Rationalizing the many uses of animals:Application of the 4N justifications beyond meat

Past research has uncovered four common justifications for using animals as food—the 4Ns—that eating meat is Natural, Normal, Necessary, and Nice. The current research investigated the extent to which the 4Ns might apply more generally to other animal uses. Two studies examined the moral justifications people spontaneously offered for various animal uses, including household products, clothing, culling, and horse racing (Study1), and in zoos, TV/film, as pets, and for medical testing (Study 2). Participants offered reasons for why it is okay to use animals and the responses were coded by independent raters. The 4N categories accounted for the majority of justifications across most uses. There was great variability in justification categories offered for each use, and some uses generated justification categories not covered within the 4N scheme, including humane treatment, prioritization of human lives, and sustainability arguments. This research provides a large-scope investigation of animal-use justifications that moves beyond meat consumption

Global and Local Connectivity Differences Converge With Gene Expression in a Neurodevelopmental Disorder of Known Genetic Origin.

Knowledge of genetic cause in neurodevelopmental disorders can highlight molecular and cellular processes critical for typical development. Furthermore, the relative homogeneity of neurodevelopmental disorders of known genetic origin allows the researcher to establish the subsequent neurobiological processes that mediate cognitive and behavioral outcomes. The current study investigated white matter structural connectivity in a group of individuals with intellectual disability due to mutations in ZDHHC9. In addition to shared cause of cognitive impairment, these individuals have a shared cognitive profile, involving oromotor control difficulties and expressive language impairment. Analysis of structural network properties using graph theory measures showed global reductions in mean clustering coefficient and efficiency in the ZDHHC9 group, with maximal differences in frontal and parietal areas. Regional variation in clustering coefficient across cortical regions in ZDHHC9 mutation cases was significantly associated with known pattern of expression of ZDHHC9 in the normal adult human brain. The results demonstrate that a mutation in a single gene impacts upon white matter organization across the whole-brain, but also shows regionally specific effects, according to variation in gene expression. Furthermore, these regionally specific patterns may link to specific developmental mechanisms, and correspond to specific cognitive deficits

Correction: Creating genetic reports that are understood by nonspecialists: a case study

An amendment to this paper has been published and can be accessed via a link at the top of the paper

Psychopathology and cognitive performance in individuals with membrane-associated guanylate kinase mutations: a functional network phenotyping study.

BACKGROUND: Rare pathogenic variants in membrane-associated guanylate kinase (MAGUK) genes cause intellectual disability (ID) and have recently been associated with neuropsychiatric risk in the non-ID population. However, it is not known whether risk for psychiatric symptoms amongst individuals with ID due to MAGUK gene mutations is higher than expected for the degree of general intellectual impairment, nor whether specific cognitive differences are associated with disruption to this gene functional network. METHODS: This study addresses these two questions via behavioural questionnaires and cognitive testing, applying quantitative methods previously validated in populations with ID. We compared males with X-linked ID caused by mutations in three MAGUK genes (PAK3, DLG3, OPHN1; n = 9) to males with ID caused by mutations in other X chromosome genes (n = 17). Non-parametric and parametric analyses were applied as appropriate to data. RESULTS: Groups did not differ in age, global cognitive impairment, adaptive function or epilepsy prevalence. However, individuals with MAGUK gene mutations demonstrated significantly higher psychopathology risks, comprising elevated total problem behaviours, prominent hyperactivity and elevated scores on an autism screening checklist. Despite these overt difficulties, individuals in the MAGUK group performed more accurately than expected for age and intelligence quotient (IQ) on computerised tests of visual attention, convergent with mouse models of MAGUK loss-of-function. CONCLUSIONS: Our findings support a role for MAGUK genes in influencing cognitive parameters relevant to psychiatric risk. In addition to establishing clear patterns of impairment for this group, our findings highlight the importance of careful phenotyping after genetic diagnosis, showing that gene functional network disruptions can be associated with specific psychopathological risks and cognitive differences within the context of ID.We thank all study participants and their families for extensive contributions to this project. This study was funded by the Academy of Medical Sciences/Wellcome Trust via a Starter Grant for Clinical Lecturers to KB. KB is funded by a National Institute for Health Research Academic Clinical Lectureship. GS is funded by a Wellcome Trust project grant and a James S. McDonnell Foundation Understanding Human Cognition Scholar Award. DEA is funded by an MRC UK intramural programme (MC-A0606-5PQ41). FLR is funded by the National Institute for Health Research (Cambridge Biomedical Research Centre).This is the final version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s11689-015-9105-

Childhood intellectual disability and parents' mental health: integrating social, psychological and genetic influences.

BACKGROUND: Intellectual disability has a complex effect on the well-being of affected individuals and their families. Previous research has identified multiple risk and protective factors for parental mental health, including socioeconomic circumstances and child behaviour. AIMS: This study explored whether genetic cause of childhood intellectual disability contributes to parental well-being. METHOD: Children from across the UK with intellectual disability due to diverse genetic causes were recruited to the IMAGINE-ID study. Primary carers completed the Development and Well-being Assessment, including a measure of parental distress (Everyday Feeling Questionnaire). Genetic diagnoses were broadly categorised into aneuploidy, chromosomal rearrangements, copy number variants (CNVs) and single nucleotide variants. RESULTS: Compared with the UK general population, IMAGINE-ID parents (n = 888) reported significantly elevated emotional distress (Cohen's d = 0.546). Within-sample variation was related to recent life events and the perceived impact of children's difficulties. Impact was predicted by child age, physical disability, autistic characteristics and other behavioural difficulties. Genetic diagnosis also predicted impact, indirectly influencing parental well-being. Specifically, CNVs were associated with higher impact, not explained by CNV inheritance, neighbourhood deprivation or family structure. CONCLUSIONS: The mental health of parents caring for a child with intellectual disability is influenced by child and family factors, converging on parental appraisal of impact. We found that genetic aetiologies, broadly categorised, also influence impact and thereby family risks. Recognition of these risk factors could improve access to support for parents, reduce their long-term mental health needs and improve well-being of individuals with intellectual disability.This work was supported by the UK Medical Research Council (grant number G101400 to K.B.), UK Medical Research Council and Medical Research Foundation (grant number MR-N022572-1 to the IMAGINE-ID study; Principle Investigators: David H. Skuse, F Lucy Raymond, Jeremy Hall, Marianne Van den Bree, Michael J. Hall) and the Baily Thomas Charitable Trust (to K.B.)

X-Rays From Massive OB Stars: Thermal Emission From Radiative Shocks

Chandra gratings spectra of a sample of 15 massive OB stars were analyzed under the basic assumption that the X-ray emission is produced in an ensemble of shocks formed in the winds driven by these objects. Shocks develop either as a result of radiation-driven instabilities or due to confinement of the wind by relatively strong magnetic field, and since they are radiative, a simple model of their X-ray emission was developed that allows a direct comparison with observations. According to our model, the shock structures (clumps, complete or fractional shells) eventually become `cold' clouds in the X-ray sky of the star. As a result, it is expected that for large covering factors of the hot clumps, there is a high probability for X-ray absorption by the `cold' clouds, resulting in blue-shifted spectral lines. Our analysis has revealed that such a correlation indeed exists for the considered sample of OB stars. As to the temperature characteristics of the X-ray emission plasma, the studied OB stars fall in two groups: (i) one with plasma temperature limited to 0.1-0.4 keV; (ii) the other wtih X-rays produced in plasmas at considerably higher temperatures. We argue that the two groups correspond to different mechanisms for the origin of X-rays: in radiative-driven instability shocks and in magnetically-confined wind shocks, respectively.Comment: 11 pages, 4 figures, 2 tables; accepted for publication in MNRA

Ceres' opposition effect observed by the Dawn framing camera

The surface reflectance of planetary regoliths may increase dramatically towards zero phase angle, a phenomenon known as the opposition effect (OE). Two physical processes that are thought to be the dominant contributors to the brightness surge are shadow hiding (SH) and coherent backscatter (CB). The occurrence of shadow hiding in planetary regoliths is self-evident, but it has proved difficult to unambiguously demonstrate CB from remote sensing observations. One prediction of CB theory is the wavelength dependence of the OE angular width. The Dawn spacecraft observed the OE on the surface of dwarf planet Ceres. We characterize the OE over the resolved surface, including the bright Cerealia Facula, and to find evidence for SH and/or CB. We analyze images of the Dawn framing camera by means of photometric modeling of the phase curve. We find that the OE of most of the investigated surface has very similar characteristics, with an enhancement factor of 1.4 and a FWHM of 3{\deg} (broad OE). A notable exception are the fresh ejecta of the Azacca crater, which display a very narrow brightness enhancement that is restricted to phase angles $< 0.5${\deg} (narrow OE); suggestively, this is in the range in which CB is thought to dominate. We do not find a wavelength dependence for the width of the broad OE, and lack the data to investigate the dependence for the narrow OE. The prediction of a wavelength-dependent CB width is rather ambiguous. The zero-phase observations allow us to determine Ceres' visible geometric albedo as $p_V = 0.094 \pm 0.005$. A comparison with other asteroids suggests that Ceres' broad OE is typical for an asteroid of its spectral type, with characteristics that are primarily linked to surface albedo. Our analysis suggests that CB may occur on the dark surface of Ceres in a highly localized fashion.Comment: Credit: Schr\"oder et al, A&A in press, 2018, reproduced with permission, \copyright ES

Epilepsy, cognitive deficits and neuroanatomy in males with ZDHHC9 mutations.

OBJECTIVE: Systematic investigation of individuals with intellectual disability after genetic diagnosis can illuminate specific phenotypes and mechanisms relevant to common neurodevelopmental disorders. We report the neurological, cognitive and neuroanatomical characteristics of nine males from three families with loss-of-function mutations in ZDHHC9 (OMIM #300799). METHODS: All known cases of X-linked intellectual disability (XLID) due to ZDHHC9 mutation in the United Kingdom were invited to participate in a study of neurocognitive and neuroimaging phenotypes. RESULTS: Seven out of nine males with ZDHHC9 mutations had been diagnosed with epilepsy, exceeding epilepsy risk in XLID comparison subjects (P = 0.01). Seizure histories and EEG features amongst ZDHHC9 mutation cases shared characteristics with rolandic epilepsy (RE). Specific cognitive deficits differentiated males with ZDHHC9 mutations from XLID comparison subjects and converged with reported linguistic and nonlinguistic deficits in idiopathic RE: impaired oromotor control, reduced verbal fluency, and impaired inhibitory control on visual attention tasks. Consistent neuroanatomical abnormalities included thalamic and striatal volume reductions and hypoplasia of the corpus callosum. INTERPRETATION: Mutations in ZDHHC9 are associated with susceptibility to focal seizures and specific cognitive impairments intersecting with the RE spectrum. Neurocognitive deficits are accompanied by consistent abnormalities of subcortical structures and inter-hemispheric connectivity. The biochemical, cellular and network-level mechanisms responsible for the ZDHHC9-associated neurocognitive phenotype may be relevant to cognitive outcomes in RE.This study was funded by the Wellcome Trust/Academy of Medical Sciences (Starter Grant for Clinical Lecturers to K. B.). K. B. is funded by the National Institute of Health Research (Academic Clinical Lectureship). J. B. and D. A. are funded by an MRC UK intramural programme (MCA0606- 5PQ41). G. S. is funded by Wellcome Trust project grant (WT079326AIA) and a James S. McDonnell Foundation Understanding Human Cognition Scholar Award. F. L. R. is funded by the National Institute of Health Research (Cambridge Biomedical Research Centre).This is the final published version. It first appeared at http://onlinelibrary.wiley.com/doi/10.1002/acn3.196/full