tbuckley/cabot-search huggingface dataset:
AB0244 Radiographic Evaluation of Large Joint Damage in Patients with Rheumatoid Arthritis Using ARASHI Scoring Method
Authors: H. Motomura, I. Matsushita, A. Kaneko, K. Kanbe, K. Arai, Y. Kuga, A. Abe, T. Matsumoto, N. Nakagawa, K. Nishida, T. Kimura
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Structural impairment of large joints in patients with rheumatoid arthritis (RA) is strongly associated with functional disabilities. Although evaluation methods of large joint damage were limited, the ARASHI study group has recently devised new radiographic scoring system (Status score; range 0-16 points, and Change score: range -11 to 12 points) [1]. <h3>Objectives</h3> To evaluate the radiographic damage of 10 large joints (bilateral shoulder, elbow, hip, knee and ankle joints) in patients with RA using the ARASHI score, and to explore factors that predict the progression of large joint damage. <h3>Methods</h3> We have prospectively examined 64 patients with RA. Radiographic findings of large joints (122 shoulder, 123 elbow, 120 hip, 98 knee, and 117 ankle joints), excluding the joints with history of surgical intervention, were evaluated at baseline using the ARASHI status score and at 1 year using the ARASHI change score. Total ARASHI status score and change score were calculated from scores of all 10 large joints in each patient. We measured CRP, MMP-3 DAS28-ESR, SDAI, CDAI and HAQ-DI at baseline and at 1 year, and then compared differences of these clinical features between total ARASHI change score &lt;1 (non-progression) group and change score ≥1 (progression) group. <h3>Results</h3> The mean total ARASHI status score of all 10 large joints in 64 patients was 8.70 (0-58) at baseline. The total ARASHI change score showed joint remodeling (change score ≤ -1) in 18 patients (28.1%) and progression of joint damage in 21 patients (32.8%) at 1 year. The age, disease duration, CRP, MMP-3, disease activity, HAQ-DI and total ARASHI status score at baseline were not significantly different between non-progression group and progression group. The CRP, disease activity and HAQ-DI at 1 year were also not significantly different in each group. However, the mean MMP-3 value at 1 year in progression group was significantly higher that in non-progression group (153.5 ng/ml vs 80.9 ng/ml, <i>P</i> &lt;0.05). <h3>Conclusions</h3> We evaluated the radiographic damage of all 10 large joints in each patient with RA using total ARASHI score. Our results showed that decrement of serum MMP-3 level was associated with the inhibition of large joint damage in RA. <h3>References</h3> Kaneko A, et al. Mod Rheumatol. 2013; 23; 1053-1062. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3961
M25 Has the new contract delivered better ambulatory oxygen devices for patients? A London perspective
Authors: C Lee, L McDonnell, C Davidson
Journal: Thorax (2013)

<h3>Background</h3> In 2012 changes in the home oxygen service (HOS) contract offered patients the potential to benefit from new technology designed to assist ambulatory oxygen (AO) use, such as liquid oxygen (LOX) and refillable cylinders (Homefill). Prior to the change in contract only three services were thought to be commissioned in London (serving approximately 10,000 HOS users, costing £10.5m), with many areas attempting to meet increasing demand with no increase in resources. <h3>Aim</h3> To determine the service provision, commissioning arrangement and assessment protocols for AO across London Establish an AO network across London <h3>Methods</h3> A telephone audit was carried out in January-March 2013 with all known oxygen assessment centres in London. Two clinicians used an agreed proforma, with email follow-up. The interview included questions regarding; commissioning/funding; location; access to service, referrals and pathway; assessment protocol; disciplines/grades; and integration with respiratory services. <h3>Results</h3> 34 interviews were performed across the 32 London boroughs. Key findings are: Access: Two boroughs had no service, some had multiple. Who: In 20 teams nursing staff assessed; 15 teams, physiotherapists; and 7 teams, respiratory physiologists. Where: 16 assessed in the hospital, 9 in the community and 7 in both. How: The majority (94%) performed the 6MWT, however teams that assessed in the home did not use validated reproducible exercise tests. Equipment for assessment: The majority had standard cylinders (88%); 53% had lightweight and conservers; and other devices were rarely (3–13%) available. Size: 16 services (47%) carried out less than 5 assessments per month. Funding: 47% have some arrangements in place, 29% had no funding or no service provided and 24% unclear. Integration: 67% were part of an integrated service, 18% stand alone, 12% unclear and 6% had no service. <h3>Conclusions</h3> Service provision for AO across London is varied, with no standardised referral pathway, assessment protocol and often limited range of equipment available for assessment. This raises concerns over access to services, clinical assessment skills/competencies and unsuitable prescriptions. Approximately half of the services have no or unclear funding arrangements and although the majority of services (67%) are integrated within a wider COPD/IRS there was no established network and many clinicians felt isolated.
Case 41-2015
Authors: Jolan E. Walter, Mary Armanios, Uzma Shah, Alison M. Friedmann, Thomas Spitzer, Steven M. Sharatz, Catherine Hagen
Journal: New England Journal of Medicine (2015)

A 14-year-old boy with a history of type 1 diabetes, learning disabilities, recurrent infections, and leukoplakia had abnormal results on liver-function tests. On evaluation, he had thrombocytopenia, anemia, splenomegaly, and liver nodularity. Diagnostic tests were performed.
Abstract 868: Regular aspirin use and risk of multiple myeloma: A prospective analysis
Authors: Brenda M. Birmann, Edward Giovannucci, Graham A. Colditz
Journal: Cancer Research (2010)

Abstract Multiple myeloma (MM) is a lethal malignancy with a poorly understood etiology and no prevention strategies. Aspirin inhibits nuclear factor (NF)-κB, a transcription factor that mediates growth factors important to MM pathogenesis. We undertook the present analysis to evaluate whether regular aspirin use is associated with MM risk and thus may offer opportunities for MM chemoprevention. We conducted prospective analyses of regular aspirin use and MM risk in the Nurses’ Health Study (NHS) and Health Professionals Follow-up Study (HPFS) populations. Questions on regular aspirin use were first asked of women in 1980 and of men in 1986, and were updated thereafter on biennial follow-up questionnaires. Participants reported height and weight at enrollment (1976 in NHS, 1986 in HPFS), and updated weight biennially. We followed participants from the year of first aspirin use questions through the earliest among a cancer diagnosis, death, or June 2006 (NHS) or January 2006 (HPFS). We excluded persons with missing baseline exposure data or a baseline history of cancer. We imposed a 4-year lag on aspirin use classification to minimize the influence of preclinical MM-related bone pain on use; exposures were updated biennially. We identified 164 women and 110 men with MM during follow-up (i.e., 1,586,035 NHS and 593,489 HPFS person-years). We obtained hazard ratios (HR) and 95% confidence intervals (CI) from Cox proportional hazard models stratified by age and adjusted for body mass index, to assess the association of updated quantity and duration of aspirin use with MM. In men, cumulative average aspirin tablets/week (tab/wk) was inversely associated with MM risk. Compared to non-users, the HR (95% CI) was 0.60 (CI=0.36-0.98) for &amp;lt;3 tab/wk, 0.33 (0.12-0.92) for 3-&amp;lt;6 tab/wk, and 0.22 (0.03-1.56) for 6-&amp;lt;10 tab/wk. Duration of continuous aspirin use was also inversely associated with MM in men: compared to non-users, the HR (95% CI) was 0.62 (0.38-0.99) for ≤5 years, 0.54 (0.30-0.95) for 6-10 years, and 0.39 (0.12-1.25) for 11-20 years continuous use. Preliminary findings among women were suggestive of an inverse association of regular aspirin use with MM risk, but were not statistically significant. Analyses stratified by duration of use and BMI are ongoing. This prospective analysis offers evidence that regular aspirin use is associated with a diminished risk of MM. Thus, NF-κB dysregulation may contribute to MM etiology as well as to pathogenesis. However, the utility of aspirin for MM chemoprevention requires further clarification. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 868.
P458Changes of pulmonary vasoactive factors and its relation with pulmonary arterial hypertension in patients with high altitude pulmonary edema
Authors: Q Zhou
Journal: Cardiovascular Research (2014)

Objective: To assess the changes of pulmonary vasoactive factors and its relation with pulmonary arterial hypertension (PAH) in patients with high altitude pulmonary edema (HAPE). Methods: The levels of plasma intermedin(IMD), adrenomedulin(ADM), endothelin-1 (ET-1), partial pressure of oxygen in artery blood (PaO2), and mean pulmonary arterial pressure (mPAP) were measured in 22 patients with HAPE before treatment and after cure.In addition,the upper mentioned parameters were meated in 30 healthy peoples. Results: Before treatment,levels of IMD, ADM, ET-1, and mPAP [(174.23±17.44)pg/mL, (77.45±6.87)pg/mL, (93.6±10.22)ng/L, (46.51±7.20)mm Hg, respectively] were markedly higher,and PaO2 [(33.82±5.66)mm Hg] was lower in HAPE patients than those in the the normal control subjects [(62.76±10.60)pg/mL, (22.04±3.15)pg/mL, (35.52±4.52)ng/L, (20.14±3.34)mm Hg, (69.27±3.35)mm Hg, respectively] (all P<0.01). The IMD ADM ET-1 was positively correled with mPAP (r= 0.752 0.733 0.812, respectively, all P<0.01,and PaO2 was netatively correlated with IMD, ADM, ET-1, mPAP(r=-0.689, -0.710, -0.741, -0.744, all P<0.01) in the HAPE patients. After cure, levels of IMD,ADM,ET-1, and mPAP[(65.33±9.88)pg/mL, (23.56±3.53)pg/mL, (36.73±3.90)ng/L,(21.22±3.63)mm Hg, respectively] were markedly lower, and PaO2 [(69.01±3.62)mm Hg] was markedly higher than those before treatment (all P<0.01) in the HAPE patients, all parameters were not markedly differcence compared with those normal control subjects (all P>0.05). Conclusion: IMD, ADM and ET-1 may play important roles in mechanism of PAH in HAPE. Imbalance of these factors had great effects on the development of hypoxic pulmonary hypertasion.
Abstract 696: Anti-NRP1 tumor uptake is impacted by normal tissue sinks in a tumor bearing mouse model
Authors: Daniela Bumbaca, Charles A. Boswell, Hong Xiang, Ruediger Port, Michelle Schweiger, Shannon Stainton, Anil Bagri, Frank-Peter Theil, Paul J. Fielder, Leslie A. Khawli, Ben-Quan Shen
Journal: Cancer Research (2010)

Abstract Neuropilin-1 (NRP1) is a VEGF165 and semaphorin receptor widely expressed by vascular endothelial cells in normal tissues and on some tumor cells. Blocking NRP1 with a human IgG1 against the b domain of NRP1 has been shown to inhibit tumor growth in several preclinical models. However, due to the wide expression of NRP1 in normal tissues, the uptake of anti-NRP1 by tumor cells may be impacted by the uptake in normal tissues. The objective of this study was to determine the normal tissue uptake of anti-NRP1 and assess its impact on tumor tissue uptake in a tumor bearing mouse model. Nude mice bearing tumors with either low, HM7, or high, SKMES, NRP1 expression were dosed with [111In]-DOTA labeled anti-NRP1 with or without excess amounts of unlabeled anti-NRP1 via single IV injection. Following dosing, blood, tumor, and several normal tissues were collected at pre-selected time points for the determination of radioactivity levels using a gamma counter. In the absence of unlabeled anti-NRP1, 3% Injected Dose (ID)/ml of radioactivity was observed in the blood at 15 minutes post-dose and decreased quickly. There was minimal radioactivity seen in tumor tissue. In contrast, the majority of radioactivity was detected in the lungs and liver. With increasing amount of unlabeled anti-NRP1, the radioactivity in the lungs/liver dropped, while increasing in blood and tumor tissue. At ∼10 mg/kg unlabeled anti-NRP1, there was no additional decrease of radioactivity in these normal tissues whereas the tumor radioactivity appeared to reach its peak. Taken together, these data suggest that the lungs/liver are tissue sinks that sequester a majority of the anti-NRP1 when given at lower doses, thus hampering tumor uptake. It is important to optimize the dose and dose regimen in order to overcome this tissue sink binding and allow for a sufficient amount of antibody to be available for tumor uptake. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 696.
Abstract 1538: Inhibition of adenosine-mediated stabilization of intercellular adhesions promotes hypoxia-stressed endometrial carcinoma cell metastasis
Authors: Jessica L. Bowser, Michael R. Blackburn, Gregory L. Shipley, Susu Xie, Russell R. Broaddus
Journal: Cancer Research (2011)

Abstract Hypoxic microenvironments are commonly encountered in multiple epithelial malignancies. Epithelial cells classically up-regulate cellular adhesive mechanisms to counter the noxious effects of hypoxia. Inhibiting these tissue protective mechanisms is necessary for carcinoma cell invasion and metastasis. Our previous studies utilizing a transgenic model deficient for 5’nucleotidase (CD73), an enzyme responsible for adenosine biosynthesis, demonstrated that adenosine is required to circumvent hypoxia-mediated disruption of cellular adhesiveness in the normal endometrium. In endometrial carcinoma (EC), CD73 is down-regulated in poorly-differentiated, invasive, and metastatic ECs, but is expressed and functional in well-differentiated and non-metastatic disease. Based on these findings, we hypothesized that the malignant progression of EC is dependant on the loss of adenosine-mediated regulation of intercellular adhesions. Modified and unmodified Boyden chambers were used to assess migration and invasion of endometrial adenocarcinoma cells HEC-1A and HEC-1B. Hypoxia (5% or 1.5% O2) significantly reduced HEC-1A and HEC-1B migration and invasion in vitro; this effect was abrogated by CD73 RNA interference and the CD73 enzymatic inhibitor, α, β- methylenediphosphate (AoPCP). The inhibitory effect of CD73 on EC cell migration and invasion was restored by the stable, receptor-targeting adenosine analog, 5’-N-ethylcarboxamido adenosine (NECA). Quantitative RT-PCR identified two adenosine receptors, A1R and A2BR, to be expressed in HEC-1A and HEC-1B. Inhibition of the A2BR by MRS1754 significantly increased HEC-1B migration and invasion, while A1R antagonism (DPCPX) had no effect. A2BR inhibition in HEC-1A monolayers also resulted in increased paracellular permeability to FITC-labeled dextrans. Moreover, A2BR antagonism lowered cellular levels of junctional adhesion proteins claudin-1 and claudin-2, and resulted in increased accumulation of β-catenin within the cytoplasm. Intracellular pools of β-catenin re-organized to the cell membrane with NECA application. In summary, we have shown that CD73-generated adenosine is necessary to maintain normal protective epithelial barrier function in the uterus. Our results demonstrate for the first time that inhibition of adenosine-mediated stabilization of intercellular adhesions promotes cancer cell invasion and metastasis in a hypoxic microenvironment. (NIH TL1RR024147 and NIH 1P50CA098258-01) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1538. doi:10.1158/1538-7445.AM2011-1538
INCIDENCE, PREDICTORS AND SHORT- AND LONG-TERM MORTALITY IN PATIENTS WITH ST-SEGMENT MYOCARDIAL INFARCTION COMPLICATED WITH ACUTE PHASE VENTRICULAR TACHYCARDIA/ VENTRICULAR FIBRILLATION IN THE PERCUTANEOUS CORONARY INTERVENTION ERA
Authors: Masaharu Masuda, Yasuhiko Sakata, Daisaku Nakatani, Shinichiro Suna, Masahiko Hara, Tetsuhisa Kitamura, Hitoshi Minamiguchi, Hiroya Mizuno, Yuji Okuyama, Takahisa Yamada, Masaaki Uematsu, Toshimitsu Hamasaki, Hiroshi Sato, Masatsugu Hori, Issei Komuro
Journal: Journal of the American College of Cardiology (2015)
AB0094 Association of TGF-beta1 - 509c/t polymorphism and TGF-beta1 serum levels with systemic lupus erythematosus
Authors: M. Ivanova Goycheva, I. Manolova, E. Aleksandrova, R. Stoilov, R. Rashkov, L. Miteva, S. Stanilova
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Recent evidences suggest a role of transforming growth factor-beta1 (TGF-beta1) in preventing autoimmune diseases, such as systemic lupus erythematosus (SLE). <h3>Objectives</h3> The aim of this study was to investigate the relationship of -509C&gt;T polymorphism of the TGF-beta1 gene and TGF-beta1 serum levels with susceptibility to SLE in Bulgarian population <h3>Methods</h3> 157 SLE patients and 134 healthy controls were studied. TGF-beta1 serum levels were measured by enzyme-linked immunosorbent assay and genotyping for the -509C&gt;T polymorphism was performed by restriction fragment length polymorphisms (RFLP) - PCR assay. <h3>Results</h3> No significant differences in allele frequencies of -509C&gt;T polymorphism of TGF-beta1 gene between SLE patients and healthy controls were observed. Although the genotype frequencies were comparable between patients and controls, higher frequency of heterozygous genotype CT (OR=1.57, 95%CI =0.96$÷ $2.59) and lower frequency of homozygous genotype TT (OR=0.63, 95%CI =0.33$÷ $21.21) was seen in cases versus controls. The -509C&gt;T polymorphism was also associated with some clinical manifestations of SLE: CT genotype was more frequent in patients with hematological manifestations (OR=2.42, 95%CI=1.1$÷ $5.32) and with antibodies to dsDNA (OR=2.0, 95%CI=0.96$÷ $4.2) compared to cases without these clinical features. Our results showed a significantly lower amount of serum TGF-beta1 in SLE patients compared to controls (p&lt;0.001). An association between high TGF-beta1 serum levels and T allele was established in healthy individuals but not in SLE patients. <h3>Conclusions</h3> The -509C&gt;T polymorphism of TGF-beta1 gene may be one of the components of genetic susceptibility to SLE in Bulgarian population. In addition, our results support the role of TGF-beta1 as key immunoregulatory cytokine in the pathogenesis of SLE. <h3>Disclosure of Interest</h3> None Declared
SP0084 Patient involvement in research on the international arena
Authors: L. Gossec
Journal: Annals of the Rheumatic Diseases (2013)

The past years have seen a growing involvement of patients in research, not as research subjects but as research partners. The other talks in this session will present in particular some of the national efforts to involve patients in research. This talk will focus on the international aspects. Building on the experience acquired when co-leading several international initiatives, the talk will address some of the specific difficulties but also strengths inherent to patient participation in international projects. <h3>Disclosure of Interest</h3> None Declared
No clear boundary between placebo and effective treatment
Authors: Dieneke Hubbeling
Journal: Journal of the Royal Society of Medicine (2013)

In a recent editorial, Justman1 discussed the use of placebos in clinical practice. Of all the GPs who used pure placebos, fewer than one in ten reported that they explained to the patient that they were prescribing a placebo, according to a study by Howick et al.2 According to the same study GPs also disapproved of deception. Justman1 suggested that GPs might well be inconsistent by disapproving of deception and not telling patients that they are prescribed a placebo.

Howick et al.2 made a difference between pure placebos (such as sugar-coated pills) and impure placebos (such as peppermint pills). However, there is no sharp dividing line between pure placebo, impure placebo and active treatment. The word ‘placebo response’ is a misnomer, because a therapeutic response to an effective treatment can consist of a placebo component.3 Research into depression suggests that patients sometimes respond to pure placebos and this correlates with changes in brain physiology.4 One can wonder whether one of the examples of impure placebos from Howick’s study,2 peppermint pills, really has no genuine therapeutic effects for pharyngitis, although it is probably the sucking on the pills and not the peppermint. Because there is no sharp dividing line between placebo and active treatment, it is more useful to think about placebo as a form of treatment, which can be effective for some conditions such as depression and not for others such as cancer.

Practising doctors face a dilemma. They have to install hope, that the treatment will work and at the same time they have to give accurate information5 about advantages and disadvantages of the proposed treatment. Mentioning the word placebo can be counterproductive, and it is not necessarily deception, if the word placebo is not used, given that even pure placebos can correlate with changes in the brain.