Development of tsunami early warning systems and future challenges

Fostered by and embedded in the general development of information and communications technology (ICT), the evolution of tsunami warning systems (TWS) shows a significant development from seismic-centred to multi-sensor system architectures using additional sensors (e.g. tide gauges and buoys) for the detection of tsunami waves in the ocean. <br><br> Currently, the beginning implementation of regional tsunami warning infrastructures indicates a new phase in the development of TWS. A new generation of TWS should not only be able to realise multi-sensor monitoring for tsunami detection. Moreover, these systems have to be capable to form a collaborative communication infrastructure of distributed tsunami warning systems in order to implement regional, ocean-wide monitoring and warning strategies. <br><br> In the context of the development of the German Indonesian Tsunami Early Warning System (GITEWS) and in the EU-funded FP6 project Distant Early Warning System (DEWS), a service platform for both sensor integration and warning dissemination has been newly developed and demonstrated. In particular, standards of the Open Geospatial Consortium (OGC) and the Organization for the Advancement of Structured Information Standards (OASIS) have been successfully incorporated. <br><br> In the FP7 project Collaborative, Complex and Critical Decision-Support in Evolving Crises (TRIDEC), new developments in ICT (e.g. complex event processing (CEP) and event-driven architecture (EDA)) are used to extend the existing platform to realise a component-based technology framework for building distributed tsunami warning systems

Recent advances in ankylosing spondylitis: understanding the disease and management

The term spondyloarthritis refers to a group of immune-mediated diseases characterised by inflammation of the axial skeleton, peripheral joints, and entheses. Ankylosing spondylitis (AS) is the most common and characteristic of these entities and even though it was first described over two centuries ago, the understanding of the underlying disease mechanism remains incomplete. It is known that around 40% of patients with AS have subclinical bowel inflammation, suggesting that the origin of the disease could be in the gut. Also, more genes and new molecules have demonstrated a role in the pathogenesis of AS. In this review, we analyse the latest therapies for spondyloarthritis and the most relevant discoveries over the last three years, together with their implications for different aspects of the disease

Prospektive Verlaufsbeobachtung einer universitären Rheumaambulanzkohorte während der ersten Welle der COVID-19-Pandemie

Background!#!In March 2020 the SARS-CoV‑2 pandemic disseminated initially especially in Bavaria. At that time data on patients with rheumatic diseases and immunomodulatory treatment was lacking.!##!Objective!#!The aim was to analyze the influence of the SARS-CoV‑2 pandemic on the clinical treatment strategy.!##!Material and methods!#!Between 16 March and 31 July 2020 all patients who consecutively presented at the rheumatology outpatient clinic of the Klinikum rechts der Isar of the Technical University of Munich were included in the study. Individual treatment adjustments were based on clinical judgment and the recommendations for action of the German Society for Rheumatology (DGRh).!##!Results!#!A total of 322 patients were included. The most frequent diagnosis was rheumatoid arthritis with 17%, ANCA-associated vasculitis (AAV) with 14% and SLE with 12%. Of the patients 262 were on DMARD treatment and 77 received oral glucocorticoids. There were 5 cases of suspected SARS-CoV‑2 infection; however, no patient verifiably became ill due to COVID-19. In 40 patients, treatment adjustments were done due to the pandemic, whereby 3 patients developed a flare of the underlying disease. In retrospect, treatment de-escalation occurred most frequently in AAV, IgG4-related disease, immunosuppressive treatment with rituximab and the simultaneous presence of malignant diseases.!##!Conclusion!#!The total lack of confirmed SARS-CoV‑2 infections in an otherwise strongly affected region could indicate that the infection risk for SARS-CoV‑2 is not substantially increased for patients with inflammatory rheumatic diseases. A continuation of most immunosuppressive medications therefore seems reasonable during the ongoing pandemic

Silencing or inhibition of endoplasmic reticulum aminopeptidase 1 (ERAP1) suppresses free heavy chain expression and Th17 responses in ankylosing spondylitis.

Objective Human leucocyte antigen (HLA)-B27 and endoplasmic reticulum aminopeptidase 1 (ERAP1) are strongly associated with ankylosing spondylitis (AS). ERAP1 is a key aminopeptidase in HLA class I presentation and can potentially alter surface expression of HLA-B27 free heavy chains (FHCs). We studied the effects of ERAP1 silencing/inhibition/variations on HLAB27 FHC expression and Th17 responses in AS. Methods Flow cytometry was used to measure surface expression of HLA class I in peripheral blood mononuclear cells (PBMCs) from patients with AS carrying different ERAP1 genotypes (rs2287987, rs30187 and rs27044) and in ERAP1-silenced/inhibited/ mutated HLA-B27-expressing antigen presenting cells (APCs). ERAP1-silenced/inhibited APCs were cocultured with KIR3DL2CD3ε-reporter cells or AS CD4+ T cells. Th17 responses of AS CD4+ T cells were measured by interleukin (IL)-17A ELISA and Th17 intracellular cytokine staining. FHC cell surface expression and Th17 responses were also measured in AS PBMCs following ERAP1 inhibition. Results The AS-protective ERAP1 variants, K528R and Q730E, were associated with reduced surface FHC expression by monocytes from patients with AS and HLA-B27-expressing APCs. ERAP1 silencing or inhibition in APCs downregulated HLA-B27 FHC surface expression, reduced IL-2 production by KIR3DL2CD3ε-reporter cells and suppressed the Th17 expansion and IL-17A secretion by AS CD4+ T cells. ERAP1 inhibition of AS PBMCs reduced HLA class I FHC surface expression by monocytes and B cells, and suppressed Th17 expansion. Conclusions ERAP1 activity determines surface expression of HLA-B27 FHCs and potentially promotes Th17 responses in AS through binding of HLA-B27 FHCs to KIR3DL2. Our data suggest that ERAP1 inhibition has potential for AS treatment.</p