Search PubMed⌕ Search

Biomedical subjects

A Ichikawa

Publications and source records attributed to A Ichikawa.

At least 307 records · Page 17Linked to original sources
PubMed1980

The ultrastructure of rapid-frozen, substitution fixed parotid gland acinar cells of the mongolian gerbil (Meriones meridianus).

The ultrastructure of gerbil parotid gland acinar cells studied by rapid freezing in liquid nitrogen and freeze-substituting with OsO4 was similar in general to conventionally prepared tissue, but different in several aspects. Acceptable preservation was limited to about 10 microgram of the surface; the secretory granule membrane was a single dense line, while all others were trilaminar; the dense-cored secretory granule had a rim of low density which was homogeneous; there were many continuous profiles between the Golgi lamellae, vesicles, and vacuoles; and mitochondria were long and arborized.

Animals↗
PubMed1980

Effect of adenosine and adenosine 5'-monophosphate on cell division of cultured mastocytoma P-815 cells.

The growth of mouse mastocytoma P-815 cells in culture (37 degrees, 42 hr) was inhibited by exogenous adenosine (0.2 to 1.0 mM) and more effectively by AMP (0.01 to 0.1 mM), but not by adenine. The inhibited growth (a 25% inhibition by 0.5 mM adenosine and a 80% inhibition by 0.25 mM AMP) was restored to a near control level by the addition of uridine (0.5 mM) to the medium. The pretreatment (37 degrees, 3 hr) of the cells with adenosine or AMP caused a 60% inhibition of incorporation (37 degrees, 2 hr) of [U-14C]aspartate into uracil nucleotides, accumulating 14C-orotate and orotidine. Both dipyridamole, an inhibitor of adenosine uptake, and exogenous adenosine deaminase suppressed the growth inhibition induced by not only adenosine but also AMP. 2-Chloroadenosine, which is resistant to the action of adenosine deaminase, was a more potent growth inhibitor, while 3'AMP and 2'-AMP, which are not hydrolyzed to adenosine by membrane 5'-nucleotidase, were ineffective. Adenosine 5'-sulfate and other 5'-substituted adenosines were also ineffective. These observations indicate that AMP inhibits the growth of mastocytoma P-815 cells as a result of its continuous conversion to adenosine and a constant exposure of the cells to a low concentration of adenosine which readily permeates the cell membrane. In addition, adenosine, AMP and their agarose-linked forms rapidly (37 degrees, 20 min) elevated cellular levels of cAMP. This effect was not suppressed by dipyridamole. Apparently adenosine and AMP also act extracellularly for growth inhibition by regulating cAMP levels.

Adenine Nucleotides↗
PubMed1980

Effect of adenosine 3',5'-monophosphate on growth and several functions of cultured mastocytoma P-815 cells.

Growth-inhibited mouse mastocytoma P-815 cells at stationary phase contained more histamine, serotonin and adenosine 3',5'-monophosphate (cAMP), and higher activities of histidine decarboxylase and adenylate cyclase than the cells during exponential growth. The elevation of endogenous cAMP levels induced by several growth-inhibiting agents such as N6, O2'-dibutyryl cAMP (Bt2cAMP), prostaglandin E1, AMP and 2-chloroadenosine stimulated several functions characteristic of mastocytoma P-815 cells in culture, elevating the synthesis of histamine and serotonin, the activity of chymotrypsin-like protease, and the incorporation of [35S]sulfate into acidic glycosaminoglycans. 1-Methyl-3-isobutyl-xanthine (MIX), a potent inhibitor of cAMP phosphodiesterase, potentiated stimulatory effect of these agents. The results indicate that cAMP regulates the growth and functions of mastocytoma P-815 cells. [35S]-Sulfated acidic glycosaminoglycans synthesized in cells at stationary phase or in cells treated with Bt2cAMP plus MIX mainly localized in the 3000-10000 x g sedimentable fraction of cell homogenates, and had a molecular weight of 200000 to 400000 based on gel filtration. This acidic glycosaminoglycan was resistant to chondroitinase ABC and the heparin-degrading enzyme present in the 20000 x g sedimentable fraction of the cells, and was identified as a highly sulfated macromolecular heparin based on behaviors on DEAE-cellulose column and on acidic electrophoresis. Cycloheximide suppressed the stimulatory effect of Bt2cAMP on the synthesis of histamine and [35S]-sulfated acidic glycosaminoglycan.

Adenosine↗
PubMed1980

Effect of D-glucosamine on growth and several functions of cultured mastocytoma P-815 cells.

In order to elucidate the biochemical basis for the selective cytotoxicity of D-glucosamine to neoplastic cells, the effect of glucosamine on the growth and several functions of mastocytoma P-815 cells were examined. Incubation of mastocytoma cells with 5 mM glucosamine resulted in a marked inhibition of growth and a significant reduction of cellular uptake and oxidation of glucose and of cellular levels of adenosine triphosphatase (ATP). Glucosamine also reduced the uridine nucleotide pool sizes, and accumulated uridine diphosphate (UDP)-N-acetylglucosamine. However, growth inhibition by glucosamine, which was reversed by glucose, was not prevented by exogenous uridine. In addition, glucosamine suppressed the phosphorylation of thymidine and its incorporation into deoxyribonucleic acid (DNA). The suppression of cell division by glucosamine was accompanied by the elevation of several functions of mastocytoma cells, including the accumulation of adenosine-3', 5'-monophosphate (cAMP), histamine, and serotonin. The incorporation of [(35)S]SO(4)(2-) into acidic glycosaminoglycan was also increased. Of these functional alterations, the elevation of cAMP levels was the earliest detectable change, indicating that growth and functions of mastocytoma cells are also regulated by cAMP. However, glucosamine did not affect the adenylate cyclase activity of plasma membrane in vitro, suggesting the necessity of intact membrane structure for the action of glucosamine.

Adenosine Triphosphate↗
PubMed1980

Aphidicolin: a specific inhibitor of DNA synthesis in synchronous mastocytoma P-815 cells.

The influence of aphidicolin on cell multiplication and DNA synthesis was examined using synchronous mouse mastocytoma P-815 cells. Aphidicolin was cytotoxic specifically to the cells of the S phase of the cell cycle. This cytotoxicity was reversed by appropriately washing the drug-treated cells, but not by the addition of deoxyribonucleosides. Aphidicolin, a potent inhibitor of DNA synthesis, selectively inhibited the activity of partially purified DNA polymerase alpha from the nucleus and the cytosol of mastocytoma cells, but did not affect the activity of DNA polymerase beta. Furthermore, aphidicolin had no effect on the synthesis of RNA and protein, and produced no changes in cell size at least for one generation.

Animals↗
PubMed1978

18p-Mosaicism: case report and review.

The case of a 5-month-old male infant with 18p- mosaic, who has intractable seizures and severe ophthalmological abnormalities in addition to many clinical manifestations usually described in the 18p- syndrome, is reported. The proportions of abnormal cells are 7-8% in blood and 55% in skin. About 35% of the short arm of chromosome 18 is deleted. to our knowledge the present report is the fifth one of 18p-mosaic. The main interest of this case resides in the fact that it shows a serious clinical picture despite the low proportion of abnormal cells in blood and the small degree of deletion of the short arm of chromosome 18.

Chromosome Deletion↗
PubMed1976

Reactivation mechanisms of thiamine with thermostable factors.

It was observed, in vitro, that the water extract of the fermented-tea customarily chewed by Thai people has a similar thermostable thiamine-inactivating factor to that found in the water extract of fern. It was also observed that the percentage of thiamine disulfide formed from thiamine with some flavones, catechol, pyrogallol, caffeic acid, dihydroxyphenylalanine, and hemin is greater at pH 7.5 than at pH 7.0. With some flavonoids, such as quercetin, rutin, and 6,7,4'-trihydroxyisoflavone, and pyrogallol, hemin, catechol and caffeic acid at pH 7.5, around 30-100% of thiamine is changed into thiamine disulfide. Water extract of shiitake, okra, coffee, black tea and fukinoto have only weak activities of thermostable thiamine-inactivating factors as a large percentage of thiamine disulfide is formed from thiamine even at pH 7.0. 2-Methyl-4-amino-5-aminomethylpyrimidine was isolated from the reaction mixture of 1 g thiamine with 20 mg catechol (1:0.5 mole) at pH 7.0, 45 degrees C, and identified with the synthesized pyrimidine.

Antimetabolites↗
PubMed1975

Penicillin-resistant mechanisms in Pseudomonas aeruginosa: binding of penicillin to Pseudomonas aeruginosa KM 338.

A comparison of the binding of radioactive penicillin G to whole cells and the membrane fraction derived from Pseudomonas aeruginosa KM 338 was made. This organism has intrinsic resistance to penicillin. The binding to the membrane fraction which catalyzed peptidoglycan synthesis followed saturation type kinetics and saturation was achieved at approximately 2 nmol of penicillin G per ml, whereas binding to the whole cells was entirely of the nonsaturation type. The binding of carbenicillin to the membrane fraction was determined by competition between radioactive penicillin G and unlabeled carbenicillin for the binding sites. It was bound at the same sites in almost the same manner. When whole cells were pretreated with high concentration of unlabeled penicillin G or carbenicillin, the subsequent binding of radioactive penicillin G to the membrane fraction from carbenicillin-treated cells was entirely nonspecific, but with penicillin G-pretreated cells it was still specific. There was apparently specific binding of radioactive penicillin G to ethylenediaminetetraacetate-treated cells. P. aeruginosa KM 338 had an extremely low activity of beta-lactamase compared with other enzyme-producing organisms. This enzyme from P. aeruginosa KM 338 was of the cephalosporinase type. These data indicate that penicillin resistance of P. aeruginosa KM 338 may be a consequence of the development of a permeability barrier which prevents the antibiotic from reaching its sites of action in the cytoplasmic membrane.

Penicillin G↗