tbuckley/cabot-search huggingface dataset:
CÁPSULA DE INTESTINO DELGADO: UNA NUEVA VISIÓN DE LA TÉCNICA ENDOSCÓPICA -
Authors: V Busto Bea, L Crespo Pérez, L Achecar Justo, C Senosiain Lalastra, R Martín Mateos, J Graus Morales, A Cano Ruiz, JA González Martín, A López San Román, D Boixeda de Miquel
Journal: Endoscopy (2011)

Resultados: La edad media de los pacientes fue 60.15 años (rango 16–89), siendo 51% varones y 49% mujeres. Los motivos de petición más frecuentes fueron anemia crónica (59,5%), sospecha de EII (12,5%) y hemorragia digestiva de origen oscuro (HDOO) (6,5%). En 58,5% se encontraron lesiones, en 12% hallazgos dudosos y el 25% resultaron normales (4.5% no valorables). Los principales hallazgos fueron angiodisplasias (26,5%), aftas-úlceras (14,5%), pólipos (10%) y lesiones submucosas (4.5%). En 4.4% la cápsula no alcanzó el ciego (porcentaje similar al descrito en otras series), sin objetivarse estenosis manifiesta ni precisar cirugía en ninguno de esos casos. Las angiodisplasias, localizadas preferentemente en yeyuno y ciego-íleon, se encontraron al alcance de la gastroscopia en 8 casos (4%) y de la colonoscopia en 15 (7,5%). En las CE solicitadas por anemia crónica y HDOO la hemoglobina media fue 10.84g/dl y el 54,8% de los pacientes precisó transfusión sanguínea, mientras que en el subgrupo de aquellas en las que se evidenciaron angiodisplasias, estos valores fueron de 10,81g/dl y 67,9%. Se detectaron aftas o úlceras en 29 pacientes (14,5%), siendo el motivo de petición anemia en 16, sospecha de EII en 7 y sospecha de enteropatía por AINES en 3.
OP0206 Efficacy of modified-release prednisone in patients with rheumatoid arthritis (RA) chronically treated with standard glucocorticoids: An italian multicenter survey:
Authors: L. Iaccarino, I. Farina, A. Sulli, A. Bortoluzzi, C. Marcassa, A. Doria, M. Govoni, M. Cutolo
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Recent studies documented the additional disease-modifying potential of low-dose glucocorticoids (GC) when added to DMARDs in the treatment of RA. Modified-release prednisone (P-MR, taken at bedtime and released 4 h after ingestion) was recently found superior to standard immediate-release GC in reducing morning stiffness and IL-6 plasma levels in a 12-week randomised double-blind trial. <h3>Objectives</h3> We assessed the efficacy of P-MR under real-life conditions in a large cohort of RA outpatients already on active treatment with GC. <h3>Methods</h3> 1928 consecutive outpatients with documented RA (average duration 76.7 months) treated with oral standard prednisone (SP) or methyl-prednisolone (MP) and referring to 100 rheumatologists from February 1st to April 30th 2011 were considered. Of them, 950 subjects (513 on SP, average dose 9.4±5.4 mg; 437 on MP, average dose 6.7±3.7 mg) were switched at physicians discretion to low-dose P-MR at corresponding dosage and followed bimonthly for 16 weeks. Clinical markers considered at first (T1) and T2-T3 follow-up visits included morning stiffness (min), pain severity (NRS, 0-10 scale), patient- and physician global assessment (GA, 0–10 scale) and DAS 28 score. Differences between/within groups were analysed by variance analysis for repeated measures (ANOVA). <h3>Results</h3> Mean patients' age was 57±13 (females 75%, bone erosions present in 55%); 83.7% were assuming methotrexate, 10.5%, leflunomide, 12.2% other DMARDs, and 15.8% were on biologics. During the follow-up, MR-P was well tolerated, 6 pts (0.6%) stopped itand 24 others downgraded to their previous GC. Among the 920 patients (96.8%) who completed the 4-month survey on MR-P, morning stiffness decreased from 58±37 min at the first visit (T1) to 32±24 min at the final T3 visit (p&lt;0.001); pain intensity was reduced from 5.4±1.8 to 3.5±1.4 (p&lt;0.001), patient- and physician- global assessment improved from 5.4±1.7 to 3.5±1.4 and from 5.1±1.7 to 3.3±1.4, respectively (p&lt;0.001). DAS28 score decreased from 4.2±1.4 to 3.3±1.2 (p&lt;0.001). Mean MR-P daily dosage was 8.2 mg at T1 and 6.7 at T3 visit. During follow-up, 33/800 (4.1%) biologics-naïve patients started them. Differences between patients who switched from MP or SP were: <h3>Conclusions</h3> In unselected RA patients chronically treated with standard GC, modified-release prednisone (given at bedtime) induced a significant improvement over a medium-term observation, particularly in those patients who switched from methyl-prednisolone. <h3>References</h3> Buttgereit F et al, Lancet 2008;371: 205–214. <h3>Disclosure of Interest</h3> None Declared
P62 Correlation Of Quantitative Chest Ct Measures With Lung Function And Functional Parameters In A Cohort Of Moderate To Very Severe Copd Patients
Authors: K. Ostridge, N. Williams, V. Kim, A. Barton, M. Wojtas, S. Harden, E. Aris, M. Peeters, J. Devaster, S. Bourne, T. Wilkinson
Journal: Thorax (2014)

<h3>Introduction</h3> COPD is a heterogeneous condition consisting of a number of different clinico-pathological subgroups (phenotypes), leading to particular challenges in managing the condition. Recognising these phenotypes may assist in directing the choice of treatment options. CT is being investigated as a tool for identifying key morphological features seen in COPD. Computer analysis of CT scans allows quantification of emphysema, bronchial wall thickening and gas trapping and offers the opportunity to study the heterogeneity of COPD. This study aims to use quantitative digital software to analyse CT scans from a cohort of COPD patients to define clinically important phenotypes. <h3>Methods</h3> Acute Exacerbation and Respiratory Infections in COPD (AERIS) is a longitudinal epidemiological study where patients with moderate to very severe COPD were followed monthly for 2 years. At enrolment subjects had pulmonary function testing and high resolution spiral CT was performed in inspiration and expiration. A sub-cohort of 36 patients is included in this analysis. CT scans were reported by a thoracic radiologist using a validated scoring system for emphysema and gas trapping. Image analysis was performed using Apollo software. Emphysema was defined as the percent of lungs with low attenuation values below -950 Hounsfield Units (%LAA) on inspiratory scan. Airway wall thickness was standardised by using the square root of the wall area for a theoretical airway with an internal perimeter of 10 mm (AWT-Pi10). Gas trapping was calculated using the relative volume change of low attenuation areas from -856 to -950 between the inspiratory and expiratory scans (RVC<sub>856–950</sub>). <h3>Results</h3> Correlation between the reported CT scores (emphysema and gas trapping) and corresponding quantitative measures (%LAA and RVC<sub>856–950</sub>) were strong: r = 0.79 and r = 0.5, respectively (p &lt; 0.05). CT scores and quantitative measures for emphysema and gas trapping were significantly correlated with pulmonary function and BODE index (Table 1). <h3>Conclusion</h3> In this study we have shown that quantitative chest CT measures correlate with a number of traditional physiological and prognostic markers in COPD. These measures have the potential to be clinically useful imaging biomarkers for the disease and further work will help validate this by investigating the longitudinal changes of the AERIS cohort.
Visualizing Myocardial Salvage: New Methods, New Insights⁎⁎Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.
Authors: Nathaniel Reichek, Visali Kodali
Journal: JACC. Cardiovascular imaging (2010)

Since the earliest days of the thrombolytic era, maximizing myocardial salvage by reperfusion of the myocardial region at risk for myocardial infarction has been the most important immediate objective in management of ST-segment elevation myocardial infarction (STEMI) ([1][1]). The roles of time to
Abstract 380: Sunitinib treatment induces up-regulation of CXCR4
Authors: Urszula Kubacka, Wouter B. Nagengast, Roeliene C. Kruizinga, Marjolijn N. Lub-deHooge, Jourik A. Gietema, Sjoukje F. Oosting, Hetty Timmer-Boscha, Geke A. Hospers, Wilfred F. den Dunnen, Elisabeth G. de Vries, Gerwin Huls, Annemiek M. Walenkamp
Journal: Cancer Research (2010)

Abstract Background: Chemokine receptors expressed on solid tumor cells and their corresponding ligands are an example of a network which is used by these cells to interact with their microenvironment to sustain survival, proliferation, invasive growth, angiogenesis, and to promote organ-specific localization of distant metastases. Indeed, CXCR4/CXCL12 signaling can induce angiogenesis and progression of tumors, for example by increasing the expression of vascular endothelial growth factor (VEGF). Inversely, it is hypothesized that anti-angiogenic treatment increases the expression of CXCR4/CXCL12 which could explain the in preclinical models observed invasive growth characteristics of tumors. Methods: A human A2780 ovarian xenograft mouse model was used. When the tumor was established, mice were treated with vehicle or sunitinib (60 mg/kg i.p.) daily for 2 weeks. CXCR4 expression was assessed by immunohistochemistry at baseline and after 1 and 2 weeks of treatment and compared with markers like HIF1α, VEGF, Ki67, VEGFR2, mean vessel density (MVD) and blood vessel diameter. In addition human plasma VEGF levels were analyzed. Results: Moderate cell membrane CXCR4 expression was seen in untreated tumors. One week of sunitinib treatment resulted in decrease angiogenice markers and tumor proliferation (Ki67) in both the tumor center and rim. Two weeks of sunitinib treatment resulted in up regulation of CXCR4 with a 2.2 fold increase (P = 0.046) particularly in the tumor rim. This coincided with normalization of blood vessel diameters, intense VEGF staining and increased tumor proliferation (Ki67) to baseline levels in the tumor rim. In contrast, an increase of HIF1α (P = 0.017) and decrease of angiogenic markers like VEGFR2 (P = 0.019) and MVD (P = 0.016) was still observed in the tumor center. Conclusion: This study shows that anti-angiogenic treatment with sunitinib up regulates CXCR4 expression, mainly in the rim of the tumor. CXCR4 is a potential target to block anti-angiogenic induced invasive growth/metastasis. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 380.
EG-07 * CELL CYCLE SIGNATURE AND TUMOR PHYLOGENY ARE ENCODED IN THE EVOLUTIONARY DYNAMICS OF DNA METHYLATION IN GLIOMA
Authors: T. Mazor, A. Pankov, B. E. Johnson, C. Hong, R. J. A. Bell, I. V. Smirnov, G. F. Reis, J. J. Phillips, M. Barnes, A. W. Bollen, B. S. Taylor, A. M. Molinaro, A. B. Olshen, J. S. Song, M. S. Berger, S. M. Chang, J. F. Costello
Journal: Neuro-Oncology (2014)

The clonal evolution of tumor cell populations can be reconstructed from patterns of genetic alterations. In contrast, tumor epigenetic states, including DNA methylation, are reversible and sensitive to the tumor microenvironment, presumably precluding the use of epigenetics to discover tumor phylogeny. Here we examined the spatial and temporal dynamics of DNA methylation in a clinically and genetically characterized cohort of IDH1-mutant low-grade gliomas and their patient-matched recurrences. WHO grade II gliomas are diffuse, infiltrative tumors that frequently recur and may undergo malignant progression to a higher grade with a worse prognosis. The extent to which epigenetic alterations contribute to the evolution of low-grade gliomas, including malignant progression, is unknown. While all gliomas in the cohort exhibited the hypermethylation signature associated with IDH1 mutation, low-grade gliomas that underwent malignant progression to high-grade glioblastoma (GBM) had a unique signature of DNA hypomethylation enriched for active enhancers, as well as sites of age-related hypermethylation in the brain. Genes with promoter hypomethylation and concordant transcriptional upregulation during evolution to GBM were enriched in cell cycle function, evolving in concert with genetic alterations that deregulate the G1/S cell cycle checkpoint. Despite the plasticity of tumor epigenetic states, phyloepigenetic trees robustly recapitulated phylogenetic trees derived from somatic mutations in the same patients. These findings highlight widespread co-dependency of genetic and epigenetic events throughout the clonal evolution of initial and recurrent glioma.
Enthusiasm for Quality-of-Life Research Rises
Authors: L. F. Anderson
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Enthusiasm for Quality-of-Life Research Rises Get access Linda F. Anderson Linda F. Anderson Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 10, 17 May 1995, Pages 712–714, https://doi.org/10.1093/jnci/87.10.712 Published: 17 May 1995
Abstract 2657: The role of NR5A2 in pancreas development and oncogenesis.
Authors: Sahar Nissim, Julia Wucherpfennig, Xiao-Xu Wang, Alec Kimmelman, Wolfram Goessling
Journal: Cancer Research (2013)

Abstract Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal cancers today. A recent genome-wide association study (GWAS) has implicated the nuclear receptor NR5A2 in modulating risk for pancreatic cancer. While a role for this gene in pancreatic cancer has not been previously recognized, it is known to have an important role in stem cell pluripotency and metabolism. Using the zebrafish model organism, we demonstrate that knockdown of nr5a2 results in absence of exocrine pancreas, while leaving endocrine pancreas unaffected, indicating an essential role in pancreas organ formation. Further, we localize expression of nr5a2 to the endodermal bud that gives rise to the exocrine pancreas, consistent with a role for nr5a2 in regulating differentiation of pancreas progenitors. In resected human PDAC specimens and in vitro cell lines, we find that NR5A2 is overexpressed compared to normal ductal epithelium. Moreover, shRNA knockdown of NR5A2 dramatically slows proliferation of PDAC cell lines, supporting the hypothesis that NR5A2 is involved in pancreatic carcinogenesis. These data support a model that NR5A2 regulates the proliferation and differentiation of exocrine pancreas progenitor cells during development. We postulate that aberrant expression of NR5A2 results in dysregulation of these processes in the adult pancreas by driving ductal epithelial cells to acquire properties of progenitor cells, and therefore may be an important step in pancreas oncogenesis. Citation Format: Sahar Nissim, Julia Wucherpfennig, Xiao-Xu Wang, Alec Kimmelman, Wolfram Goessling. The role of NR5A2 in pancreas development and oncogenesis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2657. doi:10.1158/1538-7445.AM2013-2657 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 1508: TNF-receptor 2 plays a critical role in liver metastasis by regulating sinusoidal endothelial VCAM-1 expression, LY6G+ leukocyte recruitment and transendothelial migration
Authors: Boram Ham, Patrick Auguste, Maximilien Evrard, Ni Wang, Yifan Lu, Pnina Brodt
Journal: Cancer Research (2012)

Abstract The hepatic microenvironment can play an important role in promoting liver metastasis. We and others have shown that when metastatic carcinoma cells enter the liver, a rapid inflammatory response mediated by TNF-α is triggered, enabling tumor transendothelial migration and metastasis. TNF-α binds to the cell surface through two receptors; the p55/p60 TNFR1 and the p75/p80 TNFR2. To elucidate the roles of these receptors in the inflammatory cascade and in liver colonization by tumor cells, we used mice with tnfr1, tnfr2 and combined tnfr1/tnfr2 gene deficiencies and investigated parameters of the host response and the outcome of metastasis in these mice using the highly metastatic mouse colon carcinoma MC-38 and lung carcinoma H-59 cells. We found that experimental liver metastasis following intrasplenic/portal inoculation of the tumor cells was markedly reduced in TNFR2−/− and even further in TNFR1−/−/TNFR2−/- female mice as compared to wild-type controls but no reduction was observed in TNFR1−/− mice. To identify the underlying mechanism(s), we investigated changes in the liver microenvironment following tumor inoculation using a combination of immunohistochemistry, confocal microscopy, qRT-PCR, and cytokine/chemokines profiling. We found that while in wild-type and TNFR1−/- mice, VCAM-1 expression on the sinusoidal endothelium was significantly upregulated within 16 hr post tumor injection, it was unchanged in TNFR2−/− and double negative female mice. In addition, qRT-PCR analysis revealed that the production of the neutrophil chemokine CXCL1, while upregulated in control mice, was suppressed in TNFR2−/− mice. These changes were associated with a parallel decrease in Ly6G+ neutrophil recruitment into extravascular, pro-metastatic niches 16-48 hr post tumor inoculation. Interestingly, these reductions were not observed in male TNFR2−/− mice and correspondingly, their metastatic burden was not reduced relative to control mice. Taken together, the results suggest that TNFR2 plays a critical and gender-specific role in Ly6G+ cell recruitment into the tumor-microenvironment by regulating sinusoidal endothelial VCAM-1 expression and chemokine production. In turn, the recruitment of these cells into extravascular pro-metastatic niches appears to promote liver metastasis. Supported by grant MOP-80201 from the Canadian Institute for Health Research. (to PB) and by a McGill Integrated Cancer Research Training Program fellowship (to BH). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1508. doi:1538-7445.AM2012-1508
Antileukotriene Therapy
Authors: STEPHEN T. HOLGATE, ANTHONY P. SAMPSON
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

In the early 1990s, numerous clinical trials with antileukotriene drugs confirmed Brocklehurst's hypothesis that slow-reacting substance of anaphylaxis (SRS-A) is an important bronchoconstrictor agent in asthma (1). Bronchoprovocation studies showed that inhibition of the synthesis of leukotrienes (LTs) or antagonism of cysteinyl-LT receptors partly or wholly blocks constrictor responses to a wide range of asthma triggers, including allergen, platelet-activating factor (PAF), exercise, cold air, sulfur dioxide, adenosine 5'-monophosphate, and nonsteroidal antiinflammatory drugs (NSAIDs) (2). Multiple-dose studies of patients with allergic and nonallergic asthma commonly report 10-15% improvements in baseline lung function, with 25-60% improvements in secondary outcome measures, including symptom scores, night-time awakenings, use of rescue medication (β 2 -agonists and glucocorticoids), and days lost from work and school (3). To many researchers, the clinical improvements observed after blockade of this single family of inflammatory mediators were surprising, in view of the widely accepted model that airway narrowing is caused by numerous agents acting as components of a mediator soup. Indeed, the efficacy of antileukotriene drugs is highlighted by the relative failure in clinical trials of other mediator antagonists such as histamine H 1  antagonists, thromboxane antagonists, and PAF antagonists (4), The antibronchoconstrictor efficacy of antileukotriene drugs provided the main impetus behind their introduction as the first novel class of asthma therapy in more than 20 yr. However, clinical trials also provided surprising evidence for a hitherto unsuspected role of cysteinyl-leukotrienes in promoting persistent eosinophilia in the airway and blood of patients with asthma, and possibly influencing pathways involved in airway wall remodeling (5). A better understanding of these actions of antileukotriene drugs will influence their place in asthma management.
Abstract 1457: Intraoperative contrast-enhanced ultrasonography using perflubutane for liver resection
Authors: Hiroyuki Uetake, Toshiaki Ishikawa, Yusuke Mitsunori, Shinji Tanaka, Shigeki Arii, Kenichi Sugihara
Journal: Cancer Research (2010)

Abstract [Background] Bevacizumab (Bmab) is now widely used for metastatic colorectal cancer (CRC) treatment in the world. Through the high response of metastatic CRC to Bmab combination therapy, neoadjuvant chemotherapy using Bmab plus FOLFOX is a new strategy for the treatment of liver metastasis. As liver metastases shows high shrinkage by Bmab plus FOLFOX therapy, intraoperative contrast-enhanced ultrasonography using perflubutane (SONAZOIDTM) is supposed to be effective for complete detection and resection of small metastatic lesion after chemotherapy. [Material and methods] Forty-five patients with metastatic CRC were underwent Bmab combination chemotherapy in our institute (response rate and disease control rate was 72% and 94%, respectively). Among them, 8 patient (18%) were underwent liver resection after Bmab+mFOLFOX6 treatment. Median cycle of preoperative chemotherapy was 6.5 (5-17). [Result] By CT angiography, 52 liver metastases were detected before chemotherapy and 27 after chemotherapy. By intraoperative contrast-enhanced ultrasonography using SONAZOIDTM, 31 liver tumors were detected and resected. In histological examination, 13 of the resected 31 lesion (41%) were without viable cancer cell (pCR). [Conclusion] Intraoperative contrast-enhanced ultrasonography was effective for complete resection of liver metastasis after Bmab plus FOLFOX therapy. High pCR rate for liver metastasis was observed by Bmab plus FOLFOX therapy. 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 1457.