The Experts below are selected from a list of 183 Experts worldwide ranked by ideXlab platform
Dennis W. Blick - One of the best experts on this subject based on the ideXlab platform.
-
Acute Behavioral Toxicity of pyridostigmine or soman in primates.
Toxicology and Applied Pharmacology, 1994Co-Authors: Dennis W. Blick, G C Brown, M.g. Yochmowitz, J W Fanton, Mike Murphy, Stanley L. HartgravesAbstract:Abstract Effects of a peripherally active carbamate (pyridostigmine bromide) and a centrally active organophosphate (OP) nerve agent (soman) on performance by rhesus monkeys of a compensatory tracking (primate equilibrium platform, or PEP) task were measured using a balanced Latin-square design to determine the ED50 for pyridostigmine (0.66 mg/kg) and the up-and-down (titration) method to determine the ED50 for soman (2.50 μg/kg). We concluded that the PEP performance model is a sensitive and reliable indicator of anticholinesterase (anti-ChE) Behavioral Toxicity. We also found that soman, an irreversible inhibitor of acetylcholinesterase (AChE), is more than 100 times more Behaviorally disruptive than the reversible peripheral inhibitor pyridostigmine, as indicated by the difference in ED50 doses expressed in molar terms. Soman′s Behavioral Toxicity is severe at levels of serum cholinesterase inhibition (70-80%) at which pyridostigmine does not significantly affect performance. As a prophylactic treatment for OP agent poisoning, pyridostigmine has a substantial safety factor, since Behavioral Toxicity becomes significant only at approximately four times the proposed therapeutic dose.
-
Behavioral Toxicity of anticholinesterases in primates: effects of daily repeated soman exposure.
Pharmacology biochemistry and behavior, 1994Co-Authors: Dennis W. Blick, G C Brown, Frank R. Weathersby, M R MurphyAbstract:The effects of repeated daily exposure to soman, an organophosphate nerve agent, on the performance of a well-learned, compensatory tracking task were tested in rhesus monkeys. The ED50 daily exposure required to produce a performance decrement on or before the fifth daily exposure (0.97 microgram/kg) was about 40% of the acute dose required to produce a similar performance decrement. After repeated, low-dose exposures, performance decrements appeared when serum cholinesterase (ChE) activity was inhibited 85-90%. Acute exposures that produced similar performance effects were associated with lower levels of ChE inhibition (65-70%), suggesting that repeated daily exposure may lead to the development of a tolerance (physiological or Behavioral) to low levels of ChE activity.
-
Behavioral Toxicity of anticholinesterases in primates : chronic physostigmine and soman interactions
Pharmacology biochemistry and behavior, 1993Co-Authors: Dennis W. Blick, G C Brown, Stephanie A. Miller, M R MurphyAbstract:Dose rates for continuous infusion of physostigmine salicylate required to inhibit 30 and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous physostigmine infusion at these dose rates on the Behavioral Toxicity of daily repeated low-dose soman were determined not to be deleterious; in fact, they were slightly (and variably) protective.
-
Behavioral Toxicity of anticholinesterases in primates: chronic pyridostigmine and soman interactions.
Pharmacology biochemistry and behavior, 1991Co-Authors: Dennis W. Blick, M R Murphy, G C Brown, Sandra Z. Kerenyi, S Miller, Stanley L. HartgravesAbstract:Dose rates for continuous infusion of pyridostigmine bromide required to inhibit 30% and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous pyridostigmine infusion at these dose-rates on the Behavioral Toxicity of 5 daily repeated low-dose exposures to a toxic organophosphate (soman) were determined not be deleterious; in fact, they were slightly (and variably) protective. Relative to controls (5-day soman ED50 = 0.89 micrograms/kg/day), pyridostigmine infusions producing 30% and 60% inhibition produced 5-day ED50s of 1.25 and 1.11 micrograms/kg/day, respectively. Variability in response to the pyridostigmine-soman combinations appeared to be greater than in response to daily soman exposure without pyridostigmine infusion.
M Stanley - One of the best experts on this subject based on the ideXlab platform.
-
Antidepressants and suicide risk: issues of chemical and Behavioral Toxicity.
Journal of Clinical Psychopharmacology, 1992Co-Authors: A Molcho, M StanleyAbstract:Recent reports have described several patients who experienced suicidal preoccupation while being treated with antidepressant drugs. This phenomenon has been interpreted as antidepressant-induced suicidal behavior. The association of antidepressant medication with suicide was noted early in their clinical use. Antidepressants have been a common cause of suicide when taken in overdose. Epidemiologic studies have reported that antidepressants differ from one another in the frequency with which they are associated with suicide by overdose. This differential association of antidepressants with suicide might support the possibility that certain agents may induce suicidal behavior. However, it seems that the frequency with which an antidepressant is related to suicide by overdose is correlated with each compound's inherent Toxicity. Reported cases of emergence of suicidal preoccupation during fluoxetine treatment have raised the possibility that serotonergic drugs may induce this destructive behavior. Although this hypothesis rests on only a few reported cases, large-scale clinical trials of serotonin uptake inhibitors such as fluoxetine, paroxetine, and sertraline do not support it. Thus, the decreased Toxicity of newer antidepressants such as fluoxetine and other selective serotonergic drugs makes them an attractive choice for treatment of depressed patients who are at risk for suicide. Language: en
-
Antidepressants and suicide risk: issues of chemical and Behavioral Toxicity.
Journal of clinical psychopharmacology, 1992Co-Authors: A Molcho, M StanleyAbstract:Recent reports have described several patients who experienced suicidal preoccupation while being treated with antidepressant drugs. This phenomenon has been interpreted as antidepressant-induced suicidal behavior. The association of antidepressant medication with suicide was noted early in their clinical use. Antidepressants have been a common cause of suicide when taken in overdose. Epidemiologic studies have reported that antidepressants differ from one another in the frequency with which they are associated with suicide by overdose. This differential association of antidepressants with suicide might support the possibility that certain agents may induce suicidal behavior. However, it seems that the frequency with which an antidepressant is related to suicide by overdose is correlated with each compound's inherent Toxicity. Reported cases of emergence of suicidal preoccupation during fluoxetine treatment have raised the possibility that serotonergic drugs may induce this destructive behavior. Although this hypothesis rests on only a few reported cases, large-scale clinical trials of serotonin uptake inhibitors such as fluoxetine, paroxetine, and sertraline do not support it. Thus, the decreased Toxicity of newer antidepressants such as fluoxetine and other selective serotonergic drugs makes them an attractive choice for treatment of depressed patients who are at risk for suicide.
M R Murphy - One of the best experts on this subject based on the ideXlab platform.
-
Behavioral Toxicity of anticholinesterases in primates: effects of daily repeated soman exposure.
Pharmacology biochemistry and behavior, 1994Co-Authors: Dennis W. Blick, G C Brown, Frank R. Weathersby, M R MurphyAbstract:The effects of repeated daily exposure to soman, an organophosphate nerve agent, on the performance of a well-learned, compensatory tracking task were tested in rhesus monkeys. The ED50 daily exposure required to produce a performance decrement on or before the fifth daily exposure (0.97 microgram/kg) was about 40% of the acute dose required to produce a similar performance decrement. After repeated, low-dose exposures, performance decrements appeared when serum cholinesterase (ChE) activity was inhibited 85-90%. Acute exposures that produced similar performance effects were associated with lower levels of ChE inhibition (65-70%), suggesting that repeated daily exposure may lead to the development of a tolerance (physiological or Behavioral) to low levels of ChE activity.
-
Behavioral Toxicity of anticholinesterases in primates : chronic physostigmine and soman interactions
Pharmacology biochemistry and behavior, 1993Co-Authors: Dennis W. Blick, G C Brown, Stephanie A. Miller, M R MurphyAbstract:Dose rates for continuous infusion of physostigmine salicylate required to inhibit 30 and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous physostigmine infusion at these dose rates on the Behavioral Toxicity of daily repeated low-dose soman were determined not to be deleterious; in fact, they were slightly (and variably) protective.
-
Behavioral Toxicity of anticholinesterases in primates: chronic pyridostigmine and soman interactions.
Pharmacology biochemistry and behavior, 1991Co-Authors: Dennis W. Blick, M R Murphy, G C Brown, Sandra Z. Kerenyi, S Miller, Stanley L. HartgravesAbstract:Dose rates for continuous infusion of pyridostigmine bromide required to inhibit 30% and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous pyridostigmine infusion at these dose-rates on the Behavioral Toxicity of 5 daily repeated low-dose exposures to a toxic organophosphate (soman) were determined not be deleterious; in fact, they were slightly (and variably) protective. Relative to controls (5-day soman ED50 = 0.89 micrograms/kg/day), pyridostigmine infusions producing 30% and 60% inhibition produced 5-day ED50s of 1.25 and 1.11 micrograms/kg/day, respectively. Variability in response to the pyridostigmine-soman combinations appeared to be greater than in response to daily soman exposure without pyridostigmine infusion.
Stanley L. Hartgraves - One of the best experts on this subject based on the ideXlab platform.
-
Acute Behavioral Toxicity of pyridostigmine or soman in primates.
Toxicology and Applied Pharmacology, 1994Co-Authors: Dennis W. Blick, G C Brown, M.g. Yochmowitz, J W Fanton, Mike Murphy, Stanley L. HartgravesAbstract:Abstract Effects of a peripherally active carbamate (pyridostigmine bromide) and a centrally active organophosphate (OP) nerve agent (soman) on performance by rhesus monkeys of a compensatory tracking (primate equilibrium platform, or PEP) task were measured using a balanced Latin-square design to determine the ED50 for pyridostigmine (0.66 mg/kg) and the up-and-down (titration) method to determine the ED50 for soman (2.50 μg/kg). We concluded that the PEP performance model is a sensitive and reliable indicator of anticholinesterase (anti-ChE) Behavioral Toxicity. We also found that soman, an irreversible inhibitor of acetylcholinesterase (AChE), is more than 100 times more Behaviorally disruptive than the reversible peripheral inhibitor pyridostigmine, as indicated by the difference in ED50 doses expressed in molar terms. Soman′s Behavioral Toxicity is severe at levels of serum cholinesterase inhibition (70-80%) at which pyridostigmine does not significantly affect performance. As a prophylactic treatment for OP agent poisoning, pyridostigmine has a substantial safety factor, since Behavioral Toxicity becomes significant only at approximately four times the proposed therapeutic dose.
-
Behavioral Toxicity of anticholinesterases in primates: chronic pyridostigmine and soman interactions.
Pharmacology biochemistry and behavior, 1991Co-Authors: Dennis W. Blick, M R Murphy, G C Brown, Sandra Z. Kerenyi, S Miller, Stanley L. HartgravesAbstract:Dose rates for continuous infusion of pyridostigmine bromide required to inhibit 30% and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous pyridostigmine infusion at these dose-rates on the Behavioral Toxicity of 5 daily repeated low-dose exposures to a toxic organophosphate (soman) were determined not be deleterious; in fact, they were slightly (and variably) protective. Relative to controls (5-day soman ED50 = 0.89 micrograms/kg/day), pyridostigmine infusions producing 30% and 60% inhibition produced 5-day ED50s of 1.25 and 1.11 micrograms/kg/day, respectively. Variability in response to the pyridostigmine-soman combinations appeared to be greater than in response to daily soman exposure without pyridostigmine infusion.
G C Brown - One of the best experts on this subject based on the ideXlab platform.
-
Acute Behavioral Toxicity of pyridostigmine or soman in primates.
Toxicology and Applied Pharmacology, 1994Co-Authors: Dennis W. Blick, G C Brown, M.g. Yochmowitz, J W Fanton, Mike Murphy, Stanley L. HartgravesAbstract:Abstract Effects of a peripherally active carbamate (pyridostigmine bromide) and a centrally active organophosphate (OP) nerve agent (soman) on performance by rhesus monkeys of a compensatory tracking (primate equilibrium platform, or PEP) task were measured using a balanced Latin-square design to determine the ED50 for pyridostigmine (0.66 mg/kg) and the up-and-down (titration) method to determine the ED50 for soman (2.50 μg/kg). We concluded that the PEP performance model is a sensitive and reliable indicator of anticholinesterase (anti-ChE) Behavioral Toxicity. We also found that soman, an irreversible inhibitor of acetylcholinesterase (AChE), is more than 100 times more Behaviorally disruptive than the reversible peripheral inhibitor pyridostigmine, as indicated by the difference in ED50 doses expressed in molar terms. Soman′s Behavioral Toxicity is severe at levels of serum cholinesterase inhibition (70-80%) at which pyridostigmine does not significantly affect performance. As a prophylactic treatment for OP agent poisoning, pyridostigmine has a substantial safety factor, since Behavioral Toxicity becomes significant only at approximately four times the proposed therapeutic dose.
-
Behavioral Toxicity of anticholinesterases in primates: effects of daily repeated soman exposure.
Pharmacology biochemistry and behavior, 1994Co-Authors: Dennis W. Blick, G C Brown, Frank R. Weathersby, M R MurphyAbstract:The effects of repeated daily exposure to soman, an organophosphate nerve agent, on the performance of a well-learned, compensatory tracking task were tested in rhesus monkeys. The ED50 daily exposure required to produce a performance decrement on or before the fifth daily exposure (0.97 microgram/kg) was about 40% of the acute dose required to produce a similar performance decrement. After repeated, low-dose exposures, performance decrements appeared when serum cholinesterase (ChE) activity was inhibited 85-90%. Acute exposures that produced similar performance effects were associated with lower levels of ChE inhibition (65-70%), suggesting that repeated daily exposure may lead to the development of a tolerance (physiological or Behavioral) to low levels of ChE activity.
-
Behavioral Toxicity of anticholinesterases in primates : chronic physostigmine and soman interactions
Pharmacology biochemistry and behavior, 1993Co-Authors: Dennis W. Blick, G C Brown, Stephanie A. Miller, M R MurphyAbstract:Dose rates for continuous infusion of physostigmine salicylate required to inhibit 30 and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous physostigmine infusion at these dose rates on the Behavioral Toxicity of daily repeated low-dose soman were determined not to be deleterious; in fact, they were slightly (and variably) protective.
-
Behavioral Toxicity of anticholinesterases in primates: chronic pyridostigmine and soman interactions.
Pharmacology biochemistry and behavior, 1991Co-Authors: Dennis W. Blick, M R Murphy, G C Brown, Sandra Z. Kerenyi, S Miller, Stanley L. HartgravesAbstract:Dose rates for continuous infusion of pyridostigmine bromide required to inhibit 30% and 60% of normal serum cholinesterase activity in rhesus monkeys were determined. The effects of continuous pyridostigmine infusion at these dose-rates on the Behavioral Toxicity of 5 daily repeated low-dose exposures to a toxic organophosphate (soman) were determined not be deleterious; in fact, they were slightly (and variably) protective. Relative to controls (5-day soman ED50 = 0.89 micrograms/kg/day), pyridostigmine infusions producing 30% and 60% inhibition produced 5-day ED50s of 1.25 and 1.11 micrograms/kg/day, respectively. Variability in response to the pyridostigmine-soman combinations appeared to be greater than in response to daily soman exposure without pyridostigmine infusion.