Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay for serotonin (5-hydroxytryptamine) has been developed, validated, and applied to the measurement of serotonin in blood and platelet-rich plasma. Six rabbits immunized with serotonin diazotized to a DL-p-aminophenylalanine-bovine serum albumin conjugate yielded anti-serotonin antibodies. In the radioimmunoassay, antibody-containing plasma (1:100) is incubated with 0.2 pmoles of [3H]serotonin, EDTA, and either serotonin standards or unknown samples (0.1 ml). Blood levels of serotonin are measured in a protein-free supernatant prepared by water lysis of heparinized blood followed by protein precipitation using zinc hydroxide. This assay is sensitive to 100 pg of serotonin and has demonstrated insignificant cross-reactivity with a number of serotonin analogues at their normal circulating concentrations. Validation has been achieved by obtaining comparable values for normal blood serotonin concentrations by radioimmunoassay and by spectrophotofluorometry as well as by demonstrating that dilutions of endogenous serotonin in rabbit blood and blood from a patient with the carcinoid syndrome were superimposable on a standard calibration curve. In 55 normal human subjects the mean whole blood serotonin concentration was 168 +/- 13.4 ng/ml (mean +/- SEM) (range: 31 to 442 ng/ml). In 15 normal volunteers the mean radioimmunoassayable serotonin concentrations in whole blood and platelet-rich plasma were 337 +/- 40 ng/10(9) platelets and 341 +/- 37 ng/10(9) platelets, respectively. Incubation of blood with PGE1 to inhibit in vitro platelet aggregation before radioimmunoassay resulted in a significant fall in measurable serotonin activity in platelet-poor plasma (from 15.3 +/- 3.0 to 6.4 +/- 1.2 ng/ml). Seventeen normal human volunteers demonstrated a rise in circulating serotonin activity to a mean of 362.1 +/- 16.9 ng/ml at 30 min postcibal after a standard test meal, which was significantly (P less than 0.02) greater than the mean fasting level of 198.1 +/- 37.0 ng/ml. Five fasting controls did not show a rise in circulating serotonin levels when sampled at these intervals. These data suggest release of serotonin, presumably from the intestine, after a meal and make serotonin a candidate hormone in gastrointestinal physiology.
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PMID:Validation and application of a radioimmunoassay for serotonin. 125 37

An extra oral approach was made to 26 pairs of Wistar rat incisors and a small bur used to expose the pulps which were then dressed with either calcium hydroxide paste (Pulpdent) zinc oxide-eugenol cement (Kalzinol) or a triamocinolone acetonide/tetracycline containing cement (Ledermix). Animals were sacrificed at 7 days, incisors removed, a window cut to the pulp opposite the site of exposure, soft tissues removed with 7% NaOCl for 30 minutes before teeth were dehydrated in graded concentrations of acetone and gold coated for examination under SEM. Calcium hydroxide produced rapid complete repair with a remarkably regular formation of calcospherites, except for a zone of relative inhibition perforated by nutrient canals at the periphery of each lesion. Both zinc oxide-eugenol and triamcinolone acetonide cements inhibited both bridging of the defect created by the exposure and dentine formation in the surrounding pulpal wall. Data was grouped according to the degree of hard tissue repair. The results were statistically significant (Chi-square p < or = 0.001). This method demonstrated qualitative and quantitative differences in the repair process resulting from chemical variations in the dressings applied.
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PMID:Morphology of the mineralizing front and observations of reparative dentine following induction and inhibition of dentinogenesis in the rat incisor. 130 79

GTPase activity has been measured in synaptic membranes from bovine retina, with and without muscarinic receptor stimulation. Maximal stimulation above basal levels was achieved with 5 microM oxotremorine and 100 microM carbachol. (4-Hydroxy-2-butynyl)-1-trimethylammonium m-chlorocarbanilate chloride, which is selective for the M1 muscarinic receptor, failed to stimulate GTPase activity. 4-Diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) inhibition of oxotremorine stimulation demonstrated the presence of two populations of receptors, a low-affinity site (IC50 +/- SEM, 0.63 +/- 0.18 microM) which accounted for 63% of the inhibition and a high-affinity site (IC50 less than 1 nM) which accounted for the remaining 37%. When carbachol-stimulated GTPase activity was assayed, a single 4-DAMP inhibitory site was apparent (IC50 +/- SEM, 2.0 +/- 0.9 microM). Pirenzepine inhibited GTPase activity at a single site (IC50 values +/- SEM, 46.9 +/- 11 and 25.4 +/- 6.5 microM against oxotremorine and carbachol, respectively). Methoctramine was equipotent against carbachol and oxotremorine stimulation (IC50 values, 4.2 +/- 1.8 and 6.2 +/- 1.5 microM). Inhibition of maximal carbachol and oxotremorine stimulation by muscarinic antagonists at the major site had a rank order of potency of 4-DAMP = methoctramine greater than pirenzepine. Thus, the major site for muscarinic stimulation of GTPase activity in bovine retinal membranes is pharmacologically similar to M2 receptors.
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PMID:Muscarinic receptor stimulated GTPase activity in synaptic membranes from bovine retina. 161 99

Although it is recognized that inhalation of acid aerosols by subjects with asthma can cause bronchoconstriction, the effects of the inhalation of an alkaline aerosol are unknown. When supplemental inflatable restraints (automobile air bags) are deployed an alkaline aerosol is released. This aerosol is composed of particles of sodium carbonate and sodium bicarbonate with some sodium hydroxide. The mass median aerodynamic diameter (MMAD) of the aerosol is approximately 1 micron, and the pH of the aerosol is 9.8 to 10.3. A group of 14 volunteer male subjects with mild asthma inhaled increasing concentrations of this aerosol for 20-min periods of mouth-only tidal ventilation. Pulmonary function tests were performed at baseline (preexposure), after inhalation of room air alone (control), and after each period of inhalation of the aerosol. A total of 5 subjects inhaled aerosols at nominal concentrations of 10, 20, and 40 mg/m3, whereas 11 subjects inhaled aerosols concentrations of approximately 30, 60, and 120 mg/m3. The mean changes in FEV1 and specific airways resistance (SRaw) for the 11 subjects who inhaled the higher concentrations (average highest concentration 126.6 +/- 7.5 mg/m3, mean +/- SEM) were -1.4 +/- 1.9 and +17.5 +/- 8.5%, respectively. Neither change in lung function was clinically or statistically significant. We conclude that the inhalation of relatively high concentrations of this alkaline aerosol by subjects with mild asthma does not result in bronchoconstriction.
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PMID:Inhalation of an alkaline aerosol by subjects with mild asthma does not result in bronchoconstriction. 199 Sep 50

In this randomised double-blind cross-over study the gastroduodenal tolerability of buffered acetylsalicylic acid (ASS) (Aspalox = 325 mg ASS plus 300 mg magnesium aluminium hydroxide) daily has been compared with unbuffered ASS (325 mg) daily in 12 healthy volunteers using upper Gl-endoscopy. The treatment period lasted 14 days: endoscopic controls were performed at entry and repeated at day 14. At day 0 the mean endoscopic score averaged 0.8 +/- 0.1 in both groups (MW +/- SEM). One tablet Aspalox daily induced marked gastroduodenal damage at day 14 (6.5 +/- 1.5). The median lesion score rose from 1.0 (day 0) to 7.0 at day 14. Unbuffered ASS evoked almost identical gastroduodenal injuries at day 14 (7.5 +/- 1.8). The corresponding median values were 1.0 (day 0) and 7.0 at day 14. Our data suggest, that the amount of buffering in the Aspalox preparation is not sufficient enough to protect human gastroduodenal mucosa against low dose acetylsalicylic acid.
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PMID:[Stomach tolerance of buffered and unbuffered low-dose acetylsalicylic acid: an endoscopy controlled double-blind study in volunteers]. 218 49

This study evaluates the use of calcium carbonate in chronic renal failure. Forty-eight patients (25 male, 23 female, mean age 54.3 years, six pre-dialysis. 12 CAPD, 30 haemodialysis) on phosphate restriction and requiring aluminum hydroxide (mean 2.4 +/- 0.8 g/day) to control serum phosphate, were converted to an equivalent dose of calcium carbonate (2.5 +/- 0.6 g/day). None received vitamin D analogues. Three months post-conversion there was a significant decrease in mean (+/- SEM) serum phosphate (1.86 +/- 0.08 versus 1.66 +/- 0.05 mmol/l P less than 0.01) and serum aluminum (28.3 +/- 5.4 versus 13.2 +/- 3.0 micrograms/l, P less than 0.0001): calcium/phosphate product was unchanged. Post-conversion there was an increase in serum bicarbonate, (20.6 +/- 0.5 versus 22.1 +/- 0.6 mmol/l, P less than 0.01) and serum calcium (2.32 +/- 0.02 versus 2.45 +/- 0.03 mmol/l, P less than 0.0001). No change in serum creatinine, alkaline phosphatase or parathormone occurred. No adverse effects were reported but nine (18%) patients became hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom responded to dose reduction. Hypercalcaemia did not correlate with pre-conversion serum calcium, parathyroid hormone, alkaline phosphatase or aluminium. Calcium carbonate is an effective alternative to aluminium-based phosphate binders. It produces a beneficial increase in serum calcium and bicarbonate and a significant decrease in serum aluminium. Hypercalcaemia is unpredictable but is easily reversible in the majority of patients.
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PMID:The use of calcium carbonate to treat the hyperphosphataemia of chronic renal failure. 251 82

Urinary excretion of thioethers has been used as an indicator of exposure to potentially alkylating agents in several studies. These studies, however, often had the disadvantage of high and varying background values. We have studied methods for sampling and determination of urinary thioethers. Modifications have been made making it possible to increase the sensitivity of the method substantially. The thioethers were extracted with ethyl acetate and hydrolyzed with sodium hydroxide. The thiols were then determined spectrophotometrically with the reagent of Ellman. The extraction procedure and the addition of the reagent were found to be critical steps, whereas the crude urine samples were comparatively stable during storage at -20 degrees C. Diet was found to be the most important factor. Using a standardized diet over 24 h with chicken, potatoes, bread and dairy products as the major components, excluding vegetables of the Cruciferae family, 24 subjects excreted low amounts of thioethers, 3.2 +/- 0.2 mmol/mol creatinine, (mean +/- SEM). Individual values did not exceed 6.5 mmol/mol creatinine. Without food restrictions the mean values and the standard deviations were increased up to five and ten times respectively. Ingestion of certain foodstuffs increased the thioether excretion up to 20 times. Twelve smokers (20 cig/d) excreted 6.7 +/- 0.4 mmol/mol creatinine (mean +/- SEM, afternoon samples and standardized diet). No effects of gender and age of the subject could be observed. It is recommended that diet factors be kept under strict control to increase the sensitivity of the thioether assay and to avoid misleading results due to diet effects.
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PMID:Influence of diet and other factors on urinary levels of thioethers. 319 77

In order to study the effects of vitamin D on aluminium balance when different forms of vitamin D and phosphate binders are used simultaneously for therapeutic purposes, 30 Sprague-Dawley weanling rats, weighing 44-66 g, were randomly assigned to 5 groups: (A) control, (B) aluminum hydroxide, (C) dihydrotachysterol at 16 micrograms/kg/day, (D) 1,25-dihydroxyvitamin D at 16 ng/kg/day and (E) vitamin D at 2,000 IU/kg/day. Aluminum hydroxide (60 mg/kg/day) in the feed was provided to all except the control group. The vitamin D or metabolites were fed by stomach tube daily for a period of 10 days. At the end of the study, the mean (+/- SEM) serum aluminum concentration, as determined by flameless atomic absorption spectrophotometry, was 5.0 +/- 2.4 micrograms/l; there were no significant differences in these results between groups. During the last three days of the study, 24-hour urine and stool collections were made with the usual precautions against trace mineral contamination. The means (+/- SEM) of aluminum balances for groups A, B, C, D and E were -388 +/- 261, 1,121 +/- 331; 2,316 +/- 304; 2,387 +/- 245, and 1,968 +/- 337 micrograms/day, respectively. We conclude that at therapeutic doses of aluminum hydroxide and vitamin D or its metabolites, hyperaluminemia was not observed. However, the positive aluminum balances imply retention, and the use of vitamin D, especially its potent metabolites dihydrotachysterol and 1,25-dihydroxyvitamin D, intensified this risk.
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PMID:Aluminum metabolism in rats: effects of vitamin D, dihydrotachysterol, 1,25-dihydroxyvitamin D and phosphate binders. 334 Feb 56

Commercial oral iron preparations (drops) containing trivalent iron either as a citrate (C) or hydroxide-polymaltose complex (HP) were labelled with 59Fe in the thermal neutron flux of a research reactor. No measurable differences were observed between the original commercial preparation and the neutron-activated samples. In an intraindividual comparison oral doses of 100 mg 59Fe were administered as an aqueous 59Fe(II)-ascorbate solution (= reference), C (-59Fe) and HP (-59Fe) to starved subjects with normal and depleted iron stores. Two weeks later the whole body retention of absorbed 59Fe was measured and used for the calculation of 59Fe-absorption. Subjects with normal Fe-stores absorbed means a +/- SEM +/- SD = 8.53 +/- 0.29 +/- 1.2% of the 59Fe from the aqueous 59Fe(II)-ascorbate solution, 1.58 +/- 0.12 +/- 0.49 of the C-59Fe and 0.81 +/- 0.06 +/- 0.27% of the HP-59Fe. Subjects with depleted Fe-stores absorbed means a +/- SD = 17 +/- 3% of the 59Fe from the aqueous 59Fe(II)-ascorbate solution and only 2.4 +/- 1% from the HP-59Fe. The relative bioavailabilities were reduced from 100% (reference = Fe(II)-ascorbate) to 19% for the C-Fe and to 9.5% for the HP-Fe in subjects with normal Fe-stores. In subjects with depleted iron stores the relative bioavailability was decreased from 100 to 14% for the HP-Fe. Oral iron preparations with a relative bioavailability less than 10% or less than 30% are considered to be therapeutically ineffective or insufficient, respectively.
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PMID:Intestinal absorption of 59Fe from neutron-activated commercial oral iron(III)-citrate and iron(III)-hydroxide-polymaltose complexes in man. 356 63

The influence of aluminium hydroxide (given as a suspension, Aludrox) on the oral bioavailability of feprazone was tested. The degree and speed of absorption of feprazone from capsules (400 mg feprazone as a single dose; 8 volunteers) was investigated by determining plasma levels of feprazone and one of its metabolites using an HPLC method. No statistically significant change in feprazone kinetics caused by the antacid was evident. Cmax (means +/- SEM) decreased from 40.6 +/- 2.9 to 36.25 +/- 1.4 micrograms/ml; the mean area under the plasma level time curve was somewhat higher after additional administration of aluminium hydroxide (n. s.).
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PMID:The influence of aluminium hydroxide on the bioavailability of feprazone. Single dose study. 403 47


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