.

Animals↗

Inducer-responsive expression of the cloned human interferon beta 1 gene introduced into cultured mouse cells.

A hybrid plasmid was constructed from pSV2-Ecogpt (Mulligan and Berg, 1981) and the cloned 1.8 kilobase chromosomal DNA segment which contains the human interferon (HIFN-beta 1) gene and its flanking sequences. Cultured mouse FM3A cells were transfected by the hybrid plasmid and several Ecogpt+ clones were selected. Southern blot analysis of the DNA from these mouse cell clones showed that two of them contained a few copies of the 1.8 kilobase human DNA. Synthesis of mRNA characteristic of the HIFN-beta 1 mRNA increased as measured by RNA blot analysis when those clones were treated with Newcastle disease virus or with poly(I):poly(C). In addition, the induced mouse cell clones gave rise to the synthesis of human IFN-beta 1. These results suggest the presence of a unique nucleotide sequence in the 1.8 kilobase DNA which is sufficient for the inducer-responsive expression of the human IFN-beta 1 gene.

Animals↗

Effect of chemotherapy on natural-killer activity and antibody-dependent cell-mediated cytotoxicity in carcinoma of the lung.

The effect of chemotherapy on natural killer (NK) activity and antibody-dependent cell-mediated cytotoxicity (ADCC) in 15 advanced carcinomas of the lung was examined with regard to the drug, dose, route and timing of administration. The relationship between the effect of chemotherapy on the prognosis for the patients, and the changes in NK activity and ADCC, was also analysed. The NK activity and ADCC in patients with poor prognosis were significantly subnormal, even before treatment. The NK activity and ADCC began to decrease 2 weeks after the initiation of treatment and reached the lowest level during the 3rd or 4th week in all patients. Thereafter, they returned to the pretreatment level in 8 patients with stabilized disease. In contrast, they were not restored in 7 patients with progressive disease and poor prognosis. In 4 patients it was found that the effect of chemotherapy with pepleomycin and carbazilquinone on NK activity and ADCC differed according to the drug used. From this pilot study it is suggested that NK activity and ADCC are valuable prognostic factors in patients with advanced carcinoma of the lung, and that detailed analysis of the effect of each anticancer agent on NK activity and ADCC is desirable for the establishment of better treatment regimens for advanced carcinoma of the lung.

Aged↗

Comparative studies on the structures of the carbohydrate moieties of human fibrinogen and abnormal fibrinogen Nagoya.

Human fibrinogen contains four asparagine-linked sugar chains in one molecule. All B beta and gamma subunits obtained from both normal fibrinogen and abnormal fibrinogen Nagoya contain 1 mol each of an asparagine-linked sugar chain. The sugar chains were quantitatively liberated as radioactive oligosaccharides from the polypeptide portion by hydrazinolysis followed by N-acetylation and NaB3H4 reduction. By the combination of sequential exoglycosidase digestion and methylation analysis, the structures of the sugar chains of human fibrinogen were elucidated to be NeuAc alpha 2 leads to 6Gal beta 1 leads to 4GlcNAc beta 1 leads to 2Man alpha 1 leads to 6(NeuAc alpha 2 leads to 6Gal beta 1 leads to 4GlcNac beta 1 leads to 2Man alpha 1 leads to 3)Man beta 1 leads to 4GlcNAc beta 1 leads to 4GlcNAc and Gal beta 1 leads to 4GlcNAc beta 1 leads to 2Man alpha 1 leads to 6(NeuAc alpha 2 leads to 6Gal beta 1 leads to 4GlcNAc beta 1 leads to 2Man alpha 1 leads to 3)Man beta 1 leads to 4GlcNAc beta 1 leads to 4GlcNAc. Neither quantitative nor qualitative differences were found between the sugar chain moieties of normal fibrinogen and fibrinogen Nagoya, indicating that the molecular basis of the abnormality in the latter may reside in its polypeptide moieties.

Asparagine↗

Pathogenicity of avian nephritis virus for embryonating hen's eggs.

The pathogenicity of avian nephritis virus (ANV) for embryonating hen's eggs was studied by various routes of inoculation. When inoculated with ANV by the yolk sac route, 6-day-old embryos showed the highest susceptibility and all of them died 3 to 14 days postinoculation (PI). They manifested hemorrhage and edema of the whole body (3 to 6 days PI) and stunting (7 to 14 days PI). The 50% egg-infective dose of the virus by yolk sac inoculation coincided well with the virus titer expressed in plaque-forming units determined on the monolayer of chicken kidney cell cultures. The virus could be passed serially through the chorioallantoic membrane (CAM) of embryonating hen's eggs. In these eggs the CAM presented edematous thickening at the inoculation site, and the embryo stunting. when inoculated by the CAM route, high virus doses killed all embryos, but low virus doses allowed some of the infected embryos to hatch normally. When inoculated by the allantoic cavity route, the virus did not multiply in the allantoic cavity of embryonating eggs, but some of these eggs became infected. Fluorescent antigens were present only in the kidneys and CAM of embryos infected with the virus. The virus was recovered at a low rate from cloacal swabs of chicks from normally hatched eggs inoculated with the virus by the CAM route. These chicks were variable in growth, but had antibodies against the virus and developed nephritis at 36 days of age.

Animals↗

Molecular cloning and coding nucleotide sequence of complementary DNA of cytochrome P-450 involved in metabolic activation of carcinogenic substances.

Complementary (c)DNA clones of phenobarbital-inducible cytochrome P-450 which has a strong activity toward metabolic activation of aflatoxin B1 were identified by a hybridization-arrested translation assay and a positive hybridization-translation assay. The coding nucleotide sequence of the cytochrome P-450 mRNA was determined by analysis of three cloned cDNAs and by primer extension method using a 5' terminal region fragment (62 bp) of a clone (pcP-450 pb-2) as a primer. The deduced amino acid sequence of the cytochrome is composed of 491 amino acid and its predicted molecular weight and amino acid composition concur with those determined with the purified protein. The sequence of one of the three cloned cDNAs is not completely the same as that of the other two. Fourteen nucleotide substitutions occur in their 922 overlapping nucleotides and 7 of them result in 6 amino acid replacements, therefore indicating the presence of at least two similar but distinct mRNAs for phenobarbital-inducible cytochrome P-450. These substitutions occur in a limited portion of the sequence, apparently forming some sort of a "variable regions."

Aflatoxin B1↗