Physical Activity Among Urban Children with Asthma: Does Sleep Matter?

Journal of Clinical Psychology in Medical Settings - The present study examined associations between sleep and physical activity among a diverse sample of 97 urban children (ages 7–9) with...     

Adaptive calibration of children's physiological responses to family stress: the utility of evolutionary developmental theory: comment on Del Giudice et al. (2012) and Sturge-Apple et al. (2012)

Children's physiological reactions to stress are presented from the broader theoretical perspective of adaptive calibration to the environment, as rooted in life history theory. Del Giudice, Hinnant, Ellis, and El-Sheikh (2012) focus on children's physiological responses to a stressful task as a consequence of their history of family stress. Sturge-Apple, Davies, Martin, Cicchetti, and Hentges (2012) focus on the ways that children respond to a novel laboratory manipulation as a combined function of their temperament patterns and the harshness of their parental environment. The theoretical perspective employed provides an overarching framework that not only accounts for the findings presented here but also has heuristic value for future research on responses to early environmental risk. Future work in this area will benefit by inclusion of additional sympathetic nervous system (SNS) markers and neurotransmitters, inclusion of the role of gene expression in adaptive calibration, broader consideration of protective factors in the child's environment, and longitudinal work demonstrating the effects of adaptive calibration on children's future life history strategies and outcomes.     

The relationship between blushing propensity, social anxiety and facial blood flow during embarrassment

To investigate blushing in relation to blushing propensity scores and core elements of social anxiety, facial blood flow was monitored in 86 normal volunteers during an embarrassing task (singing a children's song). Increases in facial blood flow were greater in women than men, as were scores on the Blushing Propensity and Fear of Negative Evaluation scales. In addition, high scores on the Blushing Propensity and Social Interaction Anxiety scales were associated with large increases in facial blood flow during singing. However, this appeared to be due primarily to social anxiety because the association between blushing propensity scores and changes in facial blood flow disappeared when social interaction anxiety scores were taken into account. These findings suggest that people generally base their beliefs about blushing on cues other than changes in facial blood flow. Social anxiety may augment increases in facial blood flow during embarrassment, independently of expected or perceived blushing.     

Testing compensatory health beliefs in a UK population

Compensatory health beliefs, beliefs that healthy behaviours can compensate or neutralise unhealthy behaviours, have been proposed as one way of understanding why people engage in health-risk behaviours (Kn?uper, B., Rabiau, M., Cohen, O., & Patriciu, N. (2004). Compensatory health beliefs scale development and psychometric properties. Psychology and Health, 19, 607-624). However, measuring compensatory health beliefs has proved a challenge, with several recent studies being unable to replicate the psychometric properties of Kn?uper et al.'s (2004) scales. The aims of this study were to: (1) test the factor structure of the compensatory health beliefs scale in the UK, (2) examine the predictive validity of the scale by testing the relationships between compensatory health beliefs and health behaviours over a six-month time interval and (3) assess the 6-month test-retest reliability of the scale. A total of 393 participants completed measures of compensatory health beliefs and health behaviours at two time points separated by six months. The findings were potentially problematic for research into compensatory health beliefs: the factor structure was not confirmed, there was little evidence of predictive validity, and test-retest reliability was poor. Further research is required to understand the operation of compensatory health beliefs and to develop the measurement of compensatory health beliefs.     

What do pre-adolescents and adolescents understand about HIV/AIDS?

Abstract

Pre-adolescents and adolescents (N= 80, aged 10, 12, 15, and 18 years) were tested on their knowledge of HIV/AIDS. Knowledge was assessed using a self-report questionnaire (examining levels of factual knowledge) and a semi-structured interview (examining cognitive developmental levels of understanding). Examination of the developmental shifts in understanding of HIV/AIDS revealed an increase in conceptual complexity on causal and prevention dimensions. The main conceptual changes included a shift from single cause to multiple cause solutions and a shift from identifying surface or immediate features to implicating less salient features. Additionally, with age, concepts about HIV/AIDS were increasingly organised around internal, physiological principles. Questionnaire responses yielded significant age-related increases in knowledge. Level of knowledge, as measured by the questionnaire, was higher than that assessed by the interview for the three youngest age groups. Thus, factual information acquired about HIV/AIDS is not automatically accompanied by understanding. In light of these findings the past conclusion that adolescents have high levels of knowledge of HIV/AIDS is questioned.     

Short-term memory stages in sign vs. speech: the source of the serial span discrepancy

Speakers generally outperform signers when asked to recall a list of unrelated verbal items. This phenomenon is well established, but its source has remained unclear. In this study, we evaluate the relative contribution of the three main processing stages of short-term memory – perception, encoding, and recall – in this effect. The present study factorially manipulates whether American Sign Language (ASL) or English is used for perception, memory encoding, and recall in hearing ASL-English bilinguals. Results indicate that using ASL during both perception and encoding contributes to the serial span discrepancy. Interestingly, performing recall in ASL slightly increased span, ruling out the view that signing is in general a poor choice for short-term memory. These results suggest that despite the general equivalence of sign and speech in other memory domains, speech-based representations are better suited for the specific task of perception and memory encoding of a series of unrelated verbal items in serial order through the phonological loop. This work suggests that interpretation of performance on serial recall tasks in English may not translate straightforwardly to serial tasks in sign language.     

Reactivity to Stress: When Does a History of Medical Adversity Foster Resilience Versus Vulnerability?

Young adults with (or without) a history of medical or physical disorders (MPDs) were exposed to repeated laboratory stress. The effects of MPD status on habituation (as measured by changing levels of cortisol) were found to be moderated by the extent to which respondents reported “attachment feelings” in their relationships (as measured by the Social Provisions Scale). Students in the MPD group who reported attachment feelings showed (a) cortisol increases during their first exposure to a laboratory stressor; and (b) cortisol decreases during a second exposure to the same stressor 1 week later. No equivalent benefit was found for students who lacked this medical history. Findings suggest the extent to which medical adversity—under the right interpersonal circumstances—promotes resilience.     

Increases in parental investment and child health as a result of an early intervention

Parental investment (involving time or money invested in 3-year-olds) and child health were assessed as an outcome of (a) children’s risk status (preterm vs. full-term birth) and (b) maternal resources (defined here in terms of their problem-solving skills in resolving caregiving challenges). Resources were varied systematically as a function of maternal participation in a traditional home visitation program versus a novel cognitively enhanced program that facilitated parenting skills more successfully. As predicted, mothers in the traditional home visitation condition invested preferentially in low-risk children, whereas mothers in the cognitively enhanced condition invested preferentially in high-risk children (who, in turn, showed maximal health benefits). Maternal investment of time in care provision mediated the relationship between predictor variables and children’s health. This pattern supports an evolutionary model of parental investment in which parents show discriminative solicitude based on the reproductive potential of the child and parents’ access to relevant resources.     

Cannabinoid and cholinergic systems interact during performance of a short-term memory task in the rat

It is now well established that cannabinoid agonists such as Δ⁹–tetrahydrocannabinol (THC), anandamide, and WIN 55,212-2 (WIN-2) produce potent and specific deficits in working memory (WM)/short-term memory (STM) tasks in rodents. Although mediated through activation of CB1 receptors located in memory-related brain regions such as the hippocampus and prefrontal cortex, these may, in part, be due to a reduction in acetylcholine release (i.e., cholinergic hypofunction). To determine the interaction between cannabinoid and cholinergic systems, we exposed rats treated with WIN-2 or cholinergic drugs to a hippocampal-dependent delayed nonmatch to sample (DNMS) task to study STM, and recorded hippocampal single-unit activity in vivo. WIN-2 induced significant deficits in DNMS performance and reduced the average firing and bursting rates of hippocampal principal cells through a CB1 receptor-mediated mechanism. Rivastigmine, an acetylcholinesterase inhibitor, reversed these STM deficits and normalized hippocampal discharge rates. Effects were specific to 1 mg/kg WIN-2 as rivastigmine failed to reverse the behavioral and physiological deficits that were observed in the presence of MK-801, an NMDA receptor antagonist. This supports the notion that cannabinoid-modulated cholinergic activity is a mechanism underlying the performance deficits in DNMS. Whether deficits are due to reduced nicotinic or muscarinic receptor activation, or both, awaits further analysis.Administration of both synthetic and phytocannabinoids, including Δ⁹–tetrahydrocannabinol (Δ⁹–THC), WIN 55,212-2 (WIN-2), and CP 55,940, impair working memory (WM) and short-term memory (STM) through a CB1 receptor-mediated mechanism in rats (Lichtman et al. 1995; Lichtman and Martin 1996; Hampson and Deadwyler 1998, 1999, 2000; Braida and Sala 2000; Egashira et al. 2002). This suggestive evidence for endocannabinoid involvement in memory formation was confirmed by Terranova and coworkers (1996), who demonstrated that the CB1 receptor antagonist rimonabant facilitated short-term olfactory memory, and this was partially reversed by the muscarinic receptor antagonist scopolamine. This suggests an interaction between cannabinoid and cholinergic systems such that endocannabinoid tone suppresses cholinergic transmission. Consequently, rats pretreated with eptastigmine, a second-generation cholinesterase inhibitor remained unaffected by the full CB1 receptor agonist CP 55,940 when tested in an eight arm radial maze (Braida and Sala 2000). And more recent evidence from Mishima and coworkers (2002) suggests that a block of cholinesterase with physostigmine and tetrahydroaminoacridine protects against WM impairments induced by Δ⁹–THC. These findings further support a potential role of the cholinergic system in cannabinoid-induced memory impairments.The exact mechanisms for this interaction still remain elusive, although cholinergic projection neurons from medial septum to hippocampus are likely to play an important role (Harkany et al. 2003, 2005; Fitz et al. 2008). However, the neuromodulatory action of pharmacologically active cannabinoids on septo-hippocampal cholinergic activity in vivo remains unexplored. Within the hippocampus, cannabinoids presynaptically inhibit the release of acetylcholine, possibly through the activation of CB1 receptors located on cholinergic nerve terminals given that these effects were blocked by rimonabant (Gifford and Ashby Jr. 1996; Gifford et al. 1997a, 2000; Kathmann et al. 2001a). Direct in vivo microdialysis studies in awake rats also showed cannabinoid-induced decreases in acetylcholine release in the hippocampus through a CB1 receptor-mediated mechanism (Gessa et al. 1997; Carta et al. 1998). High doses of rimonabant alone increase the amount of acetylcholine release in the hippocampus (Gessa et al. 1997, 1998) either by blocking the tonic inhibitory influence of endocannabinoids and/or through its inverse agonism at CB1 receptors. Such actions are in agreement with a 100% greater increase in electrically evoked hippocampal acetylcholine release in CB1^−/− mice (Kathmann et al. 2001b).In contrast, low doses of Δ⁹–THC (0.01–0.15 mg/kg), WIN-2 (0.01–0.5 mg/kg), and HU-210 (0.001–0.004 mg/kg) have been shown to enhance acetylcholine release (Acquas et al. 2000, 2001), indicating that cannabinoid modulation of acetylcholine release in the hippocampus is “biphasic.” This has been further supported by the work carried out by Tzavara and coworkers (2003), who demonstrated that low (0.5 mg/kg, intraperitoneally [i.p.]) and high (5 mg/kg, i.p.) doses of WIN-2 induce transient stimulation and prolonged inhibition of hippocampal acetylcholine efflux, respectively. This demonstrates that the dose of cannabinoids plays a key role in determining how much acetylcholine is released in the hippocampus.Such an interaction is likely to play an important role during the performance of a delayed nonmatch to sample (DNMS) task but has not been explored. Hence, a comprehensive pharmacological assessment was carried out here to (1) reveal the existence of such an interaction in terms of DNMS performance and (2) assess a possible cannabinoid-acetylcholine cross-talk on burst characteristics of hippocampal principal cells in CA3 and CA1.