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Biomedical subjects

A Ichikawa

Publications and source records attributed to A Ichikawa.

At least 289 records · Page 16Linked to original sources
PubMed1983

Effect of 7-fluoro prostacyclin, a stable prostacyclin analogue, on cAMP accumulation and prostaglandin binding in mastocytoma P-815 cells.

The effect of 7-fluoro prostacyclin (PGI2-F), a chemically stable analogue of prostacyclin, on cAMP accumulation in and [3H]PGE binding to mastocytoma P-815 cells was compared with those of the Na salt and methyl ester of prostacyclin (PGI2-Na or PGI2-Me), which are rapidly inactivated in aqueous solution or metabolized in the tissue. PGI-F was as effective as PGI2-Me, and slightly less effective than PGI2-Na in stimulating cAMP accumulation in mastocytoma cells and rabbit platelets. PGI2-F was also more stable than PGI2-Me or PGI2-Na, and retained its original cAMP elevating activity even after incubation with or without cells for 4 h at 37 degrees C. Cells which had been exposed to PGI2-F and then washed free of unbound reagent continued to produce cAMP for more than 3 h. PGI2-F was also as effective as PGE1 or PGE2 in displacing [3H]PGE2 bound to the cells. Non-competitive inhibition by PGI2-F or PGI2-Me of [3H]PGE2 binding to the cells, with apparent Kis of 1.29 microM and 1.13 microM, respectively, indicates the presence of different receptors for PGE2 and for PGI2-F or PGI2-Me in mastocytoma P-815 cells.

Animals↗
PubMed1983

Inhibition of cellular growth and nutrient transport induced by calcium ionophore A23187 in mastocytoma P-815 cells.

Kinetic analysis of Ca2+ metabolism in mastocytoma P-815 cells showed that at non-cytotoxic and growth-inhibitory concentrations (less than 10 micrograms/ml), the calcium ionophore A23187 did not affect the rate constant (36.2 min-1) or the compartment size (8.32 nmol/10(6) cells) of the fast phase of calcium exchange at the cell surface. In contrast, A23187 (1 to 10 micrograms/ml) dose-dependently increased the compartment size of slow phase I of the intracellular calcium uptake from 0.54 to 2.39 nmol/10(6) cells without affecting the rate constant (2.38 min-1). In addition, A23187 (5 to 10 micrograms/ml) produced an additional compartment [slow phase II] with a rate constant of 0.25 min-1 and increased its compartment size from 0.42 to 1.26 nmol/10(6) cells. A23187 (10 micrograms/ml) in the presence of Ca2+ (0.9 mM) non-competitively inhibited the membrane transport of amino acids, glucose and nucleosides; and it also reduced the cellular ATP level and the membrane fluidity. Apparently, A23187 inhibits the growth of mastocytoma cells by elevating the intracellular concentration of Ca2+, which in turn reduces the membrane fluidity and the carrier-dependent as well as the active membrane transport of various nutrients required for cellular growth.

Adenosine Triphosphate↗
PubMed1983

[Detection of learning impairment in offspring in reproduction tests].

We examined the ability of learning and its retention employing test with the water T-maze, shuttle box and passive avoidance response (PAR) in offspring from mother rats treated with N-methylnitrosourea (MNU) or chlorpromazine (CPZ). The offspring of MNU-induced learning impairments were detected only in tests with the water T-maze and PAR. On the other hand, CPZ induced impairments were detectable only in tests with the shuttle box and PAR. Thus offspring from mother rats treated with MNU or CPZ showed partially different responses. In retention tests, both MNU and CPZ caused impaired ability in the water T-maze and PAR. In the PAR test, impairment was most clearly detectable. From these results, the PAR test appears to be the most useful method in detection of impairments in learning and retention ability, especially the latter, in the reproduction test of offspring.

Animals↗
PubMed1982

Calcium uptake in mastocytoma P-815 cells.

Kinetic data of 45Ca2+ exchange in exponentially growing mastocytoma P-815 cells at 37 degree C indicated the presence of at least two calcium compartments, fast and slowly exchangeable. The fast phase of calcium exchange at the cell surface had a rate constant of 36.1 min-1 and a compartment size of 8.27 nmol/10(6) cells, while the slow phase, the intracellular calcium exchange, showed a rate constant of 2.4 min-1 and a compartment size of 0.53 nmolS/10(6) cells. The fast phase comprised two calcium binding sites of high and low affinities with dissociation constants of 0.59 and 4.88 mM, respectively, and binding maxima of 5.15 and 34.4 nmol/10(6) cells, respectively. The calcium uptake at both binding sites was inhibited by 80% on the addition of ruthenium red (0.4 mM) or lanthanum chloride (0.5 mM), but not by tetracaine (5 mM). The high-affinity site had two negative reaction enthalpy changes, delta H 0 = -1.55 (from 0 to 22 degree C) and -4.27 (from 22 degree C to 37 degree C) kcal . mol-1, while the low-affinity site showed two positive reaction enthalpy changes, delta H0 = +6.53 (below 22 degree C) and +2.05 (above 22 degree C) kcal . mol-1, suggesting the effect of membrane fluidity on calcium binding. The slow phase of calcium exchange was also inhibited by ruthenium red and lanthanum chloride resulting in a decrease of the Hill's coefficient from 1.70 to 1.28 and 1.13, respectively, but was not affected by tetracaine. Calcium efflux from 45 Ca-loaded cells was also inhibited by ruthenium red and lanthanum chloride and was also temperature sensitive. The efflux rate constant was reduced by 80% and 100% at 20 degree C and 0 degree C, respectively. As calcium uptake fluctuated during the cell cycle of synchronous mastocytoma P-815 cells with a peak at the mid S phase and the lowest level during the late M phase, the compartment size of fast phase also fluctuated, being highest at the S phase and lowest at the M phase. In contrast, the compartment size of the slow phase was highest at the G1 phase and lowest at the M phase. In parallel with these changes, the binding maximum of the high-affinity site was highest at the S phase and lowest at the M phase, while that of the low-affinity site fluctuated little throughout the cell cycle.

Animals↗
PubMed1982

Cell cycle specific fluctuations of adenosine 3',5' -monophosphate and prostaglandin binding in synchronized mastocytoma P-815 cells.

Endogenous adenosine 3',5' -monophosphate (cAMP) levels in mastocytoma P-815 cells, synchronized either at the G1/S transition by amethopterin- or double thymidine-block or in mitosis by colcemid block, were highest during late S and early G2 phases and lowest during mitosis. These cell cycle-dependent changes in cAMP levels were largely accounted for by changes in adenylate cyclase and phosphodiesterase activities. Similar fluctuations occurred simultaneously with specific prostaglandin E1 (PGE1) binding, histidine decarboxylase activity, histamine content, and [35S]SO-2(4) incorporation into glycosaminoglycans of the cells. In addition, endogenous levels of the E group of prostaglandins (PGEs) and "14C]carachiodonic acid incorporations into PGE, phosphatidylcholine and phosphatidylinositol also exhibited fluctuation patterns similar to that of cAMP levels. Since cAMP levels still fluctuated in a serum-depleted medium where DNA synthesis and cell division were inhibited, endogeneous levels of prostaglandin and cAMP appeared not to be regulated solely by serum factor(s). Exposure of cells at G1/S transition to 1-methyl-3-isobutylxanthine (MIX) resulted in 10-fold elevation of cAMP levels throughout the cell cycle without affecting DNA synthesis. On the other hand, PGE1 and/or MIX added at late S phase elevated cAMP levels, prolonged C2 phase and retarded the cell division, but these agents added at the beginning of mitosis elevated cAMP levels without affecting the cell division. These results suggest that prostaglandin newly synthesized by the increased metabolism of phospholipids promote the cAMP synthesis via their binding to the receptors and thereby control the division and phenotypic expression of mastocytoma P-815 cells.

Adenylyl Cyclases↗
PubMed1982

Asplenia and polysplenia syndrome.

This report described the morphological characteristics of seven cases of asplenia syndrome and three of polysplenia syndrome. Each syndrome has been characterized by a tendency for symmetric development of normally asymmetric organs, with varying degrees of cardiovascular anomalies. These latter anomalies are usually present in asplenia syndrome to a greater extent than in polysplenia syndrome. While, as observed in our material, the conotruncal anomalies were present more commonly in cases with asplenia, and absence of inferior vena cava with azygos continuation was seen specifically in all the cases with polysplenia. This evidence implied the presence of some pathogenetic distinction between the two syndromes.

Abnormalities, Multiple↗