tbuckley/cabot-search huggingface dataset:
FRI0540 Evaluation of bone quality using the new trabecular bone score (TBS) tool in rheumatoid arthritis patients
Authors: A Casabella, A Sulli, C Seriolo, G Botticella, L Molfetta, M Cutolo, S Paolino, B Ruaro
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Patients affected by Rheumatoid Arthritis (RA) show an increased risk of low bone mass, as a result of multi-systemic disorders including toxic drug, low vitamin D levels and physical inactivity. Trabecular Bone Score (TBS), is an index extracted from the dual-energy X-ray absorptiometry (DXA) images, that provides an indirect measurement (Score) of bone axial microarchitecture and allows to get information about bone quality (1,2). <h3>Objectives</h3> The aim of this investigation was to evaluate bone quality in RA patients (high risk population) receiving vitamin D supplementation from at least 3 month, using the TBS. <h3>Methods</h3> 108 female patients (mean age 61±8 years) affected by RA and 60 age- matched controls (CNT) (mean age 64±11 years) were enrolled. Bone Mineral Density (BMD, g/cm<sup>2</sup>) of the lumbar spine (L1-L4) was analyzed using a DXA scan (GE,Lunar Prodigy). Lumbar spine TBS (TBS iNsight Medimaps) was derived for each spine DXA examination. All patients were evaluated for serum 25 hydroxyvitamin D (25(OH)D) concentrations. <h3>Results</h3> 78 RA patients (80%) presented a bone loss that was significantly lower when compared with control group (p&lt;0.001). Likewise, lumbar spine TBS score was found significantly lower in RA patients compared with CNT (p&lt;0.001). Finally, RA patients showed lower 25(OH)D concentrations (18.4±1.3 ng/ml) than CNT (26.2±0.9 ng/ml; p&lt;0.04). <h3>Conclusions</h3> This study shows in RA patients a reduction of TBS values that seem placed side by side with reduced BMD values and 25(OH)D serum concentrations. Therefore, TBS could become a new and safe diagnostic tool for the quantification of the bone quality and related osteoporosis, in chronic systemic inflammatory rheumatic diseases, such as RA. <h3>References</h3> Sinigaglia L, et al. Rheum Dis Clin North Am. 2006;32:631–58. Avouac J, et al. Arthritis Care Res 2012;64:1871–8. <h3>Disclosure of Interest</h3> None declared
Treating anxious expectations can improve dyspnoea in patients with COPD
Authors: Andreas von Leupoldt
Journal: European Respiratory Journal (2017)

Chronic obstructive pulmonary disease (COPD) is a worldwide leading cause of morbidity and mortality and associated with great individual, societal and economic burden [1]. Dyspnoea is the threatening cardinal symptom and related to a worse course of COPD, including drastic reductions in quality of life and even increased mortality risk [2, 3]. Dyspnoea is a multi-dimensional subjective experience that encompasses not only the perception of sensory signals (dyspnoea intensity), but also important immediate and long-term affective aspects (dyspnoea unpleasantness, dyspnoea anxiety, suffering) [2–4]. In many patients, dyspnoea can be persistent, despite optimal treatment efforts, which was recently termed "chronic breathlessness syndrome" [5]. Notwithstanding, reducing dyspnoea is a major treatment goal in COPD [6] and neglecting it has previously been discussed in a thought-provoking article in this journal as a potential violation of human rights [7]. The detection and treatment of anxious expectations can improve dyspnoea in patients with COPD <http://ow.ly/jnBR30efnhj>
Infographic: Consensus statement on concussion in sport
Authors: Paul McCrory, Willem Meeuwisse, Jiri Dvorak, Mark Aubry, Julian Bailes, Steven Broglio, Robert C Cantu, David Cassidy, Ruben J Echemendia, Rudy J Castellani, Gavin A Davis, Richard Ellenbogen, Carolyn Emery, Lars Engebretsen, Nina Feddermann-Demont, Christopher C Giza, Kevin M Guskiewicz, Stanley Herring, Grant L Iverson, Karen M Johnston, James Kissick, Jeffrey Kutcher, John J Leddy, David Maddocks, Michael Makdissi, Geoff Manley, Michael McCrea, William P Meehan, Shinji Nagahiro, Jon Patricios, Margot Putukian, Kathryn J Schneider, Allen Sills, Charles H Tator, Michael Turner, Pieter E Vos
Journal: British Journal of Sports Medicine (2017)
THU0441 Synovial fluid leukocyte count and its association with crystal deposition in asymptomatic hyperuricemia: a preliminary report
Authors: M Andrés, JA Bernal, MD Arenas, E Pascual
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Joint deposits of monosodium urate (MSU) crystals in asymptomatic hyperuricemia (AH) may associate with more severe forms of atherosclerosis [1]. It likely relates with crystal-driven subclinical inflammation, a phenomenon well described in gout [2] but to date not assessed in AH. <h3>Objectives</h3> To assess the synovial fluid (SF) leukocytes count in patients with AH depending on the presence of crystals. <h3>Methods</h3> Consecutive patients with AH were selected from nephrology clinics. Hyperuricemia threshold was established at serum uric acid (SUA) ≥7mg/dL; those on current urate-lowering therapy were excluded. Ultrasound (US) of knees, ankles and first metatarsophalangeal joints was performed blinded to clinical and laboratory data, in order to perform US-guided aspiration and obtain SF samples. These samples were analyzed in fresh by two observers, using a compensated polarized light microscope equipped with two viewing stations. The second observer was in addition unaware of US findings. The presence of leukocytes and crystals was established by consensus. SF leukocyte count was performed using a Neubauer counting camera. Mann-Whitney9s U and Kruskal-Wallis9 H were used to compare difference in leukocyte counts between groups. <h3>Results</h3> To end of January 2017, 30 patients have been assessed, with SF samples available from 27 (three showed no joint effusion at US). Median age was 70 years (p25–75 59.8–75.5), and 16 of them (60%) were males. Median (p25–75) SUA and estimated glomerular filtration rate were 8.1 mg/dL (7.6–8.5) and 37.0 mL/min (31.0–47.5), respectively. Seven (25%) were on diuretics. After microscopy evaluation, MSU crystals were found in four patients (14.8%), calcium pyrophosphate (CPP) crystals in five (18.5%), and no crystals in 18 (66.7%). Figure shows median leukocytes count according to crystal group: 200/mm<sup>3</sup> (138–540) in MSU group; 60/mm<sup>3</sup> (50–235) in CPP group; and 30/mm<sup>3</sup> (10–53) in those with no crystal at SF. A statistically significant difference was found between the three groups (p=0.001), and comparing MSU crystals and no crystals groups (p&lt;0.001); no difference was found between MSU and CPP groups (p=0.111). <h3>Conclusions</h3> In a preliminary report, MSU crystal deposition in patients with AH leads to higher SF leukocyte count, indicating low-grade inflammation. Despite low numbers and being an ongoing study, this significant finding might contribute to explain the severe atherosclerosis data recently reported in AH patients with silent crystal deposits. <h3>References</h3> Arthritis Rheumatol 2016;68:1531. Arthritis Rheum 1991;34:141. <h3>Disclosure of Interest</h3> None declared
Adaptation to TKI Treatment Reactivates ERK Signaling in Tyrosine Kinase–Driven Leukemias and Other Malignancies
Authors: J. Kyle Bruner, Hayley S. Ma, Li Li, Alice Can Ran Qin, Michelle A. Rudek, Richard J. Jones, Mark J. Levis, Keith W. Pratz, Christine A. Pratilas, Donald Small
Journal: Cancer Research (2017)

Abstract FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibitors (TKI) have been tested extensively to limited benefit in acute myeloid leukemia (AML). We hypothesized that FLT3/internal tandem duplication (ITD) leukemia cells exhibit mechanisms of intrinsic signaling adaptation to TKI treatment that are associated with an incomplete response. Here, we identified reactivation of ERK signaling within hours following treatment of FLT3/ITD AML cells with selective inhibitors of FLT3. When these cells were treated with inhibitors of both FLT3 and MEK in combination, ERK reactivation was abrogated and anti-leukemia effects were more pronounced compared with either drug alone. ERK reactivation was also observed following inhibition of other tyrosine kinase–driven cancer cells, including EGFR-mutant lung cancer, HER2-amplified breast cancer, and BCR–ABL leukemia. These studies reveal an adaptive feedback mechanism in tyrosine kinase–driven cancers associated with reactivation of ERK signaling in response to targeted inhibition. Cancer Res; 77(20); 5554–63. ©2017 AACR.
The development of collagen based composite scaffolds for bone regeneration
Authors: Dawei Zhang, Xiaowei Wu, Jingdi Chen, Kaili Lin
Journal: Bioactive Materials (2017)

Bone is consisted of bone matrix, cells and bioactive factors, and bone matrix is the combination of inorganic minerals and organic polymers. Type I collagen fibril made of five triple-helical collagen chains is the main organic polymer in bone matrix. It plays an important role in the bone formation and remodeling process. Moreover, collagen is one of the most commonly used scaffold materials for bone tissue engineering due to its excellent biocompatibility and biodegradability. However, the low mechanical strength and osteoinductivity of collagen limit its wider applications in bone regeneration field. By incorporating different biomaterials, the properties such as porosity, structural stability, osteoinductivity, osteogenicity of collagen matrixes can be largely improved. This review summarizes and categorizes different kinds of biomaterials including bioceramic, carbon and polymer materials used as components to fabricate collagen based composite scaffolds for bone regeneration. Moreover, the possible directions of future research and development in this field are also proposed.
Downregulation of <i>SAFB</i> Sustains the NF-<b>κ</b>B Pathway by Targeting <i>TAK1</i> during the Progression of Colorectal Cancer
Authors: Hong-Li Jiao, Ya-Ping Ye, Run-Wei Yang, Hui-Ying Sun, Shu-Yang Wang, Yong-Xia Wang, Zhi-Yuan Xiao, Liu-Qing He, Juan-Juan Cai, Wen-Ting Wei, Yan-Ru Chen, Chun-Cai Gu, Yue-Long Cai, Yun-Teng Hu, Qiu-Hua Lai, Jun-Feng Qiu, Li Liang, Guang-Wen Cao, Wen-Ting Liao, Yan-Qing Ding
Journal: Clinical Cancer Research (2017)

Purpose: To investigate the role and the underlying mechanism of scaffold attachment factor B (SAFB) in the progression of colorectal cancer (CRC).Experimental Design: SAFB expression was analyzed in the Cancer Outlier Profile Analysis of Oncomine and in 175 paraffin-embedded archived CRC tissues. Gene Ontology analyses were performed to explore the mechanism of SAFB in CRC progression. Western blot, RT-PCR, luciferase assay, and chromatin immunoprecipitation (ChIP) were used to detect the regulation of transforming growth factor-β-activated kinase 1 (TAK1) and NF-κB signaling by SAFB The role of SAFB in invasion, metastasis, and angiogenesis was investigated using in vitro and in vivo assays. The relationship between SAFB and TAK1 was analyzed in CRC tissues.Results: SAFB was downregulated in CRC tissues, and low expression of SAFB was significantly associated with an aggressive phenotype and poorer survival of CRC patients. The downregulation of SAFB activated NF-κB signaling by targeting the TAK1 promoter. Ectopic expression of SAFB inhibited the development of aggressive features and metastasis of CRC cells both in vitro and in vivo The overexpression of TAK1 could rescue the aggressive features in SAFB-overexpressed cells. Furthermore, the expression of SAFB in CRC tissues was negatively correlated with the expression of TAK1- and NF-κB-related genes.Conclusions: Our results show that SAFB regulated the activity of NF-κB signaling in CRC by targeting TAK1 This novel mechanism provides a comprehensive understanding of both SAFB and the NF-κB signaling pathway in the progression of CRC and indicates that the SAFB-TAK1-NF-κB axis is a potential target for early therapeutic intervention in CRC progression. Clin Cancer Res; 23(22); 7108-18. ©2017 AACR.
Abstract 16761: The Relationship of Lipids and Lipoprotein Distribution With Depressive Symptoms: The Multi-Ethnic Study of Atherosclerosis
Authors: Kwok-Leung Ong, Margaret J Morris, Robyn L McClelland, Jayanthi Maniam, Matthew A Allison, Kerry-Anne Rye
Journal: Circulation (2016)

Introduction:  Previous studies suggest lower concentrations of both total and HDL cholesterol to be predictive of depression. We therefore investigated the relationship of lipids and lipoprotein distribution with elevated depressive symptoms (EDS) in healthy men and women from the Multi-Ethnic Study of Atherosclerosis (MESA).   Methods:  All MESA participants were 45-84 years old and free of clinically apparent cardiovascular disease at baseline. They were recruited from six United States communities and were followed up in person at four clinic visits over a 9.5-year period. EDS were defined as a Center for Epidemiological Studies Depression (CES-D) score ≥16 and/or use of antidepressant drugs. Lipoprotein distribution was determined from plasma by nuclear magnetic resonance spectroscopy.   Results:  Among 4938 MESA participants without EDS at baseline, 1178 participants (23.9%) developed EDS during follow-up. In multivariable Cox regression analyses, lower total, LDL, and non-HDL cholesterol concentrations at baseline were associated with incident EDS over 9.5 years (hazards ratio = 1.11-1.12 per SD decrease, all  P  P    Conclusions:  Lower baseline concentrations of total, LDL and non-HDL cholesterol were associated with a higher risk of incident EDS. However, a short-term increase in cholesterol concentrations did not help to reduce the risk of EDS. Further studies are needed to replicate our findings and clarify the contradictory relationship between lipid profile and depression.
Positive effects of combined cognitive and physical exercise training on cognitive function in older adults with mild cognitive impairment or dementia: A meta-analysis
Authors: E.G.A. (Esther) Karssemeijer, J.A. (Justine) Aaronson, W.J. (Willem) Bossers, T. (Tara) Smits, M.G.M. (Marcel) Olde Rikkert, R.P.C. (Roy) Kessels
Journal: Ageing Research Reviews (2017)
On the “Lucke Tumor”Origin of Cell Line LT-1: Reply
Authors: Louis S. Kucera, Janice Simonson, Stephen J. O'Brien, Hayden Coon
Journal: JNCI Journal of the National Cancer Institute (1978)

On the “Lucke Tumor”Origin of Cell Line LT-1: Reply Get access Louis S. Kucera, Louis S. Kucera Department of Microbiology and Immunology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103 Search for other works by this author on: Oxford Academic PubMed Google Scholar Janice Simonson, Janice Simonson Laboratory of Viral Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar Stephen J. O'Brien, Stephen J. O'Brien Laboratory of Viral Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar Hayden Coon Hayden Coon Laboratory of Cell Biology, National Cancer Institute, Bethesda, Maryland 20014 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 60, Issue 3, March 1978, Page 495, https://doi.org/10.1093/jnci/60.3.495 Published: 01 March 1978
THU0253 Triple positivity to antiphospholipid antibodies in primary antiphospholipid syndrome: increased risk of arterial thromboses and abortions
Authors: F Signorelli, G Balbi, RA Levy
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Triple positivity (TP) to antiphospholipid antibodies (aPL) has been associated with increased risk of thrombotic and gestational events in different populations of antiphospholipid syndrome (APS) patients. Nonetheless, the majority of the studies evolved APS secondary to systemic lupus erythematosus (SLE). <h3>Objectives</h3> To investigate whether TP increases the risk of criteria and non-criteria manifestations in primary APS (pAPS) patients. <h3>Methods</h3> A cross-sectional study was performed in a group of 74 outpatients who fulfilled APS classification criteria (Sydney; N=67) or with thrombocytopenia and persistent circulating aPL, but no criteria manifestations of APS (N=7), seen in our department. Clinical and serological features collected during medical examination and by chart review were correlated to the presence or not of aPL TP. <h3>Results</h3> Nineteen out of 74 pAPS patients had aPL TP (25.7%). Demographic and clinical characteristics are shown in Table 1. In a bivariate analysis, TP was associated with the presence of combined thrombotic and obstetric manifestations (p=0.008), three or more abortions (abortion 3+; p=0.043), and livedo (p=0.023). In a multivariate regression analysis, the model was adjusted to age, sex, race and variables with p&lt;0.10 in the bivariate analysis (arterial thrombosis, abortion 3+, livedo, thrombocytopenia, and thrombotic+obstetric). After the analysis, arterial thrombosis (OR 5.74; CI95% 1.31–25.05; p=0.02) and abortion 3+ (OR 12.55; CI95% 1.01–156.54; p=0.049) were associated with TP. <h3>Conclusions</h3> In our cohort of primary APS patients, triple positivity was associated with arterial thromboses and the occurrence of 3 or more abortions, with increased risk over 5 and 12 folds, respectively. <h3>Disclosure of Interest</h3> None declared
Counting Sepsis, an Imprecise but Improving Science
Authors: Kristina E. Rudd, Anthony Delaney, Simon Finfer
Journal: JAMA (2017)

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Real-world analysis of treatment patterns examining nab-Paclitaxel plus Gemcitabine (nab-P+G) versus FOLFIRINOX (FFX) in first-line (1L) treatment (tx) of metastatic pancreatic adenocarcinoma (MPAC) in a U.S. community oncology setting.
Authors: Fadi S. Braiteh, Manish Patel, Monika Parisi, Quanhong Ni, Si yeon Park, Claudio Faria
Journal: Journal of Clinical Oncology (2016)

e18130 Background: In independent phase III trials, both nab-P + G and FFX demonstrated significantly better OS, PFS, and ORR than G alone as 1L tx for MPAC. Limited real-world data exist on the effectiveness of and treatment patterns associated with nab-P + G vs FFX for 1L tx of patients (pts) with MPAC, supporting the need for the current study. Methods: A retrospective cohort study was performed using fully de-identified data from a nationally representative electronic medical record platform of 1,300 community oncologists. Pts diagnosed with MPAC between 9/10/13 and 10/6/14 and received either nab-P+G or FFX as 1L tx were included. We calculated median time to treatment discontinuation (TTD) and estimated survival (ES), proxy for OS, using the Kaplan Meier method. We also assessed incidence of adverse events (AEs), utilization of supportive care, and incidence of regimen modifications and dose delays across the two groups. Lastly, we explored outcomes associated with sequencing 1L and 2L therapy. Results: 202 pts met eligibility criteria (nab-P+G, n = 122; FFX, n = 80). Pts on nab-P+G were older than pts on FFX (mean age 67.0 vs 61.4; p < 0.01), but other baseline characteristics were comparable. TTD (3.4 vs 3.8 mos) and ES (8.6 vs 8.6 mos) were not statistically different for nab-P+G and FFX, respectively. FFX pts had a higher incidence of overall AEs vs nab-P + G pts (95% vs 84%), and utilized significantly more G-CSF (39% of pts on FFX vs 8% on nab-P + G received prophylactic G-CSF), but nab-P + G pts require significantly more ESA. Fewer pts in the nab-P+G group required a regimen modification (10.7% v 27.5%) and dose delay (39.3% v 73.8%) compared to FFX pts. For nab-P+G pts who moved to a 5-FU based 2nd line regimen (n = 25), the median ES was 12.7 mos compared to 9.3 mos (p = 0.48) for FFX pts who switched to a G based 2nd line regimen (n = 41). Conclusions: TTD and ES for pts with MPAC did not differ significantly between nab-P+G and FFX. Fewer nab-P+G pts required regimen modifications and dose delays compared to FFX pts. Pts who received 1st-line nab-P + G followed by a 5-FU-based 2nd-line therapy had a longer ES.
rSj16 Protects against DSS-Induced Colitis by Inhibiting the PPAR-α Signaling Pathway
Authors: Lifu Wang, Hui Xie, Lian Xu, Qi Liao, Shuo Wan, Zilong Yu, Datao Lin, Beibei Zhang, Zhiyue Lv, Zhongdao Wu, Xi Sun
Journal: Theranostics (2017)

Background: Epidemiologic studies and animal model experiments have shown that parasites have significant modulatory effects on autoimmune disorders, including inflammatory bowel disease (IBD). Recombinant Sj16 (rSj16), a 16-kDa secreted protein of Schistosoma japonicum (S.japonicum) produced by Escherichia coli (E. coli), has been shown to have immunoregulatory effects in vivo and in vitro. In this study, we aimed to determine the effects of rSj16 on dextran sulfate sodium (DSS)-induced colitis. Methods: DSS-induced colitis mice were treated with rSj16. Body weight loss, disease activity index (DAI), myeloperoxidase (MPO) activity levels, colon lengths, macroscopic scores, histopathology findings, inflammatory cytokine levels and regulatory T cell (Treg) subset levels were examined. Moreover, the differential genes expression after treated with rSj16 were sequenced, analyzed and identified. Results: rSj16 attenuated clinical activity of DSS-induced colitis mice, diminished pro-inflammatory cytokine production, up-regulated immunoregulatory cytokine production and increased Treg percentages in DSS-induced colitis mice. Moreover, DSS-induced colitis mice treated with rSj16 displayed changes in the expression levels of specific genes in the colon and show the crucial role of peroxisome proliferator activated receptor α (PPAR-α) signaling pathway. PPAR-α activation diminished the therapeutic effects of rSj16 in DSS-induced colitis mice, indicating that the PPAR-α signaling pathway plays a crucial role in DSS-induced colitis development. Conclusions: rSj16 has protective effects on DSS-induced colitis, effects mediated mainly by PPAR-α signaling pathway inhibition. The findings of this study suggest that rSj16 may be useful as a therapeutic agent and that PPAR-α may be a new therapeutic target in the treatment of IBD.