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Biomedical subjects

B W Wilson

Publications and source records attributed to B W Wilson.

At least 73 records · Page 4Linked to original sources
PubMed1988

Toxicity of an acute dose of agent VX and other organophosphorus esters in the chicken.

The neurotoxicities of single doses of a chemical warfare agent VX [phosphonothioic acid, methyl-S-(2-[bis(1-methylethyl)amino/ethyl) O-ethyl ester], a metabolite of the agricultural chemical parathion, paraoxon, PO (phosphonothioic acid, diethyl paranitrophenyl ester), and the known neuropathic agents DFP] phosphorofluoridic acid, bis(1-methylethyl) ester] and TOCP (phosphoric acid, tri-o-tolyl ester) were compared in the chicken. Single injections (subcutaneous, sc) of VX as high as 150 micrograms/kg (5 times the LD50, intramuscular, im) were tolerated by laying tens if atropine and 2-pralidoxime were used as antidotes before and immediately after injection. The 150 of VX for inhibition of chicken brain acetylcholinesterase was approximately 5 X 10(-10). Plasma acetylcholinesterase, but not butyrylcholinesterase, was depressed 2 h after injections of 2-20 micrograms VX/kg im without antidotes. Levels of plasma enzymes such as creatine kinase, indicative of tissue damage, were increased after exposure to both VX and PO. Injections of up to 150 micrograms/kg of VX with antidotes did not cause locomotor or histological signs of organophosphorus-induced delayed neuropathy, but single injections of 400 mg TOCP/kg did.

Acetylcholinesterase↗
PubMed1988

Toxicity of repeated doses of organophosphorus esters in the chicken.

Hens were repeatedly exposed to paraoxon (PO, phosphonothioic acid, diethyl paranitrophenyl ester), the chemical warfare agent VX/phosphorofluoridic acid, methyl-S-(2-[bis(1-methylethyl)amino/ethyl)O-ethyl ester], or the neuropathic DFP [phosphorofluoridic acid, bis(1-methylethyl)ester] as evidence was sought for nerve or other tissue damage following long-term treatments at high dose levels. Thirty-day and 90-d trials were performed in which each bird was injected 3 or 5 times per week with atropine as protection, weighed, their eggs collected, and their blood enzymes (cholinesterases creatine kinase, and lactic dehydrogenase) and locomotion periodically examined. Muscle and brain enzymes were assayed at the end of the experiments. Doses of PO and VX were at or above LD50 levels. DFP doses were lowered with each run to estimate a no-observable-effect level for organophosphate-induced delayed-neuropathy (OPIDN). No abnormalities attributable to repeated exposures to either PO or VX were found, even though acute, short-term symptoms of toxicity appeared after each injection. No evidence for OPIDN was obtained with repeated exposures to PO and VX under conditions where OPIDN was caused by DFP. Histological signs of OPIDN appeared in the spinal cord without gross symptoms of ataxia following repeated treatments of 25 mg/kg of DFP. The results of one experiment suggested that exposure to protective injections of atropine delays the appearance of the locomotor symptoms of the DFP-induced neuropathy.

Animals↗
PubMed1988

Glucocorticoids in muscular dystrophy: beneficial effects of dexamethasone on avian myopathy.

A corticosteroid with mixed glucocorticoid-mineralocorticoid actions was previously shown to improve neuromuscular function in muscular dystrophic chickens. The significance of that finding was recently underscored by reports that a mixed-action corticosteroid improved muscle function in Duchenne dystrophy patients, albeit at high doses. In the present study a pure glucocorticoid improved function and retarded muscle histopathology in the chicken, but a pure mineralocorticoid did not. These observations suggest that elucidation of mechanisms by which glucocorticoids beneficially affect dystrophic muscle could lead to development of more effective therapies.

Acetylcholinesterase↗
PubMed1988

Combined paraesophageal and sliding hiatal hernia.

We have reported a case of a large paraesophageal herniation with a small sliding component. Abnormal positioning of the esophagogastric junction or the necessity for mobilizing it during repair requires the addition of an antireflux procedure to the standard reduction and repair. Elective repair of a paraesophageal herniation, even in the absence of limiting symptoms, is warranted, since complications of nonsurgical treatment may be sudden and severe.

Esophagogastric Junction↗
PubMed1988

Inbred crosses and inherited muscular dystrophy of the chicken.

Inbred normal and genetically dystrophic chickens of New Hampshire and White Leghorn backgrounds, respectively, have been crossed to yield hybrids of normal and dystrophic genotypes in order to provide genetically homogeneous but heterozygous experimental animals. This study examined carcass and pectoral muscle weights, pectoral muscle fiber diameters, serum creatine kinase (CK) levels, muscle acetylcholinesterase (AChE), lactic dehydrogenase (LDH), and creatine kinase, and response to daily injections of corticosterone-21-acetate (C21A) of these hybrid chickens and their inbred parental lines. With the exception of pectoral muscle weight, dystrophic hybrids exhibited symptoms of dystrophy: high serum CK and high muscle AChE and low LDH levels. The results support the hypothesis that neither early muscle fiber hypertrophy nor atrophy is invariably associated with expression of the dystrophic gene; both are the result of secondary gene interactions. One experiment showed that muscle AChE levels decreased and LDH levels rose after C21A treatments.

Animals↗
PubMed1988

Atropine and DFP-induced delayed neurotoxicity.

Atropine is often given as an antidote for acute cholinergic effects in studies of a delayed neuropathy (OPIDN) caused by some organophosphorus esters. These experiments examined if atropine would also affect the onset and/or severity of signs of OPIDN. Chickens were given one to six 200 micrograms/kg doses of diisopropyl phosphorofluoridate (DFP) with or without 20 mg/kg atropine (IM). Locomotion, brain neurotoxic esterase (NTE) activity, and histology of the nervous system were examined. The results demonstrated that atropine treatments delayed onset of the signs of OPIDN and may have slightly increased brain NTE activity in vivo. Relatively high levels (Ki: approximately 3.0 mM) of atropine inhibited NTE activity in vitro.

Animals↗
PubMed1988

DFP-induced elevation of strength-duration threshold in hen peripheral nerve.

Previous research has indicated that organophosphorus agents which induce a delayed neuropathy also elevate the strength-duration threshold during the progression of the neuropathy. To establish further the correlation between strength-duration changes and delayed neuropathy, the purpose of the present study was to investigate the biochemical and electrophysiological effects of two additional agents: diisopropylflourophosphate (DFP) and phosphonothioc acid, methyl-[2-(dimethylamino)-ethyl]O-ethyl ester (VX). DFP-treated hens exhibited clinical signs of toxicity at the time of electrophysiologic recording and biochemical analysis. DFP treatment also resulted in significantly elevated thresholds of the strength-duration curves of both the sciatic and tibial nerves. The VX-treated animals exhibited no clinical signs, despite aggressive dosing, and there were no significant changes in the electrophysiologic characteristics (conduction velocity, relative refractory period, strength-duration threshold) of either peripheral nerve. Acetylcholinesterase activities of the brain and skeletal muscle were significantly reduced in the VX- and DFP-treated hens, whereas creatine phosphokinase activities in these tissues were unaffected. These results are consistent with the view that elevation of the strength-duration threshold in peripheral nerves is among the earliest indicators of organophosphorus-induced delayed neuropathy.

Acetylcholinesterase↗
PubMed1987

Chemical basis for photomutagenicity in synthetic fuels and correlation with carcinogenicity.

Photomutagens (chemicals that enhance the mutagenicity of non-ionizing radiation) have been detected in experimental coal- and oil shale-derived synthetic fuel samples using Salmonella typhimurium strain TA98 and fluorescent light. In this study, photomutagenic activity was measured among distillation and chemical class fractions from a blend of direct coal liquefaction process materials. Photomutagenicity increased with increasing boiling point and was concentrated in fractions enriched in neutral polycyclic aromatic compounds (neutral PACs). The photomutagenic activities of the materials tested correlate well with the previously reported tumorigenic activities of the same samples on mouse skin, but correlate poorly with the previously reported mutagenic activities of the same samples in the Salmonella/mammalian-microsome test (using strain TA98), in which neutral PAC-enriched fractions were not active. These data suggest that relatively high boiling neutral PACs are important chemical photomutagens in synthetic fuels and suggest the potential use of the photomutation assay as an improved, relatively simple, inexpensive and short-term bioassay for detecting carcinogens as mutagens in complex mixtures such as synthetic fuels.

Animals↗
PubMed1987

The isolation and characterisation of the ovine growth hormone gene.

The ovine growth hormone gene has been isolated and sequenced, together with about 1 kbp of DNA flanking each end of the gene. The structure of the gene is similar to that found for other growth hormone genes, particularly the bovine gene, and has a primary transcript of 1792 bp, with five exons, and with intron sizes of 264 bp, 231 bp, 227 bp and 273 bp. The gene is flanked by artiodactyl-specific middle-repetitive DNA, consisting mainly of elements belonging to the 'C-A3' family of repeated DNA. A previously unreported sequence has been found, which we have named an 'E' element.

Amino Acid Sequence↗
PubMed1987

Solubilization of Leonardite by an Extracellular Fraction from Coriolus versicolor.

Coriolus versicolor has previously been shown to degrade leonardite, an oxidized form of lignite. An extracellular fraction containing protein purified from a C. versicolor culture solubilized leonardite in vitro. Expression of the activity did not require the presence of leonardite and appeared during idiophase. During ion-exchange and gel filtration column chromatography, leonardite-biosolubilizing activity eluted with syringaldazine oxidase activity and with protein, as measured by A(280) and the biuret protein assay. Syringaldazine is a substrate of the polyphenol oxidase formed by C. versicolor. Comparison of leonardite-biosolubilizing activity with the effects of chelators and surface-active agents on leonardite showed that biosolubilization was not due to either surfactant or chelating ability. Heat treatment of the preparation at 60 degrees C for 30 min significantly reduced both syringaldazine oxidase and leonardite-biosolubilizing activities. Cyanide, azide, and thioglycolate, which are known inhibitors of syringaldazine oxidase activity of C. versicolor, also inhibited leonardite biosolubilization. From these data, we conclude that the purified protein fraction from C. versicolor contains a syringaldazine oxidase activity that participates in leonardite biosolubilization by enzymatic action.

Journal Article↗
PubMed1986

Isofenphos and an in vitro activation assay for delayed neuropathic potential.

Organophosphorus compounds (OPs) that cause organophosphorus ester-induced delayed neuropathy (OPIDN) generally inhibit neurotoxic esterase (NTE). However, the assay itself, when conducted in vitro, misses OPs that are activated into OPIDN-causing agents in the body. A preparation of liver mixed-function oxidases and brain NTE was used to rapidly detect activations of OPs. The compounds (0.1 mM or less) to be tested were incubated with microsomes isolated from livers of phenobarbital-treated chick embryos (P-450 content averaged 1.81 +/- 0.27 nmol/mg protein, means +/- SD, N = 5) and NTE (average of 13.8 nmol/min/mg protein) from untreated chick embryo brains. The NTE was separated by calcium precipitation and its activity assayed as usual. The low inhibitions of NTE of compounds that were not neurotoxic (parathion, Diazinon) did not increase in the presence of NADPH; inhibitions of NTE of compounds that required activation (leptophos, S,S,S-tri-n-butyl phosphorotrithioate, and tri-o-cresyl phosphate) greatly increased with NADPH. Both the recently identified neuropathic OP isofenphos (IFP) and its oxon required activation to inhibit NTE (inhibitions of 20 and 80%, respectively). Evidence is presented that the possible neuropathic metabolite is des-N-isopropyl IFP oxon.

Animals↗
PubMed1986

60-Hz electric-field effects on pineal melatonin rhythms: time course for onset and recovery.

Rats exposed for 3 weeks to uniform 60-Hz electric fields of 39 kV/m (effective field strength) failed to show normal pineal gland circadian rhythms in serotonin N-acetyl transferase activity and melatonin concentrations. The time required for recovery of the melatonin rhythm after cessation of field exposure was determined to be less than 3 days. The rapid recovery suggests that the overall metabolic competence of the pineal is not permanently compromised by electric-field exposure, and that the circadian rhythm effect may be neuronally mediated.

Animals↗
PubMed1986

Serum regulation of acetylcholinesterase in cultured myotubes.

A large (20S) collagen-tailed form of acetylcholinesterase associated with the neuromuscular junction appears in cultures of chick embryo muscle cells when horse serum is withdrawn from the medium. In this report, 10-day-old cultures were incubated 2 days in serum-free medium or in medium containing either horse, bovine, fetal calf, chicken, heat-treated horse or chicken serum, low (less than 100K) or high (less than 100K) molecular weight fractions of horse serum, or fibronectin. Total acetylcholinesterase activity and activity of the 20S form increased in medium without serum, with fetal calf serum and with the low-molecular-weight fraction of horse serum. The largest increase occurred with fibronectin. The results suggest that a factor(s) greater than 100K in adult sera inhibits total acetylcholinesterase production and formation of the 20S form of the enzyme.

Acetylcholinesterase↗
PubMed1986

Pulmonary histiocytosis X. Immunoperoxidase staining for HLA-DR antigen and S100 protein.

Immunoperoxidase staining for S100 protein and HLA-DR antigen was used to identify histiocytosis X (HX) cells in 23 cases of pulmonary histiocytosis X (PHX), three cases of idiopathic pulmonary fibrosis, and one case of hypersensitivity pneumonitis. S100 protein was present in HX cells in 22 of the PHX cases; HLA-DR antigen was present in HX cells from 16 cases. Varying numbers of peribronchiolar and interstitial cells were positive for either S100 or HLA-DR in two of the three cases of idiopathic pulmonary fibrosis, and in the case of hypersensitivity pneumonitis. Immunoperoxidase staining for chromogranin showed isolated neuroendocrine cells within the mucosa and wall or airways, sites in which HX cells were occasionally found. As other types of dendritic cells, as well as some neuroendocrine cells, may contain S100 protein, positive staining for S100 is not specific for HX cells.

Chromogranins↗
PubMed1985

Comparative chemical and biological analysis of coal tar-based therapeutic agents to other coal-derived materials.

In this study, methodologies developed for the analysis of synthetic fuel products were applied to the coal tar fractions isolated from coal tar-based pharmaceutical products. A pharmaceutical stock solution of 20% coal tar in alcohol, a 50% coal tar bath emulsion and a 4.3% coal tar shampoo were studied. The toxicology and chemical composition of the coal tar fractions isolated from these materials were compared with an industrial coal tar and with a direct-liquefaction coal liquid product. The coal tars and coal liquid product were fractionated into chemical classes by alumina column chromatography and individual components were identified and quantitated by high-resolution gas chromatography. The microbial mutagenicity of these materials was measured against S. typhimurium, TA 98. In addition, the industrial coal tar, coal-liquid product, and coal tar isolate from the 20% coal tar in alcohol solution were tested for initiating activity in an initiation/promotion mouse skin painting assay for carcinogenicity. The chemical compositions of the coal tar-based therapeutic agents, the industrial coal tar and direct-liquefaction coal liquid were similar. With the exception of the 50% bath emulsion, the microbial mutagenicity and tumor-initiating activity in mouse skin for those materials tested were also similar.

Animals↗
PubMed1984

Percutaneous absorption of triadimefon in the adult and young male and female rat.

The percutaneous absorption of 14C-phenoxy ring labeled triadimefon was studied in adult and young male and female Sprague-Dawley rats. Triadimefon was applied (41.1 to 46.4 micrograms/cm2) in 0.2 ml of acetone to areas comprising 3% of the body surface (7.0 to 14.5 cm2). Thirty-six animals were treated at the initiation of each study. Groups of three animals were subsequently killed at 1, 4, 8, 12, 24, 48, 72, 96, 120, 144, 168, and 192 hr after treatment. Skin from the treated area as well as blood, heart, liver, kidneys, remaining carcass, urine, and feces were analyzed for 14C by scintillation counting techniques. Based on 14C counts, triadimefon was lost more rapidly from the skin of young animals (t 1/2, 20 to 25 hr) than from the skin of adult animals (t 1/2, 29 to 53 hr). Recovery studies indicated that adult males, adult females, young males, and young females, respectively, absorbed 53, 82, 57, and 52% of the dose. The rest of the dose based on material balance was presumably lost by evaporation. Approximately 2.5 to 3.9% of the dose penetrated the skin in one hour and was available for absorption. The rate of entry triadimefon into blood was 2 to 2.5 times faster for young than that observed in adult animals. Elimination of it from blood was faster in the case of the young animals. Triadimefon was absorbed through the skins of the adult male, adult female, young male, and young female rats, respectively, at rates of 0.20, 0.50, 0.58, and 0.48 micrograms/hr/cm2 of skin.

Absorption↗
PubMed1984

Drugs in muscular dystrophy of the chicken: corticosterone-21-acetate.

In a previous series of 22-day evaluations of 31 compounds, only corticosterone-21-acetate (C-21-A) increased righting ability of genetically dystrophic chickens to a greater extent than the standard of comparison, methysergide maleate. In the present study, C-21-A was subjected to longer-term trials of up to 48 days, and additional signs of the myopathy were examined. The highest doses of C-21-A increased righting ability for the duration of the trials, decreased the typically elevated plasma levels of creatine kinase (CK) activity by more than 80%, and improved morphology of the dystrophic pectoralis major muscle at the light microscopic level. The major adverse effect of C-21-A, reduction of body weight, was consistently observed at the relatively high doses needed to increase righting ability. That alone, however, could not account for increased righting ability, and plasma CK activity was decreased even at doses that did not reduce body weight. The results show that C-21-A is the most effective compound yet tested in this system and, perhaps more significantly, provides the first evidence that it is possible to identify compounds that improve muscle morphology in a hereditary myopathy using a short-term, step-wise system.

Animals↗