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Passive Exposure (passive + exposure)
Selected AbstractsWhat neurobiology cannot tell us about addictionADDICTION, Issue 5 2010Harold Kalant ABSTRACT Molecular neurobiological studies have yielded enormous amounts of valuable information about neuronal response mechanisms and their adaptive changes. However, in relation to addiction this information is of limited value because almost every cell function appears to be involved. Thus it tells us only that neurons adapt to ,addictive drugs' as they do to all sorts of other functional disturbances. This information may be of limited help in the development of potential auxiliary agents for treatment of addiction. However, a reductionist approach which attempts to analyse addiction at ever finer levels of structure and function, is inherently incapable of explaining what causes these mechanisms to be brought into play in some cases and not in others, or by self-administration of a drug but not by passive exposure. There is abundant evidence that psychological, social, economic and specific situational factors play important roles in initiating addiction, in addition to genetic and other biological factors. Therefore, if we hope to be able to make predictions at any but a statistical level, or to develop effective means of prevention, it is necessary to devise appropriate integrative approaches to the study of addiction, rather than pursue an ever-finer reductive approach which leads steadily farther away from the complex interaction of drug, user, environment and specific situations that characterizes the problem in humans. [source] Chronic passive exposure to aggression escalates aggressiveness of rat observersAGGRESSIVE BEHAVIOR, Issue 1 2010Hideo Suzuki Abstract Previous studies have documented that exposure to aggression increases aggressiveness of human witnesses. However, the question of whether passive exposure to aggression can exclusively cause a risk of aggressive inclination for observers through a learning process, rather than mimicry effect, has not been readily addressed in the clinical literature. This study aimed to investigate this question by using a simple animal model to test the behavioral effect of chronic passive exposure to aggression. Our results indicate that observer rats that had been passively exposed to aggression for 10,min per day for 23 consecutive days exhibited more aggressive behavior than controls or those groups undergoing a single exposure to passive aggression. Furthermore, aggression levels in the group of 23-day chronic exposure to aggression lasted 16 days after the recovery from exposure to aggression. These data suggest that the development of aggression in this model occurred through a learning process because only chronic exposure to aggression resulted in this behavioral outcome in the long run. Aggr. Behav. 36:54,66, 2010. © 2009 Wiley-Liss, Inc. [source] Schedule of Passive Ethanol Exposure Affects Subsequent Intragastric Ethanol Self-InfusionALCOHOLISM, Issue 11 2009Tara L. Fidler Background:, Many studies have shown that chronic ethanol exposure can enhance later self-administration of ethanol, but only a few studies have identified critical parameters for such exposure. The present studies examined temporal and other parameters of chronic ethanol exposure on subsequent intragastric (IG) self-infusion of ethanol. Methods:, Sprague,Dawley rats implanted with IG catheters were passively infused with ethanol for 5 to 6 days and then allowed to self-infuse ethanol or water using a procedure in which infusions were contingent upon licking fruit-flavored solutions. Experiment 1 examined the time interval between consecutive periods of passive infusion (Massed Group: 12 hours vs. Spaced Group: 36 hours). Experiment 2 studied the interval between the final passive infusion and onset of self-infusion (12 vs. 36 hours). Finally, Experiment 3 tested the effect of inserting self-infusion days within the passive infusion phase. Results:, Passive ethanol exposure on consecutive days induced relatively large amounts of ethanol self-infusion (4.1 to 7.9 g/kg/d). Increasing the duration of the ethanol-free interval between periods of passive exposure to 36 hours significantly reduced ethanol self-infusion (2.2 g/kg/d; Exp. 1). The time delay between the last passive ethanol exposure and onset of self-infusion had no effect on self-infusion (Exp. 2). Moreover, inserting no-choice self-infusion days between the last few passive exposure days did not increase self-infusion (Exp. 3). Conclusions:, Measurement of withdrawal signs indicated that Massed passive exposure produced stronger dependence than Spaced passive exposure, suggesting that enhanced ethanol self-infusion in Massed Groups might be explained by the opportunity for greater negative reinforcement by ethanol. Although enhanced negative reinforcement might also explain why the Massed Group showed a weaker aversion for the ethanol-paired flavor than the Spaced Group, this observation could also be explained by the development of greater tolerance to ethanol's aversive pharmacological effects in the Massed Group. [source] Linkage between smoking and asthmaALLERGY, Issue 12 2009A. Pietinalho Smoking is one of the most important preventable public health problems. Prevalence of smoking is decreasing in the Western world but lot of work is left. We reviewed the most important papers related to smoking and asthma. Despite of decreasing smoking figures in Finland, about 15,20 per cent of pregnant women smokes. Children's exposure to harmful effects of environmental tobacco smoke (ETS) still continues. Exposure to tobacco smoke during pregnancy and in early childhood both deteriorates permanently children's lungs and increases their asthma risk. The exposure of adults to ETS also increases their asthma risk. Both passive exposure to ETS and active smoking worsen asthma. In addition, smoking asthmatics run a higher risk of developing COPD compared to non-smokers. Smoking prevalence among the population can be regulated through legislation, but the health care personnel have a central role in encouraging smoking cessation among smoking patients. [source] Leukotriene synthesis during respiratory syncytial virus bronchiolitis: Influence of age and atopy,PEDIATRIC PULMONOLOGY, Issue 4 2005Giovanni Piedimonte MD Abstract Respiratory syncytial virus (RSV) infection is the most common cause of bronchiolitis in infants and an important risk factor for the development of recurrent wheezing and asthma. Cysteinyl leukotrienes were implicated in the pathophysiology of these diseases, and are being targeted for their diagnosis and therapy. We measured urinary leukotriene E4 (LTE4) in infants with RSV bronchiolitis in comparison with controls without respiratory infection, and investigated whether medical and family history, age, and passive exposure to tobacco smoke are related to urinary leukotriene excretion. We studied 33 infants with bronchiolitis and 25 controls, 1,12 months of age. Demographic and historical data were obtained from informed-consent forms and questionnaires completed by the parents. RSV was detected in nasal secretions by enzyme-linked immunoassay. Urine samples were collected on day of admission and were analyzed for LTE4 with an enzyme-linked immunoassay. Urinary LTE4 was 8-fold higher in infants with bronchiolitis than in controls. Leukotriene excretion was significantly higher in infected infants <6 months of age with a medical history of eczema or dry cough and/or family history of asthma. Multivariate analysis revealed that eczema and dry cough are independently associated with high LTE4 excretion during bronchiolitis. Exposure to tobacco smoke did not affect urinary LTE4. Our study shows that leukotriene synthesis during bronchiolitis is particularly elevated in younger infants with an atopic/asthmatic background. Urinary LTE4 may become a valuable, noninvasive marker for the identification of patients who will benefit most from therapy with leukotriene modifiers for management of bronchiolitis. Pediatr Pulmonol. © 2005 Wiley-Liss, Inc. [source] Association of tobacco smoke exposure and respiratory syncitial virus infection with airways reactivity in early childhoodPEDIATRIC PULMONOLOGY, Issue 6 2001Alan Adler MD Abstract Exposure to infectious agents and environmental tobacco smoke are thought to induce bronchial hyperresponsiveness (BHR). This study was undertaken to determine the effects of passive exposure to tobacco smoke and respiratory syncitial virus (RSV) lower respiratory infection (LRI) during infancy on the occurrence of BHR in the first 2 years of life. Eighty-six cases of documented RSV (mean age, 188 days) and 78 controls (mean age, 162 days) were enrolled from the clinic and in-patient service of a single hospital. None had a history of prior LRI. Subjects were studied at 6-month intervals up to 19 months of age with a standardized respiratory illness and parental smoking questionnaire, partial expiratory flow-volume curves by the "hug" (rapid thoracic compression) technique, and methacholine challenge. Exposure to maternal and paternal cigarette smoking, maternal history of asthma, and mold exposure were associated with decreased levels of length-corrected maximal flow at functional residual capacity (V,maxFRC). RSV-LRI was not related to V,maxFRC. After adjustment of V,maxFRC for these factors, V,maxFRC was a significantly and positively correlated with a methacholine concentration provoking a 40% fall in V,maxFRC (PC40) and negatively correlated with dose-response slope. After adjustment for V,maxFRC, there were no independent effects of tobacco smoke exposure or RSV-LRI on methacholine responses. These data do not support a role for RSV as a risk factor for airways reactivity in childhood and indicate that exposure to tobacco smoke affects airways reactivity through its effects on airways. Pediatr Pulmonol. 2001; 32:418,427. © 2001 Wiley-Liss, Inc. [source] Altered free radical metabolism in acute mountain sickness: implications for dynamic cerebral autoregulation and blood,brain barrier functionTHE JOURNAL OF PHYSIOLOGY, Issue 1 2009D. M. Bailey We tested the hypothesis that dynamic cerebral autoregulation (CA) and blood,brain barrier (BBB) function would be compromised in acute mountain sickness (AMS) subsequent to a hypoxia-mediated alteration in systemic free radical metabolism. Eighteen male lowlanders were examined in normoxia (21% O2) and following 6 h passive exposure to hypoxia (12% O2). Blood flow velocity in the middle cerebral artery (MCAv) and mean arterial blood pressure (MAP) were measured for determination of CA following calculation of transfer function analysis and rate of regulation (RoR). Nine subjects developed clinical AMS (AMS+) and were more hypoxaemic relative to subjects without AMS (AMS,). A more marked increase in the venous concentration of the ascorbate radical (A,,), lipid hydroperoxides (LOOH) and increased susceptibility of low-density lipoprotein (LDL) to oxidation was observed during hypoxia in AMS+ (P < 0.05 versus AMS,). Despite a general decline in total nitric oxide (NO) in hypoxia (P < 0.05 versus normoxia), the normoxic baseline plasma and red blood cell (RBC) NO metabolite pool was lower in AMS+ with normalization observed during hypoxia (P < 0.05 versus AMS,). CA was selectively impaired in AMS+ as indicated both by an increase in the low-frequency (0.07,0.20Hz) transfer function gain and decrease in RoR (P < 0.05 versus AMS,). However, there was no evidence for cerebral hyper-perfusion, BBB disruption or neuronal,parenchymal damage as indicated by a lack of change in MCAv, S100, and neuron-specific enolase. In conclusion, these findings suggest that AMS is associated with altered redox homeostasis and disordered CA independent of barrier disruption. [source] Cognitive mechanisms underlying the emotional effects of bias modificationAPPLIED COGNITIVE PSYCHOLOGY, Issue 3 2010Laura Hoppitt In this study we assessed the cognitive mechanisms underlying the affective consequences of modifying emotional processing biases. During ,active' training participants selected either threatening or non-threatening meanings of emotionally ambiguous words, in contrast to ,passive' conditions in which participants read unambiguous words with equivalent valenced meanings. Both methods enhanced access to training-congruent primed emotional meanings, as assessed in a lexical decision task, although neither method displayed evidence of an induced interpretive bias as it is usually understood. However, consistent with previous research, the methods differed in their emotional consequences: Active training had greater effects on anxiety while viewing an accident video than did passive exposure. We interpret these results to suggest that both forms of training enhance priming of a valenced category, but only active conditions induce an implicit production rule to generate and/or select emotional meanings, and that it is this latter process that is critical to the modification of emotionality. Copyright © 2010 John Wiley & Sons, Ltd. [source] Prolonged stimulus exposure reveals prolonged neurobehavioral response patternsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 10 2010Brett A. Johnson Abstract Although it has been shown repeatedly that minimum response times in sensory systems can be quite short, organisms more often continue to respond to sensory stimuli over considerably longer periods of time. The continuing response to sensory stimulation may be a more realistic assessment of natural sensory responses, so we determined for how long a stimulus would evoke a response in naïve, freely moving animals. Specifically, we determined for how long such rats responded to odorants during continuous passive exposures by monitoring their sniffing with whole-body plethysmography. We found that naïve rats continue to sniff odorants vigorously for up to 3 minutes, much longer than what has been reported for highly trained, highly motivated rats. Patterns of 2-deoxyglucose (2-DG) uptake in the glomerular layer of the rat olfactory bulb also were seen after only 1,5 minutes of odorant exposure, overlapping with the period of increased respiration to odorants. Moreover, these 2-DG uptake patterns closely resembled the patterns that emerge from prolonged odorant exposures, suggesting that activity mapping over prolonged periods can identify areas of activity that are present when rats are still attending and responding to odorant stimuli. Given these findings, it seems important to consider the possibility that prolonged exposure to other sensory stimuli will reveal more realistic neural response patterns. J. Comp. Neurol. 518:1617,1629, 2010. © 2009 Wiley-Liss, Inc. [source] | ||||||||||||||||