tbuckley/cabot-search huggingface dataset:
PTH-095 Are IBD Patients Either CRP Producers or Non-Producers? a Longitudinal Study: Abstract PTH-095 Table 1
Authors: STR Powles, A Varey, T Orchard, J Tyrrell-Price
Journal: Gut (2013)

<h3>Introduction</h3> C-reactive protein (CRP) is an established marker of disease activity in inflammatory bowel disease (IBD). However not all flares in IBD are associated with an elevated CRP. This raises the possibility that some patients are not CRP producers<sup>1,2,3</sup>. In this retrospective observational study, we have assessed if patients consistently produce a low or high CRP level in response to a flare in IBD. <h3>Methods</h3> 31 patients were identified, over a 5 year period across 3 centres, with endoscopic mucosal assessments of two consecutive exacerbations of IBD which were at least 3 months apart. Patients were included if they had a CRP measurement within 7 days of each endoscopic examination (colonoscopy or flexible-sigmoidoscopy), and if they had active inflammatory colitis confirmed on mucosal biopsy. A CRP non-producer was defined as a CRP level of less than 10mg/L as according to the laboratory reference range used in the centres. <h3>Results</h3> In the cohort of 31 patients, 19 had biopsy proven UC, 3 had Crohn’s disease, 6 were unclassified, and 3 had differing classifications of Crohn’s disease and UC on successive endoscopies. There was an overall mean period of 11.3 months between successive endoscopies. 17 patients were CRP non-producers and 9 were CRP producers during successive IBD flares. The table below shows the disease classification in different CRP response groups. Disease extent was defined in both flares in 97% of patients. In the CRP non-producer group, 10 out of 17 (59%) patients had left sided disease or proctitis compared to 4 out of 8 (50%) in the CRP producer group. This difference in proportion did not reach statistical significance as assessed by Fisher’s exact test. Three of the five patients with a variable CRP response had more extensive disease at the time of the higher CRP level. <h3>Conclusion</h3> Most patients (84%) in this study had a consistent CRP response; but this was not universal. Disease extent appears to contribute to CRP, but patient specific factors also appear to play a role. <h3>Disclosure of Interest</h3> None Declared. <h3>References</h3> Gut. 2008 Nov; 57(11):1518–23. Epub 2008 Jun 19. C-reactive protein: a predictive factor and marker of inflammation in inflammatory bowel disease. Results from a prospective population-based study. Henriksen M, <i>et al.</i> IBSEN Study Group Inflamm Bowel Dis. 2005 Aug; 11(8):707–12..Correlation of C-reactive protein with clinical, endoscopic, histologic, and radiographic activity in inflammatory bowel disease. Solem CA, <i>et al.</i> Inflamm Bowel Dis. 2004 Sep; 10(5):661–5.C-reactive protein as a marker for inflammatory bowel disease. Vermeire S, <i>et al.</i>
AB1313 Survival of leflunomide treatment in a cohort of patients with rheumatoid arthritis
Authors: A.B. Rodríguez, Ó. Fontseré, R. Peña, E. Toledano, M. Blanco, E. Pato, L. Abasolo, I. Morado, J. Ά. Jover
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> after more thana decade usingLeflunomide(LFN), is widely known to be effective in the treatment of rheumatoid arthritis (RA). However, there is evidence in the literatureofa higher rate of suspension for toxicity and lack of efficacy compared to other DMARDs such as methotrexate (MTX). Although, those are series with small numbers of patients and short-term follow up. <h3>Objectives</h3> toevaluate the survival of LFN, and the causes of its suspension in a cohort of patients with RA. <h3>Methods</h3> retrospectivelongitudinal observational study. <i>Subjects:</i> patients with RA followed in our hospital, treated with LFN, from January 1, 2006 until October 1, 2011. <i>Outcomes:</i> primary outcome: LFN suspension due to: a) adverse event (AE), b) lack of efficacy, c) patient's decision; d) remission or improvement. Secondary outcomes: age, sex, date of diagnosis, date of start and end of treatment with LFN. The data sourcewas our electronic health record. <i>Statistical analysis:</i> a description of the sociodemographic and clinical characteristics of patients included and the causes for suspension using frequency distribution rates and the mean and standard deviation or median and percentiles. Survival techniques are used to estimate the suspension rate of LFN, expressing the incidence per 1000 patient-years (95% CI). <h3>Results</h3> 322 patients started treatment with LFN during the follow up. 257 were women (79.81%), the mean age at baseline was 59±15 years. The median time from diagnosis of RA was 2.37 years (p25-75: 0,56-5, 68), there were 116 suspensions (38.41%), the 68.97% of them were due to AE, 7.76% to patient's decision, 7.76% due to lack of efficacy, and 6.9% to clinical improvement. 74.78% of the patients with suspensions were women, mean age at the time of suspension was 60±15 years and the median time from diagnosis of RA was 2.64 years (P25-75: 0.73-5.68). The suspension rate was 216 per 1000 (95% CI 180.23-259.35), 277.88 per 1000 in men (95% CI 193-399.88) and 199 per 1000 in women (95% 161-245.87). 83 of the suspensions (71.5%) occurred within the first 6 months of treatment with LFN. 50% of patients had discontinued the drug 3.5 years after starting treatment. AE rate was 149.10 per 1000 (95% CI 119.76-185.636). The suspension rate associated with lack of efficacy was 16.77 per 1000 (95% CI 8.72-32.23). The suspension rate because of clinical improvement was 14.91 per 1000 (95% CI 7.45-29.81). <h3>Conclusions</h3> the survival of the treatment with LFN is less than 50% at 4 years. The suspension rate was high, mainly due to adverse events. <h3>Disclosure of Interest</h3> None Declared
Abstract 1214: TIMP-1 and the TIMP-1 interacting cell surface protein CD63 in cultured astrocytoma derived spheroids: expression and co-expression with stem cell markers
Authors: Charlotte Aaberg-Jessen, Henrik D. Schrøder, Claus Andersen, Nils Brünner, Bjarne W. Kristensen
Journal: Cancer Research (2010)

Abstract In previous studies we have shown that the immunohistochemical expression of TIMP-1 (tissue inhibitor of metalloproteinases-1) and CD63 increases with tumor grade in astrocytomas grade II-IV. Moreover, we demonstrated that a high TIMP-1 protein expression in glioblastomas was associated with a shorter overall patient survival. Recent studies have suggested that TIMP-1 can prevent chemo-induced apoptosis and in a study, using human breast epithelial cells (MCF10A), it was demonstrated that the interaction of TIMP-1 and CD63 is necessary for the TIMP-1 anti-apoptotic pathway. The aim of the present study was to investigate the expression of TIMP-1 and CD63 in cultured organotypic multicellular spheroids (OMS) and cell line spheroids (CLS) derived from astrocytomas in order to assess spheroid models for future studies involving TIMP-1, CD63 and chemo-resistance. By investigating the spheroids immunohistochemically, we wanted to elucidate if TIMP-1 and CD63 are co-expressed within the spheroids and whether they are expressed by tumor stem like-cells, since these cells are known to be more resistant to chemotherapeutic treatment. In the present study OMS from nine astrocytomas and CLS from three commercial astrocytoma cell lines were included as well as the glioblastoma tumor stem cell line SJ-1 made in our laboratory. In general high levels of CD63 protein was detected in all the original tumors, whereas TIMP-1 was moderately expressed. TIMP-1 and CD63 expression in OMS was similar to the expression in the original tumors. TIMP-1 was expressed at low to moderate levels in CLS, whereas CD63 was expressed by all tumor cells in all spheroids. TIMP-1/CD63 double immunofluorescence staining was performed on selected OMS and CLS showing tumor cells expressing both proteins. Furthermore, double staining was performed with TIMP-1 and the stem cell markers CD133, nestin and Sox2 demonstrating that a population of the tumor stem like-cells expressed TIMP-1. In conclusion, this study shows that spheroid models can be used in future studies investigating the role of TIMP-1 and CD63 in chemo-induced apoptosis. Furthermore, these results indicate that a fraction of the tumor stem like-cells could be protected by TIMP-1/CD63 interaction. 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 1214.
Thrombectomy in Volkmann's Contracture
Authors: Dean K. Crystal, Ernest Burgess, Clayton Wangeman
Journal: New England Journal of Medicine (1952)

ARTERIAL thrombectomy is a previously untested treatment for Volkmann's contracture. A review of the literature failed to reveal any earlier employment of the procedure. Griffiths1 , 2 reported segmental arteriectomy and described embolectomy in patients who are fibrillating, but he did not mention thrombectomy at the site of injury in cases of contracture. Foisie3 advocated arteriectomy for "stubborn" cases, but he did not consider thrombectomy.Orthopedic and surgical textbooks properly emphasize prophylaxis against Volkmann's contracture rather than treatment. Most conservative therapeutic measures — for example, fasciotomy, sympathetic block and removal of splints — have been disappointing and inadequate in combating fully developed . . .
Esophageal metallic stent fixation with dental floss: a simple method to prevent migration
Authors: B. da Costa Martins, B. Medrado, M. de Lima, F. Retes, F. Kawaguti, C. Pennacchi, F. Maluf-Filho
Journal: Endoscopy (2013)

Use of fully and partially covered self-expanding metallic esophageal stents (SEMS) is associated with high rates of migration [1]. Stent modification with a silk thread to permit external fixation, proposed by Shim et al., has been shown to reduce migration [2] but this stent may not be routinely available. Therefore we present another modified stent technique that can be used in patients with or at risk for stent migration.
Abstract 1290: Investigations to evaluate the role of Twist1 during tumor promotion and epithelial carcinogenesis.
Authors: Jaya Srivastava, Everardo Macias, Dharanija Rao, Kaoru Kiguchi, John DiGiovanni
Journal: Cancer Research (2013)

Abstract Recent studies have identified the involvement of receptor tyrosine kinases (RTKs) and their downstream signaling pathways, including MAPK, PI3K/Akt/mTOR, and Stat3, as key regulatory factors of epidermal proliferative capacity during skin carcinogenesis. Through development and study of transgenic mice with overexpression of a constitutively active form of Stat3 (Stat3C) in the basal cell layer, previous studies in the laboratory discovered that constitutive Stat3 activation accelerates tumor progression in the two-stage skin carcinogenesis model, which utilizes the tumor initiator 7,12-dimethylbenz[α]anthracene (DMBA) and tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Twist1, a well-known inducer of EMT, has been shown to be regulated by Stat3 in a number of systems. Western blot analysis of epidermal protein lysates from Stat3C transgenic mice indicated a two-fold induction of Twist1 expression as compared to wild type mice. In addition, immunofluorescence staining analysis of tumors from wild type mice [papillomas and squamous cell carcinomas (SCCs)] and Stat3C mice (SCCs) showed nuclear co-localization of Twist1 and Stat3. In the present study, we investigated the activation and subsequent downstream signaling of Twist1 during TPA-induced epidermal hyperproliferation. Western blot analysis of epidermal lysates from mice treated topically with multiple applications of TPA showed an initial decrease (4-6 h) followed by a subsequent rebound of Twist1 protein at 18 hours post TPA treatment. This initial decrease and then rebound coincided with that of the cell cycle regulatory proteins cyclin D1, cyclin E1, E2F-1, and c-myc. Interestingly, basal levels of Twist1 were reduced in epidermis specific Stat3 deficient mice. Furthermore, Stat3 deficient mice treated with TPA failed to show a rebound in expression of Twist1 in the epidermis. Immunofluorescence experiments of TPA treated epidermis revealed that nuclear localization of Twist1 was restricted to the proliferative compartment. Collectively, these results, combined with other data to be presented, suggest that Stat3 regulates basal levels of Twist1. This protein is localized in the nucleus of cells found primarily in the proliferative compartment of hyperplastic epidermis and skin tumors. The current results further suggest that Twist1 may play a role in cell cycle progression in keratinocytes during tumor promotion. Research supported by CA76520. Citation Format: Jaya Srivastava, Everardo Macias, Dharanija Rao, Kaoru Kiguchi, John DiGiovanni. Investigations to evaluate the role of Twist1 during tumor promotion and epithelial carcinogenesis. [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 1290. doi:10.1158/1538-7445.AM2013-1290
VTE prophylaxis across the continuum of care in U.S. cancer patients
Authors: A. Amin, J. Lin, A. Ryan
Journal: Journal of Clinical Oncology (2009)

e17510 Background: The period of VTE risk in cancer patients extends beyond the hospital stay. This analysis evaluated VTE prophylaxis patterns for US cancer patients across the continuum of care. Methods: Premier's Perspective inpatient data were cross-matched with Ingenix LabRx outpatient data from the I3 database (January 2005-December 2007) to assess VTE prophylaxis patterns in medical cancer patients at risk of VTE (according to the American College of Chest Physicians 2004 guidelines) and with no contraindications for anticoagulation. Inpatient anticoagulant groups were assigned based on the drug the patient received during hospital stay and were followed by their outpatient prophylaxis use. Patients were evaluated on drug utilization, diagnoses and clinical practice patterns during and after hospitalization. Results: Overall, 75.3% of 2,337 cancer patients did not receive anticoagulation during their hospital stay. Of the 577 patients receiving prophylaxis, 66% received UFH and 25% received enoxaparin ( Table ). The mean length of hospital stay was 3 days after which 97.9% of patients did not receive any prophylaxis within the following 30 days. Of the 50 patients who received outpatient prophylaxis, 60% received warfarin alone and 22% received both enoxaparin and warfarin. Conclusions: This unique analysis presents VTE prophylaxis patterns across the continuum of care. Most cancer patients did not receive anticoagulation in the inpatient or outpatient settings. Further efforts are needed to identify optimal VTE prevention in cancer patients, namely the duration of prophylaxis and how healthcare providers can increase awareness. Financial and editorial support was provided by sanofi-aventis US, Inc. [Table: see text] [Table: see text]
ACCURACY OF GLOBAL LONGITUDINAL STRAIN BY ECHOCARDIOGRAPHY IN THE ASSESSMENT OF LEFT VENTRICULAR FUNCTION AND MYOCARDIAL SCAR BURDEN IN PATIENTS WITH ADVANCED ISCHEMIC CARDIOMYOPATHY: COMPARISON WITH CARDIAC MRI
Authors: Samornrat Jampates, Kenya Kusunose, Zoran Popovic, Scott Flamm, Brian Griffin, Deborah Kwon
Journal: Journal of the American College of Cardiology (2015)
Past public health faculty presidents call for withdrawal of health bill
Authors: Z. Kmietowicz
Journal: BMJ (2011)

A group of leading public health specialists has written to the prime minister calling on him to withdraw the Health and Social Care Bill because of its “threat to the integrity and cohesion of the NHS” and its likely effect to “widen inequalities in health and healthcare.”

Seven past presidents of the UK Faculty of Public Health say that the bill’s proposals mark “an unprecedented marketisation of the NHS which will promote competition at the expense of collaboration.” The …
Abstract 1602: Mucinous adenocarcinoma developed from human fallopian tube epithelial cells through a combination of defined genetic modifications and tumor microenvironment
Authors: Imelda Mercado-Uribe, Weiwei Shan, Jinsong Liu
Journal: Cancer Research (2011)

Abstract Epithelial ovarian cancer includes several distinct histologic types including serous, mucinous, endometrioid, and clear cell. The cell origin of these distinct epithelial ovarian cancers has been debated for many years. Recent studies have suggested that some ovarian and pelvic serous carcinomas could originate from the fimbrial end of distal fallopian tube, although direct experimental evidence supporting this hypothesis is still lacking. To test this hypothesis, we immortalized a normal human fallopian tubal epithelial (FTE) cell line by using a retrovirus-mediated infection expressing the early region of SV40 T/t antigen and the human telomerase reverse transcriptase. These immortalized FTEs were then transformed by ectopic expression of oncogenic human HRASV12. Tumorigenicity of the immortalized and/or transformed cells was subsequently tested by anchorage-independence assay and inoculation into nude mice via subcutaneous or intraperitoneal injections. As expected, the HRASV12-transformed FTEs produced tumors through both subcutaneous and intraperitoneal injections, while no tumor growth was observed in immortalized FTEs. To our surprise, however, while histopathologic examination of resulting tumor from subcutaneous injections revealed a largely undifferentiated carcinoma with focal mucin production, tumors from intraperitoneal injections showed mucinous adenocarcinoma with rich mucin production from an undifferentiated area. The mucinous differentiation of tumors was most prominent near the peritoneal fat and other peritoneal organs including the pancreas, spleen, and intestine. Immunohistochemical staining of tumor cells showed positive staining for the epithelial cell markers cytokeratin AE1/AE3 and CA125. Our study demonstrates that FTEs can generate mucinous adenocarcinoma through genetic modifications and that such mucinous differentiation is dependent on the peritoneal microenvironment. Thus, the experiment described here provided the first experimental evidence that fimbrial epithelial cells of the fallopian tube could be a potential source of ovarian mucinous adenocarcinoma, a distinct histologic entity of epithelial ovarian cancers whose origin is largely unknown. 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 1602. doi:10.1158/1538-7445.AM2011-1602
Yield of the second surveillance colonoscopy based on the results of the index and first surveillance colonoscopies
Authors: Michael Morelli, Elizabeth Glowinski, Ravi Juluri, Cynthia Johnson, Thomas Imperiale
Journal: Endoscopy (2013)

<b>Background and study aims:</b> The risk of advanced colorectal neoplasia (ACN) after the first surveillance colonoscopy is not well quantified. The aim of the current study was to quantify the risk of ACN on the second surveillance colonoscopy based on previous colonoscopic findings. <b>Patients and methods:</b> This was a single-site study of patients with index adenomas who underwent two surveillance colonoscopies. ACN was defined as advanced adenoma (≥ 1 cm, villous histology, or high-grade dysplasia) or as "high-risk" findings (advanced adenoma or ≥ 3 non-advanced adenoma [NAA]). <b>Results:</b> Among 509 patients with low-risk index findings, 61 (12.0 %; 95 % confidence interval [CI], 9.3 % – 15.1 %) had high-risk findings on the first surveillance colonoscopy, 11 of whom (18.0 %; 95 %CI 9.4 % – 30.0 %) had high-risk findings on second surveillance colonoscopy compared with 39 (8.7 %; 95 %CI 6.3 % – 11.7 %) of the remaining 448 patients who had normal or low-risk findings on the first surveillance colonoscopy (relative risk [RR] = 2.07; 95 %CI 1.12 – 3.83). Among 456 patients with high-risk index findings, 91 (20.0 %; 95 %CI 16.3 % – 23.9 %) had high-risk findings on the first surveillance colonoscopy, 20 of whom (22.0 %; 95 %CI 14.0 % – 31.9 %) had high-risk findings on second surveillance colonoscopy compared with 40 (11.0 %; 95 %CI 8.0 % – 146 %) of the remaining 365 patients who had normal or low-risk findings on first surveillance colonoscopy (RR = 2.01; 95 %CI 1.04 – 3.32). Results were similar when only advanced adenomas were considered. <b>Conclusions:</b> Patients with high-risk findings on index and first surveillance colonoscopies require close surveillance. Those with low-risk findings on index colonoscopy and normal/non-advanced findings on the first surveillance colonoscopy have low subsequent risk of ACN. These and previous data may be useful for generating recommendations for the timing of the second surveillance colonoscopy.
AB1045 Development and Validation of Juvenile Autoinflammatory Disease Multidimensional Assessment Report (JAIMAR)
Authors: D. Konukbay, D. Yildiz, C. Acikel, B. Sozeri, B. Makay, N. Ayaz, K. Barut, A. Kisaarslan, Y. Bilginer, H. Peru, O. Erdogan, E. Unsal, O. Kasapcopur, Z. Gunduz, S. Ozen, E. Demirkaya
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> There are a lot of effects of auto-inflammatory diseases (e.g. fear of attack, pain, fever, fatigue, problems at school) that are quite important to patients but have not been measured with the outcome instruments currently included in clinical trials of autoinflammatory diseases. <h3>Objectives</h3> The aim of this study is to develop and test a new multidimensional questionnaire for assessment of children with autoinflammatory disease (AID) in standard clinical care. <h3>Methods</h3> JAIMAR includes 16 parent or patient - centered measures and four dimensions that assess functional status, pain, therapeutic compliance and health-related quality of life with disease outcome. The JAIMAR is proposed for use as both a proxy-report and a patient self-report, with the suggested age range of 7-18 years for use as a self-report. The study was conducted in children with AID and their parents in seven different paediatric rheumatology center from Turkey. To validate the JAIMAR, the Outcome Measures in Rheumatology Clinical Trials (OMERACT) filter for outcome measures in rheumatology was applied. <h3>Results</h3> Completion and scoring appeared to be quick, requiring avarage15 minutes. The analysis data set included by the parents of 250 children with FMF in 351 visits and by 179 children in 187 visits. The median age of the children was 10.64±4.38 and female to male ratio was. The JAIMAR was found to be feasible and to possess face, content, criterion and construct validity. The cronbach9s alpha coefficient for internal consistency for the JAIMAR dimensions were between for parents 0.677-0.998 and for children 0.507-0.986. Parents9 proxy-reported and children9s self-reported data were outstandingly concordant.The JAIMAR dimensions patient self-report and parent proxy-report cronbach9s alpha values were between 0.770-0.989. <h3>Conclusions</h3> The development of the JAIMAR introduces a new and multi-dimensional approach in pediatric rheumatology practice. The JAIMAR provided thorough information for the study patients about recent medical history, attack status and current health status. It is valid tool for children with autoinflammatory disease and will help enhance the quality of care of in this group of patients <h3>References</h3> Kalkan G, Demirkaya E, Acikel CH, Polat A, Peru H, Karaoglu A, Sari E, Dursun I, Gok F, Ozen S; (FAVOR). Evaluation of the current disease severity scores in paediatric FMF: is it necessary to develop a new one? Rheumatology (Oxford). 2012, 51(4):743-8. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5963