Panarchy, Transformation, and Place: Exploring Social Change and Resiliency Through an Ecological Lens

This paper uses panarchy theory, a complexity theory used in environmental management, to describe transformation in social systems. To introduce the concept of panarchy, the authors reflect on the naming of their new son and the changes that their choice of name caused in their family. They then bridge this analogy into Author 1's, (first name) preliminary dissertation research findings that invited exemplary Canadians to revisit their childhood and adolescent transformative place. Using video ethnography and participatory action research, these interviews should be simultaneously viewed when reading this article at http://www.transformativeplaces.com/. The five components of panarchy, scale, time, holarchy, cycles, and cross-scale dependency are demonstrated by the interviewees' connection to their transformative outdoor childhood or adolescent place. Observing systems and the change that arises from 'release' events supports human and social resiliency. The terminology used in panarchy theory provides an ecological approach to describing social systems and their transformation

Continuous flow mobility classifier interface with mass spectrometer

A continuous flow mobility classifier provide the ability to perform two-dimensional separation in mass spectrometry. An ionization system is used to ionize a sample. A differential mobility analyzer (DMA) (e.g., a nano-radial DMA) is coupled to the ionization system and to a mass spectrometer. The nano-RDMA is configured to separate the ionized sample by mobility for subsequent mass analysis by the mass spectrometer

Theory of mind mediates the prospective relationship between abnormal social brain network morphology and chronic behavior problems after pediatric traumatic brain injury

Childhood and adolescence coincide with rapid maturation and synaptic reorganization of distributed neural networks that underlie complex cognitive-affective behaviors. These regions, referred to collectively as the ‘social brain network’ (SBN) are commonly vulnerable to disruption from pediatric traumatic brain injury (TBI); however, the mechanisms that link morphological changes in the SBN to behavior problems in this population remain unclear. In 98 children and adolescents with mild to severe TBI, we acquired 3D T1-weighted MRIs at 2–8 weeks post-injury. For comparison, 33 typically developing controls of similar age, sex and education were scanned. All participants were assessed on measures of Theory of Mind (ToM) at 6 months post-injury and parents provided ratings of behavior problems at 24-months post-injury. Severe TBI was associated with volumetric reductions in the overall SBN package, as well as regional gray matter structural change in multiple component regions of the SBN. When compared with TD controls and children with milder injuries, the severe TBI group had significantly poorer ToM, which was associated with more frequent behavior problems and abnormal SBN morphology. Mediation analysis indicated that impaired theory of mind mediated the prospective relationship between abnormal SBN morphology and more frequent chronic behavior problems. Our findings suggest that sub-acute alterations in SBN morphology indirectly contribute to long-term behavior problems via their influence on ToM. Volumetric change in the SBN and its putative hub regions may represent useful imaging biomarkers for prediction of post-acute social cognitive impairment, which may in turn elevate risk for chronic behavior problems

Most Reported Genetic Associations with General Intelligence Are Probably False Positives

General intelligence (g) and virtually all other behavioral traits are heritable. Associations between g and specific single-nucleotide polymorphisms (SNPs) in several candidate genes involved in brain function have been reported. We sought to replicate published associations between g and 12 specific genetic variants (in the genes DTNBP1, CTSD, DRD2, ANKK1, CHRM2, SSADH, COMT, BDNF, CHRNA4, DISC1, APOE, and SNAP25) using data sets from three independent, well-characterized longitudinal studies with samples of 5,571, 1,759, and 2,441 individuals. Of 32 independent tests across all three data sets, only 1 was nominally significant. By contrast, power analyses showed that we should have expected 10 to 15 significant associations, given reasonable assumptions for genotype effect sizes. For positive controls, we confirmed accepted genetic associations for Alzheimer’s disease and body mass index, and we used SNP-based calculations of genetic relatedness to replicate previous estimates that about half of the variance in g is accounted for by common genetic variation among individuals. We conclude that the molecular genetics of psychology and social science requires approaches that go beyond the examination of candidate genes.Economic

Uncovering the neuroanatomical correlates of cognitive, affective and conative theory of mind in paediatric traumatic brain injury: a neural systems perspective

Deficits in theory of mind (ToM) are common after neurological insult acquired in the first and second decade of life, however the contribution of large-scale neural networks to ToM deficits in children with brain injury is unclear. Using paediatric traumatic brain injury (TBI) as a model, this study investigated the sub-acute effect of paediatric traumatic brain injury on grey-matter volume of three large-scale, domain-general brain networks (the Default Mode Network, DMN; the Central Executive Network, CEN; and the Salience Network, SN), as well as two domain-specific neural networks implicated in social-affective processes (the Cerebro-Cerebellar Mentalizing Network, CCMN and the Mirror Neuron/Empathy Network, MNEN). We also evaluated prospective structure–function relationships between these large-scale neural networks and cognitive, affective and conative ToM. 3D T1- weighted magnetic resonance imaging sequences were acquired sub-acutely in 137 children [TBI: n = 103; typically developing (TD) children: n = 34]. All children were assessed on measures of ToM at 24-months post-injury. Children with severe TBI showed sub-acute volumetric reductions in the CCMN, SN, MNEN, CEN and DMN, as well as reduced grey-matter volumes of several hub regions of these neural networks. Volumetric reductions in the CCMN and several of its hub regions, including the cerebellum, predicted poorer cognitive ToM. In contrast, poorer affective and conative ToM were predicted by volumetric reductions in the SN and MNEN, respectively. Overall, results suggest that cognitive, affective and conative ToM may be prospectively predicted by individual differences in structure of different neural systems—the CCMN, SN and MNEN, respectively. The prospective relationship between cerebellar volume and cognitive ToM outcomes is a novel finding in our paediatric brain injury sample and suggests that the cerebellum may play a role in the neural networks important for ToM. These findings are discussed in relation to neurocognitive models of ToM. We conclude that detection of sub-acute volumetric abnormalities of large-scale neural networks and their hub regions may aid in the early identification of children at risk for chronic social-cognitive impairment

The Promises and Pitfalls of Genoeconomics

This article reviews existing research at the intersection of genetics and economics, presents some new findings that illustrate the state of genoeconomics research, and surveys the prospects of this emerging field. Twin studies suggest that economic outcomes and preferences, once corrected for measurement error, appear to be about as heritable as many medical conditions and personality traits. Consistent with this pattern, we present new evidence on the heritability of permanent income and wealth. Turning to genetic association studies, we survey the main ways that the direct measurement of genetic variation across individuals is likely to contribute to economics, and we outline the challenges that have slowed progress in making these contributions. The most urgent problem facing researchers in this field is that most existing efforts to find associations between genetic variation and economic behavior are based on samples that are too small to ensure adequate statistical power. This has led to many false positives in the literature. We suggest a number of possible strategies to improve and remedy this problem: (a) pooling data sets, (b) using statistical techniques that exploit the greater information content of many genes jointly, and (c) focusing on economically relevant traits that are most proximate to known biological mechanisms.EconomicsSociolog

Does neighborhood fast-food outlet exposure amplify inequalities in diet and obesity? A cross-sectional study.

BACKGROUND: Greater exposures to fast-food outlets and lower levels of education are independently associated with less healthy diets and obesity. Little is known about the interplay between these environmental and individual factors. OBJECTIVE: The purpose of this study was to test whether observed differences in fast-food consumption and obesity by fast-food outlet exposure are moderated by educational attainment. DESIGN: In a population-based cohort of 5958 adults aged 29-62 y in Cambridgeshire, United Kingdom, we used educational attainment-stratified regression models to estimate the food-frequency questionnaire-derived consumption of energy-dense "fast foods" (g/d) typically sold in fast-food restaurants and measured body mass index (BMI; in kg/m(2)) across geographic information system-derived home and work fast-food exposure quartiles. We used logistic regression to estimate the odds of obesity (BMI ≥30) and calculated relative excess risk due to interaction (RERI) on an additive scale. Participant data were collected during 2005-2013 and analyzed in 2015. RESULTS: Greater fast-food consumption, BMI, and odds of obesity were associated with greater fast-food outlet exposure and a lower educational level. Fast-food consumption and BMI were significantly different across education groups at all levels of fast-food outlet exposure (P < 0.05). High fast-food outlet exposure amplified differences in fast-food consumption across levels of education. The relation between fast-food outlet exposure and obesity was only significant among those who were least educated (OR: 2.05; 95% CI: 1.08, 3.87; RERI = 0.88), which suggested a positive additive interaction between education and fast-food outlet exposure. CONCLUSION: These findings suggest that efforts to improve diets and health through neighborhood-level fast-food outlet regulation might be effective across socioeconomic groups and may serve to reduce observed socioeconomic inequalities in diet and obesity.This work was undertaken by the Centre for Diet and Activity Research (CEDAR), a UK Clinical Research Collaboration (UKCRC) Public Health Research Centre of Excellence. Funding from the British Heart Foundation, Cancer Research UK, Economic and Social Research Council, Medical Research Council, the National Institute for Health Research [grant number ES/G007462/1], and the Wellcome Trust [grant number 087636/Z/08/Z], under the auspices of the UK Clinical Research Collaboration, is gratefully acknowledged. Core MRC Epidemiology Unit support [programme numbers MC_UU_12015/1 and MC_UU_12015/5] is acknowledged.This is the final version of the article. It first appeared from the American Society for Nutrition via http://dx.doi.org/10.3945/​ajcn.115.12813

RFC1 expansions are a common cause of idiopathic sensory neuropathy

After extensive evaluation, one-third of patients affected by polyneuropathy remain undiagnosed and are labelled as having chronic idiopathic axonal polyneuropathy, which refers to a sensory or sensory-motor, axonal, slowly progressive neuropathy of unknown origin. Since a sensory neuropathy/neuronopathy is identified in all patients with genetically confirmed RFC1 cerebellar ataxia, neuropathy, vestibular areflexia syndrome, we speculated that RFC1 expansions could underlie a fraction of idiopathic sensory neuropathies also diagnosed as chronic idiopathic axonal polyneuropathy. We retrospectively identified 225 patients diagnosed with chronic idiopathic axonal polyneuropathy (125 sensory neuropathy, 100 sensory-motor neuropathy) from our general neuropathy clinics in Italy and the UK. All patients underwent full neurological evaluation and a blood sample was collected for RFC1 testing. Biallelic RFC1 expansions were identified in 43 patients (34%) with sensory neuropathy and in none with sensory-motor neuropathy. Forty-two per cent of RFC1-positive patients had isolated sensory neuropathy or sensory neuropathy with chronic cough, while vestibular and/or cerebellar involvement, often subclinical, were identified at examination in 58%. Although the sensory ganglia are the primary pathological target of the disease, the sensory impairment was typically worse distally and symmetric, while gait and limb ataxia were absent in two-thirds of the cases. Sensory amplitudes were either globally absent (26%) or reduced in a length-dependent (30%) or non-length dependent pattern (44%). A quarter of RFC1-positive patients had previously received an alternative diagnosis, including Sj\uf6gren's syndrome, sensory chronic inflammatory demyelinating polyneuropathy and paraneoplastic neuropathy, while three cases had been treated with immune therapies