tbuckley/cabot-search huggingface dataset:
Diagnosis of Complete Ectopic Lingual Thyroid with Tc-99m Pertechnetate Scintigraphy
Authors: C Aktolun, H Demir, F Berk, K Metin Kir
Journal: Clinical Nuclear Medicine (2001)

The authors present four cases of ectopic lingual thyroid disease diagnosed by Tc-99m pertechnetate scanning, which is an efficient diagnostic tool that yields high-quality images in this clinical setting.
ANÁLISIS COMPARATIVO DE 2 REGÍMENES DE PREPARACIÓN DE LA COLONOSCOPIA
Authors: R Irisarri, E Amorena, JJ Vila, F Bolado, M Basterra, M Gómez, J Urman, FJ Jiménez
Journal: Endoscopy (2010)

Introducción: La buena preparación es uno de los criterios de calidad para las colonoscopias. Nosotros realizamos colonoscopias siguiendo 2 regímenes de preparación según la colonoscopia se realice en horario de mañana (preparación la tarde anterior) o de tarde (repartida entre la tarde del día anterior y la mañana del día de la colonoscopia).
Abstract 5182: Nicotine enhanced colon cancer migration through the change of epithelial-to-mesenchymal transition biomarkers
Authors: Yu-Jia Chang, Po-Li Wei, Ming-Te Huang, Jun-Jen Liu
Journal: Cancer Research (2011)

Abstract Long-term cigarette smoking increases the risk of colorectal cancer mortality. Tobacco's addictive toxin, nicotine, was reported to increase DNA synthesis of colon cancer cells. Since metastasis is the major cause of cancer death, the influence of nicotine on the migration of colon cancer cells remains to be determined. The influence of nicotine on the migration of colon cancer cells was evaluated using trans-well assay. Nicotine receptor-mediated migration was studied by using both inhibitors and small interfering RNA (siRNA). The role of COX-2 signal was studied using pharmacological inhibitors. The expression of epithelial mesenchymal transition (EMT) marker and COX-2 signal was evaluated using real time PCR. Nicotine enhanced DLD-1 and SW480 cell migration in dose dependent manner. We used inhibitors and siRNA to demonstrate that α7-nAChR mediates nicotine-enhanced colon cancer cell migration and upregulates fibronectin expression, which is involved in nicotine-enhanced migration. Further, COX-2 signal was induced by nicotine treatment and is involved in nicotine-enhanced fibronectin expression. We concluded that nicotine, tobacco's additive toxin, enhances colon cancer metastasis through α7-nAChR and fibronectin, a mesenchymal marker for epithelial mesenchymal transition. Furthermore, COX-2 signal was also involved in the induction of fibronectin. Therefore, smoking may play role in the progression of colon cancer. 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 5182. doi:10.1158/1538-7445.AM2011-5182
SAT0230 The Influence of Anti-TNF or Rituximab on Cancer Incidence in Patients with Rheumatoid Arthritis Who Have HAD A Prior Malignancy:
Authors: L. Silva-Fernandez, M. Lunt, K.D. Watson, W.G. Dixon, B. Control Centre Consortium, D.P. Symmons, K.L. Hyrich
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> The exact relationship between biologics and cancer remains unclear. Despite no evidence to date of an overall increased risk of cancer on biological therapies, concerns remain about starting therapy in patients with prior malignancy. <h3>Objectives</h3> The aim of this study was to explore the relationship between different anti-TNF and rituximab (RTX) therapy and the incidence of cancer in patients with rheumatoid arthritis (RA) and prior malignancy. <h3>Methods</h3> The British Society for Rheumatology Biologics Register (BSRBR)-RA is a national prospective cohort study of subjects with RA starting biologic therapy. Patients receiving anti-TNF or RTX as their first biologic were included in this analysis and compared to patients who had never taken biologics. At registration, all patients were linked to the UK National Health Service Information Centre (NHS IC) which provided details of all historic cancers and any new cancers, including date of diagnosis. Analysis was limited to patients with a history of malignancy (except non melanoma skin cancer or carcinoma-in-situ) identified by the NHS IC with a diagnosis date prior to the BSRBR-RA registration date. All patients were followed by clinical and patient questionnaires every 6 months for the first 3 years and annual clinical questionnaires thereafter, in which data on drug therapy and serious adverse events were reported. Incident malignancies (IM) were defined as malignancies diagnosed after the registration date. New primaries, local recurrence and metastases were all included as incident cancers. Subjects were followed until 31/05/2013, first IM, death or switch of treatment, whichever came first. The rates of IM in the three cohorts were compared using age and gender adjusted Cox proportional hazards models. <h3>Results</h3> In total, 3787 DMARD (recruitment: 2002-2009), 14168 biologic-naive anti-TNF (recruitment: 2001-2013) and 257 biologic-naive rituximab (recruitment: 2008-2011) treated patients were recruited. Of these, 425 patients had prior malignancy (DMARDs: 159 (4.2%); anti-TNF: 243 (1.7%); rituximab: 23 (8.9%)) (see table). Overall there was a trend towards a reduced adjusted hazard ratio of new IM for patients starting anti-TNF (HR 0.55 [95% CI 0.35, 0.87]) and rituximab (HR 0.47 [95% CI 0.11, 1.94]) compared to patients receiving DMARDs. <h3>Conclusions</h3> Although numbers are still low, patients with RA and prior malignancy selected to receive biologic therapy in the UK do not seem to have an increased risk of future incident malignancy. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.1134
Abstract 3109: SOX4 and POU2F1 synergistically regulate metastasis-associated NRP1 in HCC metastasis.
Authors: Ann-Ping Tsou, Yu-Lun Liao, Yi-Ming Sun, Jorng-Tzong Horng, Michael Hsiao
Journal: Cancer Research (2013)

Abstract Gene regulation by SOX proteins depends on the presence of requisite partners which provides target specificity and combinatorial control. Previously, we have shown that SOX4 is an oncogenic transcription factor involved in human hepatocarcinogenesis. By bioinformative prediction, we identified that POU2F1 is an SOX4 co-factor and further showed that SOX4 and POU2F1 synergistically regulate metastasis-associated NRP1 expression in HCC cells. Using co-immunoprecipitation experiments, SOX4 and POU2F1 were shown to participate in direct protein-protein interaction in vitro involving assembly into a complex that required the N-terminus and HMG domain of SOX4 interacting with POU2F1. In addition, RNAi knockdown of SOX4 expression of HCC cell lines drastically reduced the expression of epithelial-mesenchymal transition (EMT) related genes, N-cadherin, MMP2 and MMP9. SOX4 knockdown also reduced the expression of VEGF related genes VEGFC, FLT1 and FLT4 and blood vessel distribution in subcutaneous tumors was decreased in shSOX4, shPOU2F1 and shNRP1-infected Mahlavu tumor cells. Our results suggest that SOX4 and POU2F1 may play a critical role in the regulation of genes involved in tumor invasion. These results support a new regulatory network from SOX4 and POU2F1 to NRP1 that occurs during liver tumor metastasis. This investigation provides relevant gene targets that are regulated by SOX4 and POU2F1 in liver tumors and these results could be used to develop effective diagnostic and alternative therapeutic strategies for the treatment of intrahepatic HCC. Keywords: SOX4; POU2F1; hepatocellular carcinoma Citation Format: Ann-Ping Tsou, Yu-Lun Liao, Yi-Ming Sun, Jorng-Tzong Horng, Michael Hsiao. SOX4 and POU2F1 synergistically regulate metastasis-associated NRP1 in HCC metastasis. [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 3109. doi:10.1158/1538-7445.AM2013-3109 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
P9 Adrenal Suppression in Difficult Asthma: A Neglected Cause For Concern
Authors: TJT Sutherland, C Hodgekiss, J Slough, JH Barth, IJ Clifton
Journal: Thorax (2012)

<h3>Introduction</h3> Inhaled corticosteroids (ICS) are the mainstay of treatment in asthma. Whilst they are felt to be safe in low doses, a number of case studies have demonstrated adrenal suppression in higher doses, particularly in paediatric patients. The relative frequency of this is largely unknown, but we believe it may be significantly under-recognised in patients with difficult to treat asthma. As part of our difficult asthma protocol we measure random cortisol levels and proceeded to further investigations if this was abnormal or the patient presented with symptoms of adrenal insufficiency. <h3>Methods</h3> Patients were assessed through the Difficult Asthma Service in Leeds which is a tertiary referral centre for West Yorkshire. Patients who had non-specific symptoms out of keeping with asthma, either had a random serum cortisol taken or had a short synacthen test. Patients were classified as: adrenal insufficient with a cortisol less than 50nmol/L or a positive short synacthen test, and adrenal sufficient with a random cortisol greater than 120nmol/L or a negative short synacthen test. A further group was defined as suboptimal if their random cortisol was between 50–120nmol/L Data were also collected on ICS dose and type, and atopic status. <h3>Results</h3> Ninety-two random cortisol samples have been taken to date. Of these, 8 patients who were not on oral corticosteroids were found to have adrenal insufficiency (8.7%). Seven patients had a random cortisol less than 50nmol/L and one had a positive short synacthen test. Of the patients with adrenal insufficiency six patients were on a combination inhaler including fluticasone, and all received a daily BDP dose over 1000mcg. None of the patients with adrenal insufficiency demonstrated evidence of atopy, except one patient with co-existent ABPA receiving itraconazole therapy. <h3>Conclusions</h3> We have identified a significant number of patients with evidence of adrenal insufficiency, with the majority identified by a random cortisol. This is likely to be under-estimated, as the 92 samples include patients on maintenance oral corticosteroids. In patients with difficult asthma, multiple or atypical symptoms, there should be a low threshold to investigate for adrenal insufficiency particularly those receiving high dose ICS.
FAVORABLE EFFECTS OF EARLY ADMINISTRATION OF TOLVAPTAN IN ELDERLY PATIENTS WITH REPEAT HOSPITALIZATIONS FOR ACUTE DECOMPENSATED HEART FAILURE
Authors: Masaki Kinoshita, Hideki Okayama, Go Kawamura, Tatsuya Shigematsu, Tatsunori Takahashi, Yoshitaka Kawada, Go Hiasa, Tadakatsu Yamada, Yukio Kazatani
Journal: Journal of the American College of Cardiology (2016)
Short Stature Caused by a Mutant Growth Hormone
Authors: Yutaka Takahashi, Hidesuke Kaji, Yasuhiko Okimura, Katsumi Goji, Hiromi Abe, Kazuo Chihara
Journal: New England Journal of Medicine (1996)

The causes of growth hormone–dependent short stature are primary pituitary disease, pituitary deficiency due to hypothalamic dysfunction, and, less often, insensitivity to growth hormone. The prototypical syndrome of growth hormone insensitivity is Laron-type dwarfism, which is characterized by absent or defective growth hormone receptors. Kowarski et al. described two children with growth retardation resulting from biologically inactive growth hormone1; additional cases were reported subsequently.2–7 This disorder is characterized by high serum concentrations of immunoreactive growth hormone, low serum concentrations of insulin-like growth factor I (IGF-I), and increases in both serum IGF-I and linear growth after the administration of . . .
Aspirin as an Antiplatelet Drug
Authors: Alastair J.J. Wood, Carlo Patrono
Journal: New England Journal of Medicine (1994)

The past 10 years have witnessed major changes in our understanding of the pathophysiologic mechanisms underlying vascular occlusion1,2 and considerable progress in the clinical assessment of aspirin and other antiplatelet agents35. The purpose of this review is to describe a rational basis for antithrombotic prophylaxis and treatment with aspirin. Basic information on the molecular mechanism of action of aspirin in inhibiting platelet function will be integrated with the appropriate clinical pharmacologic data and the results of randomized clinical trials.Mechanism of ActionAspirin induces a long-lasting functional defect in platelets, clinically detectable as a prolongation of the . . .
Abstract 1476: Cell surface nucleolin acts as a specific receptor of Tipα, a carcinogenic factor released from <i>H. pylori</i>
Authors: Masami Suganuma, Tatsuro Watanabe, Hideaki Tsuge, Kazuo Hirano, Masatoshi Beppu, Kensei Yamaguchi, Atsushi Takahashi, Hirota Fujiki
Journal: Cancer Research (2010)

Abstract TNF-α inducing protein (Tipα), a unique carcinogenic factor of H. pylori, has the potential to transform Bhas 42 (v-H-ras transfected BALB/3T3) cells. Tipα directly binds to gastric cancer cells and then induces expression of TNF-α gene, an endogenous tumor promoter, in gastric epithelial cells. H. pylori obtained from gastric cancer patients release significant amounts of Tipα into the culture medium compared with H. pylori of gastritis patients, indicating that Tipα plays important role in gastric cancer development. Recently, Tipα vaccination was reported to significantly reduce the colonization of H. pylori in mice associated with high levels of Tipα-specific antibody: All the results indicate that Tipα is a suitable molecular target for gastric cancer prevention. We recently demonstrated that nucleolin is a specific binding protein for Tipα in mouse gastric cancer cells MGT-40 using FLAG pull-down assay. Although nucleolin is known to a be non-ribosomal protein in nucleoli, we found that nucleolin is present on the cell surface of MGT-40 cells and various human gastric cancer cell lines, such as KATOIII and AGS, as determined by flow cytometry with anti-NUC295 antibody (recognizing cell surface nucleolin), and by cell fractionation. Pretreatment with anti-NUC295 antibody induced the enhancement of Tipα incorporation into the MGT-40 cells, but pretreatment with tunicamycin, an inhibitor of N-glycosylation decreased the amounts of cell surface nucleolin and inhibited internalization of Tipα, resulting in down-regulation of TNF-α gene expression. We here present evidence that cell surface localized nucleolin acts as a receptor of Tipα and shuttles Tipα from cell surface to cytosol and nuclei, and we discuss the significant roles of cell surface nucleolin in gastric cancer development by H. pylori infection. 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 1476.
Abstract 1653: Vasodilator-stimulated phosphoprotein ser157 and ser239 are antimetastatic targets in colon cancer
Authors: Mehboob Ali, Giavanni Mario Pitari
Journal: Cancer Research (2011)

Abstract Colorectal cancer is the third deadly cancer worldwide. Patient mortality is largely the result of metastatic disease progression, in which tumor cells undergo dramatic morphological changes characterized by the formation of membrane protrusive structures mediating invasion (lamellipodia, filopodia, invadopodia). These events are driven by the activity of actin-regulatory proteins, including the vasodilator-stimulated phosphoprotein (VASP), which reorganize the actin cytoskeleton to promote cell migration and invasion. In colon cancer, cAMP- and cGMP-dependent VASP phosphorylation at Ser157 (pVASP-Ser157) and Ser239 (pVASP-Ser239) represent opposing molecular switches, which regulate the invasive cell shape. Here, pVASP-Ser157 and pVASP-Ser239 differentially affected the metastatic potential of colon cancer cells, including tumor proliferation, colony formation, migration, adhesion and metastasis in vivo. Investigations employed intestinal cancer cells, human tumor cells expressing serine phosphoresistant VASP mutants, cGMP or cAMP analogs, agonists selectively elevating intracellular cGMP or cAMP levels, and orthotopic mouse models of colorectal cancer. Collectively, results demonstrated pVASP-Ser239 suppresses, while pVASP-Ser157 promoted, the metastatic phenotype of colon cancer cells. Thus, differential VASP serine phosphorylation is a novel targeted strategy to prevent colon cancer metastasis. Clinical translation of these findings may provide original therapeutic interventions to reduce mortality in patients with colon cancer. 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 1653. doi:10.1158/1538-7445.AM2011-1653
Water‐Borne Endovascular Embolics Inspired by the Undersea Adhesive of Marine Sandcastle Worms
Authors: Joshua P. Jones, Monika Sima, Ryan G. O'Hara, Russell J. Stewart
Journal: Advanced Healthcare Materials (2016)

Transcatheter embolization is used to treat vascular malformations and defects, to control bleeding, and to selectively block blood supply to tissues. Liquid embolics are used for small vessel embolization that require distal penetration. Current liquid embolic agents have serious drawbacks, mostly centered around poor handling characteristics and toxicity. In this work, a water-borne in situ setting liquid embolic agent is described that is based on electrostatically condensed, oppositely charged polyelectrolytes-complex coacervates. At high ionic strengths, the embolic coacervates are injectable fluids that can be delivered through long narrow microcatheters. At physiological ionic strength, the embolic coacervates transition into a nonflowing solid morphology. Transcatheter embolization of rabbit renal arteries demonstrated capillary level penetration, homogeneous occlusion, and 100% devascularization of the kidney, without the embolic crossing into venous circulation. The benign water-borne composition and setting mechanism avoids many of the problems of current liquid embolics, and provides precise temporal and spatial control during endovascular embolization.
Comparison of Administration of Recombinant Human Thyrotropin with Withdrawal of Thyroid Hormone for Radioactive Iodine Scanning in Patients with Thyroid Carcinoma
Authors: Paul W. Ladenson, Lewis E. Braverman, Ernest L. Mazzaferri, Françoise Brucker-Davis, David S. Cooper, Jeffrey R. Garber, Fredric E. Wondisford, Terry F. Davies, Leslie J. DeGroot, Gilbert H. Daniels, Douglas S. Ross, Bruce D. Weintraub, Ian D. Hay, Silvina Levis, James C. Reynolds, Jacob Robbins, David V. Becker, Ralph R. Cavalieri, Harry R. Maxon, Kevin McEllin, Richard Moscicki
Journal: New England Journal of Medicine (1997)

To detect recurrent disease in patients who have had differentiated thyroid cancer, periodic withdrawal of thyroid hormone therapy may be required to raise serum thyrotropin concentrations to stimulate thyroid tissue so that radioiodine (iodine-131) scanning can be performed. However, withdrawal of thyroid hormone therapy causes hypothyroidism. Administration of recombinant human thyrotropin stimulates thyroid tissue without requiring the discontinuation of thyroid hormone therapy.
Abstract 5323: Fractalkine receptor CX3CR1 regulates peritoneal dissemination of ovarian carcinoma
Authors: Maria V. Barbolina, Jia Xie, Joanna E. Burdette
Journal: Cancer Research (2012)

Abstract Epithelial ovarian carcinoma (EOC) is the deadliest gynecologic malignancy largely due to the metastatic disease. EOC metastases spread by shedding the malignant cells off of the ovarian surface and seeding tissues and organs of the peritoneal cavity. Currently used therapies, a combination of chemotherapy and surgery, fail to keep most patients in the remission. Mechanistic understanding of the biology of EOC metastasis will facilitate development of new therapeutic approaches. Our previous data demonstrated that fractalkine receptor (CX3CR1) is expressed by EOC cells and can support cell migration and proliferation. Moreover, our previous data suggested that CX3CR1-positive EOC cells can adhere to the CX3CL1-postive peritoneal mesothelial cells in in vitro assay. Thus, we hypothesized that CX3CL1/CX3CR1 axis could be important for peritoneal dissemination of metastatic EOC. To test this hypothesis, we performed short-term ex vivo and in vivo adhesion assay, as well as long-term metastasis formation assay. Expression of CX3CR1 in EOC cells was downregulated in SKOV-3 using shRNA. Both CX3CR1 shRNA-expressing and scrambled shRNA-expressing EOC cells were seeded atop of mouse peritoneum and omentum tissues in the ex vivo assay and allowed to adhere for up to 24 h. CX3CR1 shRNA-expressing and scrambled shRNA-expressing EOC cells were intraperitoneally injected into abdomens of athymic nude mice for 4 h following sacrifice of the animals and examination of the peritoneal organs and tissues for green fluorescence. Data analysis has demonstrated that downregulation of CX3CR1 in EOC cells led to a significant decrease of adhesion in these assays. Furthermore, parental SKOV-3 as well as CX3CR1 shRNA-, scrambled shRNA-, and vector shRNA-expressing cells were intraperitoneally injected into athymic nude mice and allowed to form metastasis for 10 weeks. As a result, we observed very small omental metastatic lesions in three out of six animals injected with CX3CR1 shRNA-expressing cells. In opposite, all of the control groups developed gross intraperitoneal metastasis in many organs and tissues. Our data suggest that CX3CR1 may be one of the key factors that determine peritoneal dissemination of EOC. 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 5323. doi:1538-7445.AM2012-5323
Epstein-Barr virus latent and replicative gene expression in post-transplant lymphoproliferative disorders and AIDS-related non-Hodgkin's lymphomas
Authors: D. Rea, H.-J. Delecluse, S.J. Hamilton-Dutoit, L. Marelle, I. Joab, L. Edelman, J.-F. Finet, M. Raphael
Journal: Annals of Oncology (1994)