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Biomedical subjects

M Ishida

Publications and source records attributed to M Ishida.

At least 415 records · Page 23Linked to original sources

Acromelic acid, a novel excitatory amino acid from a poisonous mushroom: effects on the crayfish neuromuscular junction.

A novel amino acid, acromelic acid, which is one of kainoids isolated from a poisonous mushroom, markedly depolarizes the crayfish opener muscle fiber in a dose-dependent manner, its potency being much greater than that of kainoids such as kainic or domoic acid. Moreover, acrolemic acid markedly potentiates the glutamate response, in spite of the fact that it reduces the quisqualate response in a dose-dependent manner. The amplitude of excitatory junctional potentials was slightly reduced by acromelic acid.

Animals↗

Enhancement of spontaneous mammary tumorigenesis at advanced age in mice by temporary stimulation of mammary growth during youth.

As a possible step to clarify the relationship between mammary gland growth during youth and mammary tumorigenesis at advanced age, the long-term effects of the temporary stimulation of mammary gland growth at youth on spontaneous mammary tumorigenesis was studied in a high mammary tumor strain of SHN virgin mice. They received a single pituitary graft under the kidney capsule or a subcutaneous implantation of progesterone for 60 days between 30 and 90 days of age. Both treatments enhanced mammary gland growth and the effect of pituitary grafting was higher. Spontaneous mammary tumorigenesis paralleled mammary gland conditions at youth. The results indicate that the stimulation of mammary gland growth during youth enhances spontaneous mammary tumorigenesis at advanced age in mice, which is quite contrary in rats, and they explain the cause of the higher mammary tumor potential in breeders than in virgin mice.

Aging↗

A new potent channel blocker: effects on glutamate responses at the crayfish neuromuscular junction.

The glutamate blocking action of 5-methyl-1-phenyl-2-(3-piperidinopropylamino)-hexane-1-ol (MLV-5860) was studied at the crayfish neuromuscular junction using electrophysiological techniques. The opener muscle of the dactyl in the first leg of the crayfish was used to examine the action of the drug on the glutamate response. MLV-5860 reduced the amplitude of repetitively-induced glutamate potentials in a dose-dependent manner at the crayfish neuromuscular junction and this reduction was time- and activity-dependent. The minimum effective concentration of MLV-5860 to reduce the glutamate response was estimated to be lower than 50 nM, and therefore MLV-5860 is the most powerful glutamate blocker known at the crayfish neuromuscular junction. Pretreatment of the muscle fiber with concanavalin A did not affect the action of MLV-5860. MLV-5860 reduced the amplitude of excitatory junctional potentials (EJPs) and increased the decay rate of extracellularly-recorded EJPs in a dose-dependent manner. Quisqualate responses were also reduced by this drug but the conductance increase of the muscle membrane induced by GABA was not affected. MLV-5860 did not cause a significant change in the input resistance of the opener muscle fiber at concentrations less than 10 microM. The action of the drug is possibly explained in part by the open channel block of the glutamate-activated ion channels. The forward rate constant for channel blockade was estimated from the difference between the decay rate constants of extracellular EJPs in the absence and presence of the drug and the estimated value was 6.5 +/- 1.4 X 10(7) M-1 s-1.

Animals↗

Parathyroid hormone increases sodium/calcium exchange activity in renal cells and the blunting of the response in aging.

Na+-dependent Ca2+ efflux was demonstrated in cells isolated from the rat renal cortex, suggestive of the presence of a Na+/Ca2+ exchange carrier in the cells. Parathyroid hormone, when incubated with the cells in vitro, increased Na+-dependent Ca2+ efflux about 60%. The effect of the hormone was specific for biologically active parathyroid hormone analogs and could be mimicked by cyclic nucleotides and forskolin. The effects of parathyroid hormone concentration on Ca2+ efflux and cyclic AMP formation were similar. These findings would be consistent with the view that the cyclic nucleotide might act as the intracellular messenger to increase Na+/Ca2+ exchange activity. Cells isolated from parathyroidectomized rats had decreased Na+-dependent Ca2+ efflux. When these cells were treated in vitro with parathyroid hormone, Na+-dependent Ca2+ efflux was enhanced to the same rate as found with cells from sham-operated animals. Parathyroid hormone-sensitive Na+/Ca2+ exchange activity was markedly blunted in cells from senescent (24 months) rats. Basal Na+-dependent Ca2+ efflux and Na+-independent Ca2+ efflux were not altered in the aged animal. Parathyroid-stimulated adenylate cyclase was also decreased in aging. In contrast, forskolin-stimulated Na+-dependent Ca2+ efflux and adenylate cyclase did not change with senescence. These findings would be compatible with a mechanism of desensitization that occurred at the level of the receptor or hormone-receptor coupling to adenylate cyclase. These results may be of physiological significance in understanding calcium homeostasis and the imbalances in mineral metabolism associated with old age.

Aging↗

Effects of amino acids on pancreatic polypeptide before and after vagotomy in the dog.

We have previously indicated a marked influence of the vagus nerve on postprandial pancreatic polypeptide secretion. The present study was designed to determine whether the vagus nerve also plays a role in the regulation of pancreatic polypeptide secretion by absorbed nutrients. The pancreatic polypeptide responses to 17 intravenously administered amino acids, as well as arginine and glucose, were measured and compared with those 1 year after truncal vagotomy in conscious dogs. In response to the infusion of a mixture of amino acids (20 g during 60 min), plasma pancreatic polypeptide concentrations decreased in normal dogs. The effect was, however, completely reversed by vagotomy, with a significant pancreatic polypeptide release being observed (p less than 0.05). Arginine (5 g during 60 min) also showed a similar, although not statistically significant, effect. After intravenous bolus-injection of glucose (0.5 g/kg body weight), a transient decrease of pancreatic polypeptide secretion was found; vagotomy abolished this response. These results suggest that the vagus nerve may have a suppressive role in the process of pancreatic polypeptide secretion induced by intravenous amino acid(s) and glucose.

Amino Acids↗

Chondrosarcoma of the ethmoidal and sphenoidal sinuses. A case of chondrosarcoma arising from postparanasal sinuses.

A case of chondrosarcoma originating within the postethmoidal and sphenoidal sinuses with intracranial invasion will be reported. The patient, a 54-year-old female, presented severe headaches and diminished visual acuity of the right eye. Angiographic findings showed both the left carotid artery to be completely occluded and the right inner carotid artery to be narrowed at the site of the carotid bifurcation. Computerized tomography scan findings showed a tumor, located mainly in the frontal base and temporal fossa, that had invaded the cranium through the skull base. Several tumor excisions were performed using a combined extranasal and transmaxillary approach. The diagnosis 'chondroma' was changed to 'chondrosarcoma' during autopsy.

Brain Neoplasms↗

Effect of 1,25-dihydroxyvitamin D3 on insulin secretion: direct or mediated?

In order to clarify the role of vitamin D (D) in regulating insulin secretion, we studied the effect of long term (10 days) and short term (3 days) supplementation with D and/or calcium (Ca) on insulin secretion from the isolated, perfused pancreas of D- and Ca-deficient rats. The influence of the nutritional state induced by D deficiency was also evaluated. The long term supplementation of either D, Ca, or both restored the body weight and improved insulin secretion induced by high glucose concentration to the same extent; thus, no significant difference in insulin secretion was found between the D-only-supplemented group and the Ca-only-supplemented group. When the insulin secretion was compared in D-deplete vs. D-replete rats given the same amount of Ca, insulin secretion was significantly higher in D-replete animals, although plasma Ca levels were also higher. In short term experiments, insulin release was significantly augmented to a similar extent in D- or Ca-replete rats as compared with D- and Ca-deficient rats, despite no significant change in body weight. In a separate experiment, the pancreas from D-deficient rats was perfused with or without 1,25-dihydroxyvitamin D3 [1,25-OH)2D3] to observe its acute effect on insulin release. The perfusion with 1,25-(OH)2D3 did not affect insulin release. This result suggests that impaired insulin secretion in D-deficient rats is caused by a decrease in Ca in the body fluid and possibly by the lack of D effect on the pancreas.

Animals↗

Inhibition of TSH binding to chicken thyroid by some cases of LATS (long acting thyroid stimulator).

TSH receptor antibody (TRAb) activity using chicken thyroid receptor (c-TRAb) and porcine thyroid receptor (p-TRAb) was determined by the incubation of 125I-bovine TSH with each receptor. Both c-TRAb and p-TRAb activity in LATS positive and negative Graves' sera were compared. 15 out of 39 LATS positive sera and 4 out of 46 LATS negative sera had positive c-TRAb activity. On the other hand, all LATS positive sera and 33 out of 46 LATS negative sera had positive p-TRAb activity. No relationship between c-TRAb and p-TRAb activity was observed, and there was also no correlation between c-TRAb and LATS activity. Changes in c-TRAb, p-TRAb and LATS activity in the clinical course of patients with Graves' disease were examined. These activities were parallel in some cases, but in others they were not. A weak c-TRAb activity was observed in 4 out of 29 Hashimoto's disease, but all cases with thyroid cancer and subacute thyroiditis showed no activity. Sera with positive c-TRAb activity did not stimulate chicken thyroid in chick bioassay. These results suggest that some cases of TRAb in Graves' disease (mainly LATS) inhibit TSH binding to chicken thyroid receptor (non-mammalian species) in the same way as mammalian thyroid, but may not have any stimulatory action on thyroid hormone synthesis. It is interesting to note that TRAb including LATS have the similar effect on TSH receptor even in nonmammalian species.

Animals↗