Characters with autism spectrum disorder in fiction : where are the women and girls?

Purpose Fiction has the potential to dispel myths and helps improve public understanding and knowledge of the experiences of under-represented groups. Representing the diversity of the population allows individuals to feel included, connected with and understood by society. Whether women and girls with autism spectrum disorder (ASD) are adequately and accurately represented in fictional media is currently unknown. The paper aims to discuss this issue. Design/methodology/approach Internet and library searches were conducted to identify female characters with ASD in works of fiction. Examples of such works were selected for further discussion based on their accessibility, perceived historical and cultural significance and additional characteristics that made the work particularly meaningful. Findings The search highlighted a number of female characters with ASD across a range of media, including books, television, film, theatre and video games. Many were written by authors who had a diagnosis of the condition themselves, or other personal experience. Pieces largely portrayed characters with traits that are highly recognised within the academic literature. However, some also appeared to endorse outdated myths and stereotypes. Existing works appear to preferentially portray high functioning autistic women, with limited representation of those whom also have intellectual disability. Originality/value This is the first exploration of the depiction of ASD in females within fiction. There is a need for more works of fiction responsibly depicting females with ASD, as this can help reduce stigma, develop public awareness and recognition and increase representation

Evaluation of Off-grid Community Managed Renewable Energy Projects in Malawi : Dedicated Study

The Evaluation of Off Grid Community Managed Renewable Energy Projects was undertaken as part of the Institutional Support Programme of the Malawi Renewable Energy Acceleration Programme (MREAP). This evaluation developed a set of 12 case studies covering the 3 regions of Malawi and included a range of renewable energy technologies (RETs) that are being used at the community and household level. These case studies were complemented by key informant interviews and a ‘round table’ with members of the Government of Malawi in March 2012. The analysis and lessons from this evaluation were designed to help inform the implementation of the MREAP itself, the ongoing development of grassroots level RET activities as well as the documentation of robust evidence and experiences that would help inform the possible development of a Renewable Energy Strategy for Malawi

The inflammatory bowel disease drug azathioprine induces autophagy via mTORC1 and the unfolded protein response sensor PERK

Background Genetic studies have strongly linked autophagy to Crohn's disease (CD) and stimulating autophagy in CD patients may be therapeutically beneficial. The aim of this study was to evaluate the effect of current inflammatory bowel disease (IBD) drugs on autophagy and investigate molecular mechanisms of action and functional outcomes in relation to this cellular process. Methods Autophagy marker LC3 was evaluated by confocal fluorescence microscopy and flow cytometry. Drug mechanism of action was investigated by PCR Array with changes in signaling pathways examined by immunoblot and RT-qPCR. Clearance of adherent-invasive Escherichia coli (AIEC) and levels of pro-inflammatory cytokine tumour necrosis factor alpha (TNFα) were evaluated by gentamicin protection assays and RT-qPCR respectively. LC3 was analysed in peripheral blood mononuclear cells (PBMC) from paediatric patients by flow cytometry. Results Azathioprine induces autophagy via mechanisms involving modulation of mechanistic target of rapamycin (mTORC1) signaling and stimulation of the unfolded protein response (UPR) sensor PERK. Induction of autophagy with azathioprine correlated with the enhanced clearance of AIEC and dampened AIEC-induced increases in TNFα. Azathioprine induced significant increase in autophagosome bound LC3-II in PBMC populations ex vivo, supporting in vitro findings. In patients, the CD-associated ATG16L1 T300A single-nucleotide polymorphism did not attenuate azathioprine induction of autophagy. Conclusions Modulation of autophagy via mTORC1 and the UPR may contribute to the therapeutic Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporatio

Measurement of erythrocyte membrane mannoses to assess splenic function

ACKNOWLEDGEMENTS This work was funded by Aberdeen University Development Trust and Friends of Anchor. The University of Aberdeen is applying for a patent based on this work. Aberdeen University Development Trust (GrantNumber(s): DB10452-11) Friends of Anchor (GrantNumber(s): RS 2018 001)Peer reviewedPublisher PD

High mannose N-glycans on red blood cells as phagocytic ligands, mediating both sickle cell anaemia and resistance to malaria

Acknowledgements We are grateful for the assistance provided by both the Microscopy and Histology Core Facility, and the Iain Fraser Cytometry Centre, at the University of Aberdeen. We thank Ann Wheeler and Matt Pearson from Edinburgh Super-Resolution Imaging Consortium for technical support with 3D SIM microscopy. We also thank Janet A. Willment and Bernard Kerscher, supervised by G.D.B., for providing the Fc fusion proteins, Jeanette A. Wagener, supervised by Neil A.R.G. Gow, for providing high purity chitin, Jan Westland for obtaining blood samples and Paul Crocker for useful discussions. Principal funding for this project was provided by Wellcome Trust grant 094847 (R.N.B, L.P.E, M.A.V). In addition, support was provided by Biotechnology and Biological Sciences Research Council grants BBF0083091 (A.D. and S.M.H.) and BBK0161641 (A.D. and S.M.H.), Wellcome Trust grant 082098 (A.D.), Wellcome Trust grants 97377, 102705 (G.D.B) and funding for the MRC Centre for Medical Mycology at the University of Aberdeen MR/N006364/1 (G.D.B).Non peer reviewe

Red blood cell mannoses as phagocytic ligands mediating both sickle cell anaemia and malaria resistance

Acknowledgements We are grateful for the assistance provided by both the Microscopy and Histology Core Facility, and the Iain Fraser Cytometry Centre, at the University of Aberdeen. We thank Ann Wheeler and Matt Pearson from Edinburgh Super-Resolution Imaging Consortium for technical support with 3D SIM microscopy. We also thank Janet A. Willment and Bernard Kerscher, supervised by G.D.B., for providing the Fc fusion proteins, Jeanette A. Wagener, supervised by Neil A.R.G. Gow, for providing high purity chitin, Jan Westland for obtaining blood samples and Paul Crocker for useful discussions. Principal funding for this project was provided by Wellcome Trust grant 094847 (R.N.B., L.P.E., M.A.V.). In addition, support was provided by Biotechnology and Biological Sciences Research Council grants BBF0083091 (A.D. and S.M.H.) and BBK0161641 (A.D. and S.M.H.), Wellcome Trust grant 082098 (A.D.), Wellcome Trust grants 97377, 102705 (G.D.B.), and funding for the MRC Centre for Medical Mycology at the University of Aberdeen MR/N006364/1 (G.D.B.).Peer reviewedPublisher PD

Tuning the Topography of Dynamic 3D Scaffolds through Functional Protein Wrinkled Coatings

Surface wrinkling provides an approach to fabricate micron and sub-micron-level biomaterial topographies that can mimic features of the dynamic, in vivo cell environment and guide cell adhesion, alignment, and differentiation. Most wrinkling research to date has used planar, two-dimensional (2D) substrates, and wrinkling work on three-dimensional (3D) structures has been limited. To enable wrinkle formation on architecturally complex, biomimetic 3D structures, here, we report a simple, low-cost experimental wrinkling approach that combines natural silk fibroin films with a recently developed advanced manufacturing technique for programming strain in complex 3D shape–memory polymer (SMP) scaffolds. By systematically investigating the influence of SMP programmed strain magnitude, silk film thickness, and aqueous media on wrinkle morphology and stability, we reveal how to generate and tune silk wrinkles on the micron and sub-micron scale. We find that increasing SMP programmed strain magnitude increases wavelength and decreases amplitudes of silk wrinkled topographies, while increasing silk film thickness increases wavelength and amplitude. Silk wrinkles persist after 24 h in cell culture medium. Wrinkled topographies demonstrate high cell viability and attachment. These findings suggest the potential for fabricating biomimetic cellular microenvironments that can advance understanding and control of cell–material interactions in engineering tissue constructs

Suppression of a Subset of Interferon-Induced Genes by Human Papillomavirus Type 16 E7 via a Cyclin Dependent Kinase 8-Dependent Mechanism

Persistent infection by human papillomaviruses (HPVs), small, double-stranded DNA viruses that infect keratinocytes of the squamous epithelia, can lead to the development of cervical and other cancers. The viral oncoprotein E7 contributes to viral persistence in part by regulating host gene expression through binding host transcriptional regulators, although mechanisms responsible for E7-mediated transcriptional regulation are incompletely understood. Type I IFN signaling promotes the expression of anti-viral genes, called interferon-stimulated genes (ISGs), through the phosphorylation and activation of STAT1. In this study, we have observed that the CR3 domain of E7 contributes to the episomal maintenance of viral genomes. Transcriptome analysis revealed that E7 transcriptionally suppresses a subset of ISGs but not through regulation of STAT1 activation. Instead, we discovered that E7 associates with Mediator kinase CDK8 and this is correlated with the recruitment of CDK8 to ISG promoters and reduced ISG expression. E7 fails to suppress ISGs in the absence of CDK8, indicating that CDK8 function contributes to the suppression of ISGs by E7. Altogether, E7/CDK8 association may be a novel mechanism by which E7 inhibits innate immune signaling