Regulation, risk assessment, and the Supreme Court: the case of OSHA's cancer policy.
Explore the source record for details and available documents.
Forensic Medicine↗
Biomedical subjects
B A Williams
Publications and source records attributed to B A Williams.
Stimulus control and associative learning.
Interest in operant research on stimulus control has declined at the same time that much interest has burgeoned in nonoperant areas. Several examples of this shift toward traditional learning theory are considered, all of which have sponsored theoretical approaches that attempt to characterize the underlying associative units. These theoretical approaches are defended on the grounds that they have generated a deeper understanding of a variety of often puzzling phenomena. My projection is that future research will be determined even more strongly by theories about the structure of associations. Particular issues for which such discussion will have major impact include (1) whether conditional stimulus control is qualitatively different than simpler forms of stimulus control, (2) whether stimulus control is organized hierarchically, and (3) the origin of categories of stimulus equivalence.
Animals↗
Thermoregulatory responses of rats to varying environmental temperatures.
The peripheral (tail) circulatory responses of six male albino rats were measured at ambient temperatures between 5 and 40 degrees C, using impedance plethysmography. Each animal was anesthetized, instrumented, and placed in a thermal environmental chamber to reach equilibrium. Tail blood flow, respiration rate, heart rate, core temperature, and tail skin temperature were then monitored at each ambient temperature. The mean tail blood flow was significantly higher (p less than 0.05) at 5 degrees C than at 10 degrees C. The mean blood flow increased significantly (p less than 0.01) at each of the temperatures above 10 degrees C. Tail skin temperature and internal body (core) temperature increased significantly with increasing ambient temperature.
Animals↗
Absence of endotoxin-fever but not hyperthermia in Brattleboro rats.
I.c.v. administration of bacterial endotoxin produced a fever in the Long-Evans rat but not in the Brattleboro rat. Similar administration of arachidonic acid, prostaglandin E2, prostacyclin, dibutyryl cAMP, norepinephrine, morphine and beta-endorphin caused hyperthermia in both Long-Evans and Brattleboro rats. Variable doses of exogenous arginine vasopressin (AVP) when centrally administered with endotoxin caused fever in the Brattleboro rat. It is suggested that AVP may play an important role in the production and release of endogenous pyrogen.
Animals↗
Cholecystokinin-octapeptide-induced hyperthermia in guinea-pigs.
Intracerebroventricular administration of cholecystokinin-octapeptide (CCK-8) at room temperature (21 degrees C) induced dose-related hyperthermia in guinea-pigs and also produced hyperthermia at low (10 degrees C) and high (30 degrees C) ambient temperatures. CCK-8-induced hyperthermia was direct and not mediated by prostaglandins, norepinephrine, cyclic AMP or naloxone-sensitive receptors.
Animals↗
Central effects of dibutyryl cyclic AMP and GMP on the temperature in conscious rabbits.
Intracerebroventricular (i.c.v.) administration of dibutyryl cyclic AMP (Db-cAMP)- and dibutyryl cyclic GMP (Db-cGMP)-induced hyperthermia in rabbits. Central administration of 4-(3-cyclopentyloxy-4-methoxyphenyl)-2-pyrrolidone (ZK 62711), a selective inhibitor of cAMP phosphodiesterase, only accentuated the hyperthermia due to Db-cAMP whereas a selective inhibitor of cGMP phosphodiesterase, 2-O-proproxyphenyl-8-azapurin-6-one (M and B 22948), only potentiated the hyperthermia caused by Db-cGMP. The hyperthermia due to Db-cAMP and Db-cGMP was not mediated through prostaglandins (PG). In contrast, central administration of an alpha-adrenergic receptor antagonist, phenoxybenzamine, or a beta-adrenergic receptor antagonist, sotalol, only attenuated the hyperthermic response to Db-cAMP while a cholinergic muscarinic receptor antagonist, atropine, specifically antagonized Db-cGMP-induced hyperthermia. I.c.v. administration of a protein synthesis inhibitor, anisomycin, did inhibit the hyperthermia due to Db-cAMP and Db-cGMP. Opiate antagonist, naloxone, did not antagonize Db-cAMP- and Db-cGMP-induced hyperthermia. These results suggest that a protein mediator is implicated in the induction of hyperthermia by Db-cAMP and Db-cGMP and that cAMP and cGMP may be involved through alpha/beta-adrenergic and cholinergic muscarinic receptors respectively in the central regulation of heat production/conservation in rabbits.
Animals↗
Peptide and non-peptide opioid-induced hyperthermia in rabbits.
Intracerebroventricular administration of all three prototype non-peptide opioid receptor (mu, kappa and sigma) agonists, morphine, ketocyclazocine and N-allyl-normetazocine (SKF 10,047) induced hyperthermia in rabbits. Similar administration of peptide opioids like beta-endorphin (BE), methionine-enkephalin (ME) and its synthetic analogue D-ala2-methionine-enkephalinamide (DAME) also caused hyperthermia. As expected, the synthetic enkephalin DAME was more potent than the parent enkephalin. Of the three anion transport systems (iodide, hippurate and liver-like or L) present in the choroid plexus, it is suggested that only the L transport system seems to be important to ventricular inactivation of BE and DAME since iodipamide (an inhibitor of the L transport system) augmented the hyperthermia produced by BE and DAME. Prostaglandins (PG) and norepinephrine (NE) were not involved in peptide and non-peptide opioid-induced hyperthermia because a PG synthesis inhibitor, indomethacin, and an alpha-adrenergic receptor blocker, phenoxybenzamine, had no thermolytic effect on them. Likewise cAMP was not required since a phosphodiesterase inhibitor, theophylline, did not accentuate the hyperthermia due to peptide and non-peptide opioids. Naloxone-sensitive receptors were involved in the induction of hyperthermia by morphine. BE, ME and DAME since naloxone attentuated them. In contrast, the hyperthermic response to ketocyclazocine and SKF 10,047 were not antagonized by naloxone.
Animals↗
Hyperthermic effects of centrally injected (D-ala2, N-Me-Phe4, Met-(O)5-ol)-enkephalin (FK 33-824) in rabbits and guinea-pigs.
Intracerebroventricular administration of (D-ala2, N-Me-Phe4, Met-(O)5-ol)-enkephalin (FK 33-824) induced dose-related hyperthermia in rabbits and guinea-pigs. Prostaglandins (PG) and norepinephrine (NE) were not involved in the hyperthermia induced by FK 33-824 because a cyclooxygenase inhibitor, indomethacin, and an alpha-adrenoceptor antagonist, phenoxybenzamine, had no antagonistic effects. Likewise, cAMP was not required since a phosphodiesterase inhibitor, theophylline, did not accentuate the hyperthermia due to FK 33-824. It is suggested that mu receptors were involved in the induction of hyperthermia by FK 33-824 in rabbits and guinea-pigs since naloxone attenuated it. These results indicate that FK 33-824-induced hyperthermia is not mediated by PG, NE and cAMP, but rather that mu receptors are involved in the induction of hyperthermia by FK 33-824.
Animals↗
Hyperthermic responses to central injections of some peptide and non-peptide opioids in the guinea-pig.
Intracerebroventricular administration of prototype non-peptide opioid receptor (mu, kappa, sigma) agonists, morphine, ketocyclazocine and N-allyl normetazocine (SKF 10,047) and an agonist at both kappa and sigma receptors, pentazocine, induced hyperthermia in guinea-pigs. Similar administration of peptide opioids like beta-endorphin (BE), methionine enkephalin (Met-E), leucine enkephalin (Leu-E) and their synthetic analogues D-ala2-methionine-enkephalinamide (D-ala2-Met-E) and D-ala2-leucine-enkephalinamide (D-ala2-Leu-E) also caused hyperthermia. Of the three anion transport systems (iodide, hippurate and liver-like) present in the choroid plexus, only the liver-like transport system seems to be important to central inactivation of beta-endorphin, D-ala2-Met-enkephalin and D-ala2-Leu-enkephalin since iodipamide (an inhibitor of the liver-like transport system) augmented the hyperthermia. Prostaglandins (PG) and norepinephrine (NE) were not involved in peptide- and non-peptide opioid-induced hyperthermia because a prostaglandin synthesis inhibitor, indomethacin, and an alpha-adrenergic receptor blocker, phenoxybenzamine, had no thermolytic effect. Likewise cAMP was not required since a phosphodiesterase inhibitor, theophylline, did not accentuate the hyperthermia due to administration of peptide and non-peptide opioids. Naloxone-sensitive receptors were involved in the induction of hyperthermia by morphine and beta-endorphin since naloxone attenuated the effect. In contrast, the hyperthermic responses to ketocyclazocine, SKF 10,047, pentazocine, Met-enkephalin, Leu-enkephalin, D-ala2-Met-enkephalin and D-ala2-Leu-enkephalin were not antagonized by naloxone. Lack of antagonism of naloxone on pyrogen, arachidonic acid, PGE2, dibutyryl cAMP and NE-induced hyperthermia indicates that endogenous opioid peptides are not likely to be central mediators of the hyperthermia induced by these agents.
Animals↗
Opposing actions of dibutyryl cyclic AMP and GMP on temperature in conscious guinea-pigs.
Intracerebroventricular administration of dibutyryl cyclic AMP (Db-cAMP), induced hyperthermia in guinea-pigs which was not mediated through prostaglandins (PG) or norepinephrine since a prostaglandin synthesis inhibitor, indomethacin, and an alpha-adrenergic receptor blocking agent, phenoxybenzamine did not antagonize the hyperthermia. In contrast, the hyperthermic response to dibutyryl cyclic AMP was attenuated by central administration of a beta-adrenergic receptor antagonist, sotalol, indicating that cyclic AMP may be involved, through beta-adrenergic receptors, in the central regulation of heat production/conservation. Central administration of dibutyryl cyclic GMP (Db-cGMP) produced hypothermia which was not mediated via histamine H1- or H2-receptors and serotonin since the H1-receptor antagonist, mepyramine, the H2-receptor antagonist, cimetidine, and the serotonin antagonist, methysergide, had no antagonistic effects. The antagonism of hypothermia induced by dibutyryl cyclic GMP and acetylcholine + physostigmine, by central administration of a cholinergic muscarinic receptor antagonist, atropine, and not by a cholinergic nicotinic receptor antagonist, d-tubocurarine, suggests that cholinoceptive neurons and endogenous cyclic GMP may regulate heat loss through cholinergic muscarinic receptors. These results support a regulatory role in thermoregulation provided by a balance between opposing actions of cyclic AMP and cyclic GMP in guinea-pigs.
Animals↗
Another look at contrast in multiple schedules.
Recent research on multiple schedule interactions is reviewed. Contrary to formulations that view contrast as the result of elicited behavior controlled by the stimulus-reinforcer contingency (e.g., additivity theory), the major controlling variable is the relative rate of reinforcement, which cannot be reduced to some combination of stimulus-reinforcer and response-reinforcer effects. Other recent theoretical formulations are also reviewed and all are found to face serious counterevidence. The best description of the available data continues to be in terms of the "context of reinforcement," but Herrnstein's (1970) formulation of the basis of such context effects appears to be inadequate. An alternative conception is provided by Catania's concept of "inhibition by reinforcement," by which rate of responding is inversely related to the average rate of reinforcement in the situation. Such a conception is related to Gibbon's recent scalar-expectancy account of autoshaping and Fantino's delay-reduction model of conditioned reinforcement, suggesting that a common set of principles determines several diverse conditioning phenomena. However, the empirical status of such a description remains uncertain, because recent evidence shows that schedule interactions are temporally asymmetric, depending primarily upon the conditions of reinforcement that follow a schedule component.
Journal Article↗
Prostacyclin-induced hyperthermia: implication of a protein mediator.
Intracerebroventricular administration of prostacyclin (PGI2) at room temperature (21 degrees C) induced dose-related hyperthermia in rabbits and also produced hyperthermia at low (4 degrees C) and high (30 degrees C) ambient temperatures. The PGI2-induced hyperthermia was not mediated by its stable metabolite 6-keto prostaglandin F1 alpha. Of the three anion transport systems (iodide, hippurate and liver-like) present in the choroid plexus, only the liver transport system seems to be important to central inactivation of pyrogen, prostaglandin E2 (PGE2) and the PGI2. Iodipamide (an inhibitor of the liver transport system) augmented the hyperthermia produced by PGI2, PGE2 and pyrogen. Phenoxybenzamine and pimozide had no thermolytic effect on PGI2-induced hyperthermia. After norepinephrine (NE) and dopamine levels were depleted by 6-hydroxydopamine, PGI2 still induced hyperthermia. Indomethacin and SC-19220 (a PG antagonist) did not antagonize PGI2-induced hyperthermia. Furthermore, the hyperthermia due to PGI2 was not accentuated by theophylline. In contrast, the hyperthermic response to PGI2 was attenuated by central administration of the protein synthesis inhibitor, anisomycin. These results indicate that PGI2-induced hyperthermia is not mediated by NE, dopamine, PGS, cyclic AMP, but, rather, that a protein mediator is implicated in the induction of fever by PGI2.
Animals↗
On the failure and facilitation of conditional discrimination.
Pigeons acquired a conditional discrimination in an autoshaping procedure in which certain stimulus combinations (form plus color) were followed by food, whereas others were not followed by food. Although the discrimination normally was acquired quickly, it was completely prevented when the color elements of the stimulus compounds were presented during the intertrial intervals preceding the trials in which both stimulus elements were available. This failure of discrimination was then prevented by having the colors serve as houselights rather than being localized on the response key and by pretraining procedures in which the colors were utilized in simpler discriminations. The results suggest that stimulus salience plays a critical role in determining whether conditional discriminations will be acquired, as the effects of all of the different operations could be understood in terms of increasing or decreasing the salience of the color elements, above or below some threshold value.
Animals↗
Determinants of contrast in the signal-key procedure: Evidence against additivity theory.
Two experiments are reported that challenge the interpretation of previous results with the signal-key procedure, in which the discriminative stimuli are located on a response key different from the key associated with the operant response requirement. Experiment 1 replicated the procedure of Keller (1974), and found that contrast effects on the operant key occurred reliably for only one of four subjects. High rates to the signal key initially occurred for only one subject, but modifications of the procedure produced substantial rates to the signal key for all subjects. In all cases, however, signal-key behavior was greatly reduced by the addition of a changeover delay which prevented reinforcement within 2 seconds of the last peck to the signal key, suggesting that signal-key pecking was maintained primarily by adventitious reinforcement. Experiment 2 modified the signal-key procedure by using three response keys, so that the discriminative stimuli on the signal key controlled different responses during all phases of training. With this modification, reliable contrast effects on the operant key occurred for all subjects, suggesting that the failure to find contrast in previous studies has been due to the confounding of changes in the discrimination requirements with changes in relative rate of reinforcement. The results challenge the additivity theory of contrast, and suggest that "elicited" behavior plays a minor role, if any, in the determination of contrast effects in multiple schedules.
Journal Article↗
The following schedule of reinforcement as a fundamental determinant of steady state contrast in multiple schedules.
Two experiments investigated whether steady-state interactions in multiple schedules depend exclusively on the following schedule of reinforcement. Experiment 1 used a four-component multiple schedule in which two components were associated with the same constant schedule of reinforcement, and where rate of reinforcement was varied in the component that followed one of these. Contrast effects were reliable only in the component that preceded the point of reinforcement variation, although some contrast did occur otherwise. In those instances where contrast other than the following-schedule effect did occur, it was accounted for by the effect of the preceding schedule, an effect for which there were consistent individual differences among subjects, and which varied with component duration. Experiment 2 used a three-component schedule, in which reinforcement rate was varied in the middle component. The results were consistent with Experiment 1, as the following-schedule effect was the only consistent effect that occurred, although an effect of the preceding schedule did occur for some subjects under some conditions, and was especially evident early in training. The conclusion from both experiments is that there is no general effect of relative rate of reinforcement apart from the sum of the effects of the preceding and following schedules, and that the following-schedule effect is the fundamental cause of steady-state interactions.
Journal Article↗
Photoincorporation of tetracycline into Escherichia coli ribosomes.
Explore the source record for details and available documents.
Escherichia coli↗
Contrast, component duration, and the following schedule of reinforcement.
Experiment 1 investigated component duration in a four-component multiple schedule designed to separate the effects of the preceding schedule of reinforcement from those of the following schedule of reinforcement. The preceding schedule in the preceding component had no consistent effect regardless of component duration. The following schedule was a powerful determinant of behavior, however, with higher response rates resulting from a following period of extinction. Moreover, the effect of the following schedule was greater with short component durations, which strongly suggests that component-duration effects previously found with multiple schedules are due generally to variation in the degree of control by the following schedule. Experiments 2--4 investigated the basis of the effects of the following schedule. In some situations differential responding in the following component was the controlling variable, but in others it was differential reinforcement in the following component. The results are consistent with the view that response rate during a stimulus is inversely related to the "value" of the following component, where the calculation of value must include both primary and conditioned reinforcement.
Animals↗
Effects on choice of reinforcement delay and conditioned reinforcement.
Pigeons chose between fixed-interval schedules of different durations presented in the terminal links of concurrent-chains schedules. The pair of schedules was always in the ratio of 2:1, but the absolute duration of the fixed intervals varied. In one set of conditions, the different terminal-link schedules were associated with different keylight stimuli (cued conditions). In a second set of conditions, the different terminal-link schedules were associated with the same stimulus (uncued conditions). Results from the cued conditions replicated previous findings that preference for the shorter fixed-interval schedule increased with fixed-interval duration. Preferences in the uncued conditions were lower than in the corresponding cued conditions but also increased with fixed-interval length. In addition, the degree of control under the uncued conditions was correlated with the extent to which the schedule during the terminal link was discriminated immediately upon entry into the terminal link. The pattern of results in both conditions was inconsistent with the notion that choice behavior matches relative immediacy of reinforcement. Reanalysis of previous evidence for matching (Chung and Herrnstein, 1967) showed that matching in fact did not occur, as the preferences of their subjects for the shorter of two delays also increased with the absolute size of the delays.
Journal Article↗