Publications by authors named "Stig-Frederikt Koelle"

Rats were given glycyl-L-glutamine (Gly-Gln) by intraaortic infusion with Alzet osmotic pumps during the 48-hr period following the intraaortic administration of diisopropyl phosphorofluoridate (DFP) (10 mumol/kg). The infusion of 1.2 mumol of Gly-Gln per 24 hr resulted in a significant increase in the acetylcholinesterase (AcChoEase; acetylcholine acetylhydrolase, EC 3.

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We developed a histochemical method for localizing neurotoxic esterase (NTE), defined as the phenylvalerate (PV)-hydrolyzing esterase that is resistant to 40 microM paraoxon (A) but inactivated by paraoxon plus 50 microM mipafox (B). NTE is considered to be the target enzyme in the production of organophosphorus ester-induced delayed neurotoxicity (OPIDN). Cryostat sections were incubated in a medium containing alpha-naphthyl valerate and 6-benzamido-4-methoxy-m-toluidine diazonium chloride (fast violet B) after treatment with the above-mentioned inhibitors, leading to formation of an aqueous insoluble precipitate at sites of enzymatic activity.

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We examined 38 patients with scleroderma, 10 with systemic lupus and 10 normal subjects for Scl-70 antibodies by the gel precipitation and by the immunoblot methods. Increased incidence of Scl-70 antibodies in scleroderma were found by the immunoblot method (55%) compared to the gel precipitation methods (40 or 42% depending on the test kits used). Immunoblot analysis of the antigen prepared with 4.

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The 24-hr intracarotid infusion of plasma-treated glycyl-L-glutamine (3 microM) produced significant enhancement of the monomeric G1 and tetrameric G4 forms of acetylcholinesterase of the cat superior cervical ganglion 48 hr after denervation, in comparison with denervated, noninfused controls. No significant effect of glycyl-L-glutamine could be demonstrated 4 or 6 days after denervation. These findings are consistent with the conclusion, drawn from a previous in vitro study, that glycyl-L-glutamine acts at a stage prior to the aggregation of the G1 form into higher polymers to maintain the acetylcholinesterase content of denervated ganglia.

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The visual fields of 30 patients (subjects) with glaucoma were sent to six experienced clinicians (observers). Each subject had at least four visual field examinations on the OCTOPUS 201 automated perimeter spanning at least one year. Each observer was asked to review the visual field data of each subject and determine whether the visual fields were stable, improved, or worse over time.

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Normal and preganglionically denervated cat superior cervical ganglia were sectioned and cultured for 24 or 48 hr, with or without preliminary inactivation of acetylcholinesterase, and in the presence or absence of 10(-5) M glycyl-L-glutamine. They were then homogenized, and the molecular forms of acetylcholinesterase were analyzed by sucrose gradient sedimentation. We observed an increased proportion of the globular monomeric G1 form, and to a lesser extent of the dimeric G2 and tetrameric membranous G4 forms, of acetylcholinesterase in the glycyl-L-glutamine-treated compared with the control cultures.

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Twenty-three selected patients presenting with massive bleeding from peptic ulcers underwent emergency parietal cell vagotomy (PCV). Nineteen patients had a duodenal ulcer, two a prepyloric ulcer, and one a gastric ulcer. The patients were studied retrospectively with regard to postoperative mortality and morbidity, early rebleeding, and recurrent ulceration.

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We analyzed the activities of acetylcholinesterase and butyrylcholinesterase, and of the metabolic enzymes enolase and lactate dehydrogenase, in the superior cervical ganglion, ciliary ganglion, dorsal root ganglion, stellate ganglion, and caudate nucleus of the cat; we found that these tissues possess very different levels of enzymic activities. The proportions of the alpha alpha, alpha gamma, and gamma gamma enolase isozymes are also quite variable. We particularly studied the molecular forms of acetylcholinesterase and butyrylcholinesterase, in normal tissues and in preganglionically denervated SCG, in comparison with earlier histochemical findings.

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Intracarotid infusion of glycyl-L-glutamine (Gly-Gln) was shown previously to oppose the fall in the acetylcholinesterase and butyrylcholinesterase contents of the cat superior cervical ganglion (SCG) that otherwise follows preganglionic denervation. However, its effect was demonstrable only on the vascularly remote left SCG but not on the directly infused right SCG. Accordingly, it was concluded that a metabolite of Gly-Gln, formed in the blood, is an active neurotrophic factor.

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Nineteen patients undergoing argon laser trabeculoplasty for open-angle glaucoma were studied prospectively. All patients had glaucomatous visual field defects with inadequate medical control of intraocular pressure (IOP) before laser treatment. All patients had two automated visual fields immediately before laser treatment.

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In continuation of previous studies, the intraarterial fusion of L-glutamic acid for 24 hr was found to oppose the decrease in acetylcholinesterase and butyrylcholinesterase in the superior cervical ganglion of the cat that otherwise occurs 48 hr after preganglionic denervation. The combination of glutamic acid and gamma-aminobutyric acid, in concentrations that were inactive individually, likewise produced the same neurotrophic effect. Inactive in this respect were glycine plus L-glutamine, pyroglutamic acid, gamma-aminobutyric acid, and L-aspartic acid.

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Because of the importance of the detection of antibodies to RNP and Sm in the diagnosis of mixed connective tissue disease, systemic lupus erythematosus and certain forms of systemic sclerosis, the various factors which influence the sensitivity of the gel precipitation method for the detection of these antibodies were investigated. The agarose concentration, thickness, well sizes and distance between wells influence the sensitivity of the precipitin reactions. Suitable conditions for a sensitive and reproducible test system are specified.

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In continuation of previous reports, it was found that the neurotrophic factor (NF) of the central nervous system of the cat for the maintenance of acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.

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Ciliary ganglia (CG) of cats were stained for acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) by the bis-(thioacetoxy) aurate (I), or Au(TA)2, method for examination by electron microscopy. Acetylcholinesterase was localized along the axolemmas of the preganglionic fibers and their terminals and on the plasmalemmas of the perikarya and dendrites of the ganglion cells, as in the cat superior cervical ganglion (SCG). In contrast to the SCG, AChE was also found in significant amounts in the rough endoplasmic reticulum of the CG cells and dendrites, and in varying but high concentrations in channels of extracellular space in the complex capsular region surrounding the perikarya and dendrites.

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The superior cervical ganglion (SCG), pineal body (PB), and liver (L) of the rat, rabbit and cat were stained for monoamine oxidase (MAO) A and B by the tetranitro blue tetrazolium (TNBT) and coupled peroxidase ( PerOx ) methods, using 5-hydroxytryptamine (5HT), tryptamine ( Tryp ), tyramine (Tyr), and benzylamine (Bz) as substrates, and clorgyline (Cl) and deprenyl (Dep), both at 10(-7) M, as selective inhibitors. The nodose ganglion (NG) and dorsal root ganglion (DRG) of the rabbit and cat were also studied. The results with rat tissues were consistent with published quantitative findings (SCG, MAO-A much greater than B; PB, MAO-A less than or equal to B; L, MAO-A = B).

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In continuation of a previously reported study, the superior cervical ganglia of cats were preganglionically denervated bilaterally under sodium pentobarbital anesthesia. The following day cats were reanesthetized and infused via the common carotid artery with an aqueous extract of cat brain, spinal cord, and sciatic nerves for periods of 24, 12, 6, and 3 hr, without ligation of the external carotid or lingual arteries as was done previously. Values for acetylcholinesterase and butyrylcholinesterase of superior cervical ganglia at 48 hr postdenervation were all considerably above those of denervated controls.

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Under sodium pentobarbital anesthesia, the superior cervical ganglia of cats were preganglionically denervated bilaterally. The following day cats were reanesthetized, the external carotid and lingual arteries were ligated bilaterally, and the right common carotid artery was infused for 24 hr with an extract prepared from cat brain, spinal cord, and sciatic nerves, with and without the incorporation of aprotinin, an inhibitor of proteases. They were sacrificed 48 hr after denervation, and the acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.

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Measurements of patient serum complement components C3 and C4 are useful indicators of complement consumption in immune complex diseases. A fluorometric quantitative immunofluorescence system was evaluated in terms of measuring these complement components, and the results were compared with those of radial immunodiffusion assays. For comparison of the two systems, 232 patient sera were evaluated for C3, and 202 specimens were tested for C4.

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Experiments were designed to test the hypothesis that ganglionic butyrylcholinesterase (BuChE) is derived from acetylcholinesterase (AChE). At 5 to 8 days following preganglionic denervation of the right superior cervical ganglion (SCG), cats were given sarin, 2.0 mumol/kg, i.

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Mouse phrenic nerve-hemidiaphragm preparations were incubated for 10 min at 37 degrees C in an oxygenated medium containing all the constituents reported as essential for the sodium-dependent high-affinity choline uptake system, including [3H]choline chloride, 3.1 Ci/mmol, 2.5 microM.

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