tbuckley/cabot-search huggingface dataset:
FRI0534 Immunization Status of Vaccine-Preventable Diseases in Children with Juvenile Idiopathic Arthritis
Authors: E. Comak, S. Akman, M. Koyun, O. Tufekci
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Immunization is the least invasive and most cost-effective approach to reduce the incidence of infections and morbidity and mortality in children. Since patients with juvenile idiopathic arthritis (JIA) are at increased risk of infections, immunisations are important. However, despite a literature about on the safety and immunogenicity of individual vaccines in the JIA patients, parental or physician9s reluctance to vaccinate because of fear of inducing flare of the disease or avoidance of vaccination during periods of active disease. <h3>Objectives</h3> To evaluate the vaccination antibody titers of patients with JIA followed at our paediatric rheumatology clinic and to determine the immunization status of vaccine-preventable diseases. <h3>Methods</h3> During the period from 1 November 2012 to 31 March 2013, consecutive patients with JIA visited at our pediatric rheumatology outpatient clinic were included. Demographic data, disease duration, physical examination findings and medications used for JIA treatment were documented. The antibody titers against measles, mumps, rubella, varicella, hepatitis A and hepatitis B were determined. <h3>Results</h3> The study included 72 children, 42 girls (58.3%), with a median age of 11.0±4.1 years and a mean follow-up period of 37.6±31.0 months. Patients were classified according to JIA subgroups as oligoarthritis in 28 (38.9%), rheumatoid factor-negative polyarthritis in 11 (15.3%), rheumatoid factor-positive polyarthritis in 1 (1.4%), systemic arthritis in 12 (16.7%), enthesitis-related arthritis in 18 (25.0%) and psoriatic arthritis in 2 (2.8%) patients. Seropositivity rate was 95.8% for rubella, 86.1% for measles, 83.3% for varicella, 73.6% for mumps and hepatitis B, and only 12.5% for hepatitis A. Median antibody titers were 169.3 IU/mL (range:15.7-1000) for hepatitis B, 87.4 IU/mL (range: 8.8-440) for rubella, 6.5 IU/mL (range: 1.2-13.7) for varicella, 4.2 IU/mL for measles (range: 1.2-12.7 IU/mL) and 2.7 IU/mL (range: 1.2-7.9) for mumps. None of the patients had protective antibodies against all tested pathogens. Only 25 (34.7%) patients showed protective antibodies against tested pathogens excluding hepatitis A. The lowest individual vaccination rate was for hepatitis A (12.5%). <h3>Conclusions</h3> Monitoring for immunization status should be a part of primary care of children with JIA. According to EULAR recommendation, JIA patients can be vaccinated safely. Our results showed the demand for continuous surveillance of specific antibody titers against vaccine-preventable diseases in children with JIA. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5204
THU0590-HPR Self-Efficacy and Positive Adaptation in Patients with Polyarthritis
Authors: E. Taal, C. Bode, R. Arends, M.A. van de Laar
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> A lack of self-efficacy, the confidence in one9s own competencies to cope with the symptoms of arthritis, has been found to be related to negative aspects of psychological functioning such as feelings of depression and anxiety. There is an increasing attention for positive adaptation to chronic diseases, inspired by the upcoming field of positive psychology. The relationships between self-efficacy and positive adaptation in patients with polyarthritis has not been investigated. <h3>Objectives</h3> To study the relationships of pain, fatigue, functional limitations and self-efficacy with indicators of positive adaptation to polyarthritis, namely purpose in life, positive affect and social and work participation. <h3>Methods</h3> 331 patients (61% women, mean age=61 years, mean disease duration=14 years) participated in a questionnaire study. Positive adaptation was measured with PIL (purpose in life), PANAS (positive affect) and IPA (social and work adaptation). Self-efficacy to cope with pain and self-efficacy to cope with other symptoms of arthritis were measured with ASES. Pain was assessed with a VAS, fatigue with SF36 Vitality scale and functional limitations with HAQ-DI. Hierarchical multiple regression analyses were applied to analyse the relationships of physical health (pain, fatigue, functional limitations) and self-efficacy with positive adaptations. <h3>Results</h3> In regression analyses physical health (pain, fatigue, functional limitations) significantly explained positive adaptation (R<sup>2</sup>: 0.15-0.50). Explained variance in positive adaptation significantly increased when Pain self-efficacy (ΔR<sup>2</sup>:0.03-0.06) or other symptoms self-efficacy (ΔR<sup>2</sup>: 0.07-0.18). In most analyses pain and other symptoms self-efficacy pain and other symptoms self-efficacy were stronger predictors of positive adaptation than pain, fatigue or functional limitations. Except for one model (purpose in life, other symptoms self-efficacy) self-efficacy was found to be partly mediating the relationship between physical health (pain, fatigue, functional limitations) and positive adaptation. <h3>Conclusions</h3> This study showed that self-efficacy is significantly related to positive adaptation in polyarthritis. A longitudinal study should be done to get more insight in the causality of the relations. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6008
SAT0127 Gout and RA: not Such A Rare Coexistence after All?
Authors: C. Petsch, E. Araujo, M. Englbrecht, A. Hueber, M. Lell, G. Schett, B. Manger, J. Rech
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> According to the current rheumatology literature, the simultaneous occurrence of rheumatoid arthritis (RA) and gout is rare and only a few cases have been reported to date.[1] However, clinical practice suggests otherwise. <h3>Objectives</h3> To investigate the prevalence of urate deposits in patients with diagnosed RA and hyperuricemia and to identify prognostic factors that could lead to the development of clinical gout in these patients. <h3>Methods</h3> 100 patients who fulfilled 2010 ACR/EULAR criteria for RA and had a serum uric acid (SUA) level above 6 mg/dl were included into the study. The presence of monosodium urate (MSU) deposits in joints and tissues was confirmed by means of dual energy computed tomography (DECT), a new imaging tool using x-ray beams of two different energies to differentiate MSU from connective tissues and from calcium containing structures by their absorption properties.[2] Automated volume measurement was used to display the amount of MSU deposition in positive DECT scans. <h3>Results</h3> 20% of scans were positive in the whole cohort in contrast to 70% in the seronegative RA subpopulation. Seronegativity was defined as negative rheumatoid factor and anti-CCP antibodies. According to a logistic regression model analysis, seronegative status showed significance for the presence of uric acid deposits (Wald χ<sup>2</sup> =5.280, Exp (B) =0.221, 95% CI=0.061 – 0.801, p=0.022) whereas SUA was not a significant predictor. Mean deposit volume was 130±60 mm<sup>3</sup>. Larger deposits were significantly associated with a higher DAS 28. <h3>Conclusions</h3> In contrast to current rheumatology literature suggesting a rare coexistence of rheumatoid arthritis (RA) and gout, we found a considerable number of RA patients with hyperuricemia presenting MSU deposits in typical locations using DECT. Seronegative status is an independent variable related to positive findings and correlation of volume and disease activity might indicate a misdiagnosis of RA in some cases. Polyarticular gout should be considered as an additional and differential diagnosis in patients with RA and hyperuricemia. <h3>References</h3> Kuo CF, Tsai WP, Liou LB. Rare copresent rheumatoid arthritis and gout: comparison with pure rheumatoid arthritis and a literature review. Clin Rheumatol 2008;27:231-235. Manger B, Lell M, Wacker J, et al. Detection of periarticular urate deposits with dual energy CT in patients with acute gouty arthritis. Ann Rheum Dis 2012;71:470-472. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2993
USE OF CAPTURE-RECAPTURE TO ESTIMATE PREVALENCE OF CONGENITAL HEART DEFECTS AMONG ADOLESCENTS AND ADULTS IN FIVE ATLANTA, GEORGIA COUNTIES: 2008-2010
Authors: Wendy M. Book, Katherine John, Cheryl Raskind-Hood, Melissa Jill Glidewell, Tiffany Riehle-Colarusso, Carol Hogue
Journal: Journal of the American College of Cardiology (2016)
P1083 VON WILLEBRAND FACTOR ANTIGEN (vWF-Ag): A NON-INVASIVE PREDICTOR OF TREATMENT RESPONSE AND SEVERE ADVERSE EVENTS IN HCV PATIENTS WITH DAA BASED TRIPLE THERAPY
Authors: K. Rutter, A. Etschmaier, M. Ferlitsch, A. Maieron, S. Hametner, P. Salzl, A. Stättermayer, S. Beinhardt, T. Reiberger, M. Peck-Radosavljevic, P. Quehenberger, H. Hofer, M. Trauner, P. Ferenci, A. Ferlitsch
Journal: Journal of Hepatology (2014)
Role of Ragulator in the Regulation of Mechanistic Target of Rapamycin Signaling in Podocytes and Glomerular Function
Authors: Yao Yao, Junying Wang, Sei Yoshida, Shigeyuki Nada, Masato Okada, Ken Inoki
Journal: Journal of the American Society of Nephrology (2016)

Aberrant activation of mechanistic target of rapamycin complex 1 (mTORC1) in glomerular podocytes leads to glomerular insufficiency and may contribute to the development of glomerular diseases, including diabetic nephropathy. Thus, an approach for preventing mTORC1 activation may allow circumvention of the onset and progression of mTORC1-dependent podocyte injury and glomerular diseases. mTORC1 activation requires inputs from both growth factors and nutrients that inactivate the tuberous sclerosis complex (TSC), a key suppressor of mTORC1, on the lysosome. Previous studies in mice revealed that the growth factor-phosphatidylinositol 3-kinase pathway and mTORC1 are essential for maintaining normal podocyte function, suggesting that direct inhibition of the phosphatidylinositol 3-kinase pathway or mTORC1 may not be an ideal approach to sustaining physiologic podocyte functions under certain disease conditions. Here, we report the role of the Ragulator complex, which recruits mTORC1 to lysosomes in response to nutrient availability in podocytes. Notably, podocytes lacking Ragulator maintain basal mTORC1 activity. Unlike podocyte-specific mTORC1-knockout mice, mice lacking functional Ragulator in podocytes did not show abnormalities in podocyte or glomerular function. However, aberrant mTORC1 activation induced by active Rheb in podocyte-specific TSC1-knockout (podo-TSC1 KO) mice did require Ragulator. Moreover, ablation of Ragulator in the podocytes of podo-TSC1 KO mice or streptozotocin-induced diabetic mice significantly blocked the development of pathologic renal phenotypes. These observations suggest that the blockade of mTORC1 recruitment to lysosomes may be a useful clinical approach to attenuate aberrant mTORC1 activation under certain disease conditions.
Mouse mammary tumor virus-related sequences in Mus musculus genome and human breast cancer tissues.
Authors: AA Lushnikova, LN Lyubchenko, AA Parokonnaya, EV Peredereeva, EB Polevaya
Journal: Cancer Research (2009)

Abstract Abstract #3087 Background: Mouse mammary tumor virus is the causative agent for breast cancer (BC) in susceptible mouse lines. MMTV –homologous sequences were detected in breast carcinoma tissue DNA samples from 14-75% BC patients in Mexico, China, USA, Australia and Tunis. However, the sequences weren't found in Japanese, Austrian, English and some other human populations. Earlier, we have found the env MMTV –homologous sequences in BC tissues and peripheral blood lymphocyte DNA samples in 39-42% sporadic and 52% familial BC as well as in 64% of BC during pregnancy and/or lactation. These population differences in MMTV-related retrovirus frequencies might associated with geographic distribution of Mus musculus sp.domesticus – native MMTV reservoir. Material and methods: To demonstrate if wild commensal mice species are MMTV carriers we investigate 11 mice ( 3 males, 8 females) related to Mus musculus sp.domesticus from Moscow region (Russia) using specific PCR and RT-PCR followed by PCR products subcloning in pGEM-T vector and sequencing. A gp52 and ITAM-coding areas of the env MMTV gene, significant for MMTV infection and epithelial cells transformation , as well as a Sag-coding area of 3'LTR were analyzed. MMTV superantigen (Sag) – mediated amplification of MMTV in lymphoid cells is required for efficient viral transformation and dissemination in the mammary gland. Results: The sequences homologous to these functionally significant MMTV genome areas were detected in the DNA samples from mouse liver, timus and peripheral blood. In 63% (7/11) animals analyzed the sequences were expressed. The sequences homology with MMTV genome (C3H strain) according BLAST was 93-96%; homology with human MMTV- related provirus detected in BC patients was 86-95%. Recently MMTV-induced human epithelial cell transformation and important role of ITAM-coding area of the env MMTV gene was demonstrated in vitro. Conclusion: MMTV-related sequences were found in wild commensal mice, Mus musculus sp.domesticus, from Moscow region. In 60% cases these sequences, homologous to functionally significant env- and Sag-coding virus genome regions were expressed. Preliminary data support the possibility of the horizontal MMTV transmission from mice to humans, except of vertical one from mother to children. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 3087.
Rupture canalaire pancréatique: intérêt du drainage transpapillaire endoscopique
Authors: R Altwegg, P Bauret
Journal: Endoscopy (2010)

Introduction: Un certain nombre de collections liquidiennes pancréatiques ou péri-pancréatiques (CLP), non résolutives, évolutives ou résistantes au traitement standard sont en fait liées à une rupture du canal principal pancréatique (RCPP). Le but de ce travail aétè d'évaluer l'intérêt du drainage endoscopique transpapillaire dans le traitement des RCPP avec CLP.
P42 PPARg AGONIST PIOGLITAZONE REDUCES PORTOSYSTEMIC COLLATERAL BLOOD FLOW VIA MODULATION OF ANGIOGENESIS AND INFLAMMATION IN PPVL RATS
Authors: P. Schwabl, B.-A. Payer, J. Grahovac, Y. Boucher, S. Klein, J. Trebicka, B. Angermayer, M. Trauner, M. Peck-Radosavljevic, T. Reiberger
Journal: Journal of Hepatology (2014)
One in Nine: The Risk of a Lifetime
Authors: N. Volkers
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article One in Nine: The Risk of a Lifetime Get access Nancy Volkers Nancy Volkers Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 8, 15 April 1992, Page 564, https://doi.org/10.1093/jnci/84.8.564 Published: 15 April 1992
IN-STENT RESTENOSIS DUE TO AN ORGANIZED THROMBUS ASSESSED WITH OPTICAL COHERENCE TOMOGRAPHY AFTER DRUG-ELUTING STENT IMPLANTATION IN HEMODIALYSIS PATIENTS
Authors: Takeshi Tada, Kazushige Kadota, Seiji Habara, Hiroyuki Tanaka, Yasushi Fuku, Tsuyoshi Goto, Kazuaki Mitsudo
Journal: Journal of the American College of Cardiology (2016)
914 INTERLEUKIN-10 SERUM LEVELS ARE LOWER IN SUSTAINED VIROLOGICAL RESPONDERS (SVR) CARRYING IL-28B CC GENOTYPE (rs12979860) COMPARED TO SVR-CT/TT
Authors: L.R.S. Vasconcelos, R.F. do Carmo, P. Moura, L.B. Pereira, M.D.S.D.M. Cavalcanti, E.R.F. de Siqueira, D.C.B.L. Aroucha, R.A. Dutra, L.M.M.B. Pereira
Journal: Journal of Hepatology (2013)
18F-FDG and FDG-Labeled Leukocyte PET/CT in Peritoneal Tuberculosis
Authors: Anish Bhattacharya, Rakesh Kochhar, Kanhaiyalal Aggrawal, Sarika Sharma, Bhagwant Rai Mittal
Journal: Clinical Nuclear Medicine (2013)

The authors present a 20-year-old patient with clinical suspicion of acute pancreatic infection. PET/CT showed significantly higher uptake of 18F-FDG alone compared with FDG-labeled autologous leukocytes in peritoneal thickening and omental deposits, with no abnormal pancreatic uptake of either tracer. Further investigation led to a diagnosis of peritoneal tuberculosis.
HOSPITAL VARIATION IN MANAGEMENT OF PATIENTS WITH HEART FAILURE PRESERVED EJECTION FRACTION
Authors: Auras R. Atreya, Mohammad Amin Kashef, Sonali Arora, Jaime Hernandez, Meng-Shiou Shieh, Penelope Pekow, Mihaela Stefan, Gregory Valania, Quinn Pack, Mara Slawsky, Peter Lindenauer, Tara Lagu
Journal: Journal of the American College of Cardiology (2015)
Mammographic Parenchymal Features and Breast Cancer
Authors: E. SONNENSCHEIN, P. TONIOLO
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Mammographic Parenchymal Features and Breast Cancer Get access ELIZABETH SONNENSCHEIN, ELIZABETH SONNENSCHEIN Laboratory of Biostatistics and Epidemiology Institute of Environmental Medicine New York University Medical CenterNew York, NY 10010 Search for other works by this author on: Oxford Academic PubMed Google Scholar PAOLO TONIOLO PAOLO TONIOLO Laboratory of Biostatistics and Epidemiology Institute of Environmental Medicine New York University Medical CenterNew York, NY 10010 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 12, 21 June 1989, Pages 962–963, https://doi.org/10.1093/jnci/81.12.962-a Published: 21 June 1989
A2.8 TNFα influences the status of B and T cells by acting on BCR and TCR pathways<i>via</i>RASGRP1 and RASGRP3 proteins
Authors: ML Golinski, M Hiron, C Derambure, C Guillou, M Fréret, O Boyer, O Vittecoq, T Lequerré
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> Rheumatoid arthritis (RA) is the most common inflammatory arthritis. B and T cells play a key role in the RA pathophysiology. RasGRP is a member of the CDC25 family of Ras guanyl nucleotide exchange factors. RasGRP1 is expressed in T and B cells whereas RasGRP3 is only expressed in B cells. In previous studies, we have shown that <i>RasGRP3 </i>gene expression level significantly decreased in peripheral blood mononuclear cells from RA patients responders to adalimumab and etanercept (anti-TNFa drugs), leading to the question of TNFα involvement in RasGRP1 and RasGRP3 pathways. <h3>Objectives</h3> To study TNFα effects on RasGRP1 and RasGRP3 expression levels <i>in vitro</i>. <h3>Materials and methods</h3> We measured, by qRT-PCR and western-blot, RasGRP1 and RasGRP3 expression levels in B and T cells isolated from buffy coat. In each condition, cells were cultured with or without TNFα for 24 or 48 h. Cell proliferation was evaluated by [3H] thymidine incorporation. To investigate the TNFα implication on signalling pathways, MAPK and apoptosis protein arrays were used. <h3>Results</h3> In B cells, TNFα induced an increase of <i>RasGRP1</i> and <i>RasGRP3</i> gene expression levels without effect on B cells proliferation and BCR pathway phosphorylations, but apoptotic pathways were inhibited. In T cells, TNFα increased <i>RasGRP1</i> gene expression level but RasGRP1 protein expression level decreased, inhibiting T cell proliferation and TCR pathway phosphorylations. <h3>Conclusions</h3> This study suggests a link, never described previously, between RasGRP1 or RasGRP3 and the TNFa effects on T and B cells. While the response to anti-TNFα treatments in RA patients modulates RasGRP3 gene expression, TNFα inhibits RasGRP1 protein expression leading to TCR pathway inhibition, <i>in vitro</i>, in pathophysiological condition. The better understanding of TNFα effects on RasGRP proteins could permit a better understanding of the mechanisms of action of TNFα blocking agents on T and B cells.
Comparison of Low-Dose Isotretinoin with Beta Carotene to Prevent Oral Carcinogenesis
Authors: Scott M. Lippman, John G. Batsakis, Bela B. Toth, Randal S. Weber, J. Jack Lee, Jack W. Martin, Granvil L. Hays, Helmuth Goepfert, Waun Ki Hong
Journal: New England Journal of Medicine (1993)

High-dose isotretinoin therapy has been determined to be an effective treatment for leukoplakia. However, a high rate of relapses and toxic reactions led us to conduct a trial of a much lower dose of isotretinoin in the hope of maintaining a response and limiting toxicity.
Abstract 3867: EGFR genotype impacts expression of chemotherapeutic target biomarkers in NSCLC
Authors: H Eugene Liu, Jacqueline M. Liu, Ming-Chih Yu, Kuan-Jen Bai, Chieh Lan
Journal: Cancer Research (2011)

Abstract BACKGROUND: Non small cell lung cancer EGFR mutations are prevalent in the East Asian population, especially in female non-smokers, the L858R and del 747-753 in exons 18-21 of the EGFR tyrosine kinase domains are activating mutations with increased sensitivity to the EGFR tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib. EGFR gene amplification also increases susceptibility to EGFR TKIs as has been reported in the IDEAL / INTACT non small cell lung cancer (NSCLC) trials. Our study evaluated chemotherapeutic target biomarkers in Chinese NSCLC patients with varying EGFR genotypes. METHODS: Seventy NSCLC patients with known EGFR genotype received chemotherapy and EGFR TKI therapy with known response and survival, their pathology specimen were retrospectively retrieved for evaluation. EGFR and KRAS were sequenced for mutations and deletions. Fluorescent in situ hybridization (FISH) was performed for EGFR genes. Immunohistochemical analyses were performed for topoisomerase 1, c-myc, RRM-1, class III beta tubulin, topoisomerase IIα, p53, thymidylate synthase, and ERCC-1. The percentage of nuclear-stained malignant cells were recorded for T IIα, T1, p53, ERCC-1, c-myc, whereas for TS, tau, RRM-1, class III beta tubulin were cytoplasmic stains, only positive or negative was reported, eventually only 63 patients had complete data for evaluation. RESULTS: Significant increase in overall survival was found in females (p=0.002), non-smokers (p=0.005), younger age (p=0.001), less advanced staging (p=0.048), EGFR mutation (p=0.038); but not with KRAS genotype, or expression of any chemotherapeutic markers. Patients in this study were consecutive patients, 60-70% received treatment. When EGFR mutant tumors were compared to EGFR wildtype tumors, the mutant tumors had lower KRAS mutation (4% vs 19%, p=0.1238), more were ERCC1- (76% vs 63%, p=0.2925), more topoisomerase 1 + (28% vs 17%, p=0.3719), less RRM1+ (24% vs 35%, p=0.4142), more TS- (93% vs 86%, p=0.4478), lower class III beta tubulin (45% vs 57%, p=0.4515). CONCLUSIONS: A difference in expression of chemotherapeutic target markers has been detected in differing EGFR genotypes, although its significance has been dampened by our small patient population, and larger patients groups will be needed to evaluate the impact of different chemotherapies on survival of the different EGFR genotype tumors. 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 3867. doi:10.1158/1538-7445.AM2011-3867
Regulation of the acute myeloid leukemia cell line OCI/AML-2 by endothelial nitric oxide synthase under the control of a vascular endothelial growth factor signaling system
Authors: P Koistinen, T Siitonen, P Mäntymaa, M Säily, V Kinnula, E-R Savolainen, Y Soini
Journal: Leukemia (2001)