[Selective venous sampling for ACTH in Cushing's disease].
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Adenoma↗
Biomedical subjects
K Ichihara
Publications and source records attributed to K Ichihara.
[Laboratory and clinical studies on ceftazidime in the field of pediatrics].
Laboratory and clinical studies on ceftazidime ( CAZ ), a new cephem antibiotic, were carried out in the field of pediatrics. The results were as follows: Antibacterial activities of CAZ against clinically isolated strains of S. pneumoniae, H. influenzae, E. coli and P. aeruginosa were compared with those of cefotaxime (CTX), ceftizoxime (CZX), latamoxef ( LMOX ), cefoperazone (CPZ) and cefmetazole (CMZ), and also with cefsulodin (CFS) and gentamicin (GM) against P. aeruginosa. Against S. pneumoniae and H. influenzae, CAZ was almost as active as CTX, CZX and CPZ. Against E. coli, it was almost as active as CTX, CZX and LMOX . Against P. aeruginosa, it was almost as active as CFS and GM. Serum concentrations and urinary excretion rates after intravenous bolus injection of CAZ at doses of 20 mg/kg and 10 mg/kg for 5 minutes in each 2 cases (4 cases in total) were determined. The mean serum concentrations of CAZ were 78.9 and 52.0 micrograms/ml at 15 minutes, 38.5 and 27.4 micrograms/ml at 1 hour, and 6.5 and 4.8 micrograms/ml at 4 hours, with serum half-lives (T 1/2) of 1.39 and 1.80 hours respectively. Mean cumulative urinary excretion rate within 6 hours after administration was 84.6%. In a patient with chronic renal failure, serum half-life was 3.22 hours and urinary excretion rate within 6 hours was 22.8% (after intravenous bolus injection of CAZ at a dose of 10 mg/kg). CAZ was administered at a dose of 55.5 mg/kg by intravenous bolus injection to a child with purulent meningitis. The levels of CAZ in the cerebrospinal fluid (CSF) at 1 hour after administration were 2.7-38.9 micrograms/ml with CSF/Serum ratios of 3.2-28.8%. Forty-two pediatric patients with various bacterial infections (pyelonephritis 14, tonsillitis 1, bronchopneumonia 3, pneumonia 17, purulent meningitis 1, bacteremia 2, SSSS 1, enterocolitis 3) were treated with CAZ at a daily dose of 49-222 mg/kg t.i.d. or q.i.d. (as a rule 60 mg/kg t.i.d.). The efficacy rate was 97.6% clinically and 97.8% bacteriologically. No adverse reactions were observed except 1 case with mild diarrhea. Abnormal laboratory findings were also only mild; eosinophilia in 1, slight elevation of GOT in 5 and that of GOT & GPT in 3 cases. These results indicate the usefulness of CAZ in the treatment of bacterial infections in children.
Age Factors↗
[Size reduction of a nonfunctioning pituitary adenoma after bromocriptine therapy: case report].
Bromocriptine therapy may cause regression of prolactinomas and GH producing adenomas, but there is only few reports about the effect of bromocriptine against nonfunctioning pituitary adenomas and there is no reports about its histopathological changes. We report a nonfunctioning pituitary adenoma, which remarkably regressed during and following bromocriptine therapy. A 47-year-old man developed blurred vision on January 20, 1981. He was pointed out of bitemporal hemianopsia and of his left palor optic fundus. His endocrinological condition was panhypopituitarism and no hypersecreting hormones were found. Cranial computerized axial tomography showed huge dumbbell shaped high density mass extending from the enlarged intrasellar area to the floor of the third ventricle. On treatment with bromocriptine, 5 mg daily for 3 days, his visual acuity and field was remarkably improved. Treatment was continued with gradually increased doses of bromocriptine to 15 mg and so, remarkable shrinkage of tumor size about 50% was seen by computerized axial tomography by a month. In addition, by eight months, the tumor reduced to 22%. Transsphenoidal surgery revealed centrally necrotic tumor mass surrounded by peripheral fibrous one. Because of fibrous and hemorrhagic tumour, we could not remove it totally. The pathological specimen was examined by light and transmission electron microscopy. The tumor was diffuse-type chromophobe adenoma partially intersected by hypertrophied fibrous interstitial materials. Some tumor cells were stained faintly eosinophilic. The cytoplasms were shrunken and the tumor cells were clumped. The immunostaining of tumor was negative to all anterior pituitary hormones. The intracytoplasmic organellae, for example, rough endoplasmic reticulum, Golgi apparatus, were scanty but prominant deformed mitochondria and small secretary granules (the size of about 90-150 nm) were found by transmission electron microscope. We think that the tumor cells had various responsiveness to this drug and the one extreme was destruction of the nucleus, the irreversible change, and the other extreme was some cytoplasmic reduction, the reversible change. The histopathological changes were almost the same as those of prolactinomas treated with bromocriptine. In conclusion, the mechanism of shrinkage of nonfunctioning pituitary adenomas treated with bromocriptine is unclear but it is worth while treating inoperable or recurrent large nonfunctioning pituitary adenomas with bromocriptine.
Adenoma↗
Ontogeny of immunoreactive CCK, VIP and secretin in rat brain and gut.
Immunoreactive cholecystokinin (iCCK), vasoactive intestinal peptide (iVIP) and secretin (iSEC) were determined in the brain and various gut regions in the developing rat between 3 and 28 days after birth and in the adult. From the different patterns observed with these three peptides, it is concluded that in rat neural tissues, peptide concentrations (iCCK in brain, iVIP in brain and gut) increase continuously until about 4 weeks. Concentrations in mucosal tissues (iSEC in gut) are equal to or higher than adult values 3 days after birth. Gut iCCK (found both in neuronal and mucosal tissues) peaks at about 2 weeks, presumably due to concentrations increasing in the former and decreasing in the latter tissues.
Aging↗
Metabolic responses to a new beta-adrenoceptor agonist, ICI 118,587, in conscious rats.
The effect of a new beta-adrenoceptor agonist, ICI 118,587, on the blood levels of cyclic AMP, glucose, lactate, and FFA was studied in conscious rats. ICI 118,587 (200 micrograms/100 g s.c.) increased the cyclic AMP level in the normal and reserpine-pretreated rat, and increased the FFA level in the reserpine-pretreated rat. Adrenaline (10 micrograms/100 g s.c.) increased the levels of cyclic AMP, glucose, and lactate in the normal rat, and increased the FFA level in the reserpine-pretreated rat. The increases in these metabolites induced by this particular dose of adrenaline were inhibited by ICI 118,587. In the normal or reserpine-pretreated rat, ICI 118,587 acts as a beta-agonist on metabolism, and is capable of antagonizing the metabolic effects of adrenaline.
Adrenergic beta-Agonists↗
Thyroid hormones in human milk and their influence on thyroid function of breast-fed babies.
Various assay methods for detection of thyroid hormones in human milk were evaluated in recovery and dilution experiments after which the concentrations of thyroxine (T4) and 3,5,3'-triiodothyronine (T3) were measured and compared with those in serum. The effect of breast feeding on pituitary thyroid function of normal babies also was studied. Competitive protein-binding analysis (CPBA) was found to be unsuitable for measurement of T4 in milk. T4 was not detected in samples of human milk by four radioimmunoassays (RIA), although more than 100% of T4 was recovered in the assays. RIA (double antibody-ANS system) seemed to be reliable for detection of T3 in milk, judging from recovery and dilution experiments. T3 was detectable in all samples obtained 1-4 months postpartum. The T3 concentration in milk was not correlated with protein concentration or daily volume. The concentration of T3 in milk was lower than that in serum and the mean ratio of serum T3 to milk T3 was 2.8 +/- 1.7 (mean +/- S.D.). No correlation was observed between the T3 concentration or daily T3 excretion in milk and the T3 concentration in serum. The total amount of T3 excreted in milk was estimated as only 5-1000 ng/day. The serum levels of thyrotropin, T4, free T4 and T3 were not significantly different between breast-fed and bottle-fed babies. These results indicate that T3 excretion in milk cannot be explained by simple diffusion from the blood into the mother's milk and that breast feeding has no influence on the pituitary thyroid axis of normal babies.
Breast Feeding↗
Subdural hematoma associated with disseminated intravascular coagulation in patients with advanced cancer.
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Adenocarcinoma↗
[II. Immunoassay as clinical test: quality control of radioimmunoassay].
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Data Collection↗
Effect of albumin concentration on the assay of serum free thyroxin by equilibrium radioimmunoassay with labeled thyroxin analog (Amerlex Free T4).
Serum free thyroxin (FT4) in normal nonpregnant and pregnant subjects was measured by radioimmunoassay (RIA) with Amerlex FT4 RIA (Amersham International) and LiquiSol FT4 RIA (Damon Diagnostics) kits. Amerlex FT4 values in serum from pregnant women were lower than those in serum from nonpregnant women, but LiquiSol FT4 values were similar in serum from both groups. Amerlex FT4 values were directly correlated with the concentrations of albumin in serum and inversely correlated with those of thyroxin-binding globulin, but not with prealbumin concentrations. No significant correlations were observed between LiquiSol FT4 values and serum concentrations of thyroxin-binding proteins. Amerlex FT4 values were normal in patients with excess, deficient, or decreased thyroxin-binding globulin. Albumin added to serum samples increased Amerlex FT4 values but not LiquiSol FT4 values. Albumin inhibited the binding of labeled thyroxin analog to the solid-phase thyroxin antibody. These data indicate that the albumin concentration influences FT4 values as measured by an RIA involving a thyroxin analog and that Amerlex FT4 values should be carefully interpreted when the patient has an abnormal concentration of serum albumin.
Female↗
Multiple forms of cytochrome P-450 from kidney cortex microsomes of rabbits treated with phenobarbital.
Two distinct forms of cytochrome P-450 (P-450), referred to as P-450a and P-450b, were separated and purified from kidney cortex microsomes of rabbits treated with phenobarbital. P-450a had a monomeric molecular weight of 53,000, and its CO-reduced difference spectral peak was at 450 nm. It catalyzed the omega-hydroxylation of prostaglandin A1 (PGA1), and the omega- and (omega-1)-hydroxylation of myristate, but it was inactive toward exogenous compounds tested. On the other hand, P-450b had a monomeric molecular weight of 49,000, and its CO-reduced difference spectral peak was at 451 nm. This cytochrome was not able to hydroxylate PGA1 at all. It hydroxylated myristate much more slowly than P-450a, and preferentially at the (omega-1)-position. Unlike P-450a, P-450b efficiently metabolized exogenous compounds such as benzphetamine, aminopyrine, 7-ethoxycoumarin and p-nitroanisole. It is suggested that P-450a and P-450b are specialized for the metabolism of PGA1 and exogenous compounds, respectively, in kidney cortex microsomes.
Animals↗
[Radioimmunoassay of free thyroxine using a T4-analog--the effect of serum albumin].
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Female↗
Separation of two forms of cytochrome P-450 with aryl hydrocarbon hydroxylase activity from intestinal mucosa microsomes of rabbits treated with 3-methylcholanthrene.
Two forms of cytochrome P-450, designated P-448a and P-448b, were purified from intestinal mucosa microsomes of rabbits treated with 3-methylcholanthrene. Both the cytochromes had absorption maxima at 448 nm in the carbon monoxide-reduced difference spectra. They exhibited comparable catalytic activities with benzo(a)pyrene, 7-ethoxycoumarin, and 7-ethoxyresorufin, when reconstituted with hepatic NADPH-cytochrome c reductase and phosphatidylserine. P-448a was apparently homogeneous on sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and its monomeric molecular weight was estimated to be 58,000. The oxidized form had absorption maxima at 416, 512 and 571 nm, indicative of the low spin state. Thus P-448a appeared to be similar to one form of P-450, which was induced in rabbit liver by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). On the other hand, SDS-PAGE of P-448b gave a single major protein band with a monomeric molecular weight of 55,500, indicating that P-448b can be distinguished from P-448a.
Animals↗
Forskolin potentiates adrenocorticotropin-induced cyclic AMP production and steroidogenesis in isolated rat adrenal cells.
Forskolin, a unique diterpene which directly activates the adenylate cyclase, stimulated production of both cyclic AMP and corticosterone in isolated rat adrenal cells, in vitro. This agent also potentiated the action of adrenocorticotropin and/or cholera toxin on cyclic AMP production and steroidogenesis at lower concentrations. It augmented both an early (cyclic AMP production) and a late (steroidogenesis) action of the hormone in the adrenal gland.
Adrenal Glands↗
Comparison of diurnal serum insulin levels during short term treatments with sulfonylurea and with insulin in non-insulin dependent diabetes.
Nine non-insulin dependent type diabetic patients were hospitalized and place on the standard diabetic diet throughout this study period. (25 cal/kg ideal weight/day). After three days of diet therapy alone, 5 mg of glibenclamide was given orally for three days, followed by an interval of four days without medication. 16 units of lente insulin was then administered subcutaneously for three days. The diurnal levels of plasma glucose (PG) and serum immunoreactive insulin (IRI) were determined on the third day of each treatment, and the integrated areas below the curves of the diurnal profile of PG and IRI were compared. The mean fasting PG level before treatment was 200 +/- 21 mg% (mean +/- SE). The initial PG area during diet therapy alone, (4,245 +/- 669 mg . h/dl) decreased significantly to similar levels both by glibenclamide (3, 317 +/- 384 mg . h/dl, P less than 0.05) and by lente insulin (3,177 +/- 552 mg . h/dl, P less than 0.01). The IRI area increased from 187 +/- 24 micromicron . h/ml during diet therapy alone to 296 +/- 65 micromicron . h/ml by glibenclamide (P less than 0.01), and to 267 +/- 43 micromicron . h/ml by lente insulin (P less than 0.05). There was no significant difference between glibenclamide and lente insulin treatments either in PG area or IRI area. These finding suggest that the hypoglycemic effect of glibenclamide treatment in the short term is mainly, if not entirely, due to augmented endogenous insulin secretion.
Adult↗
Multiple forms of cytochrome P-450 in kidney cortex microsomes of rabbits treated with 3-methylcholanthrene.
Cytochrome P-450 was purified from kidney cortex microsomes of rabbits treated with 3-methylcholanthrene. 6-Amino-n-hexyl-Sepharose 4B column chromatography of the cholate-solubilized microsomes yielded two cytochrome P-450 fractions, one of which was eluted from the column with 20 mM potassium phosphate buffer in the presence of 0.4% cholate and 0.08% Emulgen 913. This fraction was partially purified to a specific content of 4.49 nmol of cytochrome P-450/mg of protein. This P-450 fraction catalyzed myristate omega- and (omega-1)-hydroxylation with a turnover rate of 5.0 nmol/nmol of cytochrome P-450 in a reconstituted system containing NADPH-cytochrome c reductase, cytochrome b5 and phosphatidylethanolamine. It had no benzo(a)pyrene hydroxylation activity. The other cytochrome P-450 fraction, which was eluted from the column with 0.1 M potassium phosphate buffer in the presence of 0.4% cholate and 0.08% Emulgen 913, was purified to a specific content of 12.0 nmol of cytochrome P-450/mg of protein. Sodium dodecyl sulfate polyacrylamide gel electrophoresis of the final preparation gave a major polypeptide band with a molecular weight of 58,000. This cytochrome P-450 showed a maximal peak at 448 nm in the carbon monoxide difference spectrum of its reduced form. Its absolute spectrum of the oxidized form had low-spin characteristics. It catalyzed benzo(a)pyrene hydroxylation with a turnover rate of 3.63 nmol/nmol of cytochrome P-450 in a reconstituted system containing NADPH-cytochrome c reductase and phosphatidylcholine, whereas little myristate hydroxylation activity was detected. The results demonstrate the occurrence of multiple forms of cytochrome P-450 in rabbit kidney cortex microsomes.
Animals↗
Effects of cholera toxin on proliferation of cultured human keratinocytes in relation to intracellular cyclic AMP levels.
In the culture of epidermal keratinocytes, the cellular growth rate is reported to be accelerated by cholera toxin. The mechanism by which cholera toxin exerts biological effects is thought to result from changes in intracellular cyclic AMP concentrations. But in many reports cyclic AMP elevating agents appeared to inhibit growth of keratinocytes in culture. This study was done to clarify the discrepancy of this problem. Determination of cyclic AMP revealed that cholera toxin over a range of 10-14-10-8 M increased the intracellular concentration of cyclic AMP of cultured keratinocytes about 100-fold over the controls after incubation for 6 hr. When a small number (10(5)) of cells were inoculated in a 60 X 15 mm culture dish, cholera toxin strongly stimulated colony growth. When a relatively larger number (8 X 10(5)) of cells were inoculated in a dish, cholera toxin moderately accelerated cell division, and increased DNA and protein levels of the culture during early days of cultivation. But after about 20 days, of cultivation when the culture reached confluence, cholera toxin decreased both DNA and protein content in a culture dish. The cultures were pulse labeled with 3H-thyrmidine at 12 and 24 hr after the addition of 10-10 M cholera toxin, and its uptake into DNA was determined. In the early days of cultivation the uptake of 3H-thymidine increased after treatment with cholera toxin. But in the late days of cultivation, cholera toxin decreased the rate of 3H-thymidine incorporation into DNA. These results indicated that cholera toxin-cyclic AMP has effects on the proliferation of keratinocytes in culture biphasically according to cellular concentrations in culture.
Cell Count↗
Effect of the discontinuation of long-term sulfonylurea treatment on blood glucose and insulin secretion in noninsulin-dependent diabetes mellitus.
The mechanism of the hypoglycemic action of sulfonylureas during long-term treatment was investigated in twenty-four patients with noninsulin-dependent diabetes mellitus treated for 1.5 to 19 yr in the out-patient clinic. The subjects received the first oral glucose tolerance test (OGTT) while on sulfonylureas and the second OGTT one month after their withdrawal. As the degree of elevation of the fasting plasma glucose level after withdrawal varied, the subjects were classified into two groups. Fourteen subjects showing an increase of more than 15 mg/dl were arbitrarily designated as group I, and the rest as group II. The mean fasting plasma glucose of group I was 134 +/- 4 mg/dl (mean +/- SE) and 194 +/- 14 mg/dl with and without sulfonylureas, respectively. Group II did no exhibit any significant change in fasting plasma glucose. A mean fasting serum IRI of either group was not changed. In group I, a mean glucose area of 807 +/- 31 mg . h/dl on OGTT increased significantly to 1121 +/- 72 mg . h/dl (p less than 0.001) and, the same time, a mean IRI area decreased significantly from 102 +/- 10 microU . h/ml to 73 +/- 7 microU . h/ml (p less than 0.001). The ratio of IRI area to glucose area, which might indicate the responsiveness of pancreatic B cells to hyperglycemia, was reduced on an average by 48% in group I. However, group II showed no significant change in the mean value of the glucose area, IRI area or the ratio one month after the discontinuation of sulfonylurea treatment. These findings suggest that the insulinotropic action of sulfonylureas is maintained even after long-term treatment and contributes to their antidiabetic effect.
Adult↗
Crossover plot study of glycolytic intermediates in the ischemic canine heart.
Effects of regional ischemia on myocardial glycolysis were studied by measuring the levels of glycolytic intermediates in the endo- and epicardial layers of the left ventricle in dogs anesthetized with pentobarbital. Regional ischemia was induced by ligating a small branch of the left anterior descending coronary artery. The myocardial tissue samples were removed before and 1.5, 3, 7, or 30 min after coronary artery ligation. Based on a crossover plot study of the glycolytic intermediates, it is suggested that the activity of glycogen phosphorylase was accelerated, while that of phosphofructokinase was inhibited in ischemic myocardium samples removed 1.5, 3, 7, and 30 min after ligation. When the frozen myocardium was allowed to stand at room temperature for 10 min, the crossover plot study revealed acceleration of phosphofructokinase activity. The metabolic response to regional ischemia of the endocardial layers was more marked than that of the epicardial. During ischemia the levels of adenine nucleotides did not change significantly, but those of citrate and hydrogen ions increased significantly. It appears that inhibition of myocardial phosphofructokinase activity during ischemia is partly due to an increase in the levels of citrate and hydrogen ions in the ischemic tissue.
Adenine Nucleotides↗