Coexistence of a triplet nodal order-parameter and a singlet order-parameter at the interfaces of ferromagnet-superconductor Co/CoO/In junctions

We present differential conductance measurements of Cobalt / Cobalt-Oxide / Indium planar junctions, 500nm x 500nm in size. The junctions span a wide range of barriers, from very low to a tunnel barrier. The characteristic conductance of all the junctions show a V-shape structure at low bias instead of the U-shape characteristic of a s-wave order parameter. The bias of the conductance peaks is, for all junctions, larger than the gap of indium. Both properties exclude pure s-wave pairing. The data is well fitted by a model that assumes the coexistence of s-wave singlet and equal spin p-wave triplet fluids. We find that the values of the s-wave and p-wave gaps follow the BCS temperature dependance and that the amplitude of the s-wave fluid increases with the barrier strength.Comment: 5 pages, Accepted to Phys. Rev.

Requirement for the NF-kappa B family member Re1A in the development of secondary lymphoid organs

The transcription factor nuclear factor (NF)-kappaB has been suggested to be a key mediator of the development of lymph nodes and Peyer's patches. However, targeted deletion of NF-kappaB/ Rel family members has not yet corroborated such a function. Here we report that when mice lacking the RelA subunit of NF-kappaB are brought to term by breeding onto a tumor necrosis factor receptor (TNFR)1-deficient background, the trice that are born lack lymph nodes, foyer's patches, and an organized splenic microarchitecture, and have a profound defect in T cell-dependent antigen responses. Analyses of TNFR1/1RelA-deficient embryonic tissues and of radiation chimeras suggest that the dependence on RelA is manifest not in hematopoietic cells but rather in radioresistant stromal cells needed for the development of secondary lymphoid organs

Dynamic MRI lesion evolution in paediatric MOG-Ab associated disease (MOGAD)

INTRODUCTION: Myelin oligodendrocyte glycoprotein (MOG) antibodies are associated clinically with either a monophasic or relapsing disease course in both children and adults. There are few studies studying lesion evolution in children with myelin oligodendrocyte glycoprotein antibody associated disorder (MOGAD). AIM: The aim of this study was to examine MRI lesion evolution over time in a large single-centre paediatric MOGAD cohort. METHODS: We retrospectively identified patients with MOGAD from a tertiary paediatric neurosciences centre (Great Ormond Street Hospital) between 2001 to 2022. RESULTS: A total of 363 MRI scans from 59 included patients were available for analysis. Median age at presentation was 4 yrs (IQR 4-9), 32 (54.2%) were female and 34 (57.6%) were of non-white ethnicities. Twenty-seven children (45.8%) had a monophasic illness and 32 (54.2%) had a relapsing disease course. In the relapsing MOGAD group, median number of relapses was 4 (range 2-30). Initial presentation was ADEM in 27(46%), ON in 18 (31%) ADEM-ON in 4 (7%), ADEM-TM in 6 (10%) TM in 2 (3%) ADEM-TM-ON in 1 (2%) and ON-Brainstem syndrome in 1 (2%). There was no difference in demographics or clinical presentation between monophasic and relapsing groups. Fifteen patients (25.4%) had gadolinium enhancement on initial attack MRI. Seven out of 32 (21.9%) relapsing patients had persistent enhancement on follow-up MRI scans. One patient with a clinical transverse myelitis at presentation was MRI negative. New asymptomatic lesions following first clinical event were seen in 5/27 (18.5%) monophasic patients and 8/32 (25%) relapsing patients. During follow-up interval scanning,38 out of 59 have had follow up neuroimaging after their first attack whereas15/32 had relapsed before having a follow up MRI. Complete lesion resolution was reported in 9/38 (23.6%) (8 monophasic, 1 relapsing) following 1st acute attack, 3/32 (9.3%) after 2nd acute attack, and 1/32 (3.1%) following 3rd acute attack and 0/32 following 4th acute attack. Partial resolution of MRI lesions was seen in 7/20 (35%) monophasic patients and 7/32 (21.8%) relapsing patients at follow-up scans. CONCLUSIONS: Demyelinating lesions in paediatric MOGAD are dynamic and timing of MRI scanning may influence CNS region involvement. Unlike in multiple sclerosis, a significant number of MOGAD patients will have complete lesion resolution at first follow-up, although the ability to repair is reduced following multiple relapses

Preface

These proceedings contain the papers of the Third International Workshop on Recent Trends in News Informa-tion Retrieval (NewsIR\u201919) held in conjunction with the ACM SIGIR 2019 conference in Paris, France, on the25thof July 2019. Ten full papers and two short papers (one position paper and one demo paper) were selectedby the programme committee from a total of 21 submissions. Each submitted paper was reviewed by at leastthree members of an international programme committee. In addition to the selected papers, the workshopfeatures one keynote and one invited talk. The Keynote speech is given by Aron Pilhofer \u201cFrom Redlining toRobots: How newsrooms apply technology to the craft of journalism\u201d. The invited talk is given by FriedrichLindenberg \u201cMining Leaks and Open Data to Follow the Money\u201d. We would like to thank SIGIR for hostingus. Thanks also go to the keynote speakers, the program committee, the paper authors, and the participants,for without these people there would be no worksho

Monitoring T cell-dendritic cell interactions in vivo by intercellular enzymatic labelling

Interactions between different cell types are essential for multiple biological processes, including immunity, embryonic development and neuronal signalling. Although the dynamics of cell-cell interactions can be monitored in vivo by intravital microscopy, this approach does not provide any information on the receptors and ligands involved or enable the isolation of interacting cells for downstream analysis. Here we describe a complementary approach that uses bacterial sortase A-mediated cell labelling across synapses of immune cells to identify receptor-ligand interactions between cells in living mice, by generating a signal that can subsequently be detected ex vivo by flow cytometry. We call this approach for the labelling of 'kiss-and-run' interactions between immune cells 'Labelling Immune Partnerships by SorTagging Intercellular Contacts' (LIPSTIC). Using LIPSTIC, we show that interactions between dendritic cells and CD4+ T cells during T-cell priming in vivo occur in two distinct modalities: an early, cognate stage, during which CD40-CD40L interactions occur specifically between T cells and antigen-loaded dendritic cells; and a later, non-cognate stage during which these interactions no longer require prior engagement of the T-cell receptor. Therefore, LIPSTIC enables the direct measurement of dynamic cell-cell interactions both in vitro and in vivo. Given its flexibility for use with different receptor-ligand pairs and a range of detectable labels, we expect that this approach will be of use to any field of biology requiring quantification of intercellular communication

Requirement for the NF-κB Family Member RelA in the Development of Secondary Lymphoid Organs

The transcription factor nuclear factor (NF)-κB has been suggested to be a key mediator of the development of lymph nodes and Peyer's patches. However, targeted deletion of NF-κB/ Rel family members has not yet corroborated such a function. Here we report that when mice lacking the RelA subunit of NF-κB are brought to term by breeding onto a tumor necrosis factor receptor (TNFR)1-deficient background, the mice that are born lack lymph nodes, Peyer's patches, and an organized splenic microarchitecture, and have a profound defect in T cell–dependent antigen responses. Analyses of TNFR1/RelA-deficient embryonic tissues and of radiation chimeras suggest that the dependence on RelA is manifest not in hematopoietic cells but rather in radioresistant stromal cells needed for the development of secondary lymphoid organs

Isolated central nervous system familial hemophagocytic lymphohistiocytosis (fHLH) presenting as a mimic of demyelination in children

Isolated central nervous system (CNS) presentations of haemophagocytic lymphohistiocytosis (HLH), traditionally a systemic inflammatory condition, have been reported in adults and children. We identified nine patients with a diagnosis of isolated CNS familial hemophagocytic lymphohistiocytosis (fHLH) with symptom onset <18 years of age, and one asymptomatic sibling. Children with atypical chronic/recurrent CNS inflammation should be considered for immunological and genetic panel testing for fHLH even in the absence of any systemic inflammatory features. Despite haematopoietic stem cell transplantation (HSCT) being a mainstay of treatment, treatment failure and high morbidity and mortality post-HSCT suggest that alternative immune therapies may be worth considering

Computational Controversy

Climate change, vaccination, abortion, Trump: Many topics are surrounded by fierce controversies. The nature of such heated debates and their elements have been studied extensively in the social science literature. More recently, various computational approaches to controversy analysis have appeared, using new data sources such as Wikipedia, which help us now better understand these phenomena. However, compared to what social sciences have discovered about such debates, the existing computational approaches mostly focus on just a few of the many important aspects around the concept of controversies. In order to link the two strands, we provide and evaluate here a controversy model that is both, rooted in the findings of the social science literature and at the same time strongly linked to computational methods. We show how this model can lead to computational controversy analytics that have full coverage over all the crucial aspects that make up a controversy.Comment: In Proceedings of the 9th International Conference on Social Informatics (SocInfo) 201

The scavenger receptor SCARF1 mediates apoptotic cell clearance and prevents autoimmunity

Clearance of apoptotic cells is critical for control of tissue homeostasis however the full range of receptor(s) on phagocytes responsible for recognition of apoptotic cells remains to be identified. Here we show that dendritic cells (DCs), macrophages and endothelial cells use scavenger receptor type F family member 1 (SCARF1) to recognize and engulf apoptotic cells via C1q. Loss of SCARF1 impairs uptake of apoptotic cells. Consequently, in SCARF1-deficient mice, dying cells accumulate in tissues leading to a lupus-like disease with the spontaneous generation of autoantibodies to DNA-containing antigens, immune cell activation, dermatitis and nephritis. The discovery of SCARF1 interactions with C1q and apoptotic cells provides insights into molecular mechanisms involved in maintenance of tolerance and prevention of autoimmune disease