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Biomedical subjects

E Fujii

Publications and source records attributed to E Fujii.

88 records · Page 5Linked to original sources

[Changes in pentobarbital hypnosis and hepatic metabolism in streptozotocin-diabetic mice].

The present study deals with the hypnotic effect of pentobarbital (Pento) in relation to its metabolism in hepatic microsomes in streptozotocin (STZ, 170 mg/kg, i.p.) injected mice. Liver weight (mg/10 g body wt.) of STZ-treated mice was larger than that of the controls throughout the experimental period. Although the shortening of sleeping time induced by Pento (60 mg/kg, i.p.) was always observed, Pento-metabolizing enzyme activity (by the method of Kato et al., 1964) increased in mice with diabetes for 2 and 4 weeks but decreased in mice with diabetes for 8 weeks. Induction following phenobarbital (100 mg/kg, s.c.) and inhibition by SKF 525-A (10 mg/kg, i.p.) of hepatic metabolizing enzyme were found in both control and mice with diabetes for 2, 4 and 8 weeks, but these were not definitely correlated to their hepatic Pento-metabolizing enzyme activities. STZ-induced hyperglycemia and shortening of sleeping time by Pento were completely prevented by the pretreatment with nicotinamide (500 mg/kg, i.p.). NPH-insulin injection partially decreased hyperglycemia in STZ-diabetic mice, but sleeping time by Pento was not significantly affected. These results suggest that the hyposensitivity to Pento in STZ-diabetic mice is partially related to an abnormality of metabolism in liver such as the hyperglycemic state.

Animals↗

Effects of nicotinamide and insulin on glycosylated hemoglobin and blood glucose in thyroidectomized streptozotocin-diabetic rats.

The present study deals with the effects of nicotinamide and insulin on glycosylated hemoglobin (HbA1) and blood glucose in thyroidectomized streptozotocin (STZ)-diabetic male rats. Nicotinamide (500 mg/kg body wt., i.p.) significantly decreased the levels of HbA1 and blood glucose in both STZ-treated (65 mg/kg body wt., i.v.) intact and STZ-treated thyroidectomized animals. Administration of NPH-insulin recovered hyperglycemia, and the increased HbA1 in thyroidectomized STZ-diabetic rats to control levels.

Animals↗

[Changes in glucose metabolism and cardiovascular responses in thyroidectomized streptozotocin treated diabetic rats (author's transl)].

Two weeks after streptozotocin i.v. injection, changes in glucose metabolism, levels of serum and urinary calcium, magnesium and copper, and cardiovascular responses were investigated in thyroidectomized streptozotocin treated diabetic rats. These parameters were compared to those of intact rats. Serum and urinary calcium, magnesium and copper concentrations were not influenced by thyroidectomy. Glycosylated hemoglobin (HbA1) in thyroidectomized streptozotocin treated diabetic rats was higher than that in those which were thyroidectomized alone. In thyroidectomized rats that induction of hyperglycemia required dose of streptozotocin than for intact rats. Norepinephrine (0.3125, 0.625, 1.25 micrograms/kg i.v.)-induced pressor response and ACh (0.3125, 0.625, 1.25, 2.5 micrograms/kg i.v)-induced depressor responses were both reduced in streptozotocin treated diabetic rats. These reduced pressor and depressor responses tended to recover after thyroidectomy. These results suggest that hypothyroid states may partially improve glucose metabolism and cardiovascular responses in streptozotocin treated diabetic rats.

Acetylcholine↗

Expression of apoptosis in placentae from mice lacking the prostaglandin F receptor.

This study aimed to investigate the changes in apoptosis in the placenta and decidua of pregnant mice lacking the prostaglandin F receptor. Mouse placentae were removed from fetuses on days 10-23 of pregnancy. Apoptotic cells were examined by a DNA fragmentation assay and the terminal deoxynucleotidyl transferase-mediated dUDP nick end-labelling (TUNEL) technique. The placenta and decidual weight increased before day 18 and 14 of pregnancy, and then decreased with gestational day. After day 19, the fetuses gradually died in the uterus. All fetuses died in the uterus on day 23 of pregnancy. The number of apoptosis was not significantly different between wild type and FP-deficient mice before day 18 of pregnancy by DNA fragmentation and TUNEL staining. The DNA fragmentation was always more pronounced in decidual tissue on each day of pregnancy. DNA laddering on placentae was more extensive on day 22 than day 18. In placenta, most TUNEL-positive cells were detected in trophoblast and stromal cells. A higher intensity of apoptotic cells was in the decidual basalis. The main area was the centre of the decidual basalis, and was in decrease toward to margin of placenta. The index of TUNEL positive cells increased as gestation progressed toward termination. Especially, it was prominent in the placentae on day 22 compared with that day 18 of pregnancy. The increased TUNEL-positive staining in syncytiotrophoblast surface was found in placenta at post-term, compared with those at term. Apoptosis may provide insights into both normal placental development and placental dysfunction during an abnormal pregnancy from post-term pregnancy.

Animals↗

Infantile spasms: localized cerebral lesions on SPECT.

Ten infantile spasms (IS) patients had single photon emission computed tomography (SPECT) with [99mTc]HMPAO, EEG, and magnetic resonance imaging (MRI) studies. SPECT showed localized cerebral hypoperfusion in 7 infants (4 unifocal; 3 multifocal) always involving the temporal regions either unilaterally or bilaterally. EEGs obtained in near time of the SPECT studies showed focal abnormalities in all 7 infants with hypoperfusion on SPECT, with complete correspondence of the abnormalities in 5. MRI showed localized cerebral lesions in only 3 of the 10 infants, all of whom had corresponding areas of hypoperfusion on SPECT. Our study indicates that localized cerebral abnormalities (especially of the temporal lobes) may often be associated with IS and that such patients may have localized cerebral hypoperfusion on SPECT even when the MRI is normal.

Brain↗

Case of ulcerative colitis associated with oesophageal ulcer.

A case of ulcerative colitis complicated by oesophageal ulcers is reported. A woman was admitted to our hospital because of exacerbations of ulcerative colitis both in 1992 (aged 15 years) and 1995 (aged 18 years). When she was admitted in 1995 she complained of bloody diarrhoea, sore throat and pain on swallowing. Oesophagogastro-duodenoscopy revealed oesophageal ulcers. Oesophageal pH monitoring (24-h) showed no evidence of gastro-oesophageal reflux disease. After the patient was treated she with oral prednisolone showed considerable improvement clinically and endoscopically. Initial dosage was 60 mg/day, and 1 week later, the dosage was gradually dropped since the patient responded favourably. The improvement of the oesophageal lesions coincided with the remission of ulcerative colitis. The oesophageal ulcers are, therefore, thought to be an extracolonic manifestation of ulcerative colitis.

Adolescent↗

Alpha 1-adrenergic stimulation of iodide organification in mouse thyroid--inhibition by protein kinase C inhibitors.

Using mouse thyroid lobes incubated in vitro, a study was made of the subtype of alpha-adrenoceptors involved in iodide organification, induced by norepinephrine, and the possible role of protein kinase C in mediating the effect of norepinephrine. Norepinephrine and phenylephrine, alpha 1-agonists, increased the iodide organification in mouse thyroid lobes; however, clonidine, and alpha 2-agonist, showed a marginal effect. Prazosin, an alpha 1-blocker, but not yohimbine, an alpha 2-blocker, inhibited the norepinephrine-induced iodide organification. These results suggest the involvement of alpha 1-adrenoceptors. The stimulation of the iodide organification, induced by norepinephrine, was inhibited by omission of calcium from the medium and by protein kinase C inhibitors such as H 7, quercetin and trifluoperazine, but not by W-7, a calmodulin antagonist. Since tetradecanoylphorbol acetate, a stimulator of protein kinase C, mimicked the effect of norepinephrine in increasing iodide organification, extracellular calcium ion and protein kinase C would appear essential to the alpha 1-adrenergically regulated iodide organification in mouse thyroid.

Adrenergic alpha-Agonists↗