tbuckley/cabot-search huggingface dataset:
Esophageal self-expandable stent material and mesh grid density are the major determining factors of external beam radiation dose perturbation: results from a phantom model
Authors: B. Abu Dayyeh, J. VanDamme, R. Miller, T. Baron
Journal: Endoscopy (2012)

<b>Background:</b> Self-expandable esophageal stents are increasingly used for palliation or as an adjunct to chemoradiation for esophageal neoplasia. The optimal esophageal stent design and material to minimize dose perturbation with external beam radiation are unknown. We sought to quantify the deviation from intended radiation dose as a function of stent material and mesh density design. <b>Methods:</b> A laboratory dosimetric film model was used to quantify perturbation of intended radiation dose among 16 different esophageal stents with varying material and stent mesh density design. <b>Results:</b> Radiation dose enhancement due to stent backscatter ranged from 0 % to 7.3 %, collectively representing a standard difference from the intended mean radiation dose of 1.9 (95 % confidence interval [CI] 1.5 – 2.2). This enhancement was negligible for polymer-based stents and approached 0 % for the biodegradable stents. In contrast, all metal alloy stents had significant radiation backscatter; this was largely determined by the density of mesh design and not by the type of alloy used. <b>Conclusions:</b> Stent characteristics should be considered when selecting the optimal stent for treatment and palliation of malignant esophageal strictures, especially when adjuvant or neo-adjuvant radiotherapy is planned.
Abstract P4-09-12: The Effect of Age on Breast Cancer Outcomes in Women with Her-2 Positive Breast Cancer: Results from the HERA Trial
Authors: AH Partridge, S Gelber, M Piccart, F Focant, M Scullion, E Winer, R Gelber
Journal: Cancer Research (2010)

Abstract Background: Previous research has suggested that young age at diagnosis is an independent risk factor for breast cancer recurrence and death. However, young women are more likely to develop more aggressive subtypes of breast cancer and no prior studies have adequately controlled for Her-2/neu status or anti-Her-2 treatment. We sought to evaluate whether age is a prognostic factor in the HERA trial, which is a large randomized phase III trial of women with Her-2 positive early stage breast cancer who were randomized to receive trastuzumab (for one or two years) or observation following (neo)-adjuvant chemotherapy. Methods: We used 2 year median follow-up data from the HERA trial and conducted Cox proportional hazards models. Age was dichotomized at ≥40 years versus &amp;gt; 41 years to evaluate its prognostic effect on outcomes in women who received trastuzumab and those who did not. Only patients included in the 1-year trastuzumab and observation arms were included in the present analysis. Results: Of the 1703 women randomized to one-year of trastuzumab and 1698 to observation, 722 (21%) were age 40 or younger at study entry. Younger women were more likely to have node negative (33% vs 37%), estrogen receptor (ER)-negative (56 % vs 49%), and progesterone receptor (PR)-positive disease (41% vs 32%). In separate Cox models controlling for T and N stage, grade, ER and PR status, chemotherapy, endocrine therapy, and menopausal status at randomization, disease-free survival (DFS) hazard ratios were consistent for women ≥40 years compared with &amp;gt; 41 years old patients, regardless of whether they were assigned to observation or to receive trastuzumab. DFS were as follow: observation group: HR (younger/older) = 1.09, p-value = 0.62; trastuzumab group: HR (younger/older) = 1.05, p-value = 0.84. There was no statistically significant interaction between age and treatment (p=0.94). Conclusions: In women with early stage Her-2/neu positive breast cancer in a large RCT, age was not an independent predictor of risk of early recurrence. Future research to investigate whether age is a predictor of later risk of recurrence or is a predictor among women with other tumor subtypes is warranted. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P4-09-12.
A10.12 Adipokines influence the interaction between rheumatoid arthritis synovial fibroblasts and endothelial cells
Authors: R Hasseli, K Frommer, T Umscheid, M Schönburg, S Rehart, U Müller-Ladner, E Neumann
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background and objectives</h3> Rheumatoid Arthritis (RA) is a chronic polyarticular inflammatory disease. Adipose tissue, as an endocrine organ, also plays an important in inflammatory processes. RA synovial fibroblasts (SF) are able to migrate long distances <i>in vivo</i> via the vasculature as shown in a mouse model. Here, we analysed the role of adipokines, immunomodulatory factors mainly secreted by white adipose tissue, on RASF and endothelial cell (EC) adhesion. Static and dynamic adhesion and the expression of selected adhesion molecules on RASF and EC after stimulation with adipokines (adiponectin, visfatin, resistin), glucocorticoids and methotrexate (MTX) were evaluated. <h3>Materials and methods</h3> Primary RASF and EC were stimulated with adiponectin (10 µg/ml), visfatin (100 ng/ml), resistin (20 ng/ml) and TNF-α (10ng/ml) as well as inhibited with MTX (1.5 µM), the glucocorticoids prednisolone (1 µM) and dexamethasone (1 µM). The interaction of both cell types under static conditions was analysed using a cell-to-cell-binding assay. RASF adhesion to E-selectin was studied in a flow adhesion assay (flow rates: 18.4/30.5/60.5 ml/h). Selected adhesion molecule expression on RASF and EC after adipokine/MTX/glucocorticoid stimulation was analysed by real-time PCR. <h3>Results</h3> Prednisolone and dexamethasone stimulation down-regulated mRNA expression of VCAM-1 (prednisolone: -3.3-fold/dexamethasone: -8,3-fold) in RASF (n = 3). TNF-α, used as proinflammatory control, increased ICAM-1 mRNA expression (46.5 fold) in EC, while P-selectin mRNA expression (-7.7-fold) was decreased (n = 3). Under static conditions, the adipokines increased adhesion of RASF to EC (adiponectin: 37%, visfatin: 23%, resistin: 32%; n = 6), while prednisolone and MTX caused a minor decrease (-7% for both; n = 4). Dexamethasone did not change RASF adhesion to EC under static conditions. Under flow conditions, visfatin increased RASF adhesion to E-selectin (28%/87%/29%; n = 3 for each flow rate), while dexamethasone decreased their adhesion to E-selectin (-33%/-35%/-41%; n = 3 for each flow rate). <h3>Conclusion</h3> Adipokines influence the cellular expression of adhesion molecules on RASF and EC as well as their interaction. Adipokines increase adhesion of RASF to EC and may thus affect RASF migration. Therapeutics such as glucocorticoids and MTX antagonised these effects, which could reflect the protective effects seen in clinics.
Do RA or TNF inhibitors increase the risk of cervical neoplasia or of recurrence of previous neoplasia? A nationwide study from Sweden
Authors: Hjalmar Wadström, Thomas Frisell, Pär Sparén, Johan Askling
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Objectives</h3> To examine screening patterns and the risk of cervical neoplasia in women with rheumatoid arthritis (RA) treated or not with tumour necrosis factor inhibitors (TNFi). <h3>Methods</h3> We performed a nationwide register-based cohort study in Sweden of women with RA who started a first TNFi (n=9629), biologics-naive women with RA (n=34 984) and general population comparators (matched 1:10, n=300 331), followed up from 1999 to 2012. Outcomes were first cytology screening with normal outcome, first ever cervical intraepithelial neoplasia (CIN) grade 1, first ever CIN 2–3 or adenocarcinoma in situ and first ever invasive cervical cancer during follow-up. HRs were assessed through Cox regressions adjusted for age, educational level, prior cervical screens, comorbidities, marital status and prior hospitalisations. <h3>Results</h3> Biologic-naive women with RA had more screenings (HR 1.08, 95% CI 1.06 to 1.10), were at greater risk of CIN 1 (HR 1.53, 1.23 to 1.89) and CIN 2–3 (HR 1.39, 1.16 to 1.66), but not of invasive cervical cancer (HR 1.09, 0.71 to 1.65) compared with the general population. Patients who initiated TNFi therapy had similar screening patterns (HR 1.01, 0.98 to 1.05), were not at increased risk of CIN 1 (HR 1.23, 0.87 to 1.74), but were at increased risk of CIN 2–3 (HR 1.36, 1.01 to 1.82) and invasive cervical cancer (HR 2.10, 1.04 to 4.23) compared with biologics-naive women with RA. Estimates varied little with successive adjustments, but were attenuated/absent in sensitivity analyses restricted to 2006–2012 and a disease-modifying antirheumatic drugs-treated comparator. <h3>Conclusions</h3> Women with RA in general are at elevated risk of cervical dysplasia. Compared with biologics-naive patients, women treated with TNFi are at increased risk of cervical cancer. Whether this increase is causally linked with TNFi could not be fully disentangled.
AB0917 Capillaroscopic Observation as Early Biomarker of Atherosclerosis in Patients with Juvenile Idiopathic Arthritis
Authors: V. Opoka-Winiarska, A. Korobowicz-Markiewicz
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Rheumatic diseases are associated with the increased incidence of cardiovascular diseases. <h3>Objectives</h3> The aim of the study was the evaluation of early vascular disorders in children with juvenile idiopathic arthritis based on the capillaroscopic assessment of the nail microcirculation, as biomarker associated with early atherosclerosis. <h3>Methods</h3> The study was performed in 56 children with JIA, 4-16 years old, without disease activity, during therapy with at least one disease modifying drug, with or without glucocorticoid. 25 patients had oligoarticular onset of disease, 21 polyarticular onset, 8 had enthesitis-related arthritis and 2 had systemic onset of JIA. The control group consisted of 17 healthy children (age of 4-16 years). The capillaroscopic microvascular assessment using the optic microscope was performed in all patients and controls. The images were analyzed in II - V finger nails of both hands. The evaluation and measurements were made using the software. The analysis of capilaroscopic parameters such as linear capillary density, the percentage of tortuous vessels, presence of avascular areas, disorganized arrangement of capillaries, percentage of abnormal vessels, enlarged and branched vessels, number of microhemorrhages and arterial and venous capillaries width measurements in the fourth finger of non-dominant hand were performed. <h3>Results</h3> The presence of microvascular disease symptoms was demonstrated in 62.5% of patients with JIA and 52.6% of the children in the control group. The stage of microvascular complications in JIA group was significantly higher in comparison to the control group. On the basis of score, severity microvascular symptoms in the control group was defined as mild and in JIA group – mild or moderate. The hallmarks of JIA microangiopathy were the increased number of vessels, the presence of branched vessels, disorganization of arrangement of capillaries, lack of avascular areas and correct vessels width. The type of disease onset, duration of the disease, the type of the treatment had no significant effect on the severity of changes in the microcirculation. <h3>Conclusions</h3> JIA is associated with the increased capillaroscopic symptoms of microangiopathy that might suggest subclinical atherosclerosis. The severity of the JIA microangiopathy was defined as mild or moderate. It indicates the need for further monitoring. The characteristic features of microangiopathy observed in the inactive phase of JIA were an increased number of vessels, presence of branched vessels and disorganized arrangement of capillaries. The capillaroscopy is a sensitive tool for assessing the severity of microvascular complications in JIA and should be considered in a non-invasive monitoring also in the aspect of the cardiovascular disease risk. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5916
AB1126 Acute Effect on Pain and ROM of Two Different Active Movement Approaches in Knee Osteoarthritis: Table 1.
Authors: M.A. Oral, E. Ünal, E. Camci, I. Duzgun
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Movement inhibition and pain are common symptoms of osteoarthritis. Therefore, movement restoration and pain inhibition are one of the most important aims of physical therapy applications [1,2]. <h3>Objectives</h3> Aim of this study is to compare acute effects of two different active movement approaches in patients with movement inhibition due to acute knee pain associated with osteoarthritis. <h3>Methods</h3> 50 patients with knee osteoarthritis (13 men, 37 women; between 50 and 70 years-old) participated in this study. Also, all patients have complained about movement inhibition due to acute knee pain. Participants were randomly separated to two intervention groups; active movement or mobilization with active movement. Before and immediately after the application, pain severity during rest and activity were measured by visual analog scale, pain sensation was measured by algometer and knee range of motion was measured by standard goniometer [3]. <h3>Results</h3> There were significant improvements in knee flexion and extension range of motion, pain sensation and pain severity in mobilization with active movement group (p&lt;0,05). Conversely, in active movement group there were no differences in knee extension range of motion and pain sensitivity (p&gt;0,05), but the knee flexion range of motion had statistically significant improvements (p&lt;0,05). <h3>Conclusions</h3> In this study both mobilization with active movement and active movement approaches were found effective in patients with movement inhibition due to acute knee pain associated with osteoarthritis. Mobilization with active movement should be considered as an alternative method for treatment in knee osteoarthritis. <h3>References</h3> Jackson BD., W.A., Teichtal AJ. et.al. (2004) Reviewing knee osteoarthritis a biomechanical perspective. J. Science Med. Sport, 7:3, 347-357. Wu CW., K.K. (2005) New developments in osteoarthritis. Clinical Geriatr Med., 21:3, 589-601. Teys P., B.L., Vicenzino B. (2006) The inital effects of a Mulligan9s mobilization with movement technique on range of movement and pressure pain threshold in pain-limited shoulders. Manual Therapy, 13, 37-42. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3803
Abstract 2424: Interferon consensus sequence binding protein promotes epithelial to mesenchymal transition and cell motility in human osteosarcoma cells
Authors: Byung-Kiu Park, Jee Young Sung, Yoon Sook Na, Yong Nyun Kim
Journal: Cancer Research (2011)

Abstract Interferon consensus sequence binding protein (ICSBP) is a regulatory factor induced by interferon gamma (IFN-γ) and a member of interferon regulatory family (IRF). ICSBP is mainly expressed in hematopoietic cell and regulates immune response and differentiation but its role in non-hematopoietic cells is largely unknown. Here we investigated a role of ICSBP in human osteosarcoma U2OS cell line. Basal level of ICSBP expression was low but was induced by interferon-γ in U2OS cells. In addition, induced ICSBP promoted U2OS cell proliferation. To further elucidate ICSBP functions in osteosarcoma cells, we generated the U2OS stable cell line that overexpresses ICSBP. ICSBP overexpressing cells grew faster compared with mock cells and showed morphological changes. ICSBP upregulated TGF-βRI expression resulting in activation of TGF-β signaling pathways. In addition, ICSBP expression altered cell morphology and increased cell adhesion and motility. Furthermore ICSBP increased vimentin expression but decreased ZO-1 and E-cadherin expression, which is EMT related phenomena. These motility and EMT related phenomena were inhibited by TGF-βRI inhibitor. Taken together, these findings indicate that ICSBP promotes EMT and cell motility via TGF-β pathways in U2OS cells. 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 2424. doi:10.1158/1538-7445.AM2011-2424
S100 The bone morphogenetic protein type II receptor is critical for venous angiogenesis in zebrafish
Authors: J. E. Cannon, C. R. Bradshaw, J. C. Smith, N. W. Morrell
Journal: Thorax (2011)

<h3>Introduction and Objectives</h3> Pulmonary arterial hypertension (PAH) is a rare but severe condition, often fatal within 3–5 years due to right heart failure. Mutations in the bone morphogenetic protein (BMP) type II receptor (BMPR-II) underlie heritable forms of the disease but the mechanisms leading to vascular disease remain obscure from studies in mice and humans. Here we use zebrafish, which have a well-documented pattern of angiogenesis, as a model organism to address this question. <h3>Methods</h3> The transgenic Tg(<i>fli1a:egfp</i>) zebrafish line, where the <i>fli1a</i> promoter drives GFP expression in vascular endothelial and blood cells, was used throughout this work. A variety of methods were used to dissect the role of BMP signalling in vascular development including: (i) BMP receptor inhibitors (dorsomorphin and LDN193189), (ii) antisense morpholino oligonucleotides (morpholinos) and (iii) transgenic zebrafish engineered with heat shock inducible dominant-negative BMP receptors. To identify BMP responsive transcripts from vascular endothelial cells in vivo we developed a system to allow FACS isolation of GFP+ve cells dissociated from Tg(<i>fli1a:egfp</i>) zebrafish following incubation in LDN193189 or DMSO solvent control. The mRNA transcripts in GFP+ve cells were determined using massively parallel (Illumina) sequencing, mapped to the Zv8 zebrafish genome and differences in transcript abundance between LDN193189 and DMSO treated embryos were determined using cufflinks. <h3>Results</h3> Inhibition of BMP signalling with LDN193189 in zebrafish embryos after dorso-ventral patterning has occurred blocked venous but not arterial angiogenesis. This phenotype was reproduced in <i>BMPR2</i> dominant-negative zebrafish and following knockdown of the zebrafish homologues of <i>BMPR2</i>, <i>bmpr2a</i> and <i>bmpr2b</i> with morpholinos. Illumina sequencing identified the BMP responsive genes in vascular endothelial cells and the gene(s) responsible for the venous angiogenic phenotype are being determined by knockdown of these genes with morpholinos. <h3>Conclusion</h3> BMP signalling, via <i>BMPR2</i>, is critical for venous but not arterial angiogenesis in zebrafish. BMPR2 mutations are recognised as causative in patients with heritable PAH, where venous involvement is recognised, but also in pulmonary veno-occlusive disease. Our findings provide novel insights onto the potential role of the pulmonary venous system in pulmonary hypertension and implicate abnormal venous angiogenesis as a novel mechanism underlying this disease.
New York Legislation Mandates Some Off-Label Drug Coverage
Authors: L. Schwab
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article New York Legislation Mandates Some Off-Label Drug Coverage Get access Linda Schwab Linda Schwab Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 9, 1 May 1991, Pages 602–603, https://doi.org/10.1093/jnci/83.9.602 Published: 01 May 1991
PUBLICATION TRENDS IN AMERICAN PSYCHIATRY : 1844-1960
Authors: JOHN PAUL BRADY
Journal: American Journal of Psychiatry (1962)

Publication trends in American psychiatry were examined by means of a large sample of the psychiatric literature from 4 general psychiatric journals over a 117-year period. This paper concerns the general categories of subjects treated in the literature and changes in etiological emphasis. In later reports, trends in treatment, research and other categories will be traced.
Abstract 587: B-Raf status predicts response to pharmacological activation of p53 in melanoma
Authors: John T. Lee, Patricia A. Brafford, Molly B. Halloran, David C. Schultz, Meenhard Herlyn
Journal: Cancer Research (2011)

Abstract The formulation of highly-potent and specific inhibitors of the MAPK pathway has yielded several promising candidates and these are currently under advanced clinical development; however, early data suggests that inhibition of the MAPK pathway will not be sufficient to elicit sustained tumor regression in malignant melanoma. Thus, other pathways likely need to be therapeutically exploited to achieve sustained responses in melanoma patients. Because the tumor suppressor protein p53 is functional, yet inactive, in nearly 100% of melanomas, we sought to identify novel pharmacological activators of p53 in melanoma. To accomplish this goal, we employed a high-throughput screening strategy that identified hycanthone, a compound previously characterized for anti-schistosomal activity, as a specific activator of p53 function. In vitro characterization of hycanthone demonstrated that it activates the p53-transcriptional response leading to cell cycle arrest and subsequent apoptosis in a panel of melanoma cell lines harboring wild-type p53; these effects are largely absent in isogenic cells expressing p53 shRNA or alternative lines expressing mutant p53. Screening of a substantial panel of cell lines revealed that activation of p53 initiated anti-melanoma effects exclusively in cells that expressed mutant Braf, indicating that activated MAPK signaling may serve as a correlate to predict response to pharmacological activators of p53 in melanoma. However, additional experimentation has demonstrated that, instead, it is the presence of mutations in Braf, rather than the resultant MAPK activity, that predicts response to p53 activation. Studies investigating the mechanistic details governing this biological phenomenon are ongoing. Collectively, our data indicate that reactivation of p53 in melanoma, like multiple other tumors, can elicit an anti-tumor phenotype; however, this response is negatively modulated by the expression of mutant Braf, which would suggest that patients should be prospectively genotyped to identify potential responders to p53 reactivators. 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 587. doi:10.1158/1538-7445.AM2011-587
Bile intraductal aspiration (BIDA): a fast method for bile collection
Authors: G. Curcio, A. Granata, L. Barresi, I. Tarantino, F. Mocciaro, M. Traina
Journal: Endoscopy (2012)

Microbiological analysis of bile can be a valuable diagnostic tool, which may lead to better therapy and help in the establishment of local antibiotic guidelines for the management of cholangitis. However, it is not generally recommended and is rarely performed because it appears to be technically demanding, time consuming, or unnecessary in the presence of blood cultures [1]. In this report, we describe a new endoscopic technique for bile aspiration that has been devised at our institute, which we have named BIDA (Bile IntraDuctal Aspiration).
The novel biomarker-based ABC (age, biomarkers, clinical history)-bleeding risk score for patients with atrial fibrillation: a derivation and validation study
Authors: Ziad Hijazi, Jonas Oldgren, Johan Lindbäck, John H Alexander, Stuart J Connolly, John W Eikelboom, Michael D Ezekowitz, Claes Held, Elaine M Hylek, Renato D Lopes, Agneta Siegbahn, Salim Yusuf, Christopher B Granger, Lars Wallentin
Journal: The Lancet (2016)