tbuckley/cabot-search huggingface dataset:
RENDIMIENTO DE LA COLONOSCOPIA CORTA URGENTE EN PACIENTES CON ENFERMEDAD INFLAMATORIA INTESTINAL EN NUESTRA EXPERIENCIA
Authors: K Spicakova, P Ramirez De La Piscina Urraca, S Estrada Oncis, I Duca Duca, R Calderon Ramirez, L Urtasun Arlegui, I Ganchegui Aguirre, M Salvador Perez, C Marra-López, F García Campos
Journal: Endoscopy (2013)

Introducción: La endoscopia digestiva es una herramienta fundamental para el diagnóstico y manejo terapéutico de la Enfermedad Inflamatoria Intestinal (EII). Su disponibilidad inmediata en nuestra unidad ante la sospecha de debut o un brote de EII, nos permite en muchos casos un control ambulatorio, evitando complicaciones y hospitalizaciones. Objetivo: Analizar el rendimiento de las colonoscopias cortas urgentes en el manejo diagnóstico y terapéutico de la EII. Material y Método: Estudio abierto basado en el registro de colonoscopias cortas urgentes sin preparación, realizadas en menos de 24h desde la valoración en nuestra unidad de EII, desde enero de 2011 hasta enero 2013, en pacientes al debut o con diagnóstico previo de EII. Se realizaron en total 60 exploraciones: 48 (80%) presentaba diagnóstico previo de colitis ulcerosa (CU), 4 (6.6%) enfermedad de Crohn (EC) y 8 (13.3%) no tenían diagnóstico previo de EII, presentando siete de ellos CU y uno EC. Resultados: De los 60 pacientes estudiados, el 35% presentaba brote leve, 56.3% moderado y el 8.7% severo, según los índices endoscópicos (CDEIS y Mayo). Según los resultados endoscópicos se modificó la actitud terapéutica en el 36% de los pacientes. El 40% de los pacientes con brote endoscópico leve-moderado no precisó ingreso, presentando buena evolución con ajuste de tratamiento ambulatorio. En todos los pacientes con sospecha de debut de EII con afectación colónica se confirmó el diagnosticó mediante la colonoscopia corta permitiendo iniciar precozmente el tratamiento. Conclusiones: La colonoscopia corta/sigmoidoscopia urgente es fundamental y puede ser decisiva para el diagnóstico y tratamiento de EII, teniendo mayor rentabilidad en CU. Es imprescindible contar con una consulta de EII abierta y con la cooperación del Servicio de Endoscopias que permite una atención rápida del paciente, tratando de minimizar errores, reducir los ingresos y en consecuencia los gastos hospitalarios.
Relation between Levels of Plasma Thromboplastin Component (PTC) and Prothrombin Times by the P&amp;P and Quick Methods in Patients Receiving Warfarin
Authors: Samuel I. Rapaport, Sara B. Ames
Journal: New England Journal of Medicine (1962)

THE coumarin anticoagulants depress the synthesis of four clotting factors: prothrombin; proconvertin (factor VII); Stuart factor (factor X); and plasma thromboplastin component, or PTC (factor IX). Prothrombin times essentially measure an overall effect of the reduced plasma concentration of the first three of these factors. When prothrombin times are used to regulate anticoagulant therapy, one assumes that the level of the unmeasured factor, PTC, does not fall appreciably below the levels of the measured factors.This assumption has been questioned: a disproportionate fall in PTC has been suggested as a possible cause of hemorrhage in patients with prothrombin times within . . .
Abstract 551: Protein biomarkers of human prostate cancer stromal cells
Authors: Zahraa I. Khamis, Kenneth A. Iczkowski, Qing-Xiang Amy Sang
Journal: Cancer Research (2010)

Abstract In situ human prostate tumors are not lethal unless they become invasive and metastatic. For cells to become invasive, the prostate gland must undergo disruption of the basal cell layer and degradation of the basement membrane underneath the luminal epithelial cell layer. Although the roles of proteinases in breaking down the basement membrane have been well-studied, little is known about the factors that induce basal cell layer disruption, degeneration, and its eventual disappearance in invasive cancer. It is hypothesized that microenvironmental factors may affect the degradation of the basal cell layer which if protected may prevent tumor progression and invasion. In this study, we have revealed differential protein expression patterns between cells separated from different prostate pathologies and identified several important stromal proteins that may contribute to inflammation and malignant transformation of benign prostate tissues to cancerous tissues using mass spectrometry and proteomics methods. The identifications of these proteins may generate new strategies for the prevention of basal cell layer disruption leading to the eventual blockade of invasive prostate carcinomas. Furthermore, human matrix metalloproteinase-26/endometase/matrilysin-2 was also investigated and its expression in preinvasive human prostate cancer cells may be associated with the expression of some apoptotic markers. This work may contribute to our understanding of epithelial-stromal interaction in the progression of human prostate cancer. (This work was supported in part by grants DAMD17-02-1-0238 and W81XWH-07-1-0225 from DOD, US Congressionally Directed Medical Research Programs, a grant from the Elsa U. Pardee Foundation, and grants from Florida State University to Dr. Q.-X. Sang) 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 551.
CORRELACIÓN DEL GRADO DE DIFICULTAD DE LA CPRE CON LAS COMPLICACIONES POSTERIORES: ANALISIS DE LA UTILIDAD DE LA GRADUACIÓN ASGE
Authors: JJ Vila, M Basterra, M Gómez, J Rodríguez, M Kutz, C Prieto, F Bolado, J Urman, I Fernández-Urién, FJ Jiménez
Journal: Endoscopy (2011)

Introducción: La ASGE publicó una graduación de dificultad prevista por indicación de CPRE (grados I-IV) para valorar riesgo de fracaso y si se debe asumir la CPRE.
Abstract 5036: MicroRNA expression profiling potential for human breast cancer diagnosis using a bead-based microRNA-specific capturing method
Authors: Kathy Tran, Tom Xu, Junko Stevens
Journal: Cancer Research (2012)

Abstract MicroRNAs (miRNAs), a family of small, endogenous, non-coding (∼17-24 nucleotides) nucleic acids, were initially discovered in 1993, but the discovery of a second miRNA led to their use as molecular markers of disease and potential therapeutic targets. MiRNAs regulate RNA translation, play a role in cell proliferation, control timing of organism development, and are associated with carcinogenesis. Because of their regulatory function in cell differentiation and renewal during physiologic and malignant conditions, miRNAs are emerging as a new class of effective biomarkers for cancer research. The miRNA expression profiling of tumor cells will allow for the identification of prognostic markers to indicate potential targets for patient- or disease-specific therapies. Three criteria important for profiling miRNAs are ease of use, simplicity and sensitivity. We have designed and developed a new method to quickly extract and purify specific miRNAs for detection using our current reverse transcription and real-time quantitative PCR workflows. The method involved 1μm-diameter magnetic beads conjugated with anti-miRNA oligoncleotides to capture these select miRNA targets from blood, plasma, and other tissues. The miRNAs were then transcribed into cDNA and subsequently used as templates for TaqMan® qRT-PCR analysis. We used this method to evaluate the miRNA signatures from normal and cancerous human breast modeled by cell lines and represented by formalin-fixed, paraffin-embedded tissues. 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 5036. doi:1538-7445.AM2012-5036
Abstract 2095: Tunicamycin inhibits triple negative breast cancer progression
Authors: Aditi Banerjee, Elizabeth Duran, Javier A. Couto, Zhenbo Zhang, Lydia A. Espinoza, Sushanta K. Banerjee, Krishna Baksi, Dipak K. Banerjee
Journal: Cancer Research (2011)

Abstract Triple negative (ER−/PR−/EGFR−) breast cancer accounts for 15% of all breast cancers. A large percentage of them are African and African-American women who are premenopausal. Histologically, the cancers are poorly differentiated, and most fall into the basal subgroup of breast cancers. Because of the absence of specific treatment guidelines, these patients are managed with standard treatment which leaves them associated with a high rate of local and systemic relapse. Angiogenesis is crucial for breast tumor growth and progression. Our laboratory has recently established that Tunicamycin (TM; an antibiotic and a glucosamine-containing pyrimidine nucleoside) interferes with the dynamic relationship between asparagine-linked (N-linked) glycosylation and angiogenesis. As a result, the xenograft developed in athymic nude mice [Balb/c (nu/nu)] with human breast cancer cell line MDA-MB-231 is reduced ∼65% in one week when Tunicamycin was given orally (0.25 mg/Kg) twice per week. To understand if it is due to a direct effect of Tunicamycin on the tumor microvsculature or a nutritional deprivation of the tumor cells due to insufficient blood flow, we have studied the effect of Tunicamycin on MDA-MB-231 breast cancer cells. When titrated with Tunicamycin (0.1 µg/ml, 1.0 µg/ml and 10.0 µg/ml) for seven days, the cell growth was inhibited almost quantitatively at all concentrations and as a function of time. In addition, no colony was formed at 1 µg/ml of Tunicamycin, the concentration used in all our experiments. Protein expression by western blotting and the gene expression by qRT-PCR indicated down-regulation of cyclin D1, and up-regulation of wild type p53, phopspho p53(ser 392), Bcl-2 and caspase-3 with no changes in the cdk-4 expression. These results strongly supported cell cycle arrest in G1 followed by the induction of apoptosis. Our recent study has demonstrated that Tunicamycin induces ER stress and consequently the apoptosis by unfolded protein response (upr) in breast tumor microvasculature. When examined, the MDA-MB-231 cells expressed high levels of GRP-78 as well as phospho PERK, a translational attenuator. Thus, we conclude that the MDA-MB-231 breast cancer cells experienced upr-mediated apoptotic death in the presence of Tunicamycin and strongly supported Tunicamycin's potential for a glycotherapeutic for treating a triple negative breast cancer in the clinic. Supported in part by grants from Susan G. Komen for the Cure (BCTR06582) and NIH/NCRR/RCMI G12-RR03035 (KB). 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 2095. doi:10.1158/1538-7445.AM2011-2095
A rare case of double primary cancer of the colon with parotid gland metastasis
Authors: S. Kim, J. Seong, H. Jeong, K. Kim, I. Jeong, K. Ko, H. Moon, D. Kang
Journal: Endoscopy (2012)

The major modes of spread for colon cancer are local invasion and lymphatic and hematogenous metastasis, with the liver being the most common site of metastasis, followed by the peritoneum, omentum, lung, and mesentery. Parotid gland involvement by adenocarcinoma of the colon is extremely rare. We report here a patient who developed a mass in the right neck due to a metastasis from a double primary adenocarcinoma of the colon.
Postoperative Potassium Deficit and Metabolic Alkalosis
Authors: Leonard P. Eliel, Olof H. Pearson, Rulon W. Rawson
Journal: New England Journal of Medicine (1950)

POSTOPERATIVE apathy, lethargy, anorexia, weakness, abdominal distention and hypochloremia constitute a syndrome that has been described by such terms as "pancreatic asthenia"1 and "la maladie post-opératoire."2 It has been noted that these poorly understood symptoms, together with hypochloremia and alkalosis, develop in certain patients after major surgical operations in spite of the administration of glucose solutions and adequate or massive amounts of sodium chloride.3 , 4 Both symptoms and electrolyte changes were observed to improve, however, as soon as these patients began to eat. Whipple5 has reported unexplained deaths following surgery of the biliary tract and pancreas in patients who showed marked . . .
Influence of cigarette smoking on cardiac biomarkers: the Atherosclerosis Risk in Communities (<scp>ARIC</scp>) Study
Authors: Wilson Nadruz, Alexandra Gonçalves, Brian Claggett, Gabriela Querejeta Roca, Amil M. Shah, Susan Cheng, Gerardo Heiss, Christie M. Ballantyne, Scott D. Solomon
Journal: European Journal of Heart Failure (2016)
NI-21 * CONTRAST ENHANCED T1 SUBTRACTION MAPS IMPROVE DETECTION OF RESIDUAL TUMOR FOLLOWING RESECTION, REDUCES MEASUREMENT VARIABILITY, AND PREDICTS SURVIVAL AFTER ANTI-ANGIOGENIC THERAPY IN GLIOBLASTOMA
Authors: B. Ellingson, G. Kim, D. Woodworth, W. Pope, P. Nghiemphu, A. Lai, T. Cloughesy
Journal: Neuro-Oncology (2014)

BACKGROUND: Estimation of contrast enhancing tumor burden on contrast-enhanced post-contrast T1-weighted images (CE-MRI) has significant limitations due to T1 shortening from blood products or gliosis and T1 lengthening from changes in extracellular fluid concentration. As a consequence, estimation of residual tumor burden after surgical resection is often inaccurate, measurements of tumor volume vary significantly across readers, and tumor burden after anti-angiogenic therapies is often undetected. We hypothesize that contrast-enhanced T1 subtraction maps can be used to improve detection of residual tumor following surgery or anti-angiogenic therapy, reduce measurement variability, and predict response and survival. METHODS: The extent of resection was evaluated in 80 GBM patients using traditional CE-MRI and T1 subtraction after surgical resection by radiologists, imaging scientists, and neuro-oncologists. To assess measurement variability, enhancing tumor volumes were evaluated in 20 randomly-selected GBM patients before and after anti-angiogenic therapy by 3 imaging scientists in 3 multicenter trials. Lastly, response evaluation was performed using CE-MRI and T1 subtraction in a single center cohort : The extent of resection was changed from GTR to STR for almost all patients and all reviewers when comparing CE-MRI to T1 subtraction maps. Additionally, the confidence in this determination was significantly improved (t-test, P < 0.01). The coefficient of variability (COV) was significantly reduced when using T1 subtraction to define lesion volumes in all settings (paired t-test, P < 0.01), with the largest improvement after anti-angiogenic therapy. Volumetric response on T1 subtraction maps after bevacizumab predicted PFS and OS in both single-center and multicenter trials (Cox regression, P < 0.05). CONCLUSION: T1 subtraction maps improve measurement accuracy and confidence of contrast enhancing tumor burden and should be used for determining extent of resection and response to therapy.
FRI0083 Predictors for the discrepancy between patient’s and evaluator’s global assessment in rheumatoid arthritis: kurama cohort study
Authors: M. Furu, M. Hashimoto, H. Ito, T. Fujii, C. Terao, S. Matsuda, T. Mimori
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The Boolean based ACR/EULAR remission criterion is stricter than indexes based criteria. It is difficult to achieve the patient’s global assessment (PGA) as the reason. We often observe the discrepancy between the PGA and the evaluator’s global assessment (EGA) in clinical. <h3>Objectives</h3> The purpose of this study is to investigate a reason of the discrepancy between the PGA and the EGA in Kyoto University Rheumatoid Arthritis Management Alliance (KURAMA) cohort. <h3>Methods</h3> We chose the 370 of RA patients in our clinical cohort and assessed swollen joint count (SJC), tender joint count (TJC), CRP, ESR, PGA, EGA, pain score, stage, class, duration of RA, and health assessment questionnaire (HAQ). We analyzed the frequency of remission by the new ACR/EULAR remission criteria, and predictors of the discrepancy between the PGA and the EGA. <h3>Results</h3> SDAS, CDAI and the Boolean based remission are achieved in 25.1%, 25.1%, and 17.3% of patients, respectively. As for fulfilling criterion in each component, SJC were 68.4%, TJC 71.6%, PGA 24.1% and CRP 83.5%. The average of PGA minus EGA (PGA-EGA) was 18mm. The PGA had correlation with pain score (r=0.84, p&lt;0.0001), class (r=0.59, p&lt;0.0001), HAQ (r=0.54, p&lt;0.0001) and SJC(r=0.35, p&lt;0.0001). The EGA had correlation with SJC (r=0.72, p&lt;0.0001), TJC (r=0.64, p&lt;0.0001), CRP (r=0.41, p&lt;0.0001), PGA (r=0.39, p&lt;0.0001), ESR (r=0.38, p&lt;0.0001) and HAQ (r=0.38, p&lt;0.0001). The PGA-EGA had correlation with pain score (r=0.81, p&lt;0.0001), class (r=0.41, p&lt;0.0001), HAQ (r=0.32, p&lt;0.0001) and SJC (r=-0.18, p=0.0005). The main predictors for the PGA-EGA were class (p=0.002), pain score (p&lt;0.0001), TJC (p&lt;0.0001) and SJC (p&lt;0.0001). <h3>Conclusions</h3> The Boolean based remission criterion is strictest because it was difficult to achieve PGA in our clinical cohort. The most significant predictors for the discrepancy between the PGA and the EGA were pain, functional disability, TJC and SJC. Increased pain and functional disability led to discrepancy toward worse PGA, while increased TJC and SJC led to accordance toward worse EGA. Understanding the reasons for this discrepancy may help to facilitate management of RA. <h3>Disclosure of Interest</h3> None Declared
Abstract LB-93: Calculating the statistical significance of synergy in cancer drug combinations.
Authors: Erin Sult, Wei Zhao, Harry Yang, Robert Hollingsworth, Kris F. Sachsenmeier
Journal: Cancer Research (2013)

Abstract Single agent treatment in cancer often results in drug resistance and limited survival. Multi-drug treatment may overcome resistance to monotherapies given the heterogeneous nature of tumors. This may result in improved survival, increased efficacy and lower toxicity. Bliss Independence and Loewes Additivity are widely accepted methods for evaluating synergy with drug combinations, however these applications typically lack statistical significance. We have developed a novel Response-Surface (RS) method that enables us to identify statistically significant synergy at a 95% confidence level. In this presentation, the RS method will be described, compared to traditional methods, and applied to dual-drug combinations across various cancer cell models. Citation Format: Erin Sult, Wei Zhao, Harry Yang, Robert Hollingsworth, Kris F. Sachsenmeier. Calculating the statistical significance of synergy in cancer drug combinations. [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 LB-93. doi:10.1158/1538-7445.AM2013-LB-93
P3-10-01: Alternative Dosing Regimens with the EGFr Inhibitors (Gefitinib and Lapatinib) in Mammary Cancer Models: Prevention and Therapeutic Efficacy.
Authors: RA Lubet, AM Bode, E Szabo, CJ Grubbs
Journal: Cancer Research (2011)

Abstract The EGFR inhibitors are effective in treatment of lung and pancreatic cancers (erlotinib, gefitinib) and Neu overexpressing breast cancer (lapatinib) in humans; as well as preventing multiple cancers in animal models. However, the development of toxicities (Iressa, skin rashes; Lapatinib, diarrhea) limit their potential use in prevention; and perhaps even in an adjuvant setting. We examined whether alternative dosing regimens which might reduce toxicity would still achieve preventive and therapeutic efficacy. Female Sprague-Dawley rats were administered a single IV dose of methylnitrosourea (MNU) at 50 days of age. In a prevention study, MNU treated rats administered Gefitinib daily (10 mg/kg BW/day, 7x/week) or Gefitinib (70 mg/kg BW, 1x/week) beginning 5 days after MNU resulted in 94 and 75% reductions, respectively, in cancer multiplicity. Simultaneous measurements of tumor load (number of tumors x tumor weight) showed that both regimens resulted in greater than a 90% decrease. In the therapeutic study (initiating treatment when animals developed a small palpable cancer), both regimens were again highly effective. A prevention study was also performed with Lapatinib (75 mg/kg BW/day, 7x/week or 525 mg/kg BW, 1x/week). While the daily dose reduced cancer multiplicity 90%, the weekly dose caused a 70% reduction. Finally, we examined the effects of daily or weekly dosing with Iressa (100 mg/kg BW/day, 5x/week or 500 or 250 mg/kg BW, 1x/week) in an ER− mouse model (using MMTV-Neu; p53+/− mice). This study showed that while daily dosing with Iressa decreased tumor multiplicity roughly 80%, weekly dosing at either dose caused roughly a 50% decrease. These data show that even a significant alteration in the dosing of Gefitinib (EGFR 1) or Lapatinib (EGFR 2/1) still resulted in a large reduction in mammary cancers. The important clinical question will be whether this altered dosing will diminish the toxicities associated with these agents. We cannot determine this in animal models since, at the effective doses employed, the typical toxicities observed in humans are not observed. Supported by NCI contract number HHSN261200433001C. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-10-01.
Abstract 774: <i>RECK</i> silencing enhances hyperplastic phenotypes in epithelial cells through c-Myc and HIF-2α.
Authors: You Mie Lee, Keun Byeol Lee, Sun Hee Lee, Nguyen Minh Phuong
Journal: Cancer Research (2013)

Abstract Downregulation of the tumor suppressor, RECK is induced by hypoxia (Lee et al., 2010). However, the role of RECK silencing in tumorigenic hyperplastic phenotype is largely unknown. Exposure of various normal epithelial cells to hypoxia resulted in significantly increased cell proliferation. Hypoxia increased diploid S phase cells, cell cycle kinase proteins such as cyclin D1 and c-Myc involved in G1/S transition. Hypoxia promoted phosphorylation of Rb protein (p-pRb), but decreased p21cip1, p27kip1 and p16ink4A. The knockdown of RECK by small interfering (si) RNA (RECKsi) promoted cell proliferation under normoxic conditions. Furthermore, siRECK produced the same expression patterns of cell cycle kinase proteins, c-Myc, and p-pRb observed under hypoxic conditions. MMP-2, MMP-9, and MT1-MMP were activated by hypoxia, and an MMP inhibitor significantly suppressed hypoxia-induced proliferation. In addition, the siRECK-transfected cells formed larger and more numerous colonies than the control cells in vitro tumorigenic assays. Nude mice injected with stably shRECK-transfected cells developed larger tumors more rapidly than those injected with control shRNA-transfected cells. Expression of HIF-2α as well as NFκB and STAT1 was significantly increased both under hypoxic conditions and in RECK-knockdown cells. Knockdown of HIF-2α diminished hypoxia-induced proliferation of epithelial cells. Taken together, these results suggest that hypoxia-induced RECK silencing increases epithelial transformation and tumorigenicity via HIF-2α activation, in which increased metalloproteinase activity may play a role. In conclusion, the suppression of RECK may be a crucial event for achieving a hyperplastic characteristics to favor early tumorigenesis by hypoxic stress. Citation Format: You Mie Lee, Keun Byeol Lee, Sun Hee Lee, Nguyen Minh Phuong. RECK silencing enhances hyperplastic phenotypes in epithelial cells through c-Myc and HIF-2α. [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 774. doi:10.1158/1538-7445.AM2013-774