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T Ando

Publications and source records attributed to T Ando.

At least 757 records · Page 42Linked to original sources
PubMed1976

Studies on a protamine (galline) from fowl sperm. 3. The total amino acid sequence of intact galline molecule.

Of the eight fractions (G-I-G-VIII) obtained from galline, a protamine from rooster sperm nuclei, the complete amino acid sequences of two fractions G-I and G-V have already been reported. Other fractions of galline purified repeatedly on the column of Bio-Gel CM-30 were submitted to structural analyses. The complete amino acid sequences of three (G-II, G-III and G-VII) of the fractions and the partial chemical structures of two (G-VI and G-VIII) of the fractions were established from the results of analyses of the tryptic and chymotryptic peptides together with those of end groups and terminal sequences. Remarkable similarities have so far been found in the sequences of these fractions. Combining these results with those complementarily explained in the following paper, it was finally confirmed that the intact galline molecule is composed of only one molecular species (G-VIII) and that fractions (G-I-G-VII) were derived from G-VIII by the action of an inherent protease in the preparation process. Consequently, the total amino acid sequence of the intact galline is concluded to be as follows: H-Ala-Arg-Tyr-Arg-Ser-Arg-Gly-Arg-Ser-Arg-Ser-Arg-Arg-Thr-Arg-Arg-Arg-Arg-Ser-Pro-Arg-Ser-Gly-Arg-Arg-Arg-Ser-Pro-Arg-Arg-Arg-Arg-Ser-Arg-Arg-Arg-Arg-Arg-Tyr-Gly-Ser-Ala-Arg-Arg-Ser-Arg-Arg-Ser-Gly-Gly-Val-Arg-Arg-Arg-Arg-Tyr-Gly-Ser-Arg-Arg-Arg-Arg-Arg-Arg-Tyr-OH.

Amino Acid Sequence↗
PubMed1976

Studies on a protamine (galline) from fowl sperm. 4. Degradation of galline by trypsin-like protease of fowl sperm heads.

Galline, a protamine of domestic fowl, was obtained by two preparation procedures from the semen of a strain of White Plymouth Rock and submitted to fractionation by column chromatography on Bio-Gel CM-30. In the first procedure the specimen prepared from sperm heads was purified by the use of distilled water and dilute acetic acid and fractionated into almost eight fractions (G-I-G-VIII) in the same way as the specimen from a strain of New Hampshire (1,2). No difference could be found between galline specimens from the two different strains based on the amino acid and terminal analyses of each fraction. The specimen of galline from sperm heads purified with 1% citric acid (the second procedure) was composed of only one component, which was isolated as a single peak. The smaller fractions, G-I-G-VII, were found to be derived from G-VIII by the action of trypsin-like protease contained in the extract of sperm heads with 1% citric acid. This enzyme seems to originate in the acrosome of fowl spermatozoa. Consequently, it is concluded that intact galline is composed of only one molecular species and its total amino acid sequence is represented by the completed formula of G-VIII as shown in the preceding paper (4).

Amino Acid Sequence↗
PubMed1975

Structural organization of 'callosal' OBg in human corpus callosum agenesis.

The structural organization of the 'callosal' OBg was studied in Nissl and Weil stained sections of two human brains completely lacking in the corpus callosum. OBg of the normal brain contains a set of distinctive large pyramidal cells in layer III. By contrast, in the brains with absence of the corpus callosum, layer III of OBg contained a slightly reduced number of smaller pyramidal cells than normal, and the characteristic large pyramidal cells were scarsely detectable. Other layers of OBg were not definitely changed. Furthermore, 'acallosal' striate cortex revealed no specific changes. From these observations, it was suggested that the large layer III pyramids of OBg might be closely related to callosal connections.

Agenesis of Corpus Callosum↗
PubMed1975

In vitro modification and restriction of phage phi-105c DNA with Bacillus subtilis N cell-free extract.

The enzymes involved in host-controlled modification and restriction by Bacillus subtilis strain N were detected in cell free extracts. In the presenct of Mg2+ the N-specific endonucleases cleaved unmodified DNA but did not attack phi-105C. N DNA carrying N-specific modification. The restriction endonuclease required neither SAM nor ATP for its activity. The N-specific modification enzyme was active only in the presence of SAM, indicating that modification in this syteem is a methylation of DNA.

Adenosine Triphosphate↗
PubMed1975

Hyperglycinemia and propionyl coA carboxylase deficiency and episodic severe illness without consistent ketosis.

Propionyl CoA carboxylase deficiency was found in a 7-month-old boy who presented with attacks of vomiting, anorexia, weight loss, weakness, and hypotonia. He failed to thrive and had generalized seizures. He had propionic acidemia and hyperglycinemia; these are the manifestations of the ketotic hyperglycinemia syndrome. However, ketonuria was not a consistent part of his clinical picture, and he had at least two episodes of acute overwhelming illness, the latter one fatal, in which ketones were never found in the urine. Large amounts of pyrrolidone carboxylic acid were found in body fluids.

Acidosis↗
PubMed1975

Action of bleomycin on the bacteriophate T7 infection.

A decrease in production of bacteriophage T7 was observed in bleomycin-treated Escherichia coli B cells. Bleomycin was found to shorten the eclipse in phage growth. A T7 early gene product, the T7-specific RNA polymerase which catalyzed the transcription of late gene appeared more rapidly in the bleomycin-treated cells than in the non-treated cells. The rate of phage adsorption increased to some extent in drug-treated cells. A possible mechanism to explain the mode of action of bleomycin is discussed.

Bleomycin↗
PubMed1975

Studies on a protamine (galline) from fowl sperm. 2. The amino acid sequences of two components of galline.

Galline, a protamine from rooster sperm nuclei, has already been separated into its components, G-I-G-VIII. The amino acid composition of the homogeneously purified fraction G-I is determined decisively to be Arg11, Ser2, Gly3, Val1 and Tyr2, and the molecular weight is 2,908 as hydrochloride. The complete amino acid sequence was deduced as follows from the results of analyses of the tryptic and chymotryptic peptides: H-Ser-Gly-Gly-Val-Arg-Arg-Arg-Arg-Tyr-Gly-Ser-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Tye-OH. Another purified fraction, G-V, has the amino acid composition, Arg24, Thr1, Ser8, Gly3, Ala2, Pro2 and Tyr2 as described previously, and the molecular weight 6,274 as hydrochloride. The complete amino acid sequence was established by combining analytical results of tryptic, chymotryptic and thermolysin peptides as well as those of carboxypeptidase and leucine aminopeptidase digestion as follows: H-Ala-Arg-Tyr-Arg-Ser-Gly-Arg-Ser-Arg-Ser-Arg-Arg-Thr-Arg-Arg-Arg-Arg-Ser-Pro-Arg-Ser-Arg-Gly-Arg-Ser-Pro-Arg-Arg-Arg-Arg-Ser-Arg-Arg-Arg-Arg-Arg-Tyr-Gly-Ser-Ala-Arg-Arg-OH.

Amino Acid Sequence↗
PubMed1975

[Latent infection with Corynebacterium kutscheri in mice after peroral inoculation and its provocation by cortisone (author's transl)].

Latent infection with Corynebacterium kutscheri in mice and its provocation by cortisone were studied with a rifampicin-resistant strain of the organism. Mice having been infected perorally began to excrete the organisms in feces within 6 hours, and most of them were found to be carrying the organisms in the intestine, especially in the cecum even 90 days after infection. In such state of latency, however, no organisms were detected in other main organs, and neither visible lesions nor serum agglutinin was detectable. The latent infection with excretion of the organisms in feces after peroral infection was shown to become overt and fatal by cortisone treatment made even 90 days after infection. In infected mice excreting no organisms in feces and having bites on their skin, the wounds became severe ulcers after cortisone treatment resulting in septicemia.

Administration, Oral↗
PubMed1975

Recovery of a DNA-protein complex in cultured mammalian cells from damage caused by 4-nitroquinoline 1-oxide.

Treatment of FM3A cells with 4-nitroquinoline 1-oxide caused a decrease in the sedimentation velocity of a DNA-protein complex, but did not cause a dissociation of the complex, as revealed by neutral sucrose gradient centrifugation. Microscopic autoradiography of the complex spread on a Millipore filter, demonstrated that treatment of the cells with 4-nitroquinoline 1-oxide, or of the complex with Pronase E, gave rise to a relaxed mass of DNA fibers, in contrast to a compact mass of DNA from control cells. The damage to the DNA-protein compelx was repaired completely by incubation of the cells in a medium without 4-nitroquinoline 1-oxide. The following metabolic inhibitors had no effect on the repair of the complex: inhibitors of nucleic acid synthesis, alpha-amanitine, cordycepin, 2-mercapto-1-(beta-4-pyridethyl)benzimidazol, 1-beta-D-arabinofuranosylcytosine, 5-fluorodeoxyuridine, and hydroxyurea; inhibitors of protein synthesis, cycloheximide and puromycin; an inhibitor of the dark repair process in a variety of biological systems, caffeine; inhibitors of the microtubular and microfilament system, Colcemid and cytochalasin B, respectively; and inhibitors of energy metabolism, 2,4-dinitrophenol, KCN, iodoacetic acid, ouabain, and an atmosphere of nitrogen. Acriflavine and actinomycin D, which are known to intercalate into DNA, caused a decrease in the sedimentation velocity of the DNA-protein complex; therefore, the effects of these agents on the recovery process remained unsolved. The repair process of the complex was, however, demonstrated to be temperature dependent. The process was inhibited at 10 degrees, retarded at 28 degrees, but accelerated at 40 degrees as compared with the rate at 37 degrees.

4-Nitroquinoline-1-oxide↗
PubMed1975

Repair of UV-induced DNA damage in recombination-deficient strains of Bacillus subtilis.

To clarify the role of gene products for genetic recombination which might be concerned in excision repair, the repair of DNA lesions induced by ultraviolet (UV) irradiation was examined under non-growing conditions with a variety of recombination deficient (Rec-) mutants of Bacillus subtilis. The extent of repair was estimated by the recovery of transforming activity of DNA extracted from the cells during the post-irradiation incubation period (the assay method was termed as marker-repair experiment). The marker repair seemed to be accomplished by the excision repair as assumed from the effects of inhibitors. Among Rec- mutants tested, a mutant strain UVS80TH (rec-80) exhibited a normal level of marker repair activity, whereas strains GSY1025 (recA1), GSY1028 (recB2) and GSY908 (rec-4) exhibited reduced marker repair activities. These results and the data on UV sensitivity of the mutants indicate that (1) the products of all these Rec genes are related to UV resistance of the cell viability and are factors functioning through mechanisms other than excision repair, (2) the products of recA, recB and rec-4 genes display some roles in maintenance of a level of excision repair activity, and (3) the product of the rec-80 gene does not participate at all in excision repair.

Acriflavine↗