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Background: Schools provide an ideal setting for promoting healthy lifestyles in youth, but it has proven difficult to promote the adoption and implementation of evidence-based programming by school leaders. The SWITCH® (School Wellness Integration Targeting Child Health) intervention is a capacity-building process designed to help school leaders learn how to plan, implement, and sustain school wellness programs on their own. Objective: The present study evaluates the transdisciplinary approaches used in establishing an integrated research-practice partnership with the state-wide 4-H/Extension network to support broader dissemination. Method: The study used a mixed methods approach to evaluate the degree of engagement and motivation of 4-H leaders (N = 30) for providing ancillary support for local school wellness programming. Engagement from 4-H Staff was logged over a year-long period through tracking completion of training and ongoing engagement with aspects of SWITCH. They completed checkpoint surveys and an interview to provide perceptions of supporting school implementation of SWITCH programming. Data were analysed through Pearson bivariate correlations and constant comparative analysis. Results: County-level 4-H staff demonstrated high engagement in SWITCH by attending training sessions and hosting structured checkpoint sessions with schools. Interview data revealed that 4-H Staff valued connections with schools and emphasized that training on SWITCH was consistent with their existing roles related to youth programming. Conclusions: The results demonstrate the value of the sequential capacity-building process used to train 4-H Staff to facilitate school wellness programming. The transdisciplinary approaches built transferable skills and fostered relationships that directly support the broader goals of 4-H. [ABSTRACT FROM AUTHOR]

Bipolar affective disorder is a severe and debilitating psychiatric condition characterized by the alternating mood states of mania and depression. Both the molecular pathophysiology of the disorder and the mechanism of action of the mainstays of its treatment remain largely unknown. Here, 1H NMR spectroscopy-based metabonomic analysis was performed to identify molecular changes in post-mortem brain tissue (dorsolateral prefrontal cortex) of patients with a history of bipolar disorder. The observed changes were then compared to metabolic alterations identified in rat brain following chronic oral treatment with either lithium or valproate. This is the first study to use 1H NMR spectroscopy to study post-mortem bipolar human brain tissue, and it is the first to compare changes in disease brain with changes induced in rat brain following mood stabilizer treatment. Several metabolites were found to be concordantly altered in both the animal and human tissues. Glutamate levels were increased in post-mortem bipolar brain, while the glutamate/glutamine ratio was decreased following valproate treatment, and γ-aminobutyric acid levels were increased after lithium treatment, suggesting that the balance of excitatory/inhibitory neurotransmission is central to the disorder. Both creatine and myo-inositol were increased in the post-mortem brain but depleted with the medications. Lastly, the level of N-acetyl aspartate, a clinically important metabolic marker of neuronal viability, was found to be unchanged following chronic mood stabilizer treatment. These findings promise to provide new insight into the pathophysiology of bipolar disorder and may be used to direct research into novel therapeutic strategies.Molecular Psychiatry (2009) 14, 269–279; doi:10.1038/sj.mp.4002130; published online 5 February 2008 [ABSTRACT FROM AUTHOR]

Background: Whilst preterm-born individuals have an increased risk of developing attention-deficit/hyperactivity disorder (ADHD), and are reported to have ADHD-like attention and arousal impairments, direct group comparisons are scarce. Methods: We directly compared preterm-born adolescents (n = 186) to term-born adolescents with ADHD (n = 69), and term-born controls (n = 135), aged 11–23, on cognitive-performance, event-related potential and skin conductance level (SCL) measures associated with attention and arousal. The measures are from baseline and fast-incentive conditions of a four-choice reaction time task, previously shown to discriminate between the individuals with ADHD and controls. We aimed to establish whether preterm-born adolescents show: (a) identical cognitive-neurophysiological impairments to term-born adolescents with ADHD (b) possible additional impairments, and whether (c) the observed impairments correlate with ADHD symptom scores. Results: The preterm group, like the term-born ADHD group, showed increased mean reaction time (MRT) and reaction time variability (RTV) in the baseline condition, and attenuated contingent negative variation (CNV) amplitude (response preparation) in the fast-incentive condition. The preterm group, only, did not show significant within-group adjustments in P3 amplitude (attention allocation) and SCL (peripheral arousal). Dimensional analyses showed that ADHD symptoms scores correlated significantly with MRT, RTV and CNV amplitude only. Conclusions: We find impairments in cognition and brain function in preterm-born adolescents that are linked to increased ADHD symptoms, as well as further impairments, in lack of malleability in neurophysiological processes. Our findings indicate that such impairments extend at least to adolescence. Future studies should extend these investigations into adulthood. [ABSTRACT FROM AUTHOR]

BackgroundIn adults, attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BD) have certain overlapping symptoms, which can lead to uncertainty regarding the boundaries of the two disorders. Despite evidence of cognitive impairments in both disorders separately, such as in attentional and inhibitory processes, data on direct comparisons across ADHD and BD on cognitive–neurophysiological measures are as yet limited.MethodWe directly compared cognitive performance and event-related potential measures from a cued continuous performance test in 20 women with ADHD, 20 women with BD (currently euthymic) and 20 control women.ResultsThe NoGo-N2 was attenuated in women with BD, reflecting reduced conflict monitoring, compared with women with ADHD and controls (both p < 0.05). Both ADHD and BD groups showed a reduced NoGo-P3, reflecting inhibitory control, compared with controls (both p < 0.05). In addition, the contingent negative variation was significantly reduced in the ADHD group (p = 0.05), with a trend in the BD group (p = 0.07), compared with controls.ConclusionsThese findings indicate potential disorder-specific (conflict monitoring) and overlapping (inhibitory control, and potentially response preparation) neurophysiological impairments in women with ADHD and women with BD. The identified neurophysiological parameters further our understanding of neurophysiological impairments in women with ADHD and BD, and are candidate biomarkers that may aid in the identification of the diagnostic boundaries of the two disorders. [ABSTRACT FROM PUBLISHER]

Background. Substantial overlap has been reported between attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Deficits in executive function (EF) are characteristic of both disorders but these impairments have not been compared directly across pure and co-morbid cases using event-related potentials (ERPs). Method. Behavioural parameters and ERPs were recorded during a flankered cued-continuous performance test (CPT-OX) administered to 8-13-year-old boys with ASD (n = 19), ADHD (n = 18), co-morbid ASD + ADHD (n = 29) and typically developing controls (TD; n = 26). Preparatory processing (contingent negative variation, CNV) and attentional orienting (Cue-P3) at cues, response execution at targets (Go-P3), inhibitory processing at non-targets (NoGo-P3) and conflict monitoring between target and non-target trials (Go-N2 v. NoGo-N2) were examined. Results. Categorical diagnoses and quantitative trait measures indicated that participants with ADHD (ADHD/ASD + ADHD) made more omission errors and exhibited increased reaction-time (RT) variability and reduced amplitude of the Cue-P3 and NoGo-P3 compared to TD/ASD participants. Participants with ASD (ASD/ ASD + ADHD) demonstrated reduced N2 enhancement from Go to NoGo trials compared to TD/ADHD participants. Participants with ASD-only displayed enhanced CNV amplitude compared to ASD + ADHD and TD participants. Conclusions. Children with ADHD show deficits in attentional orienting and inhibitory control whereas children with ASD show abnormalities in conflict monitoring and response preparation. Children with co-morbid ASD + ADHD present as an additive co-occurrence with deficits of both disorders, although non-additive effects are suggested for response preparation. Measuring ERPs that index attention and inhibition is useful in disentangling cognitive markers of ASD and ADHD and elucidating the basis of co-occurring ASD + ADHD to guide clinical assessment. [ABSTRACT FROM AUTHOR]

BackgroundParent and teacher ratings of attention deficit hyperactivity disorder (ADHD) symptoms yield high estimates of heritability whereas self-ratings typically yield lower estimates. To understand why, the present study examined the etiological overlap between parent, teacher and self-ratings of ADHD symptoms in a population-based sample of 11–12-year-old twins.MethodParticipants were from the Twins Early Development Study (TEDS). ADHD symptoms were assessed using the Strengths and Difficulties Questionnaire (SDQ) hyperactivity scale completed by parents, teachers and children. Structural equation modeling was used to examine genetic and environmental contributions to phenotypic variance/covariance.ResultsThe broad-sense heritability of ADHD symptoms was 82% for parent ratings, 60% for teacher ratings and 48% for self-ratings. Post-hoc analyses revealed significantly higher heritability for same-teacher than different-teacher ratings of ADHD (76% v. 49%). A common pathway model best explained the relationship between different informant ratings, with common genetic influences accounting for 84% of the covariance between parent, teacher and self-rated ADHD symptoms. The remaining variance was explained by rater-specific genetic and non-shared environmental influences.ConclusionsDespite different heritabilities, there were shared genetic influences for parent, teacher and self-ratings of ADHD symptoms, indicating that different informants rated some of the same aspects of behavior. The low heritability estimated for self-ratings and different-teacher ratings may reflect increased measurement error when different informants rate each twin from a pair, and/or greater non-shared environmental influences. Future studies into the genetic influences on ADHD should incorporate informant data in addition to self-ratings to capture a pervasive, heritable component of ADHD symptomatology. [ABSTRACT FROM AUTHOR]

ADHD is a common neurodevelopmental disorder that persists into adulthood in around two-thirds of cases. Current operational definitions of ADHD focus on three core domains of inattention, overactivity and impulsivity, yet it is widely recognised that there is a wider range of psychopathology that co-occurs alongside these core symptoms. Among the most prevalent of these in adults with ADHD is mood instability, characterized by shifts in mood from ‘highs’ to ‘lows’, frustration, and chronic irritability. Mood instability may often be the main presenting symptom of ADHD and may also be one of the more impairing features of the disorder. Importantly, it has been noted that treatment for ADHD with stimulants or atomoxetine often results in improvements in mood instability symptoms in the same timescale as other core symptoms of ADHD, indicating that mood instability can be considered a symptom of ADHD just as much as inattention, impulsivity and hyperactivity. Here we report on key findings that show the very high correlation between ADHD and mood instability and the response of such symptoms to treatment with stimulant medications. Further work is aimed to clarify whether the problems with regulation of emotional responses and mood states seen in ADHD arise from the same underlying processes that lead to impaired regulation of attention and impulse control. [ABSTRACT FROM AUTHOR]

ADHD in adults is frequently associated with unstable or irritable moods reflecting difficulties with emotion regulation. Effect sizes of drug treatments on symptoms that reflect difficulties with emotion regulation, are similar to those on core ADHD symptoms, with co-variation of around 0.8 between the two types of symptoms during the treatment response. We therefore set out to investigate whether variability in mood results from the same aetiological processes that lead to variability in behaviour and cognitive performance in ADHD. Using real-time self-monitoring of emotional states and ADHD symptoms every two hours for 3-5 days, we characterised the mood changes in ADHD. Variability in both mood and ADHD symptoms (measured as the standard deviation) were significantly correlated with self-rated ADHD symptoms of inattention and hyperactivity. Subsequent analyses will link the observed symptom changes to cognitive-electrophysiological measures which are reliable indicators of core processes that underlie cognitive deficits associated with ADHD. We previously showed that a familial reaction time (mean and variability) factor explains 70% and commission and omission errors 20%, of the familial effects on ADHD. This finding concurs with the developmental model of Halperin which postulates that ADHD is linked to an early-appearing and enduring subcortical dysfunction, reflected in reaction time variability, while persistence/desistence of ADHD is dependent on maturational changes in executive control during adolescence reflected in commission and omission errors. We propose that at a behavioural level the subcortical deficit leads to dysregulation of a number of processes, including attentional, impulsive and emotional control. [Copyright &y& Elsevier]

ADHD in adults is frequently associated with unstable or irritable moods reflecting difficulties with emotion regulation. Effect sizes of drug treatments on symptoms that reflect difficulties with emotion regulation, are similar to those on core ADHD symptoms, with co-variation of around 0.8 between the two types of symptoms during the treatment response. We therefore set out to investigate whether variability in mood results from the same aetiological processes that lead to variability in behaviour and cognitive performance in ADHD. Using real-time self-monitoring of emotional states and ADHD symptoms every two hours for 3-5 days, we characterised the mood changes in ADHD. Variability in both mood and ADHD symptoms (measured as the standard deviation) were significantly correlated with self-rated ADHD symptoms of inattention and hyperactivity. Subsequent analyses will link the observed symptom changes to cognitive-electrophysiological measures which are reliable indicators of core processes that underlie cognitive deficits associated with ADHD. We previously showed that a familial reaction time (mean and variability) factor explains 70% and commission and omission errors 20%, of the familial effects on ADHD. This finding concurs with the developmental model of Halperin which postulates that ADHD is linked to an early-appearing and enduring subcortical dysfunction, reflected in reaction time variability, while persistence/desistence of ADHD is dependent on maturational changes in executive control during adolescence reflected in commission and omission errors. We propose that at a behavioural level the subcortical deficit leads to dysregulation of a number of processes, including attentional, impulsive and emotional control. [Copyright &y& Elsevier]

BackgroundTwin and sibling studies have identified specific cognitive phenotypes that may mediate the association between genes and the clinical symptoms of attention deficit hyperactivity disorder (ADHD). ADHD is also associated with lower IQ scores. We aimed to investigate whether the familial association between measures of cognitive performance and the clinical diagnosis of ADHD is mediated through shared familial influences with IQ.MethodMultivariate familial models were run on data from 1265 individuals aged 6–18 years, comprising 920 participants from ADHD sibling pairs and 345 control participants. Cognitive assessments included a four-choice reaction time (RT) task, a go/no-go task, a choice–delay task and an IQ assessment. The analyses focused on the cognitive variables of mean RT (MRT), RT variability (RTV), commission errors (CE), omission errors (OE) and choice impulsivity (CI).ResultsSignificant familial association (rF) was confirmed between cognitive performance and both ADHD (rF=0.41–0.71) and IQ (rF=−0.25 to −0.49). The association between ADHD and cognitive performance was largely independent (80–87%) of any contribution from etiological factors shared with IQ. The exception was for CI, where 49% of the overlap could be accounted for by the familial variance underlying IQ.ConclusionsThe aetiological factors underlying lower IQ in ADHD seem to be distinct from those between ADHD and RT/error measures. This suggests that lower IQ does not account for the key cognitive impairments observed in ADHD. The results have implications for molecular genetic studies designed to identify genes involved in ADHD. [ABSTRACT FROM PUBLISHER]

Abstract: Conventional neuropathological analysis for brain malignancies is heavily reliant on the observation of morphological abnormalities, observed in thin, stained sections of tissue. Small Angle X-ray Scattering (SAXS) data provide an alternative means of distinguishing pathology by examining the ultra-structural (nanometer length scales) characteristics of tissue. To evaluate the diagnostic potential of SAXS for brain tumors, data was collected from normal, malignant and benign tissues of the human brain at station 2.1 of the Daresbury Laboratory Synchrotron Radiation Source and subjected to data mining and multivariate statistical analysis. The results suggest SAXS data may be an effective classifier of malignancy. [Copyright &y& Elsevier]

Abstract: Glioblastoma multiforme (GBM) is the commonest and most aggressive primary brain tumor in humans. The high rate of tumor recurrence results in a poor prognosis despite multimodality treatment. One reason for high rate of recurrence is the invasive nature of the tumor into the surrounding normal brain tissue or multifocal occurrence at sites remote from that of the primary tumor establishment. Existing imaging demonstrates the primary tumor but fail to show the residual tumor microaggregates left behind following initial treatment. In this study, we employed diffraction-enhanced imaging (DEI) in an attempt to find an imaging modality that will provide visualization of residual disease that is not be apparent on MRI or CT scans. [Copyright &y& Elsevier]