tbuckley/cabot-search huggingface dataset:
Indolent Systemic Mastocitosis with Germline D816V Somatic c-kit Mutation Evolving to an Acute Myeloid Leukemia
Authors: L. Escribano, R. Núñez-López, M. Jara, A. García-Montero, A. Prados, C. Teodosio, A. Iglesias, M. Sanchez, A. Orfao
Journal: Journal of Allergy and Clinical Immunology (2006)
One minute urease test
Authors: G. Hao
Journal: Gut (1990)

As cancer strikes, individuals vary not only in terms of factors that contribute to its occurrence and development, but as importantly, in their capacity to respond to treatment. While exciting new therapeutic options that mobilize the immune system against cancer have led to breakthroughs for a variety of malignancies, success is limited to a subset of patients. Pre-existing immunological features of both the host and the tumor may contribute to how patients will eventually fare with immunotherapy. A broad understanding of baseline immunity, both in the periphery and in the tumor microenvironment, is needed in order to fully realize the potential of cancer immunotherapy. Such interrogation of the tumor, blood, and host immune parameters prior to treatment is expected to identify biomarkers predictive of clinical outcome as well as to elucidate why some patients fail to respond to immunotherapy. To approach these opportunities for progress, the Society for Immunotherapy of Cancer (SITC) reconvened the Immune Biomarkers Task Force. Comprised of an international multidisciplinary panel of experts, Working Group 4 sought to make recommendations that focus on the complexity of the tumor microenvironment, with its diversity of immune genes, proteins, cells, and pathways naturally present at baseline and in circulation, and novel tools to aid in such broad analyses.
Phase II Study of Gemcitabine, Carboplatin, and Iniparib As Neoadjuvant Therapy for Triple-Negative and <i>BRCA1</i>/<i>2</i> Mutation–Associated Breast Cancer With Assessment of a Tumor-Based Measure of Genomic Instability: PrECOG 0105
Authors: Melinda L. Telli, Kristin C. Jensen, Shaveta Vinayak, Allison W. Kurian, Jafi A. Lipson, Patrick J. Flaherty, Kirsten Timms, Victor Abkevich, Elizabeth A. Schackmann, Irene L. Wapnir, Robert W. Carlson, Pei-Jen Chang, Joseph A. Sparano, Bobbie Head, Lori J. Goldstein, Barbara Haley, Shaker R. Dakhil, Julia E. Reid, Anne-Renee Hartman, Judith Manola, James M. Ford
Journal: Journal of Clinical Oncology (2015)

This study was designed to assess efficacy, safety, and predictors of response to iniparib in combination with gemcitabine and carboplatin in early-stage triple-negative and BRCA1/2 mutation-associated breast cancer.This single-arm phase II study enrolled patients with stage I to IIIA (T ≥ 1 cm) estrogen receptor-negative (≤ 5%), progesterone receptor-negative (≤ 5%), and human epidermal growth factor receptor 2-negative or BRCA1/2 mutation-associated breast cancer. Neoadjuvant gemcitabine (1,000 mg/m(2) intravenously [IV] on days 1 and 8), carboplatin (area under curve of 2 IV on days 1 and 8), and iniparib (5.6 mg/kg IV on days 1, 4, 8, and 11) were administered every 21 days for four cycles, until the protocol was amended to six cycles. The primary end point was pathologic complete response (no invasive carcinoma in breast or axilla). All patients underwent comprehensive BRCA1/2 genotyping, and homologous recombination deficiency was assessed by loss of heterozygosity (HRD-LOH) in pretreatment core breast biopsies.Among 80 patients, median age was 48 years; 19 patients (24%) had germline BRCA1 or BRCA2 mutations; clinical stage was I (13%), IIA (36%), IIB (36%), and IIIA (15%). Overall pathologic complete response rate in the intent-to-treat population (n = 80) was 36% (90% CI, 27 to 46). Mean HRD-LOH scores were higher in responders compared with nonresponders (P = .02) and remained significant when BRCA1/2 germline mutations carriers were excluded (P = .021).Preoperative combination of gemcitabine, carboplatin, and iniparib is active in the treatment of early-stage triple-negative and BRCA1/2 mutation-associated breast cancer. The HRD-LOH assay was able to identify patients with sporadic triple-negative breast cancer lacking a BRCA1/2 mutation, but with an elevated HRD-LOH score, who achieved a favorable pathologic response. Confirmatory controlled trials are warranted.
Blood Flow Limitation In Vivo of Small Solute Transfer during Peritoneal Dialysis in Rats
Authors: Bert-Inge Rosengren, Bengt Rippe
Journal: Journal of the American Society of Nephrology (2003)

ABSTRACT. The aim of this study was to determine whether or to what extent transperitoneal flux of small solutes is reduced at low blood flows during peritoneal dialysis (PD) in rats. Peritoneal blood flow reductions were achieved by bleeding anesthetized (300 g) rats by 25% of their blood volume. After bleeding, a 2 h PD dwell was started using standard PD fluid. The permeability-surface area product (PS) for 51Cr-EDTA and glucose were assessed, as well as the transperitoneal clearance (Cl) of albumin. Control animals were not bled. After bleeding, peritoneal blood flow declined from 145 ± 17 perfusion units (PU) to 59 ± 12 PU (P = 0.001). Concomitant with this reduction, PS for 51Cr-EDTA fell from 0.284 ± 0.01 ml/min to 0.216 ± 0.01 ml/min (P = 0.006) and PS for glucose from 0.338 ± 0.02 ml/min to 0.294 ± 0.01 ml/min (P = 0.046). Mean arterial BP (MAP) dropped from 133 ± 4 mmHg to 61 ± 5 mmHg (P = 0.008). Cl of albumin fell largely in proportion to the estimated capillary hydrostatic pressure drop, i.e., from 6.1 ± 0.7 μl/min to 2.3 ± 0.3 μl/min (P = 0.001). The results demonstrate that the transperitoneal clearances of small solutes are blood flow limited during PD, when peritoneal perfusion is markedly reduced. The level of flow limitation was, however, much lower than expected and observed in other tissues. Albumin transport, which is not blood flow limited, was reduced largely in proportion to the calculated capillary hydrostatic pressure decrease. E-mail: [email protected]
Effect of Specific Immunotherapy With Preimmunization Against Alpha-Fetoprotein on a Mouse Transplantable Hepatoma: Brief Communication 2
Authors: Eva Engvall, Helena Pihko, Hannu Jalanko, Erkki Ruoslahti
Journal: JNCI Journal of the National Cancer Institute (1977)

Journal Article Effect of Specific Immunotherapy With Preimmunization Against Alpha-Fetoprotein on a Mouse Transplantable Hepatoma: Brief Communication Get access Eva Engvall, Eva Engvall Search for other works by this author on: Oxford Academic PubMed Google Scholar Helena Pihko, Helena Pihko Search for other works by this author on: Oxford Academic PubMed Google Scholar Hannu Jalanko, Hannu Jalanko Search for other works by this author on: Oxford Academic PubMed Google Scholar Erkki Ruoslahti Erkki Ruoslahti Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 59, Issue 1, July 1977, Pages 277–280, https://doi.org/10.1093/jnci/59.1.277 Published: 01 July 1977 Article history Received: 18 October 1976 Accepted: 23 January 1977 Published: 01 July 1977
IL-15 prevents allergic rhinitis through reactivation of antigen-specific CD8+ cells
Authors: Noriaki Aoi, Tokuko Masuda, Daisuke Murakami, Toshiki Yajima, Hiroyuki Mizubuchi, Hisakata Yamada, Hideyuki Kawauchi, Yasunobu Yoshikai
Journal: Journal of Allergy and Clinical Immunology (2006)
Ventricular tachycardia in infancy: evidence for a reentrant mechanism.
Authors: W E Gaum, D C Schwartz, S Kaplan
Journal: Circulation (1980)

Ventricular tachycardia is unusual in infancy. Three infants are described in whom this arrhythmia was documented by electrophysiologic studies. The ability to start and terminate this rhythm by critically timed premature ventricular stimulation suggests a reentrant mechanism. All three patients have remained free of arrhythmias on oral propranolol therapy.
Similar insulin secretory response to a gastric inhibitory polypeptide bolus injection at euglycemia in first-degree relatives of patients with type 2 diabetes and control subjects
Authors: Juris J Meier, Michael A Nauck, Nina Siepmann, Michael Greulich, Jens J Holst, Carolyn F Deacon, Wolfgang E Schmidt, Baptist Gallwitz
Journal: Metabolism (2003)
<i>p53</i> Mutations in Deep Tissues Are More Strongly Associated with Recurrence than Mutation-Positive Mucosal Margins
Authors: Xiaohong Huang, Stelios Pateromichelakis, Allison Hills, Martyn Sherriff, Andrew Lyons, John Langdon, Edward Odell, Peter Morgan, John Harrison, Max Partridge
Journal: Clinical Cancer Research (2007)

Abstract Purpose: Application of ultrasensitive diagnostics has shown that small numbers of p53 mutation-positive cells may signify the presence of residual tumor in histologically normal tissues after resection of squamous cell carcinomas arising in the head and neck area. To date, most studies in this area have focused on analysis of tissues at the mucosal aspect of the resection and highlighted the importance of molecular changes in the field with respect to the risk of recurrence. Experimental Design: In the present investigation, we analyzed normal tissues from mucosal and deep surgical margins, referred to as “molecular margins,” for the presence of the signature p53 mutation identified for each tumor. Results: The p53 mutation status of these carcinomas did not correlate with clinical or histopathologic variables, but these mutations provided an excellent target for ultrasensitive analysis of margin status. We found that 11 of 16 (68%) of cases with histologically tumor-free (including 9 without dysplasia), but with p53 mutation-positive molecular margins, developed recurrence. The probability of developing local recurrence was significantly higher for the group with p53 mutation-positive margins when compared with the group with clear margins (P = 0.048) and more strongly associated with p53 mutation-positive deep molecular margins than mutation-positive mucosal molecular margins or positivity at both sites (P = 0.009). Conclusions: This shows that although persistent mucosal fields may contribute to recurrence, clonal p53 mutations in deep tissues are an important cause of treatment failure, and molecular margins from both sites should be analyzed in future prospective series.
Metabolic Syndrome
Authors: James B. Meigs
Journal: Diabetes Care (2004)

The concept of a “metabolic syndrome ” conferring increased risk of incident type 2 diabetes and cardiovascular disease (CVD) has been around for more than a couple of decades. Recent publication of clinical definitions has transformed the metabolic syndrome from a physiological curiosity to a major focus of research and of clinical and public health interest (1,2). The metabolic syndrome is generally considered to be the co-occurrence of obesity (particularly central obesity); elevated glucose, triglyceride, and blood pressure levels; and/or low HDL cholesterol levels, and in many cases their co-occurrence signifies underlying insulin resistance (3). The metabolic syndrome has been most widely promoted as a means to identify patients for lifestyle interventions to reduce risk factor levels and, theoretically, incident disease, particularly CVD. However, various tools already exist for the identification of apparently healthy people at elevated risk of diabetes (4–6) or CVD (7). The degree to which a clinical diagnosis of the metabolic syndrome complements or improves upon risk prediction using existing methods has not been defined.

In this issue of Diabetes Care , Stern et al. (8) address this question using the experience of Mexican American and non-Hispanic white participants in the San Antonio Heart Study (SAHS). After a baseline examination and 7 years of follow-up, 195 subjects subsequently developed type 2 diabetes out of 1,709 subjects without baseline diabetes (defined by diabetic hyperglycemia or self-reported use of diabetes medications) and 156 experienced a CVD event out of 2,570 subjects without baseline CVD (defined as self-reported physician diagnosis of heart attack, revascularization procedure, stroke, or CVD death by death certificate). Clinical history and metabolic risk factors measured at baseline were used to categorize subjects with the metabolic syndrome by National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP-III) criteria (or World Health Organization …
Tumor Necrosis Factor Receptor–Associated Factor 1 (TRAF1) Deficiency Attenuates Atherosclerosis in Mice by Impairing Monocyte Recruitment to the Vessel Wall
Authors: Anna Missiou, Natascha Köstlin, Nerea Varo, Philipp Rudolf, Peter Aichele, Sandra Ernst, Christian Münkel, Carina Walter, Peter Stachon, Benjamin Sommer, Dietmar Pfeifer, Katja Zirlik, Lindsey MacFarlane, Dennis Wolf, Erdyni Tsitsikov, Christoph Bode, Peter Libby, Andreas Zirlik
Journal: Circulation (2010)

Background— Members of the tumor necrosis factor superfamily, such as tumor necrosis factor-α, potently promote atherogenesis in mice and humans. Tumor necrosis factor receptor–associated factors (TRAFs) are cytoplasmic adaptor proteins for this group of cytokines. Methods and Results— This study tested the hypothesis that TRAF1 modulates atherogenesis in vivo. TRAF1 −/− /LDLR −/− mice that consumed a high-cholesterol diet for 18 weeks developed significantly smaller atherosclerotic lesions than LDLR −/− (LDL receptor–deficient) control animals. As the most prominent change in histological composition, plaques of TRAF1-deficient animals contained significantly fewer macrophages. Bone marrow transplantations revealed that TRAF1 deficiency in both hematopoietic and vascular resident cells contributed to the reduction in atherogenesis observed. Mechanistic studies showed that deficiency of TRAF1 in endothelial cells and monocytes reduced adhesion of inflammatory cells to the endothelium in static and dynamic assays. Impaired adhesion coincided with reduced cell spreading, actin polymerization, and CD29 expression in macrophages, as well as decreased expression of the adhesion molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in endothelial cells. Small interfering RNA studies in human cells verified these findings. Furthermore, TRAF1 messenger RNA levels were significantly elevated in the blood of patients with acute coronary syndrome. Conclusions— TRAF1 deficiency attenuates atherogenesis in mice, most likely owing to impaired monocyte recruitment to the vessel wall. These data identify TRAF1 as a potential treatment target for atherosclerosis.
Hemin, a heme oxygenase substrate analog, both inhibits and enhances neutrophil random migration and chemotaxis
Authors: J. A. Andersson, R. Uddman, L.‐O. Cardell
Journal: Allergy (2002)

Background: Carbon monoxide (CO), is an endogenously produced gas, generated by the rate‐limiting enzyme heme oxygenase (HO), present in man throughout the respiratory tract. CO can elicit important physiological responses like bronchial relaxation and vasodilation. Both HO expression and CO levels in the airways increase in response to hypoxic challenge and to a wide variety of inflammatory stimuli, such as intermittent allergic rhinitis, asthma and upper respiratory tract infections. A role for CO in airway regulation and inflammation has therefore been suggested. However, information about CO‐induced effects on cells involved in airway inflammation is scarce. The present study was designed to investigate if the HO substrate analog hemin could affect neutrophil random migration, and N‐formyl‐L‐methionyl‐L‐leucyl‐L‐phenylalanine (fMLP) induced chemotaxis. Methods: Hemin was added to and incubated with whole blood and the effects of the anticipated CO production were then evaluated on isolated neutrophils using a chemotaxis chamber. Results: A biphasic dose–response curve emerged for both the neutrophil spontaneous random migration and the fMLP‐induced chemotaxis. Low concentrations of hemin (10 −11 m to 10 −9 m ) enhanced the migratory response, whereas higher concentrations (10 −7 m and 10 −5 m ) inhibited migration. The inhibition induced by hemin on fMLP‐induced migration was abolished after pre‐treatment with Rp‐8Br‐cyclicGMPS, an inhibitor of cyclicGMP. Conclusions: The present data indicate that endogenously produced CO can affect both spontaneous and stimulated neutrophil migration, partly via a cyclicGMP‐related process, hence strengthening the idea of a role for CO in airway inflammation.
Different thrombotic and inflammatory patterns between unstable angina and peripheral vascular disease
Authors: C. Monaco, E. Rossi, D. Milazzo, G. Liuzzo, A. Cuculo, F. Citterio, G. D'Onofrio, W. van de Greef, A. Meo, L.M. Biasucci, A. Maseri
Journal: Journal of the American College of Cardiology (1998)
Alternatives to radical behaviorism
Authors: Terry L. Smith
Journal: Behavioral and Brain Sciences (1995)

Abstract Operant psychologists are looking for alternatives to radical behaviorism. Rachlin offers teleological behaviorism, but it may pose as many difficulties as radical behaviorism. There is, however, a less drastic way to defend Rachlin's thesis of “order in the relationship between organisms and environment.” It portrays operant principles as relating distal efficient causes to behavioral effects.
gp130-Mediated Stat3 Activation in Enterocytes Regulates Cell Survival and Cell-Cycle Progression during Colitis-Associated Tumorigenesis
Authors: Julia Bollrath, Toby J. Phesse, Vivian A. von Burstin, Tracy Putoczki, Moritz Bennecke, Trudie Bateman, Tim Nebelsiek, Therese Lundgren-May, Özge Canli, Sarah Schwitalla, Vance Matthews, Roland M. Schmid, Thomas Kirchner, Melek C. Arkan, Matthias Ernst, Florian R. Greten
Journal: Cancer Cell (2009)
NKG2D-dependent effector function of bronchial epithelium-activated alloreactive T-cells
Authors: K. Kraetzel, B. Stoelcker, G. Eissner, G. Multhoff, M. Pfeifer, E. Holler, C. Schulz
Journal: European Respiratory Journal (2008)

Allogeneic haematopoietic stem cell transplantation (SCT) has emerged as a curative therapeutic option. However, the role of graft-versus-host disease in lung injury after SCT has yet to be determined. In the present study, primary bronchial epithelial cells and the bronchial epithelial cell line BEAS-2B were used to investigate immune responses of allogeneic CD8+ T-cells directed against respiratory epithelial cells. Following stimulation with irradiated bronchial epithelial cells, CD8+ T-cells produced significant amounts of interferon-gamma, upregulated alloantigen activation markers and proliferated highly compared with T-cells stimulated with interleukin-2 alone. Furthermore, cytotoxicity assays demonstrated that bronchial epithelial cell-specific and granzyme B-mediated cytolytic activity was induced in CD8+ T-cells. Generation of natural killer (NK) T-cells, NK-like T-cells, cytokine-induced killer cells or lymphokine-activated killer cells could be excluded by phenotyping, culture conditions and neglectable lytic activity following stimulation with interleukin-2 alone. Inhibition experiments showed that lysis of bronchial epithelial cells was not major histocompatibility complex-I restricted, but depended on NK group 2 member D signalling; a stimulatory receptor initially shown to be expressed on NK cells. The present data imply that the respiratory epithelium has an antigen presenting function and directly alloactivates cytotoxic CD8+ T-cells that show nonclassical effector function.
Le processus psychothérapeutique et sa relation avec le contexte réel de l’expérience psychothérapeutique
Authors: Jorge E. Garcia Badaracco
Journal: Psychotherapy and Psychosomatics (1978)

Research Articles| February 16 2010 Le processus psychothérapeutique et sa relation avec le contexte réel de l'expérience psychothérapeutique Subject Area: Psychiatry and Psychology Jorge E. Garcia Badaracco Jorge E. Garcia Badaracco Clinica Psiquiatrica O'Higgins, Buenos Aires Search for other works by this author on: This Site PubMed Google Scholar Psychother Psychosom (1978) 29 (1-4): 107–112. https://doi.org/10.1159/000287109 Article history Published Online: February 16 2010 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Jorge E. Garcia Badaracco; Le processus psychothérapeutique et sa relation avec le contexte réel de l'expérience psychothérapeutique. Psychother Psychosom 31 December 1978; 29 (1-4): 107–112. https://doi.org/10.1159/000287109 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsPsychotherapy and Psychosomatics Search Advanced Search Article PDF first page preview Close Modal 1978Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
806 TYPE OF RESPONSE TO PRIOR PEGYLATED INTERFERON ALFA-2B (12KD)/RBV PREDICTS SUBSEQUENT RESPONSE TO RETREATMENT WITH PEGINTERFERON ALFA-2A (40KD)/RBV
Authors: P. Marcellin, B. Freilich, P. Andreone, A. DiBisceglie, C.E. Brandao, K.R. Reddy, A. Craxi, A. Olveira, G. Teuber, D. Messinger, G. Hooper, M. Popescu, A. Tietz, D. Jensen
Journal: Journal of Hepatology (2008)
Nuclear Receptor COUP-TFII Controls Pancreatic Islet Tumor Angiogenesis by Regulating Vascular Endothelial Growth Factor/Vascular Endothelial Growth Factor Receptor-2 Signaling
Authors: Jun Qin, Xinpu Chen, Li-yuan Yu-Lee, Ming-Jer Tsai, Sophia Y. Tsai
Journal: Cancer Research (2010)

The significance of angiogenesis in cancer biology and therapy is well established. In this study, we used the prototypical RIP-Tag model of multistage pancreatic islet tumorigenesis to show that the nuclear receptor COUP-TFII is essential to regulate the balance between pro- and anti-angiogenic molecules that influence the angiogenic switch in cancer. Conditional ablation of COUP-TFII in the tumor microenvironment severely compromised neoangiogenesis and lymphangiogenesis during pancreatic tumor progression and metastasis. We found that COUP-TFII plays a cell-autonomous role in endothelial cells to control blood vessel sprouting by regulating cell proliferation and migration. Mechanistic investigations revealed that COUP-TFII suppressed vascular endothelial growth factor (VEGF)/VEGF receptor-2 (VEGFR-2) signaling by transcriptionally repressing the expression of VEGFR-1, thereby curtailing a central angiogenic driver of vascular growth. Taken together, our results implicate COUP-TFII as a critical factor in tumor angiogenesis through regulation of VEGF/VEGFR-2 signaling, suggesting COUP-TFII as a candidate target for antiangiogenic therapy.