tbuckley/cabot-search huggingface dataset:
Abstract 196: UHRF1 is upregulated in prostate cancer and induces epigenetic silencing of tumor suppressor genes
Authors: Paolo Kunderfranco, Laura Curti, Federica Babbio, Christian Pistore, Marco Magistri, Giovanna Chiorino, Ian Marc Bonapace, Carlo V. Catapano, Giuseppina M. Carbone
Journal: Cancer Research (2010)

Abstract Cancer of the prostate is the most common cancer and a leading cause of cancer death in Europe and North America. At the present there is a need to understand the mechanisms involved in the pathogenesis of this disease and discover alternative therapeutic targets. UHRF1 (ubiquitin-like protein containing PHD and RING domains 1), a nuclear RING finger protein, has been previously reported to acts as a dominant negative effectors of cell growth. UHRF1 is involved in epigenetic mechanisms by virtue of its interaction with DNMTs and HMTs. In this study, analysis of gene expression profiles of prostate tumors and normal prostate showed that UHRF1 is frequently over-expressed in tumors compared to normal tissues. UHRF1 expression was very low in immortalized prostate epithelial cells (LH) while it was higher in the Ras transformed counterpart LHSR cells. Furthermore, we observed low level of UHRF1 in the androgen-dependent prostate cancer cell lines LNCaP and 22Rv1, while higher levels were present in the androgen-independent cell lines PC3 and DU145. These data suggested that over-expression of UHRF1 is associated with malignant transformation and prostate cancer progression. To understand the role of UHRF1 we performed knockdown experiments with UHRF1 specific siRNA. Transient transfection in PC3 cells reduced UHRF1 mRNA and protein level. UHRF1 knock-down resulted in reversion of the transformed phenotype with significant inhibition of clonogenic growth in anchorage dependent and independent condition. Reversion of the transformed phenotype occurred concomitantly with restoration of the expression of several tumor suppressor genes relevant for prostate differentiation, proliferation and epithelial-mesenchymal transition such as CDH1 and RARB2. Moreover, chromatin immunoprecipitation showed binding of UHRF1 to these gene promoter and UHRF1 knockdown resulted in significant reduction of repressive histone marks on gene promoters. These studies suggest that deregulated UHRF1 expression results in epigenetic silencing of relevant tumor suppressor genes, contributing to prostate cancer progression. Targeting UHRF1 may result in re-expression of tumor suppressor genes and thus may be a valid strategy for therapeutic intervention. 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 196.
TCT-198 Retrograde Recanalization Of Chronic Total Occlusions In Europe: Procedural And In-Hospital Outcomes From The Multicenter ERCTO Registry
Authors: Alfredo R. Galassi, Georgios Sianos, Gerald S. Werner, Javier Escaned, Francesco Marzà, Marouane Boukhris, Salvatore D. Tomasello, Carlo Di Mario
Journal: Journal of the American College of Cardiology (2014)
TEMPORAL TRENDS IN CARDIAC REHABILITATION REFERRAL AMONG PATIENTS HOSPITALIZED WITH HEART FAILURE: ANALYSIS FROM AMERICAN HEART ASSOCIATION GET WITH THE GUIDELINES-HEART FAILURE REGISTRY
Authors: Harsh Golwala, Ambarish Pandey, Christine Ju, Javed Butler, Clyde Yancy, Deepak Bhatt, Adrian Hernandez, Gregg Fonarow
Journal: Journal of the American College of Cardiology (2015)
PTU-167 The role of proton pump inhibitors in patients with Barrett's oesophagus following laparoscopic fundoplication can only be determined after the level of residual reflux has been quantified
Authors: A Bond, D Wilson, A Hastings, F Rowley, D Veeramootoo, K K Singh
Journal: Gut (2012)

<h3>Introduction</h3> Laparoscopic fundoplication is carried out for pathological Gastro Oesophageal Reflux in patients with and without Barrett9s oesophagus. It has been suggested that in patients with Barrett9s, only those patients with no physiological evidence of reflux post surgery have any reduction in risk of transition to cancer. The aim of this study is to quantify and compare residual reflux post fundoplication in patients with and without Barrett9s Oesophagus. <h3>Methods</h3> Data were collated from January 2002 to December 2011, using the hospital coding database for a single consultant surgeon. Each case was studied for patient demographics, indication, operative findings and outcomes. Prospectively collected data on pre and post operative pH manometry was assessed for evidence of reflux. Total percentage time less than pH 4 was used to determine reflux and a paired t-test was used to compare reflux between the groups. <h3>Results</h3> 78 patients had a Nissen Fundoplication, 32 with Barrett9s oesophagus. There was no significant difference between age and sex of the Barrett9s and non Barrett9s groups. There is seen to be a significant difference in reflux between the pre operative groups (p=0.0227) when looking at reflux, but a very significant difference (p=0.0038) when comparing reflux postoperatively between those with and those without Barrett9s. <h3>Conclusion</h3> There is a significantly higher level of residual reflux in patients with Barretts oesophagus following fundoplication even when patients report no symptoms. Therefore those with Barrett9s should continue with Proton Pump Inhibitors until there is confirmed evidence of no reflux. <h3>Competing interests</h3> None declared.
Health Promotion and the State
Authors: Meredith B. Rosenthal, Thomas Farley, Steven Gortmaker, Cass R. Sunstein
Journal: New England Journal of Medicine (2013)

Policymakers at all levels of government are searching for ways to promote wellness and reduce unhealthy behaviors without overstepping or infringing on personal liberties. Thomas Farley, Steven Gortmaker, and Cass Sunstein address these issues in a roundtable discussion moderated by Meredith Rosenthal.
LIPID LOWERING INTENSITY AT DISCHARGE AFTER ACUTE MYOCARDIAL INFARCTION: TEMPORAL CHANGES AND IMPACT ON 3 YEAR MORTALITY. RESULTS FROM THE FAST-MI 2005 AND FAST-MI 2010 REGISTRIES
Authors: Francois Schiele, Jean Ferrieres, Nicolas Meneveau, Etienne Puymirat, Pierre Coste, Nicolas Delarche, Marion Chatot, Fiona Ecarnot, Tabassome Simon, Nicolas Danchin
Journal: Journal of the American College of Cardiology (2016)
Abstract 1592: Silibinin inhibits UVB-induced DNA-damage and apoptosis by enhancing interleukin-12 expression in JB6 cells and SKH-1 mouse skin
Authors: Sreekanth C. Narayanapillai, Mallikarjuna Gu, Chapla Agarwal, Rajesh Agarwal
Journal: Cancer Research (2012)

Abstract Ultraviolet-B (UVB) radiation plays a pivotal role in non-melanoma human skin cancers (NMSCs) by inducing cellular DNA damage, mutations and immunosuppression. Decades of research has demonstrated silibinin efficacy against UVB-induced skin carcinogenesis by regulating different molecular pathways in various cell lines and animal models; however, the role of silibinin in regulating interleukin-12 (IL-12), an immunomodulatory cytokine with the capacity to reduce UVB-induced DNA damage and apoptosis, has not been studied. Here, we report that UVB irradiation caused a dose- and time-dependent caspase 3 and PARP cleavage as well as apoptosis in JB6 cells. Addition of recombinant IL-12 or silibinin immediately after UVB significantly protected UVB-induced apoptosis in JB6 cells, and antibody-mediated blocking of IL-12 activity compromised the protective effect of both IL-12 and silibinin. In addition, both silibinin and IL-12 accelerated the repair of UVB-caused cyclobutane-pyrimidine dimers (CPDs) in JB6 cells. Additional studies confirmed that indeed silibinin causes a significant increase in IL-12 levels in UVB-irradiated JB6 cells as well as in the SKH-1 hairless mouse epidermis, and that similar to in vitro findings, silibinin topical application immediately after UVB exposure causes a very strong protection against UVB-induced TUNEL positive cells in epidermis possibly through a significantly accelerated repair of UVB-caused CPDs in skin epidermis. Together, these findings for the first time identify an important insight regarding the pharmacological mechanism wherein silibinin induces endogenous IL-12 in its efficacy against UVB-caused skin damages. Considering the fact that millions of people get constantly exposed to solar UVB radiation and live with persistent UVB-induced DNA lesions, the post-damage use of silibinin as an inducer of endogenous IL-12 in UVB-damaged human skin for the rapid repair of DNA damage could be a more practical and translational approach in reducing sunlight-caused damages in human skin which eventually lead to NMSCs. 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 1592. doi:1538-7445.AM2012-1592
SAT0139 Gender Differences in the Choice of Coping Strategies for Patients with Rheumatoid Arthritis
Authors: E.V. Muslimova, S.P. Yakupova, E.Z. Yakupov, R.Z. Abdrakipov
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Strategies for dealing with chronic pain designed to overcome chronic pain syndrome and adapt patients to their condition. <h3>Objectives</h3> To study coping strategies (CS) in patients with rheumatoid arthritis (RA) with regard to their gender characteristics, to reveal interrelation between CS, DAS 28 and RA duration in female and male patients. <h3>Methods</h3> A cross-sectional survey included 82 patients with RA ( male to female ratio 4.5:1 (82% women), mean age 49,1±11,3 years, mean duration of RA disease ranged from 4 months to 41 years (Me 8 (3, 12)). RA diagnosis based on ACR criteria of 1987. Pain was recorded using a visual analog scale (VAS). Chronic Pain Coping Questionnaire was used in determing coping strategies. According with gender, patients were divided into 2 groups. Significance of independent variables differences determined by the Kolmogorov-Smirnov test, differences were considered significant at p&lt;0,05. For correlation analysis Spearman method was performed. <h3>Results</h3> There were no significant differences in VAS scores between male and female patients. Women were significantly more frequently used coping strategies than men (p&lt;0,05). Both groups preferred maladaptive strategies in case of pain syndrome. Gender differences emerged in the maladaptive strategies "protection" and "relaxation" and adaptive strategy "self-persuasion" (p&lt;0,05). The correlations between adaptive strategy "exercises" and DAS 28 (r=0,55, p=0,03), between duration of the disease and "self-persuasion" strategy (r=0,83, p=0,0001) were revealed on men. In case of female patients such correlations weren9t found. <h3>Conclusions</h3> Gender preferences in using different types of CS were detected. The findings may be used in individual gender approach in educating patients on how to deal with the chronic pain and decrease its activity. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5555
Significance of Fluid Levels in X-Ray Films of the Abdomen
Authors: John K. Donahue, Charles Hunter, Henry H. Balch
Journal: New England Journal of Medicine (1958)

AMONG many surgeons and radiologists it is an axiom that the appearance of fluid levels in the intestine on a roentgenogram of the abdomen is pathognomonic of intestinal obstruction.As long ago as 1911, Schwarz,1 of Vienna, described the presence of gaseous shadows in loops of distended bowel and indicated their significance in the diagnosis of acute obstruction. He advocated the administration of a small amount of a contrast medium for the production of fluid levels and suggested that the erect position of the patient be used in order that fluid levels might be demonstrated. Assmann,2 in 1913, reported 5 . . .
Abstract 5362: Mechanisms involved in hormone promoted growth of preneoplastic mammary lesions
Authors: Arunkumar Arumugam, Rajkumar Lakshmanaswamy
Journal: Cancer Research (2010)

Abstract Carcinogenesis is a complex process, which involves initiation, promotion and progression. Copenhagen strain of rat is a well known animal model which is resistant to carcinogen-induced mammary carcinogenesis. In our laboratory, we were able to induce a very high incidence of mammary cancers in these rats using combination of carcinogen N-methyl-N-nitrosourea (MNU), followed by estradiol and progesterone treatment. We have demonstrated that the resistance to mammary carcinogenesis in these rats is not due to inhibition of initiation but due to reduced hormone promotional environment and we further extend our research to investigate the molecular mechanisms involved behind this hormone-induced promotion. We used both in vivo and in vitro experimental system to understand the mechanisms involved in mammary cancer promotion and progression. Seven week old female Copenhagen rats were administered a single dose of MNU at a dose of 50 mg/kg body weight intraperitoneally. Four weeks post carcinogen administration, the rats were killed and preneoplastic lesions were excised and used for further in vitro experiments. The preneoplastic lesions were cultured and were treated with estradiol, progesterone or a combination of both hormones. Changes in survival and cell death pathways in the cultured preneoplastic lesions in response to different hormone treatments were analyzed using different molecular techniques. Our result indicates that hormone treatment induces alterations in cell survival and cell death pathways of the preneoplastic lesions demonstrating the significance of hormones in promotion and progression of breast cancer. 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 5362.
929 PHARMACOGENETICS OF AZATHIOPRINE IN AUTOIMMUNE HEPATITIS: RELATIONSHIP OF THIOPURINE METHYLTRANSFERASE AND INOSINE TRIPHOSPHATE PYROPHOSPHATE POLYMORPHISMS TO AZATHIOPRINE METABOLITE LEVELS AND TO ADVERSE EVENTS
Authors: H.K. Dhaliwal, E. McFarlane, D. Gleeson, L. Lennard
Journal: Journal of Hepatology (2013)
Abstract 2155: Inhibition of the ERK1/2 pathway by RanBPM
Authors: Elnaz Atabakhsh, Caroline Schild-Poulter
Journal: Cancer Research (2012)

Abstract Ran binding protein-M (RanBPM, also called RanBP9) is a nucleo-cytoplasmic protein that has been implicated in a multitude of cellular roles, including the regulation of transcription, protein modifications and stability, and extracellular receptor signaling pathways. However its function within the cell remains largely unknown. Previous studies in our lab have identified RanBPM as a pro-apoptotic protein that mediates its effects through modulation of Bcl-2 and Bcl-XL levels. Here we present evidence that RanBPM functions to regulate apoptotic activation through regulation of the ERK1/2 signaling pathway. First, we determined that siRNA-mediated knockdown of RanBPM expression led to elevated Bcl-2 and Bcl-XL mRNA expression, suggesting regulation by RanBPM at the transcriptional level. Additionally, expression of RanBPM affected ectopically expressed Bcl-2 protein levels. Together, these findings suggested that RanBPM regulated the expression of Bcl-2 and Bcl-XL at both the transcriptional and post-translational levels. The ERK1/2 signaling cascade has previously been shown to regulate the expression of Bcl-2 and Bcl-XL at both the transcriptional and post-translational levels. We found that that RanBPM-deficient cells exhibited enhanced ERK1/2 phosphorylation and activation, while re-expression of RanBPM led to a marked decrease in the levels of phosphorylated ERK1/2. Furthermore, enhanced ERK1/2 activation in RanBPM-deficient cells contributed to the elevated levels of Bcl-2 expression observed in these cells, as inhibition of ERK1/2 activation correlated with decreased Bcl-2 protein expression. We characterized regulation of ERK1/2 signaling by RanBPM, and identified that RanBPM targets this pathway downstream of Ras, through modulation of c-Raf stability. Our studies revealed that downregulation of RanBPM expression promotes phosphorylation and stabilization of c-Raf, leading to elevated c-Raf protein expression. Finally we observed that downregulation of RanBPM expression promotes cellular transformation, as RanBPM-deficient cells exhibit increased cell growth rates and enhanced cell migration. Together, these findings suggested that RanBPM acts as a novel inhibitor of ERK1/2 signaling, and that downregulation of RanBPM expression leads to oncogenic transformation. 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 2155. doi:1538-7445.AM2012-2155
Competing risk: a potential risk factor for misleading results of length of stent patency
Authors: T. Hamada, Y. Nakai, H. Isayama, T. Sasaki, K. Koike
Journal: Endoscopy (2012)

We read with great interest the article by Kim et al. [1] about a retrospective study evaluating the effects of chemotherapy on the patency of self-expandable metal stents (SEMS) for malignant outlet obstruction caused by gastric cancer. Kim et al.’s analysis showed that greater time-to-progression (TTP) and first-line chemotherapy were associated with significantly longer SEMS patency. Better local tumor control in patients with a better response to chemotherapy theoretically provides longer SEMS patency. However, these “reasonable” results regarding SEMS patency and its association with chemotherapy should be interpreted with caution due to the presence of competing risks.
Will Optimality Theory colonize all of higher cognition?
Authors: Tamás Biró
Journal: Behavioral and Brain Sciences (2010)

Abstract To establish Optimality Theory as a framework in anthropology, or as a general model of higher human cognition, researchers have to demonstrate OT is convincing in a number of ways. This commentary summarizes some of them – based on experience obtained in contemporary linguistic OT – including factorial typologies, exact formulation of candidate sets and constraints, and computational plausibility.
Inferior-Mesenteric-Artery Syndrome after Translumbar Aortography
Authors: Paul H. Guilfoil
Journal: New England Journal of Medicine (1963)

THE use of translumbar aortography is sufficiently widespread so that a considerable literature has appeared in which indications, technic and complications have been thoroughly discussed. It is generally recognized that the procedure is not innocuous and that major complications, and even death, may attend its use. The most common serious complications are either renal or neurologic in origin, and an occasional death has been reported after the injection of contrast material directly into the superior mesenteric artery.In a considerable experience with translumbar aortography, no complication similar to that described below had been encountered; for that reason the literature was . . .
Abstract 2417: Oncogenic properties shared by all Snail family members
Authors: Baptiste Gras, Christelle Chassot, Alain Puisieux, Stéphane Ansieau
Journal: Cancer Research (2012)

Abstract The epithelial to mesenchymal transition (EMT) is a latent embryonic process promoting cell migration by transiently affording epithelial cells a mesenchymal phenotype, motility and a survival advantage. The inappropriate activation of this program in adult cells is associated with several pathologies including tumor development where EMT promotes cancer cell dissemination and multidrug resistance development. We have recently demonstrated that EMT-inducers, beyond their prometastatic potential, facilitate the malignant transformation of human mammary epithelial cells in vitro and promote breast carcinogenesis in vivo. Although their ability to alleviate senescence and apoptosis failsafe program induction unquestionably contributes to their oncogenic potentials, we sought to investigate whether EMT inducers share additional properties. To this end, the activities of all three Snail members were examined. Likewise SNAI1 and SNAI2, SNAI3 expression is aberrantly activated in cancers, especially in mammary carcinomas. Ectopic expression of all three proteins in mammary epithelial cells induces their commitment into EMT, provides cells with a survival advantage in low adherent conditions and promotes their neoplastic transformation, with a similar gradient of efficiencies. Interestingly, this efficiency parallels with their ability to upregulate intracellular signaling pathways. We will update on the progress of our work aimed at understanding how these dysregulations impact on their oncogenic and prometastatic potential. 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 2417. doi:1538-7445.AM2012-2417
Antibiotic-associated hemorrhagic colitis with ischemic change
Authors: Koichiro Abe, Yu Kawashima, Hitoshi Aoyagi, Satoshi Kimura, Akari Isono, Tadahisa Ebato, Takatsugu Yamamoto, Hiroto Kita, Yasushi Kuyama
Journal: Endoscopy (2014)

A 67-year-old woman presented with abdominal pain and hematochezia. She had never used non-steroidal anti-inflammatory drugs, but had been started on amoxicillin, clarithromycin, and lansoprazole 3 days earlier as Helicobacter pylori eradication therapy. On admission, white blood cell count was 21 600/µL and C-reactive protein level was 2.8 mg/dL. Computed tomography showed thickening of the intestinal wall from the ascending to transverse colon ([Fig. 1]). No occlusion of the superior mesenteric artery was found.
Antibodies against Human Herpesvirus 8 in Black South African Patients with Cancer
Authors: Freddy Sitas, Henri Carrara, Valerie Beral, Rob Newton, Gillian Reeves, Diana Bull, Ute Jentsch, Rosana Pacella-Norman, Dimitra Bourboulia, Denise Whitby, Chris Boshoff, Moosa Patel, Paul Ruff, Werner R. Bezwoda, Edna Retter, Martin Hale, Robin Weiss
Journal: New England Journal of Medicine (1999)

Infection with human herpesvirus 8 (HHV-8) has been consistently linked to Kaposi's sarcoma, but its mode of transmission, association with other cancers, and interaction with the human immunodeficiency virus type 1 (HIV-1) are largely unknown.