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Biomedical subjects

T Aoyagi

Publications and source records attributed to T Aoyagi.

At least 415 records · Page 23Linked to original sources
PubMed1980

Effects of hydrocortisone on the adrenaline-adenylate cyclase system of the skin.

Using pig skin slices, we investigated the effects of hydrocortisone on the adenylate cyclase system of the skin. In short-term experiments, hydrocortisone, when added singly or in combination with other stimulators of adenylate cyclase in the skin (adrenaline or histamine), had no effect on cyclic AMP accumulation. However, when skin slices were incubated with hydrocortisone for more than 6 h, the response to adrenaline differed, with a greater accumulation of cyclic AMP in the hydrocortisone-treated skin. This effect was seen at a concentration of more than I micrometer hydrocortisone and was most marked 48 h later, while responses to adrenaline in control skin gradually decreased and remained low. Histamine, which is another stimulator of adenylate cyclase of the skin, did not cause a greater cyclic AMP accumulation in response to this hydrocortisone treatment. There was no significant difference in either low Km or high Km cyclic AMP phosphodiesterase activities as a result of this hydrocortisone treatment. Hydrocortisone seems to act by protecting the adrenaline-adenylate cyclase system of the skin.

Adenylyl Cyclases↗
PubMed1980

Cyclic GMP system in the epidermis.

A great deal of knowledge has been gained concerning the activation of adenylate and guanylate cyclase in epidermal cells. Adenylate cyclase is activated by 4 different independent receptors-responding respectively to catecholamine (beta), to prostaglandins (E), to histamine (H2), and to adenosine and it phosphorylated derivatives. Upon activation, each of these receptors becomes unresponsive to further stimulation by its specific stimulator. Guanylate cyclase, on the other hand, is activated by histamine (H1) and epidermal growth factor (EGF). Unlike EGF, the histamine activation is extremely rapid (less than 5 minutes). Epidermal cells are permeable (leak) to cyclic GMP but not cyclic AMP. When the skin is traumatized or injured in any way (even by intradermal injection) there is a sudden catastrophic change in the intracellular levels of the cyclic nucleotides (and of ATP). Cyclic AMP rapidly rises to perhaps 5-10 times its normal resting level while cyclic GMP falls to 10-20% of its level in vivo. The rise in cyclic AMP is due to activation of adenylate cyclase while the fall in cyclic GMP is due in major part to activation of cyclic GMP phosphodiesterase (and perhaps the fall in ATP is due to activation of ATPase). The changes in ATP and cyclic AMP can be reversed by incubating the tissue in a buffered salt solution containing glucose, but this does not normalize the cyclic GMP content. The fall in cyclic GMP can be prevented by a phosphodiesterase inhibitor (IBMX ). This series of events has been called the "ischemia effect." However, it implies that a lack of oxygen is at fault, and that has not been shown to be the case. Its underlying cause and possible physiologic significance are not known. Do these changes in cyclic nucleotides have effects on epidermal proliferation? And does EGF? Agents which increase cyclic AMP do inhibit the epidermal outgrowth and mitotic activity of explant cultures of pig skin. Cyclic GMP does increase outgrowth at a particular concentration. Histamine, which elevates both cyclic nucleotides, has a biphasic action depending on its concentration. These findings imply that these nucleotides do act as one of the controls of epidermal proliferation. The action of cyclic GMP is not accompanied by detectably increased phosphorylation of epidermal proteins. On the other hand, EGF action which also enhances epidermal outgrowth is characterized by an increased protein phosphorylation that precedes any increase in cellular cyclic GMP. We conclude that the action of EGF is independent of the cyclic nucleotide system.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1980

Effect of bestatin on mouse immune system and experimental murine tumors.

Effect of bestatin on the establishment of delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) and oxazolone was examined in normal and immunity-impaired mice. Administration of a low dose of bestatin (0.1 approximately 100 microgram/mouse) augmented DTH to SRBC and restored their impaired DTH to oxazolone. The effect of bestatin in the mouse was age-dependent. Bestatin retarded the growth of slow growing solid tumors of Gardner lymphosarcoma and IMC carcinoma and the effect was influenced by the time of the administration and the number of cells inoculated. Bestatin enhanced the antitumor action of the antitumor antibiotics, bleomycin and adriamycin. Bestatin also retarded the induction of skin cancer by 20-methylcholanthrene.

Aminopeptidases↗
PubMed1979

Studies on relationships between the structure and the glycosidase-inhibiting activity of HPAAO and its analogs.

p-Hydroxyphenylacetaldoxime (HPAAO) (anti and syn forms) obtained by fermentation and its analogs chemically synthesized were tested for their activities to inhibit various glycosidases. HPAAO inhibited bovine liver beta-galactosidase in a competitive manner at pH 7.0 with an apparent Ki value of 8 x 10(-8) M. HPAAO also inhibited various mammalian beta-glycosidases which had pH optima between 6.0 and 8.0. The syn form of HPAAO was found to be more active than the anti form against bovine liver neutral beta-galactosidase. It was concluded that the oxime moiety of HPAAO and its analogs was essential for their enzyme-inhibiting activity and the activities of aromatic or aliphatic oxime derivatives were dependent on the number of carbon atoms in their alkyl-chains.

Acetylglucosaminidase↗
PubMed1979

beta-Galactosidase-inhibiting new isoflavonoids produced by actinomycetes.

Six isoflavonoids having beta-galactosidase inhibiting activity were isolated from the culture filtrate of Streptomyces xanthophaeus. Their structures were determined by spectral analyses to be daidzein, daidzein 7-alpha-L-rhamnoside, daidzein 4',7-di-alpha-L-rhamnoside, genistein, genistein 7-alpha-L-rhamnoside and genistein 4',7-di-alpha-L-rhamnoside.

Actinomycetales↗