Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Red cell sodium (RBC-Na+) concentrations were measured using 23Na nuclear magnetic resonance (NMR), without the destruction of erythrocyte membranes. Subjects were categorized into four groups: 20 normotensive subjects (NT group), 20 age-matched essential hypertensive patients (EHT group), 10 patients with primary aldosteronism (PA group), and 18 patients treated with digoxin (DIG group). Although RBC-Na+ concentrations were similar between the NT group (6.14 +/- 0.80 (Mean +/- SD) mmol/l) and the EHT group (5.92 +/- 0.99), they were significantly higher in both the PA group (7.55 +/- 0.88, p less than 0.001) and the DIG group (8.43 +/- 3.81, p less than 0.02). In the PA group, RBC-Na+ concentrations decreased significantly after resection of the adenoma, and there was an inverse relationship between serum potassium and RBC-Na+ concentrations (r = -0.65, p less than 0.01). In the DIG group, RBC-Na+ concentrations tended to increase in proportion to serum digoxin levels (r = 0.53, p less than 0.05). These results support the view that RBC-Na+ concentrations are determined primarily by Na+/K+-pump activity of red cell membranes. This study showed also that Na+ NMR is an useful method determining intracellular Na+ concentrations.
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PMID:Clinical application of sodium-23 nuclear magnetic resonance for measurement of red cell sodium concentrations. 259 44

Transformation of normal human colonocytes makes them sensitive to new mitogenic signals. Long-chain diglycerides (LCDGs) found in the human colon are mitogens selective for colon tumor cells, inducing mitogenesis in premalignant cells from each of 13 adenomas and in malignant cells from two of four carcinomas, but having no mitogenic effects on normal colonocytes (E. Friedman, P. Isaksson, J. Rafter, B. Marian, S. Winawer, and H. Newmark, Cancer Res., 49:544-548, 1989). Parallel to this biological activity pattern, LCDGs induce protein phosphorylation only in adenomas and carcinomas. Immunoblotting with an anti-phosphotyrosine monoclonal antibody demonstrated that the LCDG dimyristin, at concentrations found within the body, induced a 6-fold increase of tyrosine phosphorylation of an Mr 63,000 protein found in the particulate fraction of colon carcinoma cells. Tyrosine phosphorylation was maximal 0.5 min after addition of the LCDG, then fell, but remained elevated 40% over constitutive levels for at least 6 h. The Mr 63,000 tyrosine phosphoprotein was found in each of four colon carcinoma cell lines and an adenoma, but not in normal colonocytes, suggesting that the tyrosine kinase is activated only in tumor cells. Constitutive levels of the Mr 63,000 substrate were enhanced 2-fold by incubation of cells for 20 h with sodium orthovanadate, a tyrosine phosphatase inhibitor. This result suggested that carcinoma cells continually phosphorylate and dephosphorylate this tyrosine kinase substrate during growth. Thus, the colon tumor cell mitogen, dimyristin, utilizes a signal transduction pathway, containing the Mr 63,000 tyrosine kinase substrate, which is already in use during cell growth, possibly by other mitogens or growth factors.
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PMID:Tyrosine phosphorylation of a Mr 63,000 protein induced by an endogenous mitogen in human colon carcinoma cells, but not in normal colonocytes. 274 9

The rare tyrosine-rich crystalloids (TRC) of salivary gland pleomorphic adenoma (PA) give a positive Million reaction indicating the presence of tyrosine. Their varied histochemical reactions, however, suggest a more complex composition. Two cases of TRC were encountered in a series of 144 PA (1.4%). Both were studied with several histochemical stains, and one tumor particularly rich in TRC was further examined with transmission and scanning electron microscopy and subjected to biochemical analysis using fresh-frozen tissue. TEM showed amorphous, electron-dense masses with no discernable internal structure. SEM revealed a geodelike structure of radially arranged, interlocking plates. Amino acid analysis of normal parotid, tumor with TRC, and a similar tumor without TRC indicated a slightly elevated level of tyrosine and arginine in the tumor with TRC. Polyacrylamide gel electrophoresis of tissue dissolved in sodium dodecyl sulfate revealed dense banding corresponding to polypeptides of a relative molecular weight of approximately 17,000 only in the TRC-rich sample. These bands on further analysis contained relatively large amounts of arginine. Tyrosine was present in only small amounts. TRC appear to be small proteins containing some tyrosine but rich in arginine.
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PMID:Tyrosine-rich crystalloids in pleomorphic adenoma: SEM findings and partial biochemical characterization. 285 75

The withdrawal effect of spironolactone treatment on natriuresis was studied in relation to atrial natriuretic peptide (ANP) in five patients with primary aldosteronism due to adenoma. The patients had been treated with spironolactone for 2-3 months before they were admitted. After admission, blood pressure, body weight, and urinary excretion of sodium were measured daily. Venous samples were obtained twice a week for measurements of plasma levels of ANP, plasma renin activity (PRA), and plasma concentrations of aldosterone (PAC), cortisol, and deoxycorticosterone. The study was performed for 7 days during the treatment with spironolactone and for 18 days after stopping the administration. Plasma volume was determined two times, during the control period and on the 13th day after stopping spironolactone. Urinary sodium excretion decreased initially and returned to the control levels successively. Body weight and plasma volume increased, and blood pressure rose steadily. PRA and the plasma concentrations of cortisol and deoxycorticosterone decreased significantly (P less than 0.05); however, high levels of PAC did not alter significantly. Plasma ANP levels increased significantly (P less than 0.05) from 26 +/- 4 pg/ml during the control period to 195 +/- 47 pg/ml on the 13th day after stopping spironolactone. The data of the urinary sodium excretion showed the escape from sodium-retaining effect of aldosterone, and this escape could be explained by the increase in plasma ANP. Furthermore, ANP might contribute to the decrease in cortisol and deoxycorticosterone in plasma because of the direct inhibitory action of ANP on steroidogenesis.
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PMID:Role of atrial natriuretic peptide in mineralocorticoid escape phenomenon in patients with primary aldosteronism. 295 9

Excessive production of an as yet unidentified aldosterone-stimulating factor may cause idiopathic hyperaldosteronism (IHA). This putative factor may be related to proopiomelanocortin-derived peptides, some of which have aldosterone-stimulating properties. The present study evaluated plasma beta-endorphin, ACTH, cortisol, and aldosterone levels in patients with IHA (n = 10), aldosterone-producing adenomas (n = 4), essential hypertension (n = 11), and normal subjects (n = 10). Plasma and urinary hormone measurements were obtained at timed intervals during an isocaloric, fixed electrolyte intake (Na+, 128 meq/day; K+, 80 meq/day) in a metabolic unit. Plasma for beta-endorphin assay was preincubated with sepharose-bound anti-beta-lipotropin to remove beta-lipotropin that cross-reacted with the beta-endorphin RIA. Mean +/- SE plasma beta-endorphin levels at 0800 h were elevated in IHA patients (47 +/- 13 fmol/ml) compared to those in aldosterone-producing adenoma (25 +/- 9), essential hypertension (16 +/- 1), and normal control (20 +/- 2; P less than 0.05) subjects. Plasma ACTH, plasma cortisol, and urinary cortisol levels were not different in these four groups. These data support the hypothesis that excess production of either beta-endorphin or related proopiomelanocortin-derived peptides may function as aldosterone secretogogue(s) in IHA.
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PMID:Plasma beta-endorphin levels in primary aldosteronism. 298 Dec 43

An enzyme immunoassay for serum 18-hydroxycorticosterone was established using alkaline phosphatase as a label. The antiserum for 18-hydroxycorticosterone was produced by immunization of rabbits with 18-hydroxycorticosterone 3-(o-carboxymethyl) oxime conjugated to bovine serum albumin. Sephadex LH-20 column chromatography was used to separate 18-hydroxycorticosterone from other steroids in serum samples. The minimal detectable amount of 18-hydroxycorticosterone was 50 pg/tube, and the measurable range was from 5 to 1000 ng/dl when a 1.0 ml serum sample was used. Intra- and inter-assay coefficients of variance were 5.0% (n = 6), and 5.8% (n = 6), respectively. In normal controls the serum 18-hydroxycorticosterone level was 4.8 approximately 34.0 ng/dl (mean +/- S.D. = 17.1 +/- 9.0 ng/dl) on an unrestricted diet. Seven out of 8 patients with aldosterone-producing adenoma had above-normal serum 18-hydroxycorticosterone levels. Serum 18-hydroxycorticosterone increased and decreased significantly following ACTH and dexamethasone administration, respectively. In essential hypertensive patients, serum 18-hydroxycorticosterone was high during a low-sodium diet and was suppressed remarkably by captopril. These observations support the previous reports that adrenal 18-hydroxycorticosterone synthesis is dependent on both ACTH and the renin-angiotensin system. The present method is sufficiently sensitive and producible, avoids the use of radioisotopes and is quite satisfactory for clinical use.
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PMID:[Enzyme immunoassay for serum 18-hydroxycorticosterone and its clinical application]. 300 75

ACTH-secreting pituitary adenoma cells were cultured from specimens obtained by transphenoidal hypophysectomy in five patients with Cushing's disease. The majority of adenoma cells (90%) stained specifically with antiserum against human ACTH. The electrophysiological properties and response to hormones of these cells were studied with intracellular recording techniques under current clamp and voltage clamp conditions. Most (80%) of the cells fired action potentials that were Ca2+-dependent inasmuch as they were blocked by Co2+ (5 mM) and by removal of Ca2+ from the medium, but were unaffected by tetrodotoxin (0.3 mM) and by Na+ removal. The cells responded to factors known to stimulate ACTH release, including high K+, CRF, and angiotensin II (AII). High K+ (50 mM) induced a membrane depolarization in association with an increase in conductance. CRF (100 nM) produced a depolarization, a decrease in conductance, an increase in spike firing, and an increase in spike duration. Although AII was inactive in ordinary recordings, in cells loaded with lithium (Li+) to promote the phospholipid-dependent second messenger system, the peptide produced an increase in spike firing and spike duration with no change in membrane potential. The combination of CRF and AII (CRF + AII; 100 nM each) in Li+-loaded cells caused a greater excitatory effect than either peptide alone. Under voltage clamp, the response either to CRF or to CRF + AII could be attributed, at least in part, to the inhibition of a slow, voltage-dependent K+ current that is persistently active at resting potential. These results indicate that modulation of action potential firing may be an early step in the regulation of ACTH release from pituitary cells by known secretagogues. Since action potentials in these cells are associated with Ca2+ entry, the resulting changes in intracellular Ca2+ levels could mediate the effects of the hormones on secretion.
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PMID:Electrical properties of cultured human adrenocorticotropin-secreting adenoma cells: effects of high K+, corticotropin-releasing factor, and angiotensin II. 303 72

Patients with primary aldosteronism do not have distinctive clinical features. However, the associated hypertension is invariably high and often resistant to drug therapy. The recommended initial test in suspected primary aldosteronism is the determination of aldosterone excretion rate after salt loading. Patients in whom aldosterone excretion rates exceed 14.0 micrograms per 24 hours when the urinary sodium is at least 250 mEq per 24 hours are prime candidates for additional studies. The presence of hypokalemia and/or suppressed plasma renin activity provides corroborative evidence of primary aldosteronism, but the absence of either or both does not preclude the diagnosis. Spontaneous, moderately severe hypokalemia (less than 3.0 mEq per L), an anomalous postural decrease in plasma aldosterone concentration, and increased plasma 18-hydroxycorticosterone values (greater than 100 ng per dl) indicate the presence of an adenoma. For localization of an adenoma, an adrenal CT scan should be obtained first and is considered diagnostic if an adrenal mass is clearly identified. When the CT scan is inconclusive, adrenal venous sampling can be done for more definitive localization. In the presence of an adenoma, surgical excision is the recommended approach but only after pharmacologic normalization of arterial pressure and correction of metabolic abnormalities. Sustained salt and water depletion is the most important therapeutic goal for these patients, and cure can be achieved despite prolonged and severe hypertension.
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PMID:Primary aldosteronism. 306 43

Differential-diagnosis tests for low-renin hypertension viz essential hypertension and arterial hypertension due to Conn's syndrome (adrenocortical adenoma or hyperplasia) have been assessed. The examined patients showed considerable humoral and metabolic differences, as compared to patients with high and normal plasma renin activity (PRA). For example, patients with essential hypertension and low PRA showed depressed noradrenalin and PGE2 secretion, increased PGF2 alpha secretion, low triglyceride level, and elevated erythrocyte sodium content. Patients with adrenocortical adenoma exhibited increased secretion of adrenalin, dopamine and PGF2 alpha, and a higher erythrocyte sodium level. Enhanced dopamine synthesis in patients with Conn's syndrome may be an adaptive response to a high aldosterone level.
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PMID:[Activity of the sympathetic nervous system and the levels of prostaglandins and intracellular electrolytes in patients with arterial hypertension and low plasma renin activity]. 307 43

Spontaneous (not experimentally induced) systemic hypertension was detected in 5 male dogs that were examined because of apparent blindness caused by intraocular hemorrhage and/or retinal detachment. Secondary causes of hypertension, including renal, adrenal, and thyroid disease, were investigated. Four of the dogs had glomerulonephropathy, renal insufficiency, and proteinuria. Four dogs had compensatory cardiac hypertrophy. Hypertension in 4 of 5 dogs was associated with glomerulosclerosis with chronic renal insufficiency, bilateral adrenocortical hyperplasia, adrenocortical adenoma with renal amyloidosis, and immune-mediated glomerulonephritis with chronic renal insufficiency, respectively. The fifth dog was determined to have essential hypertension. The dogs were treated for their primary diseases. Sodium restriction alone was inadequate to reduce blood pressure; 4 of the dogs also required antihypertensive medications.
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PMID:Spontaneous systemic hypertension in dogs: five cases (1981-1983). 317 Mar 25


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