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Biomedical subjects

H Kawashima

Publications and source records attributed to H Kawashima.

At least 325 records · Page 18Linked to original sources
PubMed1985

Aspirin inhibition of 1 alpha-hydroxyvitamin D3 or parathyroid hormone induced hypercalcemia in vivo in rats. A mechanism independent of prostaglandin biosynthesis inhibition.

The interactions of calcium-regulating hormones, active forms of vitamin D and parathyroid hormone, and aspirin were studied in rats. Aspirin, a prostaglandin biosynthesis inhibitor, abolished the hypercalcemia induced by 1 alpha-hydroxyvitamin D3 at 20, 50 and 100 mg/kg p.o. in parathyroidectomized or thyroparathyroidectomized rats with or without vitamin D deficiency, and in thyroparathyroidectomized plus nephrectomized rats. Aspirin did not affect the stimulation of intestinal calcium absorption by 1 alpha-hydroxyvitamin D3. By contrast, indomethacin, another prostaglandin biosynthesis inhibitor, did not affect hypercalcemia or stimulation of intestinal calcium absorption by 1 alpha-hydroxyvitamin D3. Aspirin also abolished the hypercalcemic action of parathyroid hormone in rats with or without intact thyroparathyroid glands. Moreover, aspirin alone caused hypocalcemia in rats with intact thyroparathyroid glands. Indomethacin had no effect in either of these systems. These data suggest that aspirin may inhibit bone resorption by the active form of vitamin D or parathyroid hormone via a mechanism independent of prostaglandin biosynthesis inhibition.

Animals↗
PubMed1985

[Study on the function of the sphincter of Oddi in patients with gallstone disease by dynamic hepatobiliary scintigraphy].

By using hepatobiliary scintigraphy, function of the sphincter of Oddi in 88 patients undergoing cholecystectomy with or without common bile duct exploration and T-tube drainage for gallstone disease was studied. These patients consisted of three groups; 57 patients with gallbladder stones (Group I), 25 with common duct stones migrated from the gallbladder (Group II) and 6 with primary common duct stones (Group III). Time-activity curves (T-A curve) obtained from the region of terminal end of the common bile duct were classified into 4 types which were different from each other. On the T-A curve, the rate of decrease (ROD, %) was defined as the difference between the count rate in the maximum and that at the 20 min after the maximum. The ROD in Group I was significantly greater than that in Group II or III (p less than 0.01). The ROD in Group II was also significantly greater than that in Group III (p less than 0.05). The increase of ROD in Group III after cholecystokinin-pancreozymin administration was less remarkable as compared with that in Group II. Thus, we conclude that the function of the sphincter of Oddi in these three groups may be different from each other.

Ampulla of Vater↗
PubMed1984

Functional domains of Escherichia coli recA protein deduced from the mutational sites in the gene.

The sites of recA mutations of Escherichia coli, recA441 (tif-1), recA1, recA430 (lexB30) and recA44, were determined by analyses of the nucleotide sequences. All mutations are single point missense mutations within the coding region of the recA gene. In the recA441, recA1, recA430 and recA44 proteins, the 38th, 160th, 204th, and 246th amino acids, respectively, from the amino terminal ends are altered. Based on the properties of these mutant proteins and modified forms of recA protein, the locations of various regions of the recA protein that are involved in binding with ATP, binding with single-stranded DNA, hydrolysis of ATP, interaction between the recA protein molecules and interaction with the lambda cI or lexA repressors are mapped on the primary structure of the protein.

Amino Acid Sequence↗
PubMed1982

Relationship between enhancement of morphine analgesia and inhibition of enkephalinase by 2S, 3R 3-amino-2-hydroxy-4-phenylbutanoic acid derivatives.

The effects of nineteen AHPA* derivatives were examined on morphine analgesia by tail-flick test in rats and on enkephalinase inhibition which was based on the formation of tyrosyl-glycyl-glycine from met-enkephalin. The correlation between the enhancement of morphine analgesia in vivo and enkephalinase inhibition in vitro was analyzed. The different analogs varied considerably in the degree of enhancement of morphine analgesia and inhibition of enkephalinase. A close relationship between enkephalinase inhibition expressed by IC50 in vitro and enhancement of morphine analgesia in vivo was observed in thirteen out of nineteen AHPA derivatives examined. One of other six AHPA derivatives which showed weak effectiveness in potentiating on morphine analgesia but was highly potent as an enkephalinase inhibitor, caused potent analgesic action when it was applied intracisternally indicating poor penetration of the blood brain barrier. The possibility was discussed that some of other compounds excluded from the linear relationship might act on other enkephalin degrading enzymes such as aminopeptidase.

Aminopeptidases↗
PubMed1982

Metabolic acidosis suppresses 25-hydroxyvitamin in D3-1alpha-hydroxylase in the rat kidney. Distinct site and mechanism of action.

Effect of metabolic acidosis on two distinct 25-hydroxyvitamin D(3)-1alpha-hydroxylase (1alpha-hydroxylase) systems was studied in the kidneys of vitamin D-deficient rats; one is localized in the proximal convoluted tubule (PCT), is activated in vitamin D deficiency, and is regulated primarily by parathyroid hormone (PTH) via cyclic AMP; the other is localized in the proximal straight tubule (PST), is latent in vitamin D deficiency, and is selectively stimulated by calcitonin via a cyclic AMP-independent mechanism. The 1alpha-hydroxylase activities were measured in the PCT and PST microdissected from the kidney of vitamin D-deficient rats with or without metabolic acidosis of varying duration. The 1alpha-hydroxylase activity decreased in the PCT from 0.74+/-0.07 fmol/mm per h to 0.24+/-0.02 at day 3 of metabolic acidosis without a further decline at day 7. Neither metabolic acidosis of 16 h duration nor reduction of the incubation medium pH from 7.4 to 7.0 affected the enzyme activity in the PCT. To examine the underlying mechanism for the suppression of 1alpha-hydroxylase activity, PTH, cyclic AMP, or calcitonin was given to rats with metabolic acidosis of 3 d duration. Although PTH failed to augment the suppressed 1alpha-hydroxylase activity in the PCT, cyclic AMP restored it to the level of control rats. The 1alpha-hydroxylase activity in the PST remained undetectable in control rats and in acidotic rats with or without PTH or cyclic AMP treatments. However, calcitonin stimulated the 1alpha-hydroxylase activity in the PST equally from undetectable to 0.75+/-0.09 fmol/mm per h in control and to 0.78+/-0.10 in acidotic rats. The data suggests that metabolic acidosis suppresses 1alpha-hydroxylase only in the PCT by inhibiting PTH-dependent adenylate cyclase, and that cellular events beyond cyclic AMP in the PCT and the events responsive to calcitonin in the PST are unaffected. The results show the definite advantage of using defined single nephron segments to study the hormonal and ionic control of the 1alpha-hydroxylase system in the kidney.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗