Self-referential cognition and empathy in autism.

BACKGROUND: Individuals with autism spectrum conditions (ASC) have profound impairments in the interpersonal social domain, but it is unclear if individuals with ASC also have impairments in the intrapersonal self-referential domain. We aimed to evaluate across several well validated measures in both domains, whether both self-referential cognition and empathy are impaired in ASC and whether these two domains are related to each other. METHODOLOGY/PRINCIPAL FINDINGS: Thirty adults aged 19-45, with Asperger Syndrome or high-functioning autism and 30 age, sex, and IQ matched controls participated in the self-reference effect (SRE) paradigm. In the SRE paradigm, participants judged adjectives in relation to the self, a similar close other, a dissimilar non-close other, or for linguistic content. Recognition memory was later tested. After the SRE paradigm, several other complimentary self-referential cognitive measures were taken. Alexithymia and private self-consciousness were measured via self-report. Self-focused attention was measured on the Self-Focus Sentence Completion task. Empathy was measured with 3 self-report instruments and 1 performance measure of mentalizing (Eyes test). Self-reported autistic traits were also measured with the Autism Spectrum Quotient (AQ). Although individuals with ASC showed a significant SRE in memory, this bias was decreased compared to controls. Individuals with ASC also showed reduced memory for the self and a similar close other and also had concurrent impairments on measures of alexithymia, self-focused attention, and on all 4 empathy measures. Individual differences in self-referential cognition predicted mentalizing ability and self-reported autistic traits. More alexithymia and less self memory was predictive of larger mentalizing impairments and AQ scores regardless of diagnosis. In ASC, more self-focused attention is associated with better mentalizing ability and lower AQ scores, while in controls, more self-focused attention is associated with decreased mentalizing ability and higher AQ scores. Increasing private self-consciousness also predicted better mentalizing ability, but only for individuals with ASC. CONCLUSIONS/SIGNIFICANCE: We conclude that individuals with ASC have broad impairments in both self-referential cognition and empathy. These two domains are also intrinsically linked and support predictions made by simulation theory. Our results also highlight a specific dysfunction in ASC within cortical midlines structures of the brain such as the medial prefrontal cortex

reval: A Python package to determine best clustering solutions with stability-based relative clustering validation.

Determining the best partition for a dataset can be a challenging task because of the lack of a priori information within an unsupervised learning framework and the absence of a unique clustering validation approach to evaluate clustering solutions. Here we present reval: a Python package that leverages stability-based relative clustering validation methods to select best clustering solutions as the ones that replicate, via supervised learning, on unseen subsets of data. The implementation of relative validation methods can contribute to the theory of clustering by fostering new approaches for the investigation of clustering results in different situations and for different data distributions. This work aims at contributing to this effort by implementing a package that works with multiple clustering and classification algorithms, hence allowing both the automation of the labeling process and the assessment of the stability of different clustering mechanisms

reval: A Python package to determine best clustering solutions with stability-based relative clustering validation.

Determining the best partition for a dataset can be a challenging task because of the lack of a priori information within an unsupervised learning framework and the absence of a unique clustering validation approach to evaluate clustering solutions. Here we present reval: a Python package that leverages stability-based relative clustering validation methods to select best clustering solutions as the ones that replicate, via supervised learning, on unseen subsets of data. The implementation of relative validation methods can contribute to the theory of clustering by fostering new approaches for the investigation of clustering results in different situations and for different data distributions. This work aims at contributing to this effort by implementing a package that works with multiple clustering and classification algorithms, hence allowing both the automation of the labeling process and the assessment of the stability of different clustering mechanisms

The ASD Living Biology: from cell proliferation to clinical phenotype.

Autism spectrum disorder (ASD) has captured the attention of scientists, clinicians and the lay public because of its uncertain origins and striking and unexplained clinical heterogeneity. Here we review genetic, genomic, cellular, postmortem, animal model, and cell model evidence that shows ASD begins in the womb. This evidence leads to a new theory that ASD is a multistage, progressive disorder of brain development, spanning nearly all of prenatal life. ASD can begin as early as the 1st and 2nd trimester with disruption of cell proliferation and differentiation. It continues with disruption of neural migration, laminar disorganization, altered neuron maturation and neurite outgrowth, disruption of synaptogenesis and reduced neural network functioning. Among the most commonly reported high-confidence ASD (hcASD) genes, 94% express during prenatal life and affect these fetal processes in neocortex, amygdala, hippocampus, striatum and cerebellum. A majority of hcASD genes are pleiotropic, and affect proliferation/differentiation and/or synapse development. Proliferation and subsequent fetal stages can also be disrupted by maternal immune activation in the 1st trimester. Commonly implicated pathways, PI3K/AKT and RAS/ERK, are also pleiotropic and affect multiple fetal processes from proliferation through synapse and neural functional development. In different ASD individuals, variation in how and when these pleiotropic pathways are dysregulated, will lead to different, even opposing effects, producing prenatal as well as later neural and clinical heterogeneity. Thus, the pathogenesis of ASD is not set at one point in time and does not reside in one process, but rather is a cascade of prenatal pathogenic processes in the vast majority of ASD toddlers. Despite this new knowledge and theory that ASD biology begins in the womb, current research methods have not provided individualized information: What are the fetal processes and early-age molecular and cellular differences that underlie ASD in each individual child? Without such individualized knowledge, rapid advances in biological-based diagnostic, prognostic, and precision medicine treatments cannot occur. Missing, therefore, is what we call ASD Living Biology. This is a conceptual and paradigm shift towards a focus on the abnormal prenatal processes underlying ASD within each living individual. The concept emphasizes the specific need for foundational knowledge of a living child's development from abnormal prenatal beginnings to early clinical stages. The ASD Living Biology paradigm seeks this knowledge by linking genetic and in vitro prenatal molecular, cellular and neural measurements with in vivo post-natal molecular, neural and clinical presentation and progression in each ASD child. We review the first such study, which confirms the multistage fetal nature of ASD and provides the first in vitro fetal-stage explanation for in vivo early brain overgrowth. Within-child ASD Living Biology is a novel research concept we coin here that advocates the integration of in vitro prenatal and in vivo early post-natal information to generate individualized and group-level explanations, clinically useful prognoses, and precision medicine approaches that are truly beneficial for the individual infant and toddler with ASD

How to get from imaginary to real chemical potential

Using the exactly solvable Gross-Neveu model as theoretical laboratory, we analyse in detail the relationship between a relativistic quantum field theory at real and imaginary chemical potential. We find that one can retrieve the full information about the phase diagram of the theory from an imaginary chemical potential calculation. The prerequisite is to evaluate and analytically continue the effective potential for the chiral order parameter, rather than thermodynamic observables or phase boundaries. In the case of an inhomogeneous phase, one needs to compute the full effective action, a functional of the space-dependent order parameter, at imaginary chemical potential.Comment: revtex, 9 pages, 10 figures; v2: add more references, modify concluding sectio

Sex/gender differences and autism: setting the scene for future research.

OBJECTIVE: The relationship between sex/gender differences and autism has attracted a variety of research ranging from clinical and neurobiological to etiological, stimulated by the male bias in autism prevalence. Findings are complex and do not always relate to each other in a straightforward manner. Distinct but interlinked questions on the relationship between sex/gender differences and autism remain underaddressed. To better understand the implications from existing research and to help design future studies, we propose a 4-level conceptual framework to clarify the embedded themes. METHOD: We searched PubMed for publications before September 2014 using search terms "'sex OR gender OR females' AND autism." A total of 1,906 articles were screened for relevance, along with publications identified via additional literature reviews, resulting in 329 articles that were reviewed. RESULTS: Level 1, "Nosological and diagnostic challenges," concerns the question, "How should autism be defined and diagnosed in males and females?" Level 2, "Sex/gender-independent and sex/gender-dependent characteristics," addresses the question, "What are the similarities and differences between males and females with autism?" Level 3, "General models of etiology: liability and threshold," asks the question, "How is the liability for developing autism linked to sex/gender?" Level 4, "Specific etiological-developmental mechanisms," focuses on the question, "What etiological-developmental mechanisms of autism are implicated by sex/gender and/or sexual/gender differentiation?" CONCLUSIONS: Using this conceptual framework, findings can be more clearly summarized, and the implications of the links between findings from different levels can become clearer. Based on this 4-level framework, we suggest future research directions, methodology, and specific topics in sex/gender differences and autism.Dr. Lai has received grant or research support from the William Binks Autism Neuroscience Fellowship, the European Autism Interventions— A Multicentre Study for Developing New Medications (EU-AIMS), and Wolfson College, Cambridge University. Dr. Lombardo has received grant or research support from the British Academy, the Wellcome Trust, and Jesus College, Cambridge University. Dr. Auyeung has received grant or research support from the Wellcome Trust. Dr. Chakrabarti has received grant or research support from the UK Medical Research Council. Dr. Baron-Cohen has received grant or research support from the Wellcome Trust, the EU-AIMS, the UK Medical Research Council, and the Autism Research Trust.This is the final published version. It first appeared at http://www.sciencedirect.com/science/article/pii/S0890856714007254#

Induced P-wave Superfluidity in Asymmetric Fermi Gases

We show that two new intra-species P-wave superfluid phases appear in two-component asymmetric Fermi systems with short-range S-wave interactions. In the BEC limit, phonons of the molecular BEC induce P-wave superfluidity in the excess fermions. In the BCS limit, density fluctuations induce P-wave superfluidity in both the majority and the minority species. These phases may be realized in experiments with spin-polarized Fermi gases.Comment: published versio

The thermal QCD transition with two flavours of twisted mass fermions

We investigate the thermal QCD transition with two flavors of maximally twisted mass fermions for a set of pion masses, 300 MeV \textless $m_\pi$ \textless 500 MeV, and lattice spacings $a$ \textless 0.09 fm. We determine the pseudo-critical temperatures and discuss their extrapolation to the chiral limit using scaling forms for different universality classes, as well as the scaling form for the magnetic equation of state. For all pion masses considered we find resonable consistency with O(4) scaling plus leading corrections. However, a true distinction between the O(4) scenario and a first order scenario in the chiral limit requires lighter pions than are currently in use in simulations of Wilson fermions.Comment: 11 pages, 11 figure