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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With regard to pH measurement of biological fluids in vivo with metal-metal oxide microelectrodes, the effect of temperature and partial pressure of oxygen on antimony (Sb) microelectrodes was examined, and pH of blood was estimated in the bullfrog. The temperature coefficient (dE/dt) of electromotive force (EMF) of Sb-microelectrodes in the range of 7 to 37 degrees C was -1.18 +/- 0.113 mV/degrees C (mean +/- SEM) in Ringer solution, whereas that of the pH glass electrode in the same solution was -0.43 +/- 0.035 mV/degrees C. When estimated in Tris buffer solution, it was -0.06 +/- 0.063 mV/degrees C for Sb-microelectrodes and 1.05 + 0.036 mV/degrees C for glass electrodes. The change of slope constant (alpha in -mV/pH) in the Sb-microelectrode due to temperature change could be predicted empirically from: alpha = 0.40 (t-25) + 55.3, where t represents the measuring temperature in degrees C. The resultant deviation of pH reading between Sb and glass electrodes, delta pHSb-Glass, may be expressed by: delta pHSb-Glass = 0.00183 (t-25) +0.016. In the range of 45 to 760 mmHg of oxygen partial pressure it fixed pH, the EMF increased linearly with the increase of Po2, the slope (dE/dlog(Po2)) being 11.7 +/- 0.42 (SEM) mV (n = 13, t = 25 degrees C). In consideration of the above effects, the blood pH of bullfrog was estimated to be 7.697 +/- 0.092 (SD) and 7.729 +/- 0.111 with glass and Sb-microelectrodes respectively, the difference between the two being relatively minor.
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PMID:Temperature coefficient of and oxygen effect on the antimony microelectrode. 697 Feb 92

Immunoreactive plasma motilin concentrations were studied following a variety of stimuli in 24 healthy fasting subjects. Plasma motilin was measured by a radioimmunoassay using antibody GP 71 (J. C. Brown) and natural porcine motilin as standard. Basal motilin levels ranged from undetectable to 365 pg/mL. Antral and intraduodenal infusion of 50 mL o.1 N HCl (pH 1.2) at 5 mL/min failed to alter significantly plasma motilin levels but duodenal acid infusions at 17 mL/min caused a significant increase (70.8 +/- 29.5 pg/mL, mean +/- SEM; n = 6), maximal at 40 min. Duodenal alkalinization with 50 mL 0.3 M Tris buffer (pH 8.0) infused at 5 mL/min produced no change in plasma motilin. A mixed meal did not affect plasma motilin levels. Ingestion of 60 g fat significantly increased plasma motilin (n = 13; maximal increase 150.3 +/- 43.3 pg/mL at 30 min) but duodenal infusions of fat failed to increase plasma motilin levels. These results suggest that motilin secretion induced by fat requires that the fat be present initially within the stomach for secretion to occur. We conclude that ingested fat is a potent stimulus of motilin release. As duodenal acidification (50 mL 0.1 N HCl over 10 min) induces duodenal activity resembling migrating motor complexes but does not release motilin, our data argue against the release of motilin following duodenal acidification as a trigger for the initiation of these complexes in man.
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PMID:Changes in plasma motilin concentration in response to manipulation of intragastric and intraduoduenal contents in man. 722 46

Studies were initiated to determine whether resident nuclear estrogen receptors with unfilled binding sites existed in the nuclear fraction of uteri from untreated immature rats. These studies revealed a small population (mean +/- SEM, 0.087 +/- 0.017 pmol/uterus) of unfilled estrogen-binding sites in the uterine nuclear fraction from untreated immature rats, which bound [3H]estradiol in the absence of added cytoplasmic receptor. These nuclear estrogen-binding sites occurred in addition to the 0.60--1.2 pmol estrogen-binding activity/uterus in the uterine cytoplasmic fraction of these animals. [3H]Estradiol bound reversibly with high affinity (apparent Kd = 1.4 x 10(-10)M to these binding sites, and only estrogenic compounds competed for this binding. Binding studies done at a variety of temperatures (0--37 C) showed that there were no estradiol-filled receptor sites associated with the nuclear fraction. In addition, these unfilled nuclear estrogen-binding sites remained unfilled 15 min after injections of either 1.0 or 0.1 micrograms estradiol/rat. Extraction of these sites was achieved with 0.4 M KCl, and when this extract was centrifuged on a 5--20% linear 0.010 M Tris-HCl, 0.0015 M Na2EDTA, and 0.40, M KCl sucrose gradient, the binding activity exhibited a sedimentation coefficient of 3.6S. These unfilled nuclear estrogen-binding sites did not appear to have arisen as a contaminant from the estrogen-binding proteins present in either uterine cytoplasm or serum during tissue homogenization. The existence of these unfilled nuclear estrogen-binding sites does not represent a major exception to the classical two-step theory of estrogen action; instead, they seem to be novel forms of the estrogen receptor whose physiological role has not been determined.
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PMID:Characterization of a unique population of unfilled estrogen-binding sites associated with the nuclear fraction of immature rat uteri. 737 93

Calcium phosphate (Ca,P) precipitation behavior on the surface of two bioactive glasses and four bioactive glass composites--two with hydroxylapatite (Ca10(PO4)6 (OH)2) and two with rhenanite (CaNaPO4)--were studied in simulated body fluid (SBF) and in Tris-Buffer at 5, 8, 16, 24, 48, 72, and 144 h. The weight loss of the materials was measured and the amount of precipitation was estimated using scanning electron microscopy with electrochemical detection (SEM-EDX) analysis. The test was repeated for one glass and its respective rhenanite composite every 3 h until 60 h and thereafter every 10 h until 150 h in SBF. Atomic absorption spectroscopy, spectrophotometry, SEM-EDX analysis, and pH measurements were performed on these samples. It is shown that in vitro the composite materials have a higher capacity for Ca,P precipitation than the glasses. Weight losses of the materials correlate well with their composition. Both the glass and Ca,P phases influence the precipitation mechanism and rate. Precipitation begins preferably from the glass phase. Ca,P particles clearly influence the time of onset and rate of precipitation. Cross-sectional EDX analysis of the samples revealed an absence of a clear Si-rich layer in glass A0B0 (SiO2 53.9 mol %, Na2O 27.5, CaO 12.4, P2O5 6.2, Al2O3 0.0 and B2O3 0.0) composites. This was attributed to the presence of extra calcium and phosphate ions on the surface of the material. The ion-concentration and pH change curves offered insight into the mechanism of precipitation. A connection was established between SEM-EDX results and the release curves. Formation of an Si,Ca,Na film was observed that seemed to initiate the Ca,P precipitation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissolution and scanning electron microscopic studies of Ca,P particle-containing bioactive glasses. 824 37

During human pregnancy, plasma CRH immunoreactivity (CRH-IR) rises progressively, peaking during labor and falling after delivery. Among animal species, only higher primates have elevated CRH-IR during pregnancy. This study examines whether changes in plasma CRH-IR in the baboon (Papio hamadryas) are similar to those in the human. CRH-IR was determined by RIA in 16 baboons at different stages of gestation (44 samples) and in 3 males. Assays were performed on Vycor extracts of plasma and CRH-IR diluted in parallel to synthetic human (h) CRH-41 standard. Reverse phase high pressure liquid chromatography and size-exclusion chromatography with Sephadex G-50 showed that baboon CRH-IR eluted in a position similar to that of hCRH-41. Regression analysis revealed a cubic association between plasma CRH-IR and gestational age, with peak concentrations occurring at 60 days gestation (term = 182 days). Although greatly elevated concentrations persisted throughout pregnancy, concentrations in the first half (1-91 days) were significantly higher (mean +/- SEM, 1.9 +/- 0.3 nM/L; n = 27) than in the second half (92-182 days; 1.0 +/- 0.2 nM/L; n = 11; P < 0.003 by t test). CRH-IR fell to low levels by day 1 postpartum. The concentration of total cortisol in nonpregnant animals was 1370.9 +/- 134.9 nM/L (n = 5), which was similar to pregnancy levels (1346.3 +/- 356.1 nM/L; n = 28); there was no gestational age-related pattern evident. Plasma corticosteroid-binding globulin was estimated by RIA, and plasma free cortisol was calculated to be 73 +/- 14 nM/L in pregnant animals and showed no gestational age-related changes. The mean progesterone concentration in the pregnant baboon was 12.5 +/- 2.2 nM/L (7-169 days; n = 27). There was no significant change in progesterone levels during the period of gestation studied; however, they were higher than nonpregnant levels. Baboon and human plasma (0.1 mL each) were incubated with [125I]Tyr-hCRH in Tris-HCl buffer (pH 7.5) and chromatographed with Sephadex G-75, using the same buffer. The radioactivity of fractions was determined, and no CRH-binding protein was identified in baboon plasma. This study indicates that gestational changes in CRH-IR in the baboon are different from those observed in humans. There is a dissociation between maternal plasma CRH and cortisol. The apparent lack of bioactivity of baboon plasma CRH is not due to a circulating binding protein, which is absent in this species.
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PMID:Corticotropin-releasing hormone in baboon pregnancy. 847 82

Previous studies have implicated the neuronal L-type voltage-sensitive Ca2+ channel (VSCC) as a target site for i.v. anaesthetic agents. It is unclear if these agents interact with the L-channel alpha-subunit 1,4-dihydropyridine (DHP) binding site. In this study, we have examined the interaction of thiopentone, pentobarbitone, ketamine, etomidate, propofol and alphaxalone, and the non-anaesthetic barbiturate, barbituric acid, with the DHP binding site on rat cerebrocortical membranes. Binding assays were performed in 1-ml volumes of Tris-HCl 50 mmol litre-1, pH 7.4, for 90 min at room temperature containing 200 micrograms of membrane protein with [3H]PN200-110 as a radiolabelled DHP. Non-specific binding was defined in the presence of nifedipine 10(-5) mol litre-1. The interaction of i.v. anaesthetics was determined by displacement of [3H]PN200-110 0.2 nmol litre-1. All i.v. anaesthetics showed some interaction with the DHP binding site. The concentrations of anaesthetic producing 25% inhibition of specific binding (corrected for the competing mass of [3H]PN200-110), K25 were (mumol litre-1): thiopentone 48 (SEM 2), pentobarbitone 95 (7), propofol 40 (2), etomidate 25 (2), alphaxalone 17 (3) and ketamine 198 (16). Barbituric acid was ineffective. With the exception of ketamine, there was a significant correlation between K25 and peak serum concentration during anaesthesia (P = 0.033) and serum concentrations on wakening (P = 0.018), suggesting that the L-channel DHP binding site may be a target for i.v. anaesthetic agents.
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PMID:I.v. anaesthetic agents inhibit dihydropyridine binding to L-type voltage-sensitive Ca2+ channels in rat cerebrocortical membranes. 913 39

In this study we have examined if the i.v. anaesthetic agents thiopentone, pentobarbitone, ketamine, etomidate, propofol and alphaxalone interact with the verapamil binding site on L-type voltage-sensitive Ca2+ channels in rat cerebrocortical membranes. Binding assays were performed in 1 ml volumes of Tris HCl 50 mmol litre-1, pH 7.4, for 90 min at 20 degrees C, with cerebrocortical membranes (200 micrograms of protein), the verapamil binding sites of which were radiolabelled with [3H]verapamil. Non-specific binding was defined in the presence of verapamil 10(-6) mol litre-1. The interaction of i.v. anaesthetics was determined by displacement of [3H]verapamil 0.2 nmol litre-1. The mean concentrations of anaesthetic producing 25% inhibition of specific binding (corrected for the competing mass of [3H]verapamil), K25, were (mmol litre-1): thiopentone 0.68 (SEM 0.14); pentobarbitone 1.22 (0.13); propofol 0.66 (0.10); etomidate 0.24 (0.03); alphaxalone 0.19 (0.02); and ketamine 0.75 (0.04). These concentrations exceeded those seen during anaesthesia and suggest that the neuronal verapamil binding site may not be an important target for i.v. anaesthetic agents.
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PMID:I.v. anaesthetic agents do not interact with the verapamil binding site on L-type voltage-sensitive Ca2+ channels. 894 16

This study examined the effects of tetracycline hydrochloride (TCN) and chlorhexidine gluconate (CHX) on the growth and viability of Candida albicans. Subcultures of Candida albicans on Sabouraud's agar, were divided into 5 treatment groups: group 1, untreated control; group 2, 0.12% CHX; group 3, 3.0 mg/ml TCN adjusted to pH 4.5; groups 4 and 5, sodium azide free Tris buffer adjusted to pH 4.5 and pH 7.4, respectively. All groups were incubated for 10 days, and sampled and subcultured daily to determine the viability of each group. Additional samples from group 2 (day 4), group 4 (day 7) and all groups at day 10 were selected for SEM and TEM examination. Visual, SEM and TEM results showed that for groups 1, 3, 4, and 5 there was a heavy and constant uniform growth of Candida albicans throughout the period of the study. However, group 2 (CHX), showed decreasing viability and attachment from day 3 to day 10, with SEM and TEM revealing decreased blastospores and profound changes in the ultrastructural morphology, indicating inhibition of normal cell growth and replication. These results show that TCN even when used at high concentrations, in vitro, will allow uninhibited growth of Candida albicans whereas CHX inhibits cell growth and replication.
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PMID:Effects of tetracycline hydrochloride and chlorhexidine gluconate on Candida albicans. An in vitro study. 935 May 60

We have examined the binding of the local anaesthetic agent [3H]amethocaine to rat cerebrocortical membranes. All studies were performed in Tris buffer 50 mmol litre-1 at pH 7.4. Bound and free radioligand were separated by rapid vacuum filtration. [3H]Amethocaine binding at room temperature was dose-dependent and saturable, with mean Kd and Bmax values of 153 (SEM 18) nmol litre-1 and 9.4 (1.6) pmol/mg protein, respectively. [3H]Amethocaine binding was displaced in a dose-dependent manner (pIC50) by unlabelled amethocaine (6.89), procaine (5.20), lignocaine (3.46) and prilocaine (2.81). Ropivacaine and bupivacaine did not produce 50% displacement at the highest concentrations used (10(-4) and 10(-3) mol litre-1, respectively). We examined the nature of the binding site further with a range of ion channel antagonists (nifedipine, verapamil, diltiazem, omega-conotoxin, tetrodotoxin, tetraethylammonium and 4-aminopyridine) and ion channel coupled receptor ligands (L-glutamate, MK801, GABA, glycine and nicotine). With the exception of tetraethylammonium (pIC50 3.07) and 4-aminopyridine (pIC50 3.68), all non-anaesthetic agents failed to displace [3H]amethocaine. Collectively our data suggest that it is unlikely that there is a single target site for all local anaesthetic agents.
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PMID:Studies on the binding of [3H]amethocaine to rat cerebrocortical membranes. 938 74

In an attempt to determine if there is any overlap in local and general anaesthetic binding sites, we have examined the effects of thiopental, phenobarbital, pentobarbital, propofol, ketamine (racemic and R(+)/S(-)), alfaxalone, etomidate and halothane on [3H]tetracaine binding to rat cerebrocortical membranes. Membranes were prepared in Tris HCI 50 mmol litre-1, pH 7.4, by homogenization and centrifugation. Binding assays were performed in 1-ml volumes of Tris HCI buffer at room temperature or 37 degrees C for halothane. Binding of [3H]tetracaine was displaced dose-dependently by unlabelled tetracaine with a mean pIC50 value of 6.91 (SEM 0.07) (123 nmol litre-1). With the exception of propofol (at high concentrations), all i.v. anaesthetic agents failed to displace the binding of [3H]tetracaine. In contrast, halothane produced a dose-dependent and statistically significant reduction in total [3H]tetracaine binding at clinically achievable concentrations (0.289, 0.885 and 1.484 mmol litre-1 equivalent to 1.0, 3.1 and 5.1 rat MAC) without markedly affecting the pIC50. Collectively these data may suggest some overlap in the binding sites for [3H]tetracaine and volatile but not i.v. general anaesthetic agents.
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PMID:Effects of i.v. anaesthetic agents and halothane on [3H]tetracaine binding to rat cerebrocortical membranes. 950 82


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