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Biomedical subjects

N Tomori

Publications and source records attributed to N Tomori.

At least 37 records · Page 2Linked to original sources
PubMed1986

Characterization of immunoreactive corticotropin and corticotropin-releasing factor in human adrenal and ovarian tumours.

The distribution of immunoreactive ACTH (I-ACTH) and corticotropin-releasing factor (I-CRF) in the human adrenal was determined and these peptides were indentified in adrenocortical adenomas from patients with primary aldosteronism. Cushing's syndrome, and ovarian tumours and compared with the results in phaeochromocytomas. I-ACTH and I-CRF, mainly localized in the adrenal medulla from patients without endocrine disorders, showed a good correlation with the epinephrine concentrations. I-ACTH and I-CRF were present in all the above-mentioned tumours. Gel filtration of I-ACTH and I-CRF from these tumours showed the presence of large molecular weight forms of these peptides as well as authentic peptides. The trypsinization study of I-CRF from phaeochromocytoma suggested that such large molecular weight forms were the precursors of authentic CRF. High performance liquid chromatography showed I-CRF in these tumours to be similar to hypothalamic CRF. Phaeochromocytoma tissue slices incorporated [3H]leucine into ACTH and CRF. These findings raised the possibility that I-ACTH and I-CRF are synthesized and processed in phaeochromocytoma.

Adenoma↗
PubMed1985

In vitro study of immunoreactive corticotropin-releasing factor release from the rat hypothalamus.

Immunoreactive corticotropin-releasing factor (I-CRF) release from rat hypothalami was studied in vitro utilizing a perifusion of rat hypothalami and a rat CRF RIA. Basal release of I-CRF from the hypothalamus of adrenalectomized or hypophysectomized rats was higher than in that of normal rats. K+-induced I-CRF release was completely suppressed by omission of Ca++ from the medium. Dexamethasone suppressed I-CRF release from hypothalami, but not from median eminence (ME). C-AMP and angiotensin II had mild stimulatory effects on I-CRF release. These results suggest that 1) the feedback mechanism acts mainly on a higher level than ME, and 2) c-AMP and angiotensin II may be involved in CRF-releasing mechanism(s).

Adrenalectomy↗
PubMed1985

Immunoreactive corticotropin-releasing factor in human plasma.

Plasma immunoreactive corticotropin-releasing factor (I-CRF) levels were determined by using a human CRF radioimmunoassay and an immunoaffinity procedure. The basal plasma I-CRF level in normal subjects was 6 +/- 0.5 pg/ml (mean +/- SD). We found that most plasma I-CRF levels were affected by stress, negative feedback, and circadian rhythm. Basal I-CRF levels were high in patients with Addison's disease, Nelson's syndrome, hypopituitarism stemming from pituitary macroadenoma, and CRF- and adrenocorticotropic hormone-producing tumors. A very low, but significant, amount of I-CRF was detected (1-3 pg/ml) in patients with Cushing's syndrome, in corticosteroid-treated patients, and in a patient with hypothalamic hypopituitarism. These results suggest that a major component of plasma I-CRF is of hypothalamic origin, however, other extrahypothalamic tissues cannot be ruled out as a minor source of plasma I-CRF.

Adrenal Gland Diseases↗
PubMed1984

Presence of immunoreactive dynorphin in human cerebrospinal fluid.

Immunoreactive dynorphin (I-dynorphin) was measured by radioimmunoassay in human cerebrospinal fluid (CSF). I-dynorphin concentration in CSF was 30 +/- 2 pg/ml. Sephadex G-25 column chromatography showed the main peak eluted at the position of dynorphin-(1-17). HPLC elution profile of this major peak from gel filtration showed a large peak corresponding to the position of dynorphin-(1-17) and small peaks corresponding to the positions of dynorphin-(1-13), dynorphin-(1-12) and other unknown peptides.

Chromatography, High Pressure Liquid↗
PubMed1984

Effect of dexamethasone on immunoreactive corticotropin-releasing factor in the rat median eminence and intermediate-posterior pituitary.

Immunoreactive ACTH (I-ACTH) concentrations in the anterior pituitary, intermediate-posterior pituitary (IP), and plasma and immunoreactive corticotropin-releasing factor (I-CRF) concentrations in the median eminence and IP were determined in rats receiving dexamethasone for various periods from 16 h to 10 days. Plasma I-ACTH concentrations were decreased 16 h after a single injection of dexamethasone. Anterior pituitary I-ACTH concentrations did not decrease until 4 days after the start of dexamethasone medication. IP I-ACTH concentrations did not change throughout these periods. I-CRF concentrations in median eminence and IP rapidly decreased after dexamethasone administration. These results raise the possibility that the source of I-CRF in the IP is hypothalamic.

Adrenocorticotropic Hormone↗
PubMed1984

Immunoreactive corticotropin and corticotropin-releasing factor in human hypothalamus, adrenal, lung cancer, and pheochromocytoma.

Immunoreactive corticotropin-releasing factor (I-CRF) and ACTH (I-ACTH) were examined using RIA, immunoaffinity chromatography, and gel filtration chromatography in human hypothalamus, adrenal (cortex and medulla), lung cancer, and pheochromocytoma. I-CRF and I-ACTH were present in these tissues. Gel filtration of I-ACTH in the adrenal, pheochromocytoma, and lung cancer showed the presence of larger amounts of I-ACTH with large molecular weight forms in contrast to the hypothalamus. Gel filtration of I-CRF in these tissues showed the main peak eluted at the position of synthetic rat CRF. High performance liquid chromatography of this main peak showed two components which eluted in the positions of synthetic rat CRF and oxidized CRF. These elution positions were the same in all tissues and identical with those in the hypothalamus. These results suggest the presence of I-ACTH and I-CRF in these tissues and that CRF outside the brain is identical to hypothalamic CRF.

Adrenal Gland Neoplasms↗
PubMed1984

Effects of corticotropin-releasing factor and other materials on adrenocorticotropin secretion from pituitary glands of patients with Cushing's disease in vitro.

ACTH responsiveness in vitro to synthetic corticotropin-releasing factor (CRF), lysine-8-vasopressin, and cAMP was examined using superfusion of pituitary adenoma tissue and the nonadenomatous tissue from 16 patients with Cushing's disease. Sensitivity of adenomas to lysine-8-vasopressin and cAMP was similar to that of nonadenomatous tissues; however, sensitivity of adenomas to CRF was lower than that of nonadenomatous tissues in 7 of 16 patients. CRF-induced ACTH secretion from adenomas was inhibited by Ca2+-free medium in all instances and by dexamethasone and somatostatin in some. Angiotensins I and II stimulated ACTH secretion from both adenomas and nonadenomatous tissues, while angiotensin I-induced ACTH secretion was inhibited by angiotensin-converting enzyme inhibitor. These results suggest that the sensitivity of the pituitary corticotroph adenomas to CRF in some patients is low. This may be due to an abnormality of the step(s) before cAMP formation, such as the CRF receptor.

Adenoma↗
PubMed1984

Distribution and characterization of immunoreactive corticotropin-releasing factor in human tissues.

The distribution and characterization of immunoreactive corticotropin-releasing factor (I-CRF) in human tissues were examined using a rat CRF RIA, immunoaffinity chromatography, gel filtration chromatography, and high performance liquid chromatography. High concentrations of I-CRF were found in the hypothalamus and pituitary stalk. In addition, I-CRF was found in the posterior pituitary, thalamus, cerebral cortex, cerebellum, pons, medulla oblongata, spinal cord, and outside the brain and in the adrenal, lung, liver, stomach, duodenum, and pancreas. The major component of I-CRF from these tissues eluted in the position of rat CRF on gel filtration chromatography. High performance liquid chromatography of this major component showed two main peaks which eluted in the positions of CRF and oxidized CRF. These elution positions were the same in all tissues. These results indicate the presence of I-CRF outside the brain and suggest that this CRF is identical to hypothalamic CRF.

Adrenal Glands↗
PubMed1983

Effects of bilateral adrenalectomy on immunoreactive corticotropin-releasing factor in the rat median eminence and intermediate-posterior pituitary.

Immunoreactive ACTH (I-ACTH) concentrations in the anterior pituitary (AP), intermediate-posterior pituitary (IP) and plasma, and immunoreactive corticotropin-releasing factor (I-CRF) concentrations in the median eminence (ME) and IP, were determined in adrenalectomized rats from 3 h till 14 days after surgery. Plasma I-ACTH concentrations showed the typical triphasic response over time. AP I-ACTH concentrations decreased immediately after surgery, then increased to high concentrations 3 days after surgery. I-ACTH concentrations in IP did not change through these periods. I-CRF concentrations in ME and IP decreased immediately after surgery, then gradually increased to high concentrations (ME) or to control levels (IP) 14 days after surgery. These results raise the possibility that the I-CRF in IP is of hypothalamic origin.

Adrenalectomy↗
PubMed1983

Modulating effect of glutathione disulfide on thyroxine-5'-deiodination by rat hepatocytes in primary culture: effect of glucose.

To investigate whether an increase in the intracellular glutathione disulfide (GSSG) concentration actually regulates T4-5'-deiodination in intact cells, rat hepatocytes in primary culture were exposed to glutathione-oxidizing agents (diamide and tertiary butylhydroperoxide) or vinblastine, and their effects on 5'-deiodination of T4 were studied. Deiodinating activity was determined from the 125I- fraction released from [3',5'-125I]T4 added to the serum-free culture medium. Total glutathione (T-GSH) and GSSG levels were determined enzymatically. Diamide (1 mM) and tertiary butylhydroperoxide (0.5 mM) increased the GSSG fraction to approximately 40% of the T-GSH at 5 min, followed by a rapid decrease in GSSG. Glucose deprivation of the medium caused a greater GSSG level at 5 min, followed by a delayed normalization of the increased GSSG level. T4-5'-deiodinating activity was minimally decreased in hepatocytes exposed to 1 mM diamide in the presence of glucose in the medium, but was significantly inhibited in the absence of glucose. Vinblastine, in contrast, gradually and steadily increased the GSSG fraction, and by 3 h, GSSG exceeded 20% of T-GSH (at 10(-4) M vinblastine). This was accompanied by a significant inhibition of 5'-deiodinating activity. When the enzyme activity was inhibited, the T-GSH level was decreased to 40-80% of the control level, which per se cannot account for the decreased T4-5'-deiodinating activity, as reported previously. These data suggest that the increased GSSG level, but not the T-GSH concentration, modulates T4-5'-deiodination in intact cells, and that glucose stimulates the enzyme activity by maintaining glutathione in the reduced form, probably through supplying NADPH, a cofactor for GSSG reductase.

Animals↗
PubMed1983

Immunoreactive corticotropin-releasing factor concentrations in cerebrospinal fluid from patients with hypothalamic-pituitary-adrenal disorders.

The concentrations of immunoreactive corticotropin-releasing factor (I-CRF) in human cerebrospinal fluid (CSF) were measured utilizing immunoaffinity chromatography and RIA in patients with no endocrine disease, patients with Cushing's disease, Nelson's syndrome, Sheehan's syndrome, Addison's disease and steroid treated patients. On high performance liquid chromatography, the elution profile and retention time of I-CRF in CSF were not identical with ovine CRF. I-CRF concentrations in CSF from patients with Cushing's disease and Sheehan's syndrome were lower than those from normal subjects, however those from patients with Nelson's syndrome and Addison's disease were within the normal range. I-CRF concentrations in CSF from patients with Cushing's disease returned to normal levels 2-9 months after pituitary adenomectomy. These results suggest that CSF I-CRF concentrations are reduced by increased plasma corticosteroid levels.

Addison Disease↗
PubMed1981

[Clinical studies of cefotiam in the field of pediatrics (author's transl)].

UNLABELLED: The therapeutic effects of cefotiam (CTM) in the pediatric field were studied, and the following results were obtained: 1. Absorption and excretion: After 30 minutes intravenous drip infusion of 250 mg (14.7 mg/kg) of CTM to a 5-year old child weighing 17 kg, the serum levels and urinary excretion were measured. The serum levels were 47.8 mcg/ml at 30 minutes after administration, 23.9 mcg/ml after 1 hour, 12.5 mcg/ml after 1 hour and 30 minutes, 5.2 mcg/ml after 2 hours and 30 minutes, 0.3 mcg/ml after 6 hours and 30 minutes. Excretion rate in the urine was 48.8% at 6 hours after administration. 2. CLINICAL RESULTS: CTM was administered at a daily dose of 35 to 91 mg/kg b.i.d. to q.i.d. by intravenous or intravenous drip injection for 2 to 6.5 days to six patients i.e. two with bronchopneumonia, one with acute bronchitis, one with acute enteritis, one with impetigo and atopic dermatitis one with acute tonsillitis and acute cervical lymphadenitis. The responses were excellent in 2 cases and good in 4 cases. The response rate was 100%. No side effect was observed.

Age Factors↗
PubMed1981

[Therapeutic experience with cefadroxil syrup in acute infections, especially scarlet fever, in pediatric field (author's transl)].

Clinical effects were investigated on cefadroxil powder for syrup (containing 100 mg of cefadroxil per 1 g) for acute bacterial infections (mostly scarlet fever) in the field of pediatrics, and the results were obtained as follows. Cefadroxil was applied in 100 cases of scarlet fever. Among 49 cases administered 30-39 mg/kg/day, the results were excellent in 34 cases and good in 15 cases, efficacy ratio being thus 100%. Among 38 cases administered 40-49 mg/kg/day, the results were excellent in 33 cases, and good in 5 cases, efficacy ratio being thus 100%. Out of 4 cases administered 20-29 mg/kg/day, the results were excellent in 3 cases and good in 1 case, while out of 9 cases administered 50-59 mg/kg/day, excellent in 4 cases and good in 5 cases. Among 78 cases of scarlet fever from which beta-hemolytic Streptococcus was proven from swab liquid of palatal tonsil, 67 cases received cefadroxil at a daily dose of 30-49 mg/kg, and the bacteria turned to negative the next day of administration in 72 cases, 2 days later in 6 cases. Cefadroxil was administered at a daily dose of 46 mg/kg for 7 days in 1 case of SSS syndrome of which Staphylococcus aureus was proven from skin lesion, and local bacteria turned to negative, as well as clinical effect was excellent. No pathogen was proven in 1 case of acute tonsillitis, maybe because ampicillin (ABPC) and cefazolin (CEZ) were administered before cefadroxil treatment, and yet a clinical efficacy was judged by administering cefadroxil at a daily dose of 46 mg/kg, though no clinical improvement was observed with the prior antibiotics. As to the side effects of cefadroxil in 102 cases, a slight vomiting was noticed in 6 cases, though the administration could be continued, and a slight rise of GOT or GPT was observed respectively in 3 cases and 1 case, all of which were recovered without abnormal clinical findings. Among the patients of scarlet fever, after beta-hemolytic Streptococcus became negative, reelimination or recurrence was noticed in 2 cases, but these patients were cured completely by readministration of cefadroxil or administration of amoxicillin (AMPC). Cefadroxil powder for syrup was absorbed quite well, its serum levels were maintained for long, and it was easily administered in children. Considering from its superior antibacterial activity, cefadroxil may be expected to be useful for a remedy in slight or middle infections of children.

Cefadroxil↗