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)

To evaluate the effects of physiological concentrations of estrogen on plasma concentrations of somatomedin-C (Sm-C) and GH, 16 chronic castrate female baboons were implanted either with blank Silastic capsules (n = 5) or capsules containing crystalline estradiol (E2; n = 11), which remained in place for 7 days. By day 7, serum E2 levels in treated animals rose into the physiological adult female range (mean +/- SEM, 96 +/- 9.2 pg/ml) and were greater (P less than 0.0005) than those in control animals (27.5 +/- 3.4 pg/ml). Sm-C concentrations rose significantly by day 7 in treated animals compared to those in control animals, whether assayed from unprocessed plasma (96% increase; P less than 0.01), plasma pretreated with glycine-HCl (99% increase; P less than 0.01), or plasma extracted with acid-ethanol (72% increase; P less than 0.02). GH concentrations in these animals were low and were not significantly different in E2-treated and control animals. To evaluate the effects of pharmacological doses of E2 on Sm-C and GH concentrations, six intact adult female baboons were treated with six daily injections of 1 mg E2 benzoate in oil. Serum E2 rose to a mean level of 1669 +/- 320 pg/ml on day 7. The plasma Sm-C concentration by day 7 was significantly higher than the pretreatment value whether assayed in untreated plasma (4.3-fold increase; P less than 0.01), plasma pretreated with glycine-HCl (2-fold increase; P less than 0.01), or plasma extracted with acid-ethanol (1.7-fold increase; P less than 0.01). Mean serum GH concentrations rose significantly from 3.3 ng/ml on day 0 to 23.6 ng/ml by day 7 (P less than 0.02). Evaluation of the chromatographic profile of native baboon plasma suggested a marked increase in [125I]Sm-C binding to plasma proteins after in vivo pharmacological E2 treatment; a broad peak of [125I]Sm-C binding over a size range from that of albumin to gamma-globulin was found. These results indicate that estrogen treatment of castrate or intact female baboons with both physiological and pharmacological doses results in an increase in plasma Sm-C concentrations that, at least in pharmacological doses, are mediated through an increase in GH concentrations. Although pharmacological E2 treatment results in a stimulation of plasma proteins that bind Sm-C, the effects on plasma Sm-C concentrations were found after procedures that diminish interference from circulating binding proteins. These data support the concept that estrogen may play a role in the physiological increase in plasma concentrations of Sm-C associated with normal puberty.
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PMID:Estrogen stimulates growth hormone and somatomedin-C in castrate and intact female baboons. 619 64

When observed by SEM, after being treated with the HCl-collagenase method, the odontoblast processes extended throughout the whole thickness of dentin in intact teeth and the whole thickness of normal and the inner carious dentin in carious teeth. Small holes and depressions were found on the processes in the transparent layer.
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PMID:The extent of the odontoblast process in normal and carious human dentin. 630 79

The effects of chronic treatment with methadone, a long-acting opiate agonist, and naltrexone, a long-acting opiate antagonist on brain immunoreactive beta-endorphin (IR-beta-EP) concentrations were studied in the rat. Male rats were treated for 30 days with either methadone, 2.5 mg/kg/day; naltrexone 2 mg/kg/day, or saline. In a repeat experiment, rats were treated for 36 days with either methadone 2.5 mg/kg/day; naltrexone 4 mg/kg/day, or saline. Brain regions were homogenized in 0.2 N HCl and assayed for IR-beta-EP by RIA. No change in the IR-beta-EP content of the hypothalamus, thalamus, midbrain, or amygdala was measured in either experiment after methadone treatment. Naltrexone, however, significantly lowered brain IR-beta-EP in both experiments. In the first study hypothalamic IR-beta-EP fell from 189 +/- 17 (SEM) to 132 +/- 7.0 ng/g wet weight of tissue after naltrexone treatment (p less than 0.01). In the second experiment naltrexone lowered IR-beta-EP in the hypothalamus from 23.4 +/- 3.6 to 15.5 +/- 1.2 ng/mg protein (p less than 0.005). Similar decreases in the IR-beta-EP content of the thalamus (from 6.74 +/- 0.59 to 4.59 +/- 0.38 ng/mg protein) and amygdala (from 1.31 +/- 0.08 to 0.90 +/- 0.10) were also measured (p less than 0.01). We conclude that occupancy of opiate receptors by an opiate antagonist reduces brain levels of IR-beta-EP and suggests that chronic opiate receptor blockade may result in a compensatory increase in brain beta-EP release.
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PMID:Effect of chronic naltrexone and methadone administration on brain immunoreactive beta-endorphin in the rat. 631 67

To evaluate the role of nonsteroidal, follicular fluid proteins in folliculogenesis, the 10-55% saturated ammonium sulfate fraction of pooled human follicular fluid was dialyzed against 0.025 M Tris/HCl (pH 7.5) using 10,000 molecular weight exclusion membranes, then passed through agarose immobilized textile dye. Activity was determined by test fraction inhibition of human menopausal gonadotropin (2 U human LH/FSH . day), induced ovarian weight, and serum estradiol increase in hypophysectomized, diethylstilbesterol-treated, 25-day-old female rats. Specific inhibition (89 +/- 6.8% SEM) of ovarian weight increase was found in the material (2 ml) eluted from an Orange A column with KCl (1.5 M, pH 6.8). Inhibitory activity of the Orange A-bound material, which eluted through a standardized Sephadex G-50 column, corresponded to a molecular weight of 13,000-25,000. Isoelectric focusing on a Sephadex G-15 support bed or ampholyte displacement chromatography of Orange A bound material demonstrated inhibitory activity at pH 3.5-4.5 and 6.5-7.0. No demonstrable activity was found in similar fractions eluted through a Concanavalin A-Sepharose 4B column before or after addition of alpha-methyl-D-mannoside (2 M, pH 7). When active fractions were heated (56 C, 1 h) or exposed to trypsin (10 mg/100 ml), activity was lost. When aliquots of the saturated ammonium sulfate-extracted, dialyzed, Orange A-bound eluent were separated by high performance liquid chromatography using gel exclusion columns, activity in the bioassay was recovered in the 13,000-35,000 molecular weight range. Although confirmatory data await further studies, it is tempting to speculate that this protein(s) may be an important inter- and/or intraovarian regulator of follicular response to gonadotropins.
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PMID:Identification of proteins in pooled human follicular fluid which suppress follicular response to gonadotropins. 640 Nov 85

Fluoride is widely used for the prevention of dental caries. Very low concentrations of fluoride are routinely ingested in optimally fluoridated drinking water of many communities. Higher concentrations of fluoride in toothpastes, mouthrinses and topically applied gels also may be ingested, especially by children. The potential effect of ingested fluoride on the gastric mucosa was the subject of this investigation. Solutions of 0, 1, or 10 mM NaF in 0.1 N HCl were placed in rat stomachs in vivo for up to one hour. The effects of fluoride on the structure and function of the gastric mucosa were determined. Histologic and SEM examinations revealed dose- and time-dependent damage to the surface mucous cells. The 10 mM, but not the 1 mM, NaF solution increased gastric mucosal permeability to small but not to large molecules.
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PMID:The effects of fluoride on the gastric mucosa of the rat. 643 19

To study the effects of acute myocardial infarction on its pharmacokinetics a single oral dose of 400 mg mexiletine HCl was administered to seven patients. The study was performed within 24 h of the onset of pain (Study I) and was repeated 10-14 days later, during the recovery phase (Study II). Mexiletine in plasma and urine was quantified by a GLC method. The peak plasma concentrations of mexiletine were 0.65 +/- 0.05 (SEM) microgram ml and 1.08 +/- 0.11 micrograms/ml (p less than 0.05) in Studies I and II, respectively. The corresponding peak times were 4.68 +/- 2.04 h and 1.46 +/- 0.17 h (N.S.). The lag time averaged 0.48 +/- 0.08 h in Study I and 0.39 +/- 0.05 h in Study II (N.S.). The area under the plasma concentration-time curve remained unchanged. The elimination half-life was 15.03 +/- 0.61 h and 11.75 +/- 0.80 h (p less than 0.01) in Studies I and II, respectively. The recovery of unchanged mexiletine in urine and its renal clearance was also the same in both studies. The plasma protein binding of mexiletine was similar in Studies I and II (61 +/- 2% and 63 +/- 3%; N.S.). Thus, the rate of gastrointestinal absorption of mexiletine was definitely slowed in the acute phase of myocardial infarction, whereas the extent of absorption was not altered. The prolongation of the elimination half-life of mexiletine in the acute phase of myocardial infarction is probably related to an increase in its volume of distribution.
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PMID:Pharmacokinetics of oral mexiletine in patients with acute myocardial infarction. 666 76

To characterize the pancreatic islet cell responses to adrenergic stimulation, membrane potentials have been recorded from isolated, perifused mouse islets of Langerhans exposed to a steady glucose level of 200 mg/dl. Various doses of epinephrine HCl from 5 to 10,000 nM have been applied for 10--15-min test periods separated by 10--15-min control periods. Epinephrine produced a dose-dependent suppression of glucose-induced membrane electrical activity. Adding epinephrine (50--100 nM) reduced the plateau fraction (the fraction of each plateau/silent phase cycle spent in the plateau phase) from 0.41 +/- 0.03 (X +/- SEM, N = 13) to 0.28 +/- 0.08 (N = 5, P = 0.05) and more markedly reduced the plateau frequency from 2.56 +/- 0.32 (N = 13) to 0.80 +/- 0.23 min-1 (N = 5, P less than 0.02). Adding 10- and 100-fold higher concentrations of epinephrine had little additional effect. There was no effect of epinephrine on the membrane potential levels of the plateau and silent phase after a new steady state was achieved and no effect on the amplitude and waveform of the rapid spikes. The pattern of inhibition of the plateau/silent phase cycles by epinephrine is qualitatively different from the pattern seen during inhibition of electrical activity by reducing glucose level. This suggests that the electrical rhythm is controlled by more than one pathway. The persistence of electrical activity at very high levels of epinephrine (to 10,000 nM) suggests that electrical activity and, therefore, Ca2+ uptake can exist in the absence of insulin release.
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PMID:Islet electrical pacemaker response to alpha-adrenergic stimulation. 675 17

We have previously reported that hyperosmotic solutions of sodium chloride or of xylitol possess potent anti-ulcer activity and reduce gastric acidity in the rat. They also stimulate gastric prostaglandin (PG) biosynthesis, which may bear a causal relationship to the above effects. In the present investigation we studied the effect of intragastric hyperosmolarity on the transmucosal potential difference (PD) and on the permeability to H+ ions in the rat stomach. We also studied the effect of the prostaglandin synthetase inhibitors, indomethacin and flufenamic acid, on these parameters. Rat stomach was perfused in vivo, under urethane anesthesia, by xylitol solutions made up in 0.01 N HCl. While moderately hyperosmotic (13%) xylitol was without effect, the perfusion of intensely hyperosmotic xylitol (34.5%) resulted in a long lasting reduction of the transmucosal PD from a mean (+/- SEM) of -63 +/- 4 mV to a trough value of -40 +/- 3 mV. This depression of transmucosal PD was inhibited in a dose-related fashion by prior treatment with the PG-synthetase inhibitors. Acid recovery in the effluent was significantly reduced by the 34.5% xylitol solution and indomethacin pretreatment did not modify the effect of hyperosmotic xylitol. It is concluded that, although intensely hyperosmotic xylitol produces some of the characteristic effects of a barrier breaker, i.e. depression of transmucosal PD and acid back diffusion, these two phenomena probably involve different mechanisms, as indicated by their differential response to indomethacin.
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PMID:Hyperosmotic xylitol, prostaglandins and gastric mucosal barrier. 679 43

Kinetics and sedative and psychomotor effects of diphenhydramine were investigated in elderly Caucasian women (greater than 64 yr. old). In a double-blind trial, each of 12 healthy subjects received on one of three occasions 50 mg/70 kg IV or oral diphenhydramine HCl or oral placebo. Plasma levels of diphenhydramine were measured in six subjects and tests of sedation and psychomotor performance were performed hourly for 8 hr in all subjects. Kinetic analysis showed that the volume of distribution (295 +/- 50 [SEM] l/70 kg), clearance (42 +/- 5 l/70 kg/hr), and plasma t1/2 (4.9 +/- 0.7 hr) were of the same order as in young adults. As in young adults, there was minimal psychomotor impairment after oral and after intravenous diphenhydramine. In contrast to young adults, however, elderly women did not report significant sedation after diphenhydramine. These results suggest that diphenhydramine may not be an effective sedative/hypnotic in elderly women.
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PMID:Diphenhydramine: kinetics and psychomotor effects in elderly women. 704 3

Five men who smoked parsley cigarettes containing 100 micrograms of [3H]-phencyclidine hydrochloride (PCP.HCl) inhaled 69 +/- 5(SEM) % of the total radioactivity in the cigarette. Both PCP and its pyrolysis product, 1-phenylcyclohexene (PC), were found and measured in plasma. Calculations based on the assumption that the ratio of these two products was the same as in simulated smoking studies and based on either area under the curve or urinary excretion of PCP indicated that most of the PCP in smoke was absorbed. Mean half-life (t1/2) of PCP (24 +/- 7 hr, harmonic mean 18 hr) and ratios of metabolites in plasma and urine were close to those previously reported after intravenous and oral doses. A second peak in PCP plasma concentrations was observed, possible due to show efflux from the lungs. PC plasma concentrations (maximum 0.35 +/- 0.06 pmol/ml) were lower than those of PCP (maximum 0.62 +/- 0.09 pmol/ml) and its mean t1/2 (14 +/- 3 hr, harmonic mean 12 h) was shorter than that of PCP. Only traces of PC were found in urine. Only small amounts of metabolites from PC were found nonconjugated in plasma (to about 0.1 pmol/ml) or urine (less than 2% of radioactivity), but larger quantities were found as enzyme-hydrolyzable conjugates in urine (6% of radioactivity). Conjugates were also found in plasma (to about 0.12 pmol/ml).
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PMID:Phencyclidine and phenylcyclohexene disposition after smoking phencyclidine. 707 12


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