Post-natal development of EEG responses to noxious stimulation in pigs (Sus scrofa) aged 1-15 days

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Template-Stripped Multifunctional Wedge and Pyramid Arrays for Magnetic Nanofocusing and Optical Sensing

We present large-scale reproducible fabrication of multifunctional ultrasharp metallic structures on planar substrates with capabilities including magnetic field nanofocusing and plasmonic sensing. Objects with sharp tips such as wedges and pyramids made with noble metals have been extensively used for enhancing local electric fields via the lightning-rod effect or plasmonic nanofocusing. However, analogous nanofocusing of magnetic fields using sharp tips made with magnetic materials has not been widely realized. Reproducible fabrication of sharp tips with magnetic as well as noble metal layers on planar substrates can enable straightforward application of their material and shape-derived functionalities. We use a template-stripping method to produce plasmonic-shell-coated nickel wedge and pyramid arrays at the wafer-scale with tip radius of curvature close to 10 nm. We further explore the magnetic nanofocusing capabilities of these ultrasharp substrates, deriving analytical formulas and comparing the results with computer simulations. These structures exhibit nanoscale spatial control over the trapping of magnetic microbeads and nanoparticles in solution. Additionally, enhanced optical sensing of analytes by these plasmonic-shell-coated substrates is demonstrated using surface-enhanced Raman spectroscopy. These methods can guide the design and fabrication of novel devices with applications including nanoparticle manipulation, biosensing, and magnetoplasmonics

Human Cytomegalovirus glycoprotein UL16 causes intracellular sequestration of NKG2D ligands, protecting against NK cell cytotoxicity.

The activating receptor, NKG2D, is expressed on a variety of immune effector cells and recognizes divergent families of major histocompatibility complex (MHC) class I-related ligands, including the MIC and ULBP proteins. Infection, stress, or transformation can induce NKG2D ligand expression, resulting in effector cell activation and killing of the ligand-expressing target cell. The human cytomegalovirus (HCMV) membrane glycoprotein, UL16, binds to three of the five known ligands for human NKG2D. UL16 is retained in the endoplasmic reticulum and cis-Golgi apparatus of cells and causes MICB to be similarly retained and stabilized within cells. Coexpression of UL16 markedly reduces cell surface levels of MICB, ULBP1, and ULBP2, and decreases susceptibility to natural killer cell-mediated cytotoxicity. Domain swapping experiments demonstrate that the transmembrane and cytoplasmic domains of UL16 are important for intracellular retention of UL16, whereas the ectodomain of UL16 participates in down-regulation of NKG2D ligands. The intracellular sequestration of NKG2D ligands by UL16 represents a novel HCMV immune evasion mechanism to add to the well-documented viral strategies directed against antigen presentation by classical MHC molecules

Optimising student learning on international placements in low income settings

This paper challenges the assumption that student visits to low resource settings inevitably promote the acquisition of cultural competence. Much of the literature and marketing rhetoric advocating the expansion of such ‘exposures’ lists numerous positive outcomes with an emphasis on ‘cultural learning’. With important exceptions, the concept of cultural learning remains uncontested, nestling in the fluffy haze of an inherently benevolent multi-culturalism. The emphasis in current research is on ‘learning’ or ‘competency’ at the expense of definitional clarity around the concept of culture itself. This results in a tendency to overemphasise (and essentialise) difference rather than commonality and conflates cultural learning with narrow (stereotypical) concepts of race, ethnicity and religion. The paper discusses the experiences of students undertaking placements in Uganda through Knowledge For Change, a UK charity hosting the Ethical Educational Placements project, to identify and critique this dimension of ‘learning’. Using an action-research approach combining observational research with qualitative interviews and surveys the paper uncovers the nuance of cultural learning. In important respects the behaviour that students are witnessing and attributing to culture is connected more to the specific organisational contexts that they are placed in and the patient groups they ‘serve’ than any connection to an homogenous ‘national’ culture. Poverty and gender inequality, amongst many other forms of structural inequality, result in ‘othering’ behaviour on the part of health workers towards patients that is a fundamental characteristic of public health organisations in residualised welfare systems. In this complex environment, cultural learning is not so much about celebrating difference. It is more about understanding social context and accepting that you don’t and can’t possibly know a person’s situation; and with that in mind you should treat everyone with the same degree of humility and respect. Adopting and practising ‘epistemic humility’ (Hanson et al 2011; Ahmed, Ackers-Johnson & Ackers 2017) is crucial to meaningful learning in any context. Further, a lack of understanding of the broader structural processes perpetuates inequalities between the Global North and South (Husih, 2012; Ahmed, Ackers-Johnson & Ackers, 2017) and impedes knowledge acquisition, particularly cultural learning. Moreover, hubris – or Western students’ assumptions of superiority over host health care workers (Bauer, 2017; Elit et al, 2011, Ahmed, Ackers-Johnson & Ackers, 2017) – may act as a further obstacle to cultural learning. Cultural learning is as much about learning about ourselves and what it feels like to be ‘othered’ as it is learning about others. International placements in LMICs create critical opportunities for relevant student learning. But achieving this and guarding against the risks of ‘mis-learning’ requires the level of cultural brokerage provided by ‘More Knowledgeable Others’ that we take for granted with clinical learning

Dynamics of Fundamental Matter in N=2* Yang-Mills Theory

We study the dynamics of quenched fundamental matter in $\mathcal{N}=2^\ast$ supersymmetric large $N$ SU(N) Yang-Mills theory at zero temperature. Our tools for this study are probe D7-branes in the holographically dual $\mathcal{N}=2^\ast$ Pilch-Warner gravitational background. Previous work using D3-brane probes of this geometry has shown that it captures the physics of a special slice of the Coulomb branch moduli space of the gauge theory, where the $N$ constituent D3-branes form a dense one dimensional locus known as the enhancon, located deep in the infrared. Our present work shows how this physics is supplemented by the physics of dynamical flavours, revealed by the D7-branes embeddings we find. The Pilch-Warner background introduces new divergences into the D7-branes free energy, which we are able to remove with a single counterterm. We find a family of D7-brane embeddings in the geometry and discuss their properties. We study the physics of the quark condensate, constituent quark mass, and part of the meson spectrum. Notably, there is a special zero mass embedding that ends on the enhancon, which shows that while the geometry acts repulsively on the D7-branes, it does not do so in a way that produces spontaneous chiral symmetry breaking.Comment: 24 pages, 8 figures. Corrected typos, added comment about counterterm. To appear in JHE

Learning Shape Priors for Single-View 3D Completion and Reconstruction

The problem of single-view 3D shape completion or reconstruction is challenging, because among the many possible shapes that explain an observation, most are implausible and do not correspond to natural objects. Recent research in the field has tackled this problem by exploiting the expressiveness of deep convolutional networks. In fact, there is another level of ambiguity that is often overlooked: among plausible shapes, there are still multiple shapes that fit the 2D image equally well; i.e., the ground truth shape is non-deterministic given a single-view input. Existing fully supervised approaches fail to address this issue, and often produce blurry mean shapes with smooth surfaces but no fine details. In this paper, we propose ShapeHD, pushing the limit of single-view shape completion and reconstruction by integrating deep generative models with adversarially learned shape priors. The learned priors serve as a regularizer, penalizing the model only if its output is unrealistic, not if it deviates from the ground truth. Our design thus overcomes both levels of ambiguity aforementioned. Experiments demonstrate that ShapeHD outperforms state of the art by a large margin in both shape completion and shape reconstruction on multiple real datasets.Comment: ECCV 2018. The first two authors contributed equally to this work. Project page: http://shapehd.csail.mit.edu

c-jun is essential for sympathetic neuronal death induced by NGF withdrawal but not by p75 activation.

Sympathetic neurons depend on NGF binding to TrkA for their survival during vertebrate development. NGF deprivation initiates a transcription-dependent apoptotic response, which is suggested to require activation of the transcription factor c-Jun. Similarly, apoptosis can also be induced by selective activation of the p75 neurotrophin receptor. The transcriptional dependency of p75-mediated cell death has not been determined; however, c-Jun NH2-terminal kinase has been implicated as an essential component. Because the c-jun-null mutation is early embryonic lethal, thereby hindering a genetic analysis, we used the Cre-lox system to conditionally delete this gene. Sympathetic neurons isolated from postnatal day 1 c-jun-floxed mice were infected with an adenovirus expressing Cre recombinase or GFP and analyzed for their dependence on NGF for survival. Cre immunopositive neurons survived NGF withdrawal, whereas those expressing GFP or those uninfected underwent apoptosis within 48 h, as determined by DAPI staining. In contrast, brain-derived neurotrophic factor (BDNF) binding to p75 resulted in an equivalent level of apoptosis in neurons expressing Cre, GFP, and uninfected cells. Nevertheless, cycloheximide treatment prevented BDNF-mediated apoptosis. These results indicate that whereas c-jun is required for apoptosis in sympathetic neurons on NGF withdrawal, an alternate signaling pathway must be induced on p75 activation

Prevalence of Avian-Pathogenic Escherichia coli Strain O1 Genomic Islands among Extraintestinal and Commensal E. coli Isolates

Escherichia coli strains that cause disease outside the intestine are known as extraintestinal pathogenic E. coli (ExPEC) and include pathogens of humans and animals. Previously, the genome of avian-pathogenic E. coli (APEC) O1:K1:H7 strain O1, from ST95, was sequenced and compared to those of several other E. coli strains, identifying 43 genomic islands. Here, the genomic islands of APEC O1 were compared to those of other sequenced E. coli strains, and the distribution of 81 genes belonging to 12 APEC O1 genomic islands among 828 human and avian ExPEC and commensal E. coli isolates was determined. Multiple islands were highly prevalent among isolates belonging to the O1 and O18 serogroups within phylogenetic group B2, which are implicated in human neonatal meningitis. Because of the extensive genomic similarities between APEC O1 and other human ExPEC strains belonging to the ST95 phylogenetic lineage, its ability to cause disease in a rat model of sepsis and meningitis was assessed. Unlike other ST95 lineage strains, APEC O1 was unable to cause bacteremia or meningitis in the neonatal rat model and was significantly less virulent than uropathogenic E. coli (UPEC) CFT073 in a mouse sepsis model, despite carrying multiple neonatal meningitis E. coli (NMEC) virulence factors and belonging to the ST95 phylogenetic lineage. These results suggest that host adaptation or genome modifications have occurred either in APEC O1 or in highly virulent ExPEC isolates, resulting in differences in pathogenicity. Overall, the genomic islands examined provide targets for further discrimination of the different ExPEC subpathotypes, serogroups, phylogenetic types, and sequence types