Search PubMed⌕ Search

Biomedical subjects

A Hirose

Publications and source records attributed to A Hirose.

At least 91 records · Page 5Linked to original sources

Established macrophagelike cell lines synthesize interleukin-1 in response to toxic shock syndrome toxin.

Toxic shock syndrome toxin is already known to induce the production of interleukin-1 (IL-1) by preparations of monocytes and macrophages that are presumably contaminated with other types of cells. The response is enhanced by increasing the density of such monocytes, suggesting that the monocyte's response to toxic shock syndrome toxin may be augmented by its interaction with some other cell. Nevertheless, we now show that several human and murine macrophagelike cell lines (U937, J774, P388D1, and WEHI 3) produce IL-1 when exposed to toxic shock syndrome toxin, and therefore the basic response does not require the presence of cells of other lineages. The cultured cells generally produce less IL-1 than do monocytes, but considerably more IL-1 is induced from cells that have undergone a terminal differentiation as a result of exposure to 1 alpha,25-dihydroxyvitamin D3. High concentrations of cultured cels suppress the production of IL-1; this effect is apparently not due to long-lived inhibitors of IL-1 production or of IL-1 activity, but may be due to a short-lived inhibitor of production.

Animals↗

Concomitant increase by peroxisome proliferators of fatty acid-binding protein, peroxisomal beta-oxidation and cytosolic acyl-CoA hydrolase in liver.

Inductions of FABP in hepatic cytosol by administration of tiadenol and clofibric acid were studied in rats, mice and guinea-pigs. In rats and mice, [1-14C]oleic acid-binding capacity of hepatic cytosol was increased, in association with induction of peroxisomal beta-oxidation, by the administration of either the two peroxisome proliferators. The increase in [1-14C]oleic acid binding capacity was responsible for the increase in the content of FABP in livers. The peroxisome proliferators caused an induction of acyl-CoA hydrolase of lower-molecular-weight form alone in hepatic cytosol of mice, although inductions of two long-chain acyl-CoA hydrolases (higher- and lower-molecular-weight form) were brought about in hepatic cytosol of rats. Guinea-pigs lacked the peroxisome proliferator-caused inductions of FABP, peroxisomal beta-oxidation and acyl-CoA hydrolase. There was no essential difference in the inductions of FABP, acyl-CoA hydrolases and peroxisomal beta-oxidation between tiadenol and clofibric acid, despite a marked difference in their chemical structures. These results suggest that the induction of FABP is correlated with the inductions of both peroxisomal beta-oxidation and cytosolic long-chain acyl-CoA hydrolase of lower-molecular-weight form.

Animals↗

Modification by clofibric acid of acyl composition of glycerolipids in rat liver. Possible involvement of fatty acid chain elongation and desaturation.

Administration of p-chlorophenoxyisobutyric acid (clofibric acid) to rats induced a marked change in acyl composition of hepatic glycerolipids; a considerable increase in the proportion of octadecenoic acid (18:1) was accompanied by a marked decrease in the proportion of octadecadienoic acid (18:2). Among the glycerolipids, the changes in the proportions of 18:1 and 18:2 were the most marked in phosphatidylcholine. The change in the acyl composition of phosphatidylcholine paralleled the change in free fatty acid composition in microsomes. The treatment of rats with clofibric acid resulted in a 2.3-fold increase in activity of microsomal palmitoyl-CoA chain elongation and a 4.8-fold increase in activity of stearoyl-CoA desaturation. The activities of acyl-CoA synthetase, 1-acylglycerophosphate acyltransferase and 1-acylglycerophosphorylcholine acyltransferase in hepatic microsomes were increased approx. 3-, 1.7- and 3.6-times, respectively, by the treatment of rats with clofibric acid. These findings are discussed with respect to the role of fatty acid modification systems in the regulation of acyl composition of phosphatidylcholine.

Acyl Coenzyme A↗

Selective increase in acylation of 1-acylglycerophosphorylcholine in livers of rats and mice by peroxisome proliferators.

Rats were fed a diet containing p-chlorophenoxyisobutyric acid (clofibric acid). Activity of microsomal 1-acylglycerophosphorylcholine (1-acyl-GPC) acyltransferase in liver was increased approx. 3-fold by the treatment with clofibric acid. The treatment of rats with clofibric acid did not increase activity of microsomal 2-acyl-GPC acyltransferase. Feeding a diet containing 2,2'-(decamethylenedithio)diethanol (tiadenol), di(2-ethylhexyl)phthalate or acetylsalicylic acid also resulted in a selective increase in the activity of 1-acyl-GPC acyltransferase in rat liver. Treatment with clofibric acid increased the activity of 1-acyl-GPC acyltransferase in liver of mouse as well as rat, but did not change the activity in liver of guinea-pig. The relative rate of acylation of 1-acyl-GPC with various acyl-CoAs by hepatic microsomes was not changed by the treatment of rats with clofibric acid.

1-Acylglycerophosphocholine O-Acyltransferase↗

Anterior discectomy and interbody fusion for lumbar disc herniation. A review of 350 cases.

Based on the follow-up evaluation of 350 patients in whom lumbar disc herniation was treated by anterior discectomy and interbody fusion from 1955 to 1982, 94.3% of the patients obtained bony union and justified the principle of interbody stabilization of the spine. The normalization of the myelographic pattern observed after surgery indicates that sufficient nerve decompression can be obtained by this procedure. The good clinical results may be attributed to the restoration of disc height and to the correction of spinal alignment. The good results observed in long-term follow-up evaluation of 223 patients and the fact that most of the patients resumed their former work after surgery provide further testimony of the value of interbody fusion. The procedure is indicated in young adults, physical laborers with low back pain and sciatica, and patients with spinal instability.

Adolescent↗

[Pharmacological effects of dobutamine and several catecholamines on various smooth muscles (author's transl)].

Pharmacological effects of dobutamine (DOB), a positive inotropic drug, on smooth muscles were compared with those of catecholamines such as norepinephrine (NE), epinephrine (E), isoproterenol (ISO) and dopamine (DA). DOB acted as a partial agonist and simultaneously as an antagonist on alpha-adrenergic receptors in the thoracic artery. Large doses of DOB induced uterine contraction in rabbits, but antagonised the contraction of the vas deferens of guinea pigs, as was induced by electrical stimulation. However, DOB showed a potent activity, similar to that seen with NE or E as an alpha-adrenergic agonist, on the portal vein. Doses of DOB required to produce a relaxation in the trachea of guinea pigs both in vitro and in vivo were 1/250 and 1/600 of ISO, respectively, and were considerably less regarding inhibition of uterine motility in rats. Inhibiting activity of DOB on the transport rate of intestinal contents in mice and gastro-intestinal motility of rabbits was much less than the activity seen with ISO, E and NE. Spasmolytic activity of DOB was also less than that of ISO, NE and E, but was more than that of DA. It is concluded that DOB is a more selective beta 1-agonist than ISO because of its weaker activity on alpha- and beta 2-receptors. The alpha-agonist activity of DOB in the portal vein was however, potent.

Animals↗