tbuckley/cabot-search huggingface dataset:
High-Density Lipoproteins Exert Pro-inflammatory Effects on Macrophages via Passive Cholesterol Depletion and PKC-NF-κB/STAT1-IRF1 Signaling
Authors: Emiel P.C. van der Vorst, Kosta Theodorou, Yongzheng Wu, Marten A. Hoeksema, Pieter Goossens, Christina A. Bursill, Taghi Aliyev, Leonie F.A. Huitema, Sander W. Tas, Ine M.J. Wolfs, Marijke J.E. Kuijpers, Marion J. Gijbels, Casper G. Schalkwijk, Debby P.Y. Koonen, Shahla Abdollahi-Roodsaz, Kimberly McDaniels, Chih-Chieh Wang, Michael Leitges, Toby Lawrence, Jogchum Plat, Miranda Van Eck, Kerry-Anne Rye, Lhousseine Touqui, Menno P.J. de Winther, Erik A.L. Biessen, Marjo M.P.C. Donners
Journal: Cell Metabolism (2016)
Scavenger Receptor-Mediated Targeted Treatment of Collagen-Induced Arthritis by Dextran Sulfate-Methotrexate Prodrug
Authors: Modi Yang, Jianxun Ding, Xiangru Feng, Fei Chang, Yinan Wang, Zhongli Gao, Xiuli Zhuang, Xuesi Chen
Journal: Theranostics (2016)

Rheumatoid arthritis (RA) is a chronic autoimmune disorder implicated in multiple joint affection and even disability. The activated macrophages perform a predominant role in onset and persistence of RA. Scavenger receptor (SR), one of several receptors overexpressed on the activated macrophages, is a specific biomarker for targeted therapy of numerous chronic inflammation diseases like RA. In this work, dextran sulfate-
Whole-Body Positron Emission Tomography (PET) Using 2-18Fluoro-2-Deoxy-D-Glucose (FDG) for Monitoring Lymphadenopathy in Autoimmune Lymphoproliferative Syndrome (ALPS).
Authors: V. Koneti Rao, Jorge A. Carrasquillo, Janet K. Dale, Stephen Bacharach, Millie Whatley, Faith Dugan, Jean Tretler, Elaine S. Jaffe, Wyndham Wilson, Nilo Avila, Stephen E. Straus
Journal: Blood (2004)
Alemtuzumab in Combination with Interferon-α or Gemcitabine in Aggressive and Advanced Cutaneous T-Cell Lymphomas: Report of Preliminary Results
Authors: Serena Rupoli, Gaia Goteri, Paola Picardi, Stefano Pulini, Antonello Costagliola, Lucia Canafoglia, Simonetta Mulattieri, Andrea Stronati, Anna Rita Scortechini, Marco Ottaviani, Massimiliano Nicolini, Stefano Serresi, Andreina Cellini, Anna Maria Offidani, Pietro Leoni
Journal: Blood (2008)
OP0252-PARE Increasing The Interest in Research in Rheumatology
Authors: K. Blidberg
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> The Swedish Rheumatism Association has a research fund which distributes money to research in rheumatology but also research on pain, osteoarthritis and other conditions related to musculoskeletal disease. Our long term commitment is to reduce the burden of rheumatic disease, increase the quality of life for people with rheumatic disease and ultimately prevent the onset of rheumatic disease and its consequences. The fund distributes about 20 million Swedish krona yearly. In 2015 the Swedish Rheumatism Association published a report on the research that is financed by their fund. <h3>Objectives</h3> The report had several objectives 1) to increase the awareness of the Swedish Rheumatism Association9s function as a funder of research 2) to interest decision makers in different parts of society in the field 3) to be used for fundraising. <h3>Methods</h3> The Swedish Rheumatism Association worked together with a content agency (OTW, Stockholm, Sweden) in the production of the report. The report was based around six major areas of research, rheumatoid arthritis, juvenile arthritis, juvenile idiopathic arthritis, systemic autoimmune rheumatic disease, pain, osteoarthritis and life style. Each theme contained a number of articles on different projects that the Swedish Rheumatism Association has helped to fund. The different articles were written by, or in collaboration with, the principal investigator. <h3>Results</h3> The report contains 18 articles on research. It addition, it contains four cases where four patients tell their story. The report was printed and first released to the public during a research seminar arranged by the Swedish Rheumatism Association. The report is also distributed as a PDF via the Swedish Rheumatism Association9s webpage and a few of the individual articles have been reworked to suit the web better. <h3>Conclusions</h3> The Swedish Rheumatism Association have published a report on the research they finance in order to use it both for lobbying purposes and for fundraising. For the coming year a series of activities will be arranged around the report. For example it will be used at a research seminar that is arranged for young medical students in order to interest them in research as a career path. It will also be used in different meetings with various decision makers as well as for fundraising purpose. <h3>Disclosure of Interest</h3> None declared
PTH-051 Influence of Iron Supplementation on The Natural History of Colitis
Authors: A Mahalhal, BJ Campbell, DM Pritchard, CS Probert
Journal: Gut (2016)

<h3>Introduction</h3> Iron deficiency anaemia is common in IBD. Iron supplementation may induce or exacerbate colitis in rats (<i>APT</i> 2001;15:1989–99).Dysbiosis of the microbiota is common in IBD and iron contributes to this as it is a growth factor for pathogenic bacteria.We investigated the effect of dietary iron supplementation and/or reduction on the severity of chronic colitis in a murine model using clinical, histological and biochemical parameters. <h3>Methods</h3> Studies were performed on 6 groups of 8 wild type (WT) C57BL/6 mice.Chronic colitis was induced with 1.25% Dextran Sodium Sulphate (DSS) for 5 days,followed by16 further days on water [for 3 consecutive cycles]. DSS-treated mice were fed one of three diets:low iron [LI] (100 ppm), normal iron [NI] (200 ppm) and high iron[HI] (400 ppm) supplemented chow. Also, 3 non-DSS-treated groups were studied and fed similarly. Half of the mice in each control group were treated with 1 cycle of acute 2% DSS for 5 days at day 53, followed by 5 further days on water. All mice were sacrificed at day 63. Daily weights and clinical features were recorded. Histological colitis was scored using the Bauer score(<i>Gut </i>2010; 59:1192–99).Faecal calprotectin was measured by ELISA and faecal iron by immunoassay at various time points [day (d) 1, 21, 42 &amp; 63]. Statistical analyses used the Kruskal–Wallis test with post-hoc analysis. <h3>Results</h3> Oral DSS administration induced colitis in all treated mice. While chronic DSS colitis was not associated with weight loss, there was severe weight loss in acute DSS mice which was greatest in the low iron diet group (p = 0.001 LI vs. HI; p = 0.01 for LI vs. NI). Histologically, the colitis features were more prominent in acute DSS-treated mice ingesting low and high iron diets, with median colitis scores 6 &amp; 5.5 respectively.Cyclic administration of DSS in drinking water resulted in a significant rise in faecal calprotectin, from baseline to d63 in LI (p = 0.05) and for HI (p = 0.01), but this was not significant in the NI group. In acute DSS, the rise was greater in LI and HI (p = 0.001) and less in NI (p = 0.01).Total faecal iron was increased in a dose-dependent manner within 9 weeks in all non-DSS groups. Nevertheless, in chronic DSS groups, p = 0.001 at d1 vs. d63 for all groups [382% change for LI, 331% for NI and 355% for HI].However, in acute DSS p = 0.05 for LI, p = 0.001 NI &amp; HI (d1 vs. d10). <h3>Conclusion</h3> Changes in nutritional luminal iron exacerbate colitis.Oral administration of DSS causes a reproducible acute colitis, followed by a slow recovery phase with a concomitant chronic inflammation. Chronic colitis was worse in mice fed low or high iron diets, as shown by elevated calprotectin. Faecal iron rose equally in all 3 groups: with iron increases likely arising from diet and bleeding during colitis. Dysbiosis may be a consequence of this change in luminal iron. <h3>Disclosure of Interest</h3> None Declared
Outcomes and Management of Red Blood Cell Transfusions in Multiple Myeloma Patients Treated with Daratumumab
Authors: Ajai Chari, Toshihisa Satta, Amit Tayal, Sundar Jagannath, Hearn Jay Cho, Samir Parekh, Kenneth Lau, Gillian Morgan, Donna Catamero, Juliet Escalon, Erika Florendo, Daniel Verina, Parul Doshi, Huaibao Feng, Clarissa Uhlar, Imran Khan, Tahamtan Ahmadi, Peter M. Voorhees, Maria-Victoria Mateos, Suzanne Arinsburg
Journal: Blood (2015)
Mutations of TET2 and JAK2 but Not CBL Are Detectable in a High Portion of Patients with Refractory Anemia with Ring Sideroblasts and Thrombocytosis (RARS-T).
Authors: Johanna Flach, Sonja Schindela, Frank Dicker, Susanne Schnittger, Alexander Kohlmann, Tamara Weiss, Wolfgang Kern, Torsten Haferlach, Claudia Haferlach
Journal: Blood (2009)
SP0098 For Whom Are Joint Replacements Most Successful? An Overview of The Current Literature
Authors: L. Mandl
Journal: Annals of the Rheumatic Diseases (2016)

Total hip and knee replacements are are some of modern medicine9s biggest success stories. They are, in general, extremely successful procedures, providing patients witih end stage arthritis significant improvements in pain, function and qualify of life. However, these procedures are not universal panaceas; in fact, it is estimated that up to 25% of total knee replacement patients may have residual chronic pain years after their original surgery. As aging babyboomers-who expect to continue an active lifestyle at higher rates than previous generations-increase the demand for joint replacements, it will become even more important to understand the risks and benefits of arthroplasty. This lecture will discuss outcomes of hip and knee replacements, with an emphasis on which patients are most likely to derive benefit. <h3>Disclosure of Interest</h3> L. Mandl Grant/research support from: Boehringher-Ingelheim
THU0126 Dose Titration of Biologics for The Treatment of Rheumatoid Arthritis and Ankylosing Spondylitis: A Systematic Literature Review: Table 1.
Authors: C.S. Lau, A. Gibofsky, N. Damjanov, S. Lula, L. Marshall, H. Jones, P. Emery
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Increasingly, clinicians treating rheumatoid arthritis (RA) or ankylosing spondylitis (AS) are trying to dose-titrate biologics, due to cost, patient preference, and safety. Recent clinical guidelines recommend down titration for RA. However, evidence of safety and efficacy is limited. <h3>Objectives</h3> Conduct a systematic literature review to assess breadth and quality of published data and evaluate whether sufficient evidence exists to support dose titration of biologics in RA or AS. <h3>Methods</h3> Medline, Embase, and the Cochrane library were electronically searched on February 2, 2015, and conference abstracts from 2010 to November 2015 were hand searched. Eligible studies included: randomized controlled trials (RCTs), non-RCTs, observational, and pharmacoeconomics. Biologics included: abatacept, adalimumab, certolizumab, etanercept, golimumab, infliximab, rituximab and tocilizumab. Outcomes were (1) efficacy and sustained remission, (2) flares and retreatment, (3) economic impact. <h3>Results</h3> The search yielded 21,585 records; after screening, 73 studies in 90 publications/abstracts were retained, including 15 full-text RCTs, 15 full-text non-RCTs and 43 conference abstracts. Efficacy and economic data were limited. Heterogeneity in disease duration, dosing strategies, and definition of treatment success/failure complicated the interpretation and comparison of regimens. Dose titration rationale varied greatly, and few studies used established definitions of flare (table). Level of evidence was low, with most studies presented as conference abstracts. <h3>Conclusions</h3> Studies evaluating dose titration of biologics are heterogeneous in design and lack standardized definitions. Little evidence of safety and efficacy exists to support dose titration of biologics in RA or AS; RCTs with defined indicators of treatment success and failure are needed. <h3>Disclosure of Interest</h3> C. S. Lau Consultant for: Abbvie, Astrazeneca, GlaxoSmithKline and Human Genome Sciences, Pfizer, Roche, UCB, A. Gibofsky Shareholder of: AbbVie, Angen, Celgene, Pfizer, GSK, J&amp;J, Regeneron, Consultant for: AbbVie, Celgene, Pfizer, Iroko, Horizon, Samumed, Relburn, Speakers bureau: Amgen, AbbVie, Pfizer, Celgene, Iroko, Horizon, N. Damjanov Consultant for: Pfizer, Roche, MSD, Abbvie, Gedeon-Richter, Boehringer Ingelheim, S. Lula Employee of: Envision Pharma, L. Marshall Shareholder of: Pfizer, Employee of: Pfizer, H. Jones Shareholder of: Pfizer, Employee of: Pfizer, P. Emery Consultant for: Pfizer,MSD,Abbvie,BMS,UCB,Roche,Novartis,Samsung, Sandoz and Lilly
Comparison of the Management of Anemia in Patients with Solid Versus Hematological Malignancies Treated with Erythropoiesis Stimulating Agents (ESAs): Findings from the European Anemia Cancer Treatment (A.C.T.) Study
Authors: Heinz Ludwig, Matti Aapro, Carsten Bokemeyer, Pierre Soubeyran, Michael Muenzberg, Matthew Turner, Karen MacDonald, Tara Albrecht, Ivo Abraham
Journal: Blood (2008)
FRI0512 IGG4-Related Disease Is Associated with A History of Malignancy
Authors: Z. Wallace, C. Wallace, L. Lu, H. Choi, J. Stone
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> IgG4-related disease (IgG4-RD) is a fibroinflammatory disease of unclear etiology<sup>1</sup>. Some studies suggest that IgG4-RD predisposes patients to malignancy or is a <i>forme fruste</i> of cancer<sup>2</sup>, but we have frequently observed IgG4-RD patients with a history of malignancy preceding the clinical onset of IgG4-RD. <h3>Objectives</h3> We sought to determine whether a history of malignancy was more common among patients at the onset of IgG4-RD compared to controls. <h3>Methods</h3> We identified IgG4-RD patients with a history of invasive malignancy from a well-defined cohort of 125 patients and compared their malignancy history to those of two reference groups. First, we calculated a standardized prevalence ratio against general US population estimates from the Surveillance, Epidemiology, and End Results (SEER) database. Second, we identified up to five age- and gender-matched controls for each case and calculated the odds of malignancy among those with IgG4-RD compared to controls using conditional logistic regression. <h3>Results</h3> The mean age at IgG4-RD onset was 50.3±14.9 years and 61% of the patients were male. Twenty (16%) had been diagnosed with 21 malignancies before the diagnosis of IgG4-RD. The observed prevalence of malignancy in this cohort was 2.5 times higher (95% CI:1.1–3.6) than expected compared to the SEER database. Compared with matched controls, a history of malignancy was more than three-fold higher in IgG4-RD (OR 3.1;95% CI:1.6–6.2). <h3>Conclusions</h3> Our findings suggest that malignancy is associated with the subsequent development of IgG4-RD in a subset of patients with IgG4-RD. Potential explanations include shared risk factors for both IgG4-RD and cancer, the triggering by cancer of autoantigen expression leading to IgG4-RD, and an increased risk of IgG4-RD resulting from cancer treatment. <h3>References</h3> Stone JH, Zen Y, Deshpande V. IgG4-related disease. N Engl J Med. 2012;366(6):539–551. Hart PA, Law RJ, Dierkhising RA, Smyrk TC, Takahashi N, Chari ST. Risk of cancer in autoimmune pancreatitis: A case-control study and review of the literature. Pancreas. 2014;43(3):417–421. <h3>Disclosure of Interest</h3> None declared
P0611 : Trajectories of hepatitis B surface antigen and associations with hepatocellular carcinoma, liver cirrhosis, and HBsAg seroclearance among chronic hepatitis B carriers with low viral loads
Authors: J. Liu, H.-I. Yang, M.-H. Lee, R. Batrla-Utermann, C.-L. Jen, S.-N. Lu, L.-Y. Wang, S.-L. You, C.-J. Chen
Journal: Journal of Hepatology (2015)
FRI0019 Divergent Effects of Free Fatty Acids on Cells of Bone Metabolism
Authors: K. Frommer, A. Schäffler, U. Lange, S. Rehart, J. Steinmeyer, M. Rickert, U. Müller-Ladner, E. Neumann
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Adipose tissue secretes numerous bioactive substances, which contribute to inflammation. Chronically elevated free fatty acid (FFA) levels are known to be associated with numerous inflammatory cardiovascular and metabolic diseases such as atherosclerosis, coronary heart diseases and type 2 diabetes. Conversely, inflammation can contribute to bone loss. FFA may therefore be a contributing factor in bone loss in osteoarthritis (OA) and/or rheumatoid arthritis (RA). Interestingly, obesity is associated with a higher risk of OA also in non-weight bearing joints and increased amounts of visceral fat are associated with lower bone density. <h3>Objectives</h3> To test the hypothesis that FFA affect cells of bone metabolism in the context of rheumatic diseases in a way that promotes bone loss. <h3>Methods</h3> Primary osteoblasts (OB) were isolated from cancellous bone of OA and RA patients undergoing knee joint surgery. Osteoclasts (OC) were differentiated from peripheral blood mononuclear cells (PBMC). OB and OC were stimulated with the saturated FFA palmitic acid (PA) and the unsaturated FFA linoleic acid (LA). Immunoassays were used to quantify protein secretion. mRNA expression levels were quantified by real-time PCR. Mineralization activity was quantified using Alizarin Red S staining, differentiated OC were quantified by counting TRAP-positive multinuclear cells. Toll-like receptor (TLR) 4 and TLR2 were blocked by neutralizing antibodies. <h3>Results</h3> Both PA and LA increased the secretion of the proinflammatory cytokine IL-6 (up to 9-fold) and the chemokines IL-8 (up to 221-fold), GRO-a (from below detection level to detectable levels) and MCP-1 (up to 16-fold). The degree of response was highly dependent upon the patient. RANKL as well as OPG, important regulators of osteoclastogenesis and OC activity, remained unaffected by FFA on protein and mRNA level. OB activity markers alkaline phosphatase (ALP) and collagen type I as well as markers of OB differentiation (e.g. osteocalcin) also remained unchanged after FFA stimulation. PA-induced IL-8 secretion by OB could be significantly reduced by TLR4 blockade (by 93%), while blocking TLR2 had no effect. Upon stimulation with PA and LA, secretion of IL-8 by RA OC was increased and MMP-9 reduced and the number of TRAP positive multinuclear cells decreased (by around 50%). Further markers of osteoclast activity (CLCN7, CTSK, TCIRG) remained unchanged. <h3>Conclusions</h3> The effect of FFA on cells of bone metabolism appears to be divergent: While FFA promote a pro-inflammatory phenotype in OB and may thus indirectly contribute to bone loss, the effects on OC mainly suggest an inhibitory effect on bone resorption. <h3>Disclosure of Interest</h3> None declared
Atypical Presentations of EBV Reactivation and EBV-Associated PTLD Post-HSCT: Implication for Routine EBV Surveillance after Allogeneic HSCT?.
Authors: Christiane E. Dobbelstein, Haytham M. Kamal, Elke Dammann, Bernd Hertenstein, Eva M. Weissinger, Arnold Ganser
Journal: Blood (2005)
PWE-044 Inter-Tumour Heterogeneity in Hepatitis C Virus (HCV) Related Multi-Focal Hepatocellular Carcinoma (HCC)
Authors: W Fateen, H Wood, S Berri, J Wyatt, M El- Meteini, C Millson, P Quirke
Journal: Gut (2016)

<h3>Introduction</h3> Curative therapies improve overall survival by more than 60 months on a small proportion of patients with HCC however the majority of patients are diagnosed with non curable, mostly multi-focal HCC. There are two theories for the development of multifocal HCC. First is intrahepatic metastasis where the new cancer would inherit genetic properties from the index cancer. Second is de novo development of HCC where both cancers are expected to have genetically diverse properties. We aimed to evaluate the presence and frequency of intrahepatic metastasis versus de novo carcinogenesis in HCV related multi-focal HCC. <h3>Methods</h3> We studied DNA copy number profiles of 70 HCV-related hepatocellular cancers found in 19 surgically removed liver specimens from 18 patients. Differences in copy number patterns were objectively analysed using Pearson’s correlations between normalised, non-smoothed, non-segmented ratios (n = 27,180 per each sample). Fisher r to z to r transformation was used in calculation of the average coefficients. <h3>Results</h3> Livers containing 2 or 3 nodules (n = 10 livers) had an average cancer correlation coefficient of 0.395 and only 20% of them (n = 2/10) harboured cancers with coefficients &gt;0.5. Livers containing 4 or more nodules (n = 9 livers) had an average cancer correlation coefficient of 0.620 and 89% of them (n = 8/9) harboured cancers with coefficients &gt;0.5. The higher correlation coefficient may indicate that livers with a larger number of nodules are more likely to harbour genetically similar cancers then liver with a smaller number of nodules. This implies that intrahepatic metastasis starts to occur at a more advanced stage of liver disease and that de novo carcinogenesis takes place at an earlier stage. <h3>Conclusion</h3> This study confirms that both processes exist. The occurrence of de novo carcinogenesis leads to emergence of genetically diverse cancers within the same liver. Our data suggests that this occurs at an earlier stage of multifocal spread. Intrahepatic metastasis leads to occurrence of genetically similar cancers within the same liver. This possibly occurs when HCC’s are more established. More cases are needed to validate the sequence of events in hepatocarcinogenesis. This is knowledge is clinically relevant as cancers with diverse genetic profiles are practically more difficult to manage. <h3>Disclosure of Interest</h3> W. Fateen: None Declared, H. Wood: None Declared, S. Berri Employee of: Illumina, J. Wyatt: None Declared, M. El- Meteini: None Declared, C. Millson: None Declared, P. Quirke: None Declared