102,576 research outputs found
Response to: 'Idiopathic inflammatory myopathies and antisynthetase syndrome: Contribution of antisynthetase antibodies to improve current classification criteria' by Greco et al
No full textIn an effort to improve and harmonise the classification of ASSD, the CLASS (classification criteria of ASSD) project
has recently been funded by the American College of Rheumatology and the European League Against Rheumatism. It will be interesting to see if similar results can be repeated using a large
and carefully selected cohort
COVID-19 revisiting inflammatory pathways of arthritis
No full textCoronavirus disease 2019 (COVID-19) is an infectious disease, caused by severe acute respiratory syndrome coronavirus 2, which predominantly affects the lungs and, under certain circumstances, leads to an excessive or uncontrolled immune activation and cytokine response in alveolar structures. The pattern of pro-inflammatory cytokines induced in COVID-19 has similarities to those targeted in the treatment of rheumatoid arthritis. Several clinical studies are underway that test the effects of inhibiting IL-6, IL-1β or TNF or targeting cytokine signalling via Janus kinase inhibition in the treatment of COVID-19. Despite these similarities, COVID-19 and other zoonotic coronavirus-mediated diseases do not induce clinical arthritis, suggesting that a local inflammatory niche develops in alveolar structures and drives the disease process. COVID-19 constitutes a challenge for patients with inflammatory arthritis for several reasons, in particular, the safety of immune interventions during the pandemic. Preliminary data, however, do not suggest that patients with inflammatory arthritis are at increased risk of COVID-19
Stunning of neutrophils accounts for the anti-inflammatory effects of clodronate liposomes.
No full textClodronate liposomes (Clo-Lip) have been widely used to deplete mononuclear phagocytes (MoPh) to study the function of these cells in vivo. Here, we revisited the effects of Clo-Lip together with genetic models of MoPh deficiency, revealing that Clo-Lip exert their anti-inflammatory effects independent of MoPh. Notably, not only MoPh but also polymorphonuclear neutrophils (PMN) ingested Clo-Lip in vivo, which resulted in their functional arrest. Adoptive transfer of PMN, but not of MoPh, reversed the anti-inflammatory effects of Clo-Lip treatment, indicating that stunning of PMN rather than depletion of MoPh accounts for the anti-inflammatory effects of Clo-Lip in vivo. Our data highlight the need for a critical revision of the current literature on the role of MoPh in inflammation.This work was supported by the Deutsche Forschungsgemeinschaft (FG 2886 “PANDORA” – B01/B02/A03/
B04 to G. Kronke, F. Nimmerjahn, G. Schett, and M.H. Hoff- ¨
mann, respectively, and the CRC1181-A03/A01/A02/A07/C03 Z2
to G. Kronke, G. Schett, F. Nimmerjahn, and M.H. Hoffmann), ¨
the Emerging Field Initiative of the Friedrich-Alexander University Erlangen-Nürnberg (EFI_Verbund_Med_05_MIRACLE
to G. Kronke), the Bundesministerium für Bildung und For- ¨
schung (MASCARA to G. Kronke and G. Schett; MelAutim to G. ¨
Kronke), and the European Union (Horizon 2020 ERC-2014-StG ¨
640087 – SOS and ERC-2020-CoG 101001866 – INSPIRE to G.
Kronke; and ERC-2018-SyG nanoSCOPE and RTCure to G. ¨
Schett). This work was supported by grants R01AI165661
from the National Institutes of Health/National Institute of
Allergy and Infectious Diseases, H2020-FET-OPEN-2018-
2020 (no. 861878) from the European Commission to A. Hidalgo and M.H. Hoffmann, and HR17_00527 from Fundacion
La Caixa to A. Hidalgo. The CNIC is supported by the Ministerio de Ciencia e Innovacion and the Pro-CNIC Foundation and is a Severo Ochoa Center of Excellence (MICINN
award CEX2020-001041-S).S
Bibliographie Hilarion G. Petzold 1958 – 2009 mit Anhang als Einführung
No full textDieses Archiv enthält die Gesamtbibliographie der Werke des Autors nebst einiger Texte „Über H. G. Petzold“ im Schlussteil der Bibliographie sowie einen Anhang mit einer Einführung in die Architektur des Werkes in seinem wissenslogischen Aufbau als Ausarbeitung seines „Tree of Science Modells“ (2007).This archive contains the complete bibliography of the author and some texts about H. G. Petzold, moreover an epilogue with an introduction to the architecture of the works in its epistemological structure and composition and as an elaborations of Petzold’s „Tree of Science Modell (2007).https://www.fpi-publikation.de/polyloge/01-2009-petzold-h-g-gesamtbibliographie-h-g-petzold-1958-2009-updating-november2009/peerReviewedpublishedVersio
Dispelling the Myths Behind First-author Citation Counts
No full textWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
Recommended from our members
3346: Samuel G. Freedman, author, 2013
No full textPhotograph of author Samuel G. Freedman, at NT Daily Slash meeting in the Mayborn School of Journalism at UNT
Fine-Tuning the Treatment of Psoriatic Arthritis: Focus on the IL-23 Pathway
No full textThe symposium ‘Fine-tuning the treatment of PsA: Focus on the IL-23 pathway’ took place during the 2019 European League Against Rheumatism (EULAR) Annual Congress in Madrid, Spain. The presentations covered the rationale for targeting IL-23 in psoriatic arthritis (PsA), details of the IL-23 pathway relevant to psoriatic disease, practical implications and consequences of targeting IL-23, and experiences of targeting IL-23 in psoriasis from the dermatologists’ perspective. Dr Stefan Siebert set the scene by outlining the pathophysiology of psoriatic diseases, particularly PsA, describing disease heterogeneity, explaining the role of inflammation, and highlighting the rationale for targeting the IL-12/23 pathway. He summarised key findings on the IL-12/23 inhibitor ustekinumab in PsA from clinical trials and real-world data available to date. Delving deeper into the IL-23 pathway, Prof Georg Schett explained the function of IL-23 and its role in inflammatory disease and autoimmunity. After briefly describing the history of the relatively recent discovery of this cytokine, Prof Schett discussed preclinical and clinical studies underlying today’s understanding of IL-23 and why it is an appropriate target in PsA. Multiple biologic or small-molecule treatments for PsA have been investigated in clinical trials. Prof Peter Taylor discussed the practical implications of targeting IL-23 and provided more details about the specific effects of targeting not only IL-23 (with risankizumab, tildrakizumab, or guselkumab) but also IL-12/23 (with ustekinumab) and IL-17 (with ixekizumab, secukinumab, or brodalumab). In the final presentation, Prof Lluís Puig described clinical experience of targeting IL-23 in psoriasis and provided an overview of findings from several clinical trials, including: VOYAGE 1 and 2 (guselkumab versus the TNF inhibitor [TNFi] adalimumab); NAVIGATE (guselkumab versus ustekinumab); and the head-to-head ECLIPSE study (guselkumab versus secukinumab). The symposium concluded with a lively panel discussion in which the speakers addressed a variety of questions and comments from the audience
IL-17-22-23 PATHWAYS IN PSORIATIC ARTHRITIS AND PSORIASIS
No full textAnnual European Congress of Rheumatology -- JUN 14-17, 2017 -- Madrid, SPAIN[Abstract Not Available
The Right to Strike under the United States Constitution: Theory, Practice, and Possible Implications for Canada
No full textAnswering critics of the Canadian Supreme Court's judgment in B.C. Health, the author argues that the Court laid the foundation for a principled and durable doctrine protecting constitutional labour rights, one that goes directly to the heart of the matter — the inequality of workers’ power in the employment relation. In the author’s view, two paths could lead from B.C. Health to the recognition of Charter protec- tion for a right to strike: one that treats the right as an accessory to col- lective bargaining, and one that upholds the right directly on the basis of the Charter values of equality and participation. The author supports the latter approach, contending that constitutional rights should be defined in relation to fundamental values, in a way that is not contingent on time-bound or fact-sensitive assessments about the role of strikes within a particular collective bargaining regime. Although a Charter right to strike may involve the courts in difficult choices about when to defer to legislative policy decisions, and courts may lack the institutional capac- ity to deal effectively with labour law issues, the author points out that judges can look to ILO standards for expert guidance. Noting that the U.S. experience in this area might be of considerable use to Canadians, the author concludes by providing an overview of American case law concerning a constitutional right to strike.Peer reviewe
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