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N Takeda

Publications and source records attributed to N Takeda.

At least 523 records · Page 29Linked to original sources
PubMed1987

Evidence for neurosecretory control of the optic gland in terrestrial pulmonates.

The optic gland in terrestrial pulmonates secretes gonadotropic hormone. The present study investigates the fine structure of the optic gland to clarify the control of secretion. Animals used were the slug, Limax marginatus, and the snail, Euhadra peliomphala. The optic gland cell has a process and the cytoplasm is filled with large granules about 750-1300 nm in diameter with a thin cortex in L. marginatus and 800-1700 nm delimited by a thick peripheral layer in E. peliomphala. These gland cells are characterized by well-developed granular endoplasmic reticulum. Granule formation was seen in the region of the Golgi apparatus. During the breeding season, the medial neurosecretory cells of the brain are active in the production and release of secretory materials. Although no neurosecretory cell bodies occur in the tentacular ganglion, neurosecretory axons penetrate into the optic gland cells. Cobalt filling reveals that axons of the medial neurosecretory cells project to the tentacular ganglion, near the optic gland. These results suggest that the optic gland is controlled by a neurohormone originating from the medial neurosecretory cells of the brain.

Animals↗
PubMed1987

Increased insulin binding of erythrocytes and insulin sensitivity in adrenal insufficiency.

We have studied 125I-insulin binding to erythrocytes (RBC) in five patients with hypoadrenocortisolism, and compared to 17 normal subjects and in nine patients with Cushing's syndrome. In another study insulin sensitivity index (ISI) was measured by the IV insulin tolerance test in four patients with hypoadrenocortisolism (1.82 +/- 0.15 mg/dL/min), and compared to 19 normal subjects and 23 patients with Cushing's syndrome (1.56 +/- 0.1 mg/min/dL). Mean insulin binding in hypocortisolism was 17.9 +/- 0.7%, and was significantly higher (P less than .01) than in normal subjects (12.0 +/- 1.4%) and was significantly (P less than .001) decreased toward normal (11.8 +/- 1.47) during replacement therapy. Increased binding in untreated hypoadrenocortisolism was due to elevated high affinity site receptor concentration as compared to the treated patients (0.10 +/- 0.015 v 0.053 +/- 0.003 nmol/L,P less than .01). These results suggest that increased insulin binding in chronic hypoadrenocortisolism may be attributed to increased insulin binding to the receptor, which can revert to normal by replacement therapy. The role of increased insulin binding to increased insulin sensitivity in hypoadrenocortisolism is discussed.

Adrenal Insufficiency↗
PubMed1987

Effect of tumor promoter TPA on spontaneous and mitomycin C induced mitotic recombination in Drosophila melanogaster.

It has been proposed that mitotic recombination is involved in tumor promotion. To test this idea, we investigated the effect of a tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), on spontaneous and mitomycin C (MMC)-induced mitotic recombination in Drosophila melanogaster. The test system used was the wing-spot assay. Third instar larvae (mwh+/+flr) were treated with MMC (0-0.3 mM) for 6 h and fed media containing TPA (0-10 micrograms/ml), and the wings of surviving adults were analyzed for the presence of mutant spots. The results are: (1) MMC induced twin spots as well as single spots dose dependently (0.03-0.3 mM). (2) TPA itself did not induce twin spots or single spots in the range of doses examined (0.1-10 micrograms/ml). (3) TPA did not enhance the frequencies of twin or single spots induced by MMC. These results indicate that TPA induced neither mitotic recombination nor mutations under these experimental conditions. Thus the results would not support the mitotic recombination theory in tumor promotion. Rather, in this study, TPA posttreatment resulted in reduced frequencies of mutant single spots induced by MMC.

Animals↗
PubMed1987

Uridylylation of the genome-linked protein of poliovirus in vitro is dependent upon an endogenous RNA template.

The properties of an in vitro replication system derived from a membrane fraction (crude replication complex, CRC) of poliovirus-infected HeLa cells were examined. This system was capable of producing the nucleotidyl-proteins VPg-pU and VPg-pUpU. Due to high intrinsic phosphoesterase(s) activity and endogenous nucleoside triphosphate pools the yield of labeled product was low. Treatment of CRC with DEAE-cellulose and addition of an ATP generating system resulted in a dramatic increase in the level of nucleotidyl-proteins formed. The capacity to form VPg-pU and VPg-pUpU could be completely abolished by pretreatment of CRC with nuclease, an observation suggesting that the uridylylation of VPg is a template-dependent reaction.

Genes, Viral↗
PubMed1987

Analysis of RNA synthesis of type 1 poliovirus by using an in vitro molecular genetic approach.

Membranous crude replication complexes (CRC) were isolated from poliovirus-infected HeLa cells as recently described (N. Takeda, R.J. Kuhn, C.-F. Yang, T. Takegami, and E. Wimmer, J. Virol. 60:43-53, 1986). Viruses used to produce the CRC were poliovirus type 1 (Mahoney), [PV-1(M)], poliovirus type 1 (Sabin) [PV-1(S)], and four in vitro recombinants that were constructed from infectious cDNA clones. RNA synthesis in CRC was studied. No end-linked, full-length double-stranded poliovirus RNA was detected in CRC regardless of whether nonionic detergent (Nonidet P-40) was added prior to incubation. Synthesis of VPg-pU and VPg-pUpU, two nucleotidyl proteins presumed to be involved in the initiation of RNA synthesis, was slower at 30 degrees C in CRC induced by PV-1(S) than by PV-1(M). This observation was used to design a pulse-chase experiment whose result suggested that synthesis of VPg-pUpU occurred by uridylylation of VPg-pU. Synthesis of VPg-pU(pU) was thermosensitive in CRC induced by PV-1(S). With CRC of recombinant viruses, the thermosensitive block covaried to nucleotide substitutions in PV-1(S) that mapped to the virus-induced RNA polymerase 3Dpol. We conclude that plus-stranded RNA synthesis in CRC does not proceed via hairpin structures. The results of VPg-pU----VPg-pUpU synthesis are consistent with a model in which VPg-pU is the primer of RNA synthesis mediated by 3Dpol. The data suggest that uridylylation of VPg or a precursor thereof may be catalyzed by 3Dpol itself, a mechanism resembling events occurring in adenovirus DNA replication.

HeLa Cells↗
PubMed1987

A case of frosted branch angiitis.

We report a case of frosted branch angiitis in a 16-year-old-girl. She noted a sudden and severe visual disturbance in both eyes, without other systemic symptoms. Diffuse retinal oedema and unusual sheathing of retinal veins were characteristic in both fundi. Fluorescein angiography showed no occlusion of the sheathed retinal veins, but some paravenous extravasation of dye was found in the late phase. With high doses of systemic corticosteroids her fundi and visual acuity improved greatly, though the vessels continued to show severe narrowing. At three months the pattern visually evoked cortical potentials were found to be normal, while flash electroretinograms were absent. No systemic abnormality has been found to explain the aetiology of this condition.

Adolescent↗
PubMed1987

Response of plasma adrenal steroids to synthetic ACTH under ketoconazole in man.

We have investigated the effect of a single oral administration of 600 mg ketoconazole, an imidazole derivative used in clinical practice as an antimycotic agent, on the response of plasma adrenocortical steroids to 1-24 ACTH in 5 normal male subjects pretreated with dexamethasone. The 2 mg of dexamethasone was administered orally at 2300 h on the preceding night, and then a rapid ACTH test was started at 0830 h. After a 1 week interval, the ACTH test was repeated in the same manner under the same dexamethasone pretreatment, but 600 mg of ketoconazole was given orally at 0500 h. The absolute plasma concentration and the increase over the basal level of each steroid after ACTH were evaluated and compared in both conditions with and without ketoconazole administration. A single ingestion of ketoconazole caused a decrease in both indices of the responsiveness of plasma dehydroepiandrosterone and a rise in the plasma level of 17 alpha-hydroxypregnenolone. The response of plasma aldosterone was clearly blunted by ketoconazole administration, whereas that of plasma corticosterone was clearly increased. Ketoconazole also blocked the response of plasma cortisol with concomitantly increased responses of plasma 11-deoxycortisol and 11-deoxycorticosterone. The increased response of plasma corticosterone seemed to be likely due to the severe inhibitory action of ketoconazole on the conversion of corticosterone to aldosterone. These results imply the inhibitory effect of ketoconazole on C17-20-lyase activity and on the conversion of corticosterone to aldosterone, and suggest an inhibitory action on 11 beta-hydroxylase activity. The effects of ketoconazole on the other enzyme activities in adrenal steroid biosynthesis were also discussed.

17-alpha-Hydroxypregnenolone↗
PubMed1987

The effect of triiodothyronine (T3) and thyroxine (T4) upon insulin secretion from isolated rat pancreatic islets.

In order to observe the effect of triiodothyronine (T3) or thyroxine (T4) on glucose-induced insulin release from pancreatic islets, isolated pancreatic islets from Wistar male rat were incubated in modified Krebs-Ringer bicarbonate solution (0.2% BSA, pH 7.4) with 3 mM, 5 mM or 10 mM glucose for 60 min with or without exposure to T3 (2.5 micrograms/ml or 7.5 micrograms/ml) or T4 (2.5 micrograms/ml or 7.5 micrograms/ml). Direct exposure of isolated pancreatic islets to T3 or T4 did not have any effect on glucose-induced insulin release from pancreatic islets during 60 min incubation. But, in successive 60 min incubations following 60 min rest periods after exposure to T3 or T4 in the first incubation, glucose-induced insulin release from isolated pancreatic islets previously exposed to T4 was reduced at 5 mM and 10 mM glucose concentrations and previous exposure to T3 had no effect on glucose-induced insulin release. A delayed effect of T4 on the mechanism of insulin secretion from pancreatic islets was suggested.

Animals↗
PubMed1987

[Multiple glioma].

Explore the source record for details and available documents.

Brain Neoplasms↗
PubMed1987

[A case of dural arteriovenous malformation in the anterior fossa].

UNLABELLED: Dural arteriovenous malformations (AVMs) are not uncommon. But most of dural AVMs are located in the cavernous portion or the transverse-sigmoid portion. Dural AVMs in the anterior fossa and very rare. We experienced a case of dural AVM in the anterior fossa and review 17 cases of dural AVM in the anterior fossa in the literature. CASE: a 62-year-old male was admitted to our center because of unconsciousness and vomiting on Sept. 28; 1985. For nineteen months he had been on anticoagulant therapy after aorto-coronary bypass. Neurological examination on admission revealed somnolence and right-hemiparesis. CT scan revealed intracerebral hematoma in the left frontal lobe with ventricular perforation. Enhanced CT scan revealed patchy enhancement in the tip of the left frontal lobe. Selective angiographies were performed. Dural AVM, fed by both anterior ethmoidal arteries and drained by the cortical veins into the superior sagittal sinus and left superficial middle cerebral vein, was found. Selective external carotid angiography failed to visualize any AVM. MRI revealed spotty low signal intensity in the frontal tip by inversion recovery and spin echo. After admission his consciousness and right-hemiparesis improved completely. Left frontal craniotomy was done. On opening the dura, aneurysmal dilatation was found in the left frontal lobe, arising from the inner surface of the dura at the antero-medial corner of the left anterior fossa. From this aneurysmal dilatation a few veins entered the superior sagittal sinus. Red veins including aneurysmal dilation was removed from its origin together with the intracerebral hematoma. (ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral Angiography↗
PubMed1987

Identification and quantification of a protein-bound ligand in uremic serum.

A major protein-bound ligand in the serum of chronic hemodialysis patients was isolated from heat-deproteinized uremic serum by "high-performance" liquid chromatography (HPLC). The isolated compound was identified as 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid by use of liquid secondary-ion mass spectrometry and gas chromatography-mass spectrometry. On HPLC, an authentic sample of this compound showed a retention time identical to that of the protein-bound ligand peak. The concentration of the furancarboxylic acid in serum, as estimated by HPLC, is markedly greater in chronic hemodialysis patients than in normal subjects.

Blood Proteins↗
PubMed1986

[Clinical investigation on the mechanism of glucose intolerance in Cushing's syndrome].

We investigated the mechanism of glucose intolerance in 51 patients with Cushing's syndrome. In an oral 100g glucose tolerance test, although prevalence of decreased glucose tolerance was very high as revealed in 36 of 47 patients (77%) studied, impairment was rather mild in the majority of patients and only 10 patients (21%) were judged as diabetic. Plasma insulin was measured in 12 patients and the mean values of these patients reached above normal levels after oral glucose load. When insulin secreting capacity was assessed by measuring the ratio of the incremental area of insulin above fasting level to the corresponding area of glucose during the test, Cushing's syndrome as a whole exhibited a normal ratio compared to 9 control subjects (113 +/- 115 vs. 144 +/- 78 microU/mg, M +/- SD, ns), but in 3 patients with severe impairment of glucose tolerance reaching the diabetic range, the ratio was lower than normal (27 +/- 20 vs. 144 +/- 78 microU/mg, M +/- SD, p less than 0.05). The hypoglycemic effect of iv insulin was studied in 23 patients and was demonstrated to have decreased. Thus, we confirmed the presence of decreased insulin sensitivity, i.e. insulin resistance in Cushing's syndrome. The age of patients showed positive correlation with the degree of impairment in glucose tolerance and insulin secreting capacity, but not with that of insulin sensitivity, that is, in patients with advanced age, glucose intolerance appeared to be severe with decreased insulin secreting capacity. 125I-insulin binding to red blood cells in 8 patients was examined to elucidate the mechanism of insulin resistance in Cushing's syndrome. Percent specific binding at tracer concentration of insulin in Cushing's syndrome was not different from the value obtained in 19 normal subjects (8.2 +/- 3.0 vs. 7.7 +/- 1.0%, M +/- SD, ns). Receptor concentration and affinity were also normal. From these observations, it is likely that glucose intolerance in Cushing's syndrome is primarily due to the effects of chronic glucocorticoid excess on tissue metabolism of glucose as characterized by the presence of insulin resistance, which is not due to a defect in insulin-receptor binding but rather caused by the alteration in post-receptor mechanism, and increased secretion of insulin can be considered as a compensatory mechanism. In some patients, however, a decrease in insulin secreting capacity, the cause of which is not clear but at least related to the patient's age, is found and seems to lead to severe glucose intolerance.

Adenoma↗
PubMed1986

The presence of a calcitonin gene-related peptide in the olivocochlear bundle in rat.

The origins of calcitonin gene-related peptide immunoreactive (CGRPI) fibers in the cochlea were examined in rats. Parasagittal transection of the brain just medial to the principal sensory trigeminal nucleus resulted in the ipsilateral disappearance of CGRPI fibers in the cochlea, indicating that the origins of these fibers lie in the central nervous system. Next, we used a highly sensitive method combining retrograde tracing and immunohistochemistry to identify the origins of the CGRPI fibers in the cochlea. After injection of biotin-wheat germ agglutinin (b-WGA) into the cochlea, CGRPI neurons in the ipsilateral lateral superior olivary nucleus also contained b-WGA granules. These findings indicated that CGRPI efferent fibers are major components of the olivocochlear bundle.

Animals↗