tbuckley/cabot-search huggingface dataset:
Effect of Plasma Transfusions on the Prothrombin Time and Clotting Factors in Liver Disease
Authors: Israel Spector, Milton Corn, Howard E. Ticktin
Journal: New England Journal of Medicine (1966)

PATIENTS with liver disease have multiple coagulation defects. Although excessive fibrinolysis, thrombocytopenia, and deficiencies of factors IX (plasma thromboplastin component) and XI (plasma thromboplastin antecedent) may be present in these patients, the most consistent abnormality is a prolonged prothrombin time.1 2 3 This abnormal prothrombin time is usually due to combined deficiencies of factors II (prothrombin), V (proaccelerin), VII (proconvertin) and X (Stuart factor). Treatment for the correction of abnormal clotting mechanisms in patients with severe liver disease is limited. Epsilon aminocaproic acid, steroids and heparin are of value only in occasional patients who exhibit excessive fibrinolysis or disseminated intravascular coagulation.4 , 5 Improvement . . .
Pelvic Exenteration for Carcinoma of the Cervix
Authors: Francis M. Ingersoll, Howard Ulfelder
Journal: New England Journal of Medicine (1966)

Pelvic exenteration for carcinoma of the cervix uteri carries a 15 per cent operative mortality and a 23.3 per cent five-year survival. Total exenteration, not anterior exenteration or modified exenteration, is the operation of choice in the heavily irradiated patient. The criteria for operability are proof of persistence of disease, proof of no extension of disease beyond the pelvis, proof of freedom of disease at the lateral margins of resection and proof that pelvic-lymph-node metastases are minimal. Only 2 of 33 patients with positive pelvic lymph nodes survived for five years. Ileal-loop urinary diversion has been a major factor in diminishing the complications and deaths from this procedure.
P3-05-06: Progression of Breast Cancer Molecular Subtypes through Different Clinical Stages.
Authors: EM Ciruelos, CA Castaneda, E Andrés, HL Gomez, D Castellano, C Mendiola, L Manso, I Ghanem, C Farfan, H Cortes-Funes
Journal: Cancer Research (2011)

Abstract Purpose : Molecular classification of breast cancer (BC) through immunohistochemistry classifies patients globally in 4 subtypes with similar features and prognosis. The present study was designed to compare features of BC subtypes in early versus locally advanced clinical stages. A secondary objective was compare molecular subtypes of the primary vs recurrences. Methods : The study included 1621 patients with non-metastatic invasive BC that were consecutively diagnosed at Hospital Universitario 12 de Octubre, Madrid, between 1997 and 2007. Luminal A was defined as ER+ and PR+, HER2−negative and Ki67 &amp;lt; 14%. Luminal B was defined as PR-negative, HER2−positive or ki67≥14%. HER2 was defined as ER and PR-negative, and HER2−positive.Triple negative (TN) were tumors with ER, PR and HER2 -negativity. Clinicopathological characteristics and outcomes were retrospectively reviewed. Variables were compared with the X2 test, and survival curves were evaluated with Kaplan-Meier method. Results : Most patients were diagnosed as T1 (48%) and T2 (39.7%) clinical stages, and classified as Luminal B (49%) and Luminal A (29%). GIII frequency increased from T1 to T3-4 in Luminal A (p=0.002), and Luminal B (p=0.051) subtypes, but not in HER2 (p=0.867) or TN (p=0.53). Molecular subtypes carry significant different prognosis (DFS and OS) in all T stages except for T1a cases. When T3-4 and T1 stages of the same molecular subtype were compared, a significant shorter DFS were found for more advanced stages in the Luminal A (p=0.0002), Luminal B (0.0001) and TN (0.0017), but not for HER2 (p=0.54) subtype. And, similar results were found for OS. We compared molecular subtypes in the primary tumor and in the metastatic site in 83 cases (excluding contralateral recurrences) and found change of phenotype in 54% of the cases. Changes from Luminal A to a more aggressive phenotype were more frequent than in the opposite situation (14 vs 2 cases). Conclusion : Despite the molecular classification of early-stage BC that classifies patients in well-defined prognostic subgroups, tumors are continuously changing and tumor behavior becomes more aggressive through progression. Therefore, even tumors with favorable phenotype could loss their good prognosis in locally advanced stages. Obtention of tumor tissue at metastatic sites is also mandatory to a better selection of systemic therapies in relapsed patients. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-05-06.
638 3-NITRO-TYROSINE AS A PERIPHERAL BIOMARKER OF MINIMAL HEPATIC ENCEPHALOPATHY IN PATIENTS WITH LIVER CIRRHOSIS
Authors: O. González-López, A. Urios, O. Cauli, B. Piedrafita, F. Ordoño, C. Gimenez-Garzó, N. El Mlili, R. Giner-Duran, M.A. Serra, J. Salazar, C. Carda, V. Belloch, V. Felipo, C. Montoliu
Journal: Journal of Hepatology (2012)
Cohort Studies of Fat Intake and the Risk of Breast Cancer — A Pooled Analysis
Authors: David J. Hunter, Donna Spiegelman, Hans-Olov Adami, Lawrence Beeson, Piet A. van den Brandt, Aaron R. Folsom, Gary E. Fraser, R. Alexandra Goldbohm, Saxon Graham, Geoffrey R. Howe, Lawrence H. Kushi, James R. Marshall, Aidan McDermott, Anthony B. Miller, Frank E. Speizer, Alicja Wolk, Shiaw-Shyuan Yaun, Walter Willett
Journal: New England Journal of Medicine (1996)

Experiments in animals, international correlation comparisons, and case-control studies support an association between dietary fat intake and the incidence of breast cancer. Most cohort studies do not corroborate the association, but they have been criticized for involving small numbers of cases, homogeneous fat intake, and measurement errors in estimates of fat intake.
Abstract 4007: Defining the role of ERG-mediated repression of HPGD in prostate tumorigenesis
Authors: Mohamed Ahmed, Shyh-Han Tan, Chen Sun, Syed Shaheduzzaman, Ying Hu, Gyorgy Petrovics, Yongmei Chen, Hua Li, Isabell Sesterhenn, Taduru Sreenath, David G. McLeod, Albert Dobi, Shiv Srivastava
Journal: Cancer Research (2011)

Abstract Activation of the ETS Related Gene (ERG) was originally identified in subsets of Ewing sarcomas, myeloid leukemias and, recently, in the majority of prostate cancers (CaP). Emerging studies in experimental models underscore functions of ERG in prostate tumorigenesis. However, biological functions of ERG in CaP remains to be better understood. Evaluation of ERG downstream targets identified 15-hydroxyprostaglandin dehydrogenase gene (HPGD) in response to ERG knockdown. Several recent studies have indicated that HPGD, the main catabolizing enzyme of prostaglandins and lipoxins and a tumor suppressor, is down-regulated in a majority of lung, colon, breast, and bladder cancers. However, the regulation of HPGD within the biological context of ERG expressing prostate tumors remains to be defined. The objective of this study was to evaluate the effects of ERG on the prostaglandin signaling pathway in prostate cancer. Correlation between HPGD and ERG expression was evaluated at the mRNA and protein levels in prostate cancer specimens and cell lines by Western blot, QRT-PCR, and immunofluorescence assays. Small interference RNA against human ERG and HPGD were used to knock-down their respective expressions. Functional consequences of ERG and HPGD knockdown in VCaP cells harboring TMPRSS2-ERG fusions were assessed by ChIP and BrdU cell proliferation assays. The experiments showed that loss of ERG expression leads to a robust overexpression of HPGD in prostate cancer cells. Furthermore, we observed altered PGE2 production, decreased expression of prostaglandin E2 receptor 4 (EP4), and inhibition of prostaglandin E2 induced cell growth. Chromatin immunoprecipitation experiments revealed direct binding of ERG protein to the HPGD core promoter. Comparison of HPGD expression in TMPRSS2-ERG positive and negative prostate tumors indicated a trend towards decreased HPGD expression. In conclusion ERG activation, as a consequence of TMPRSS2-ERG fusions, may influence the components of the prostaglandin signaling pathway in prostate tumorigenesis disrupting the tumor suppressor functions of HPGD. These findings suggests for a new biological role of ERG in CaP that may be further evaluated as a target for prevention, as well as early therapeutic intervention in CaP. 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 4007. doi:10.1158/1538-7445.AM2011-4007
Transtibial vs anatomical single bundle technique for anterior cruciate ligament reconstruction: A Retrospective Cohort Study
Authors: Bekir Eray Kilinc, Adnan Kara, Yunus Oc, Haluk Celik, Savas Camur, Emre Bilgin, Yunus Turgay Erten, Turker Sahinkaya, Osman Tugrul Eren
Journal: International Journal of Surgery (2016)
SAT0412 Patients with Psoriatic Arthritis HAD Better TNFI Survival than Ankylosing Spondylitis: HÜR-BİO REAL Life Results
Authors: U. Kalyoncu, O. Karadag, L. Kilic, S.A. Bilgen, A. Akdogan, S. Kiraz, I. Ertenli
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> TNFi drug survival is one of the valid outcome measure in rheumatological diseases. Patients with psoriatic arthritis (PsA) usually have both joint/back pain diseases and skin disorders. Thus, efficacy of TNFi may be related with joint and skin disease. In fact, PsA patients have different way from ankylosing spondylitis. <h3>Objectives</h3> Objective of this study was to compare TNFi drug survival in PsA and ankylosing spondylitis (AS). <h3>Methods</h3> HÜR-BİO (Hacettepe University Rheumatology Biologic Registry) is a single center biological registry since 2005 in Turkey. Data collected includes demographic data, co-morbidities, smoking, switch ratio, baseline and follow-up disease activity parameters (such as BASDAI, BASFI, CRP, ESR, global VAS, swollen joint count ad tender joint count). If patients took TNFi drugs last 6 months, patient accepted as ongoing TNFi treatment. Kaplan-Meier plots and log rank tests were used to assess drug survival. <h3>Results</h3> There were 630 AS and 119 PsA [30 (25.2%) psoriatic spondylitis] patients with TNFi in this database. Mean age in PsA and AS were 45±11 vs 41±11 years (p=0.005). Mean disease duration in PsA and AS were 7.1±5.6 vs 9.7±7.2 years (p&lt;0.001). AS patients were more frequently male 415/630 (65.8%) vs 34/119 (28.6%), p&lt;0.001. Mean TNFi duration was similar in PsA and AS patients 29±29 vs 34±31 months, p&gt;0.05. TNFi drugs in PsA and AS patients were adalimumab (36.1% vs 23.1%), etanercept (27.7% vs 38.1%), infliximab (26.9% vs 34.4.%) and golimumab (8.4% vs 4.1%), p&lt;0.001. PsA patients were used more frequetly DMARDs than AS patients [methotrexate 48.2% vs 6.9%, p&lt;0.001, leflunomide 20.1% vs 0.9%, p&lt;0.001, sulphasalazine 14.0% vs 25.4%, p&gt;0.05]. Patients with PsA had higher TNFi switch rate than AS patients 45/116 (38.8%) vs 154/578 (26.6%), p=0.008. Baseline ESR 30±26 vs 33±23 mm/hour, CRP 2.39±3.27 vs 3.70±7.24 mg/dl, BASDAI score 5.6±2.0 vs 5.6±1.8 and BASFI score 4.2±2.9 vs 4.4±2.6 were similar in PsA and AS patients. However, tender joint counts 5.2±5.4 vs 0.29±0.96, p&lt;0.001 and swollen joit counts 2.54±2.73 vs 0.58±0.27 p&lt;0.001 were higher in PsA patients. Patients with PsA had better drug survival than AS patients (log rank 0.012) (Fig. 1). <h3>Conclusions</h3> TNFi drug survival is better in PsA than AS patients. Distribution of TNFi and DMARDs, switch rates may be responsible from those results. However, we thought that, improvement of peripheral arthritis and skin lesions are also reflect good TNFi survival in PsA. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4155
P955 IN VITRO COMPARISON OF Octaplas-LG, STANDARD Octaplas AND FRESH FROZEN PLASMA IN THE TREATMENT OF COAGULOPATHY DUE TO LIVER DISEASE
Authors: M.A. Connaughton, J.L. Chin, P.A. Mc Cormack, P. O'Brien, J.M. Fitzgerald
Journal: Journal of Hepatology (2014)
Combined Tc-99m Sestamibi First-Pass Radionuclide Angiography and Cardiac SPECT Imaging During Arbutamine Infusion Delivered by a Computerized Closed-Loop System
Authors: SALVADOR BORGES-NETO, MARY A. CURTIS, EDWARD I. MORRIS, MICHAEL W. HANSON, RALPH E. COLEMAN
Journal: Clinical Nuclear Medicine (1999)

This study evaluated the feasibility, hemodynamic responses, and relation of combined Tc-99m sestamibi SPECT imaging and first-pass radionuclide angiography during the infusion of a new beta agonist arbutamine.Arbutamine was administered to 15 patients and constantly adjusted by a closed-loop computerized system. Rest and arbutamine Tc-99m sestamibi radionuclide angiography was performed with a multicrystal gamma camera followed by SPECT imaging with a rotating triple-head, single-crystal gamma camera.The mean differences (paired t-test) between rest and arbutamine studies for heart rate (HR), end-diastolic volume (EDV), stroke volume (SV), cardiac output (CO), and ejection fraction (EF) were as follows: 55 bpm for HR (P < 0.001), 5 ml for EDV (P=ns), 7.5 ml for SV (P=0.04), 4.4 l/min for CO (P < 0.001), and 6.4% for EF (P < 0.001), respectively. The results of SPECT studies were abnormal in six patients and normal in nine. Findings of radionuclide angiography were normal in 12 patients and abnormal in three. Interpretation of the perfusion and functional studies were concordant in 10 and discordant in five patients.Simultaneous cardiac radionuclide angiography and SPECT imaging are feasible during arbutamine infusion. This potent beta agonist increases cardiac output through a chronotropic effect with no significant changes in EDV. The discordance in SPECT and radionuclide angiography results may represent incremental diagnostic and prognostic information provided by both studies.
Abstract 1139: Complete characterization of prostate cancer genomes by massively parallel sequencing
Authors: Michael F. Berger, Michael S. Lawrence, Kristian Cibulskis, Dorothee Pflueger, Francesca Demichelis, Carrie Sougnez, Robert C. Onofrio, Lauren Ambrogio, Timothy Fennell, Melissa Parkin, Scott L. Carter, Gordon Saksena, Andrey Sivachenko, Douglas Voet, Jane Wilkinson, Sheila Fisher, Wendy Winckler, Kristin Ardlie, John Chant, Jennifer Baldwin, Mark Gerstein, Todd R. Golub, Matthew Meyerson, Ashutosh K. Tewari, Stacey B. Gabriel, Eric S. Lander, Gad Getz, Mark A. Rubin, Levi A. Garraway
Journal: Cancer Research (2010)

Abstract Prostate cancer is the most common type of cancer diagnosed among men in the United States, accounting for 200,000 new cases and 27,000 deaths per year. Prior genetic studies have shown that chromosomal rearrangements comprise a major mechanism of oncogene activation in prostate cancer. For example, androgen-regulated gene fusions involving ETS family transcription factors are present in the majority of prostate cancers, yet the full repertoire of genomic alterations driving prostate carcinogenesis and progression remains unknown. Toward this end, recent technological advances have made it possible to characterize the full complement of somatic mutations in a single tumor through whole genome sequencing. We are using massively parallel sequencing technology to characterize the complete genomes of several primary prostate adenocarcinomas at &amp;gt;30x coverage. All samples are high-grade primary tumors (Gleason grade 7 to 9) and include cases with and without known ETS family translocations. For each tumor, we are also obtaining &amp;gt;30x sequence coverage of matched normal DNA from blood of these same patients in order to determine the somatic component of the overall variation we observe. Our results indicate that translocations and other chromosomal rearrangements occur frequently in prostate cancer, at a rate of &amp;gt;100 per genome. Further, we have discovered many nonsynonymous sequence mutations (point mutations and indels) in each tumor, some of which may represent novel candidate drivers of tumor progression. The overall rate of somatic point mutations is approximately 1 per Megabase. Integrated analysis of all genomes reveals both recurrent and private alterations. Together, these results illuminate potential avenues for target discovery and demonstrate the unparalleled value in performing complete genome sequencing in this malignancy. 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 1139.
A2.29 Immature dendritic cells are potent osteoclasts precursors in ra and are targeted by ra-specific antibodies
Authors: A Krishnamurthy, M Sun, B Rethi, V Joshua, H Wähämaa, N Tarasova, K Amara, V Malmström, J Ytterberg, AI Catrina
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background and purpose</h3> We have recently shown that the immature dendritic cells (iDC) developing in dense cultures in presence of high lactic acid levels can efficiently differentiate into osteoclasts (OC). We aimed to investigate influence of Anti-citrullinated protein antibodies (ACPA) on iDC differentiation to OC in rheumatoid arthritis (RA). <h3>Methods</h3> CD14<sup>+</sup> monocytes from PB of ACPA+ RA patients and healthy individuals were first used to generate iDC and MΦ and these cells were then differentiated to OC with RANKL and M-CSF. Mass spectrometry analysis was performed on different stages of differentiation of iDC and MΦ derived OC. ACPA positive and negative polyclonal IgGs were isolated from synovial fluid (SF, n = 26) and peripheral blood (PB, n = 38) samples of RA patients and the effects of these antibodies was tested in OC cultures. Cytokines were measured by CBA in cultures supernatants. Immunoflourescence was done on OCs with monoclonal ACPAs derived from single SF derived B cells. The effect of IL-8 and PAD inhibition was tested on OC differentiation. <h3>Results</h3> Principal component analysis confirmed distinct proteomics profiles in sparse or dense DC cultures and in MΦ but both DC and MΦ precursors differentiated into OC with similar protein composition. Citrullinated-actin was identified during iDC-OC maturation and citrullinated-vimentin in matured OC. With immunofluorescent staining we demonstrated the presence of citrullinated proteins on the surface of both iDC precursors and iDC-derived mature OCs. PAD2 and PAD4 showed faint staining in CD14 monocytes with increased staining intensity in both iDC precursors and more mature OCs. Polyclonal ACPAs enhanced osteoclastogenesis and bone resorption from iDC (fold increase 1.6 ± 0.2 for OC number and 2.0 ± 0.3 for bone resorption area). Similar effect was observed when the iDC were derived from ACPA+ RA patients (fold increase of 2.3 ± 0.9 for OC number and 2.6 ± 0.1 for bone resorption area). The importance of citrullination and PAD enzymes for ACPA mediated iDC transdifferentiation to OC was confirmed by a dose-dependent inhibition of OC differentiation using the PAD inhibitor Cl-Amidine. Increased osteoclastogenesis was associated with significantly higher levels of IL-8 levels in cultures supernatants (fold increase of 2.4 ± 0.5). <h3>Conclusion</h3> iDC can efficiently transdifferentiate in to OC in RA and this process is enhanced by ACPA.
Diagnosis of Recurrent Astrocytoma with Fludeoxyglucose F18 PET Scanning
Authors: Siroos Mirzaei, Peter Knoll, Horst Kohn
Journal: New England Journal of Medicine (2001)

To the Editor: The recent report of an astrocytoma following the pyramidal tract (Dec. 7 issue)1 was quite interesting. We report on the use of fludeoxyglucose F18 positron-emission tomography (PET...
An Outbreak of Streptococcal Puerperal Sepsis
Authors: William R. McCabe, Archie A. Abrams
Journal: New England Journal of Medicine (1965)

HISTORICALLY, streptococcal puerperal sepsis has been one of the most frequent and devastating forms of hospital-acquired infections. Treatises on this subject appeared in the English literature as early as 1795,1 and some authorities, notably Holmes,2 were early believers in the contagiousness of the disease. Person-to-person transmission, however, was not clearly established until the classic studies of Semmelweis.3 Prevention and some degree of control of epidemics of puerperal sepsis was achieved by the introduction of antiseptic, aseptic and isolation technics,4 but the number of deaths from this cause still varied from 1.5 to 2.1 per 1000 births in England between 1925 . . .
Abstract 1060: Regulation of SDF-1 (CXCL12) production by mesenchymal stromal cells in the tumor microenvironment
Authors: Sohrab Amiri, Siang-Yo Lin, Sonia Picinich, Christopher DeRenzo, Jiadong Li, Debabrata Banerjee, John W. Glod
Journal: Cancer Research (2010)

Abstract The tumor microenvironment is made up of a number of cell types including fibroblasts, pericytes, endothelial cells, macrophages, and neoplastic cells. The interaction between cellular components of the microenvironment is critical for processes such as tumor growth, angiogenesis, and metastasis. Mesenchymal stromal cells (MSCs) are an important component of the tumor microenvironment with roles in key aspects of tumor progression such as cell growth and metastasis. Stromal-derived factor −1 (SDF-1) has been identified as a key signaling molecule in the interaction between MSCs and neoplastic cells. SDF-1 acting through its cognate receptors CXCR4 and CXCR7 is known to mediate diverse processes such as chemotaxis, angiogenesis, hematopoiesis, metastasis, and tumor growth. In this study we investigated the regulation of SDF-1 production by MSCs. We show that the tumor suppressor p53 is one of the major regulators of SDF-1 signaling in MSCs within the tumor stroma. We also illustrate that a decrease in p53 function leads to increased SDF-1 production by MSCs which results in increased migration of MSCs. Decreased p53 expression by MSCs leads to increased SDF-1 production with and increased recruitment to the tumor microenvironment. An improved understanding of the molecular mechanisms controlling SDF-1 production by MSCs may identify novel ways of therapeutically targeting tumor - stromal interactions. 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 1060.
Malignant esophagobronchial fistula with severe esophageal stenosis, successfully treated by transbronchial occlusion with cyanoacrylate glue
Authors: T. Iwata, K. Chung, M. Toda, A. Hiraoka, H. Hagiwara, S. Hanada, T. Yokota, K. Inoue, T. Miura
Journal: Endoscopy (2012)

A 68-year-old man with advanced esophageal cancer was receiving chemotherapy. On day 6, he suddenly complained of massive greenish-black watery sputa that looked like stomach contents. A chest radiograph showed right hilar infiltration ([Fig. 1]). Chest computed tomography (CT) demonstrated a small cavitary lesion next to the esophageal tumor ([Fig. 2]). The patient soon fell into respiratory failure and needed artificial respiration. Bronchoscopy showed massive black sputa, continuously coming up from the right B6a bronchus. Malignant esophagobronchial fistula due to necrotizing perforation of the esophageal cancer following chemotherapy was then diagnosed.