Characteristics of control group participants who increased their physical activity in a cluster-randomized lifestyle intervention trial

<p>Abstract</p> <p>Background</p> <p>Meaningful improvement in physical activity among control group participants in lifestyle intervention trials is not an uncommon finding, and may be partly explained by participant characteristics. This study investigated which baseline demographic, health and behavioural characteristics were predictive of successful improvement in physical activity in usual care group participants recruited into a telephone-delivered physical activity and diet intervention trial, and descriptively compared these characteristics with those that were predictive of improvement among intervention group participants.</p> <p>Methods</p> <p>Data come from the Logan Healthy Living Program, a primary care-based, cluster-randomized controlled trial of a physical activity and diet intervention. Multivariable logistic regression models examined variables predictive of an improvement of at least 60 minutes per week of moderate-to-vigorous intensity physical activity among usual care (n = 166) and intervention group (n = 175) participants.</p> <p>Results</p> <p>Baseline variables predictive of a meaningful change in physical activity were different for the usual care and intervention groups. Being retired and completing secondary school (but no further education) were predictive of physical activity improvement for usual care group participants, whereas only baseline level of physical activity was predictive of improvement for intervention group participants. Higher body mass index and being unmarried may also be predictors of physical activity improvement for usual care participants.</p> <p>Conclusion</p> <p>This is the first study to examine differences in predictors of physical activity improvement between intervention group and control group participants enrolled in a physical activity intervention trial. While further empirical research is necessary to confirm findings, results suggest that participants with certain socio-demographic characteristics may respond favourably to minimal intensity interventions akin to the treatment delivered to participants in a usual care group. In future physical activity intervention trials, it may be possible to screen participants for baseline characteristics in order to target minimal-intensity interventions to those most likely to benefit. (Australian Clinical Trials Registry, <url>http://www.anzctr.org.au/default.aspx</url>, ACTRN012607000195459)</p

Children, parents and pets exercising together (CPET) : exploratory randomised controlled trial

Levels of physical activity (PA) in UK children are much lower than recommended and novel approaches to its promotion are needed. The Children, Parents and Pets Exercising Together (CPET) study is the first exploratory randomised controlled trial (RCT) to develop and evaluate an intervention aimed at dog-based PA promotion in families. CPET aimed to assess the feasibility, acceptability and potential efficacy of a theory-driven, family-based, dog walking intervention for 9-11 year olds

Tracking of dietary intakes in early childhood : the Melbourne InFANT program

Background/Objectives: The objectives of the present study were to describe food and nutrient intakes in children aged 9 and 18 months, and to assess tracking of intakes between these two ages.Subjects/Methods: Participants were 177 children of first-time mothers from the control arm of the Melbourne Infant Feeding Activity and Nutrition Trial (InFANT) Program. Dietary intake was collected at 9 and 18 months using three 24&thinsp;h diet recalls. Tracking was assessed for food and nutrient intakes using logistic regression analysis and estimating partial correlation coefficients, respectively.Results: Although overall nutrient intakes estimated in this study did not indicate a particular risk of nutrient deficiency, our findings suggest that consumption of energy-dense, nutrient-poor foods occurred as early as 9 months of age, with some of these foods tracking highly over the weaning period. Intakes of healthier foods such as fruits, vegetables, dairy products, eggs, fish and water were also relatively stable over this transition from infancy to toddlerhood, along with moderate tracking for riboflavin, iodine, fibre, calcium and iron. Tracking was low but close to &rho;=0.3 for zinc, magnesium and potassium intakes.Conclusions: The tracking of energy-dense, nutrient-poor foods has important implications for public health, given the development of early eating behaviours is likely to be modifiable. At this stage of life, dietary intakes are largely influenced by the foods parents provide, parental feeding practices and modelling. This study supports the importance of promoting healthy dietary trajectories from infancy.<br /

Activation of mGlu3 Receptors Stimulates the Production of GDNF in Striatal Neurons

Metabotropic glutamate (mGlu) receptors have been considered potential targets for the therapy of experimental parkinsonism. One hypothetical advantage associated with the use of mGlu receptor ligands is the lack of the adverse effects typically induced by ionotropic glutamate receptor antagonists, such as sedation, ataxia, and severe learning impairment. Low doses of the mGlu2/3 metabotropic glutamate receptor agonist, LY379268 (0.25–3 mg/kg, i.p.) increased glial cell line-derived neurotrophic factor (GDNF) mRNA and protein levels in the mouse brain, as assessed by in situ hybridization, real-time PCR, immunoblotting, and immunohistochemistry. This increase was prominent in the striatum, but was also observed in the cerebral cortex. GDNF mRNA levels peaked at 3 h and declined afterwards, whereas GDNF protein levels progressively increased from 24 to 72 h following LY379268 injection. The action of LY379268 was abrogated by the mGlu2/3 receptor antagonist, LY341495 (1 mg/kg, i.p.), and was lost in mGlu3 receptor knockout mice, but not in mGlu2 receptor knockout mice. In pure cultures of striatal neurons, the increase in GDNF induced by LY379268 required the activation of the mitogen-activated protein kinase and phosphatidylinositol-3-kinase pathways, as shown by the use of specific inhibitors of the two pathways. Both in vivo and in vitro studies led to the conclusion that neurons were the only source of GDNF in response to mGlu3 receptor activation. Remarkably, acute or repeated injections of LY379268 at doses that enhanced striatal GDNF levels (0.25 or 3 mg/kg, i.p.) were highly protective against nigro-striatal damage induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice, as assessed by stereological counting of tyrosine hydroxylase-positive neurons in the pars compacta of the substantia nigra. We speculate that selective mGlu3 receptor agonists or enhancers are potential candidates as neuroprotective agents in Parkinson's disease, and their use might circumvent the limitations associated with the administration of exogenous GDNF

An Updated Meta-Analysis of Risk of Multiple Sclerosis following Infectious Mononucleosis

Background: Multiple sclerosis (MS) appears to develop in genetically susceptible individuals as a result of environmental exposures. Epstein-Barr virus (EBV) infection is an almost universal finding among individuals with MS. Symptomatic EBV infection as manifested by infectious mononucleosis (IM) has been shown in a previous meta-analysis to be associated with the risk of MS, however a number of much larger studies have since been published.Methods/Principal Findings: We performed a Medline search to identify articles published since the original meta-analysis investigating MS risk following IM. A total of 18 articles were included in this study, including 19390 MS patients and 16007 controls. We calculated the relative risk of MS following IM using a generic inverse variance with random effects model. This showed that the risk of MS was strongly associated with IM (relative risk (RR) 2.17; 95% confidence interval 1.97-2.39; p<10(-54)).Discussion: Our results establish firmly that a history of infectious mononucleosis significantly increases the risk of multiple sclerosis. Future work should focus on the mechanism of this association and interaction with other risk factors

Parallel Driving and Modulatory Pathways Link the Prefrontal Cortex and Thalamus

Pathways linking the thalamus and cortex mediate our daily shifts from states of attention to quiet rest, or sleep, yet little is known about their architecture in high-order neural systems associated with cognition, emotion and action. We provide novel evidence for neurochemical and synaptic specificity of two complementary circuits linking one such system, the prefrontal cortex with the ventral anterior thalamic nucleus in primates. One circuit originated from the neurochemical group of parvalbumin-positive thalamic neurons and projected focally through large terminals to the middle cortical layers, resembling ‘drivers’ in sensory pathways. Parvalbumin thalamic neurons, in turn, were innervated by small ‘modulatory’ type cortical terminals, forming asymmetric (presumed excitatory) synapses at thalamic sites enriched with the specialized metabotropic glutamate receptors. A second circuit had a complementary organization: it originated from the neurochemical group of calbindin-positive thalamic neurons and terminated through small ‘modulatory’ terminals over long distances in the superficial prefrontal layers. Calbindin thalamic neurons, in turn, were innervated by prefrontal axons through small and large terminals that formed asymmetric synapses preferentially at sites with ionotropic glutamate receptors, consistent with a driving pathway. The largely parallel thalamo-cortical pathways terminated among distinct and laminar-specific neurochemical classes of inhibitory neurons that differ markedly in inhibitory control. The balance of activation of these parallel circuits that link a high-order association cortex with the thalamus may allow shifts to different states of consciousness, in processes that are disrupted in psychiatric diseases

Fragile x syndrome and autism: from disease model to therapeutic targets

Autism is an umbrella diagnosis with several different etiologies. Fragile X syndrome (FXS), one of the first identified and leading causes of autism, has been modeled in mice using molecular genetic manipulation. These Fmr1 knockout mice have recently been used to identify a new putative therapeutic target, the metabotropic glutamate receptor 5 (mGluR5), for the treatment of FXS. Moreover, mGluR5 signaling cascades interact with a number of synaptic proteins, many of which have been implicated in autism, raising the possibility that therapeutic targets identified for FXS may have efficacy in treating multiple other causes of autism

Medical conditions in autism spectrum disorders

Autism spectrum disorder (ASD) is a behaviourally defined syndrome where the etiology and pathophysiology is only partially understood. In a small proportion of children with the condition, a specific medical disorder is identified, but the causal significance in many instances is unclear. Currently, the medical conditions that are best established as probable causes of ASD include Fragile X syndrome, Tuberous Sclerosis and abnormalities of chromosome 15 involving the 15q11-13 region. Various other single gene mutations, genetic syndromes, chromosomal abnormalities and rare de novo copy number variants have been reported as being possibly implicated in etiology, as have several ante and post natal exposures and complications. However, in most instances the evidence base for an association with ASD is very limited and largely derives from case reports or findings from small, highly selected and uncontrolled case series. Not only therefore, is there uncertainty over whether the condition is associated, but the potential basis for the association is very poorly understood. In some cases the medical condition may be a consequence of autism or simply represent an associated feature deriving from an underlying shared etiology. Nevertheless, it is clear that in a growing proportion of individuals potentially causal medical conditions are being identified and clarification of their role in etio-pathogenesis is necessary. Indeed, investigations into the causal mechanisms underlying the association between conditions such as tuberous sclerosis, Fragile X and chromosome 15 abnormalities are beginning to cast light on the molecular and neurobiological pathways involved in the pathophysiology of ASD. It is evident therefore, that much can be learnt from the study of probably causal medical disorders as they represent simpler and more tractable model systems in which to investigate causal mechanisms. Recent advances in genetics, molecular and systems biology and neuroscience now mean that there are unparalleled opportunities to test causal hypotheses and gain fundamental insights into the nature of autism and its development