Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of propofol, etomidate, midazolam, and fentanyl on motor evoked responses to transcranial stimulation (tc-MERs) were studied in five healthy human volunteers. Each subject, in four separate sessions, received intravenous bolus doses of propofol 2 mg.kg-1, etomidate 0.3 mg.kg-1, midazolam 0.05 mg.kg-1, and fentanyl 3 micrograms.kg-1. Electrical tc-MERs (tce-MERs) were elicited with anodal stimuli of 500-700 V. Magnetic tc-MERs (tcmag-MERs) were elicited using a Cadwell MES-10 magnetic stimulator at maximum output. Compound muscle action potentials were recorded from the tibialis anterior muscle. Duplicate tce-MERs and tcmag-MERs were recorded before and up to 30 min after drug injection. Reproducible baseline tce-MERs (amplitude 4.7 +/- 0.43 (SEM) mV, latency 29.4 +/- 0.35 ms) and tcmag-MERs (amplitude 3.7 +/- 0.43 mV, latency 31.1 +/- 0.39 ms) were obtained in all subjects. Pronounced depression of tce-MER amplitude to 2% of baseline values (P less than 0.01) was observed 2 min after injection of propofol. Thirty minutes after injection of propofol, amplitude depression to 44% of baseline (P less than 0.05) was still present, despite an apparent lack of sedation. Midazolam caused significant (P less than 0.01) amplitude depression, e.g., tcmag-MER to 16% of baseline values 5 min after injection. Significant depression persisted throughout the 30-min study period. Fentanyl did not cause any statistically significant amplitude changes in this small population. Etomidate caused significant but transient depression of tc-MER amplitude. However, there was considerable intersubject variability. Latency did not change significantly after any drug.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of propofol, etomidate, midazolam, and fentanyl on motor evoked responses to transcranial electrical or magnetic stimulation in humans. 155 Feb 74

To determine whether exogenously administered neutral endopeptidase (NEP; enkephalinase, EC 3.4.24.11) inhibits the substance P-induced increase in vascular permeability in the skin, we examined the effects of recombinant human NEP on plasma extravasation induced by intradermal injection of substance P in guinea pig skin. Injection of substance P (2.5 X 10(-8) M) induced significant plasma extravasation in the skin (53 +/- 4 mm2 of Evans blue extravasation; mean +/- 1 SEM). In vitro incubation of substance P with recombinant human NEP prior to injection prevented the substance P-induced plasma extravasation in the skin in a dose-dependent fashion. Intradermal preinjection of recombinant human NEP partially inhibited plasma extravasation induced by subsequent injection of substance P (52 +/- 9% of the control without NEP). The H1 and H2 histamine antagonists pyrilamine and cimetidine, and a muscarinic antagonist, atropine, had no effects on substance P-induced responses. Two products of substance P degradation by NEP containing the carboxy-terminal portion, substance P7-11 and substance P8-11, were also without effect. These findings suggest that recombinant human NEP can attenuate substance P-induced increases in vascular permeability in guinea pig skin and, therefore, may be useful in treating dermatologic disorders in which abnormal responses to substance P or other neuropeptides cleaved by NEP may occur.
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PMID:Recombinant neutral endopeptidase attenuates substance P-induced plasma extravasation in the guinea pig skin. 169 12

The influence of an SPUU-PEO-Heparin (B-PEO-HEP) copolymer coated blood contacting surface on patency and platelet deposition in small diameter (4 mm i.d.) Biomer grafts was investigated using a canine model. Grafts were implanted in the bilateral carotid and femoral arteries. B-PEO-HEP coated grafts still showed patency after 3 days. Control Biomer grafts occluded before 24 hr. (postoperatively). SEM of the luminal surfaces of the Biomer grafts demonstrated large amounts of adherent platelets with distorted morphologies, while B-PEO-HEP grafts did not. In platelet studies, B-PEO-HEP grafts showed significantly less platelet adhesion than Biomer grafts. The improved blood compatibility of B-PEO-HEP graft co-polymer coatings attests to their usefulness for coating or casting.
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PMID:SPUU-PEO-heparin graft copolymer surfaces. Patency and platelet deposition in canine small diameter arterial grafts. 175 Oct 86

In the present study, increasing amounts of the anti-estrogen 1-(p-2-diethylaminoethoxyphenyl)-1-phenyl-2-p-methoxyphenoletha nol (MER-25) were administered to pregnant baboons (Papio anubis) to block the action of endogenous estrogen and to determine effect on placental low-density lipoprotein (LDL) uptake. Pregnant baboons were untreated (n = 8) or received MER-25 orally at a dosage of 25 (n = 10), 50 (n = 8), or 75 (n = 4) mg/kg BW daily on Days 140-170 of gestation (term = 184 days). Placentas were removed on Day 170 of gestation and villous tissue was dispersed with 0.1% collagenase. Placental cells (10(6] were incubated in Medium 199 for 12 h at 37 degrees C with increasing amounts of 125I-LDL, with or without a 100-fold excess of unlabeled baboon LDL. Mean (+/- SEM) placental uptake (ng/micrograms cell protein) of 125I-LDL was 55% (6.4 +/- 1.0), 75% (3.6 +/- 0.7), and 81% (2.7 +/- 0.2) lower (p less than 0.001) in baboons that received MER-25 in doses of 25, 50, and 75 mg/kg BW, respectively, than in untreated baboons (14.2 +/- 1.3 ng/micrograms cell protein). Maximal effect occurred with 50 mg MER-25, because LDL uptake was not further decreased with greater levels of MER-25. Dissociation constants for placental LDL uptake, as determined by Scatchard analysis, were unaltered by anti-estrogen treatment. The amount of 125I-LDL degradation by placental cells of untreated and MER-25-treated baboons was proportional to LDL uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of placental low-density lipoprotein uptake in baboons by estrogen: dose-dependent effects of the anti-estrogen ethamoxytriphetol (MER-25). 187 35

Nine mongrel dogs were anesthetized, paralysed, ventilated, and placed in an iron lung. Each animal was transiently connected to a spirometer and the respiratory system compliance measured by applying negative or positive extrathoracic pressures (from -20 cm H2O to +20 cm H2O in 5 cm H2O steps). A sub-lobar bronchus was wedged with a 5.5 mm bronchoscope, and a 5f Swan-Ganz catheter was inserted into the lumen of the bronchoscope; one port served to introduce a 200 ml.min-1 flow of 5% CO2 in air, the other to measure the pressure in the wedged segment. Rcoll was measured with extrathoracic pressures in the iron lung ranging from 0 to -20 cm H2O (NEP) and 0 to +20 cm H2O (PEP) in 5 cm H2O steps, and under expiratory positive airway pressure (EPAP) of 5, 10, 15, and 20 cm H2O. The maximal changes in FRC were an increase of 1009 +/- 49 ml (mean +/- SEM) with NEP and a decrease of 397 +/- 33 ml with PEP. Increasing FRC decreased Rcoll while decreasing FRC markedly increased it. EPAP induced similar decreases in Rcoll as NEP of equal pressure. This effect of EPAP was inhibited by simultaneously applying PEP of equal pressure. We conclude that resistance to collateral flow is highly dependent on lung volume, and that positive airway pressure decreases Rcoll by its effects on lung volume.
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PMID:Effects of lung volume and positive airway pressure on collateral resistance. 236 48

An investigation was undertaken to evaluate the effect of both photoinitiators (camphor-quinone-amine systems) and the adhesion promoting monomer (4-MET) on photopolymerization of bonding liners and their adhesion to dentin. Photopolymerization of bonding liners was measured with differential scanning calorimetry (DSC). The bonding liner containing 2-(dimethylamino)ethyl methacrylate (DMAEMA) as a reducing agent decreased the rate of polymerization in the presence of 4-MET. On the other hand, the bonding liners containing N-phenylglycine (NPG) and N,N-dimethylaniline derivatives as a reducing agent showed good polymerization in the presence of 4-MET. The results of the tensile bond test suggested that bonding liners containing NPG and 4-(dimethylamino)benzoic acid (DMABA), one of the N,N-dimethylaniline derivatives, with or without 4-MET bonded well to dentin treated with EDTA 3-2. NPG and DMABA are recommended not only as reducing agents but also as aids in the diffusion of monomers into the dentin substrate. The relationship between the strength of the bond to dentin and photoirradiation of the bonding liner and composite resin was studied. Elongation of photoirradiation of both the bonding liner and composite resin was effective in impacting the strength of the bond to dentin. Furthermore, sufficient photoirradiation of the bonding liner prior to any filling of composite resin was especially important to obtain high bond strengths. SEM and TEM observations supported good adhesion being achieved by hybrid formations between photocurable bonding liners and dentin.
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PMID:[Formulation of photocurable bonding liner and adhesion to dentin. Effect of photoinitiator, monomer and photoirradiation]. 248 1

The natriuretic effects of atrial peptide hormones have been attributed, at least in part, to their stimulation of guanylate cyclase activity in renal cell membranes. The effects of atrial natriuretic factor (ANF) on stimulation of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) accumulation were investigated in cloned human kidney tumor (hKT) cells and parent cells from a human renal tumor epithelial cell line (SK-NEP-1). Human ANF-(99-126) (10(-6)M) stimulated (p less than 0.001) cellular cGMP accumulation in a dose-dependent manner from a basal level of 0.26 +/- 0.04 to 3.73 +/- 0.81 pmol/mg protein/5 mi (mean +/- SEM, n = 13). ANF stimulation of cGMP accumulation was specific, in that high concentrations (10(-6)M) of atriopeptin I [rat ANF-(103-123)], angiotensin II, arginine vasopressin, and amiloride (10(-4)M) did not increase basal cGMP. Amiloride (10(-4)M) enhanced (p less than 0.01, n = 6) the ANF stimulation of cGMP accumulation (1.24 +/- 0.39 pmol/mg protein/5 min), particularly at low doses of ANF (10(-10)M) where stimulation by ANF without amiloride (0.34 +/- 0.08 pmol/mg protein/5 min) was barely distinguishable from a basal level (0.19 +/- 0.02 pmol/mg protein/5 min) of cGMP accumulation. The stimulatory effect of ANF (1.59 +/- 0.07 pmol/mg protein/5 min) was attenuated (0.75 +/- 0.06 pmol/mg protein/5 min, p less than 0.01, n = 6) by preincubation of the cells with pertussis toxin but not by cholera toxin. ANF (4.56 +/- 0.93 pmol/mg protein/5 min, n = 8) did not affect cAMP accumulation (4.32 +/- 0.98 pmol/mg protein/5 min) in hKT cells. This is the first report of an ANF responsive human renal cell line, and its use should facilitate investigation of ANF-receptor interactions.
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PMID:Atrial natriuretic factor effects on cyclic nucleotides in a human renal cell line. 256 5

This paper reports in vivo protein adsorption onto polymers, including Biomer, PEO grafted Biomer (B-PEO-4K), heparin immobilized Biomer with PEO spacers (B-PEO-4K-HEP), and HEMA-Styrene block copolymer (H-S). Vascular grafts (6 mm ID, 7 cm in length) were fabricated with Biomer, coated on their luminal surfaces with test polymers, and implanted into the abdominal aorta of dogs. After 3 weeks-1 month, the grafts were retrieved and processed for TEM and SEM. TEM measured the thickness of adsorbed protein layers stained with a OsO4 solution, and the distribution pattern of adsorbed proteins (albumin, IgG and fibrinogen) using the immunoperoxidase technique. Retrieved grafts of Biomer and B-PEO-4K showed mural thrombi along the graft length, while thrombus formation on B-PEO-4K-HEP and H-S grafts was limited to the anastomotic sites. SEM pictures of B-PEO-4-HEP and H-S surfaces demonstrated clear morphology, with minimal platelet adhesion and activation, and microthrombi. Biomer and B-PEO-4K demonstrated a thick proteinaceous layer (1000-2000 A), whereas B-PEO-4K-HEP and H-S showed what can be described as a monolayer protein thickness (200-300 A). B-PEO-4K-HEP and H-S showed a monolayer-like adsorbed protein pattern, with high concentrations of albumin and IgG, and less fibrinogen, while Biomer and B-PEO-4K showed multilayered patterns with relatively high concentrations of fibrinogen, and less albumin. These results suggest that the surface properties of polymer may control protein adsorption pattern, and the composition of adsorbed protein is essential to in vivo long-term blood compatibility.
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PMID:In vivo protein adsorption onto polymers: a transmission electron microscopic study. 268 16

Histamine (HA) may participate in the neuroendocrine regulation of pituitary hormone secretion. HA diphosphate infused iv for 120 min in a dose of 9, 18, 30, or 50 micrograms/kg BW.h to six normal men stimulated PRL secretion in a dose-dependent manner [absolute change in PRL (delta PRL) area = 52 X (HA dose) - 618; r = 0.9926; P less than 0.001]. The stimulatory effect of HA was modest and occurred during the second hour of infusion. This increase might be due to the opposing effects of HA on PRL secretion, specifically stimulation via H1 receptors and inhibition via H2 receptors. The PRL-releasing effect of 11 micrograms HA dihydrochloride was not significantly different from that of an equimolar dose of HA diphosphate (18 micrograms). Selective activation of H2 receptors by combined infusion of HA and the H1 receptor antagonist mepyramine inhibited PRL secretion compared to the effect of NaCl [delta PRL, -55 +/- 23 (+/- SEM) vs. -20 +/- 17 microIU/ml; P less than 0.01; n = 6). Mepyramine infused alone had no effect (delta PRL, -43 +/- 22 vs. -33 +/- 30 microIU/ml; n = 6). Selective activation of H1 receptors by combined infusion of HA and the H2 receptor antagonist cimetidine stimulated PRL secretion (delta PRL, 193 +/- 40 vs. -20 +/- 17 microIU/ml; P less than 0.0005; n = 6). When infused alone, cimetidine had only a modest and late stimulatory effect (delta PRL, 35 +/- 22 vs. -27 +/- 15; P less than 0.025; n = 6). Dopamine receptor blockade with metoclopramide (MET; 10 mg, three times daily, orally) did not prevent the PRL-inhibiting action of H2 receptor activation (delta PRL, -374 +/- 70 vs. -184 +/- 107 microIU/ml; P less than 0.01; n = 6), whereas the PRL-stimulating effect of H1 receptor activation was abolished by the drug (delta PRL, -249 +/- 64 vs. -174 +/- 54 microIU/ml; n = 6). The latter effect of MET was not due to exhaustion of the lactotrophs, since 200 micrograms TRH stimulated PRL secretion during MET treatment. These findings suggest that the H1 receptor-mediated PRL-stimulating effect of HA occurs through an inhibition of the dopaminergic system, whereas the H2 receptor-mediated PRL-inhibiting effect of HA does not involve dopaminergic neurons.
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PMID:Histaminergic regulation of prolactin secretion: dose-response relationship and possible involvement of the dopaminergic system. 394 33

Temperature-sensitive (ts) mutants of the rhabdoviruses vesicular stomatitis virus and Chandipura virus have been used to measure the appearance of virus antigen on the surface of infected cells by the technique of surface analysis by bacterial adherence and scanning electron microscopy (SABA/SEM). The number of staphylococci specifically adhering to antiserum-treated infected PTK-2 or BSC-1 cells at permissive (31 degrees C) and restrictive (39 degrees C) temperatures was followed in time-course experiments and a close correspondence was observed between the proportion of staphylococci bound at 39 degrees C and the known phenotypic properties of the ts mutants. Virus surface antigen was undetected in cells infected by transcription- and replication-defective ts mutants with thermolabile L proteins under restrictive conditions up to an input multiplicity of infection of 50, and in cells infected by a replication-defective NS protein mutant. Some surface antigen was detected late in infection in PTK-2 cells infected by a replication-defective N protein mutant. Surface antigen accumulated normally in maturation-defective mutants with lesions in envelope proteins. These results establish the suitability of the SABA/SEM technique for quantitative estimation of virus antigen on the surface of infected cells.
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PMID:Measurement of surface antigen by specific bacterial adherence and scanning electron microscopy (SABA/SEM) in cells infected by vesiculovirus ts mutants. 627 72


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