tbuckley/cabot-search huggingface dataset:
Preconditioning, postconditioning and their application to clinical cardiology
Authors: R KLONER, S REZKALLA
Journal: Cardiovascular Research (2006)

Ischemic preconditioning is a well-established phenomenon first described in experimental preparations in which brief episodes of ischemia/reperfusion applied prior to a longer coronary artery occlusion reduce myocardial infarct size. There are ample correlates of ischemic preconditioning in the clinical realm. Preconditioning mimetic agents that stimulate the biochemical pathways of ischemic preconditioning and protect the heart without inducing ischemia have been examined in numerous experimental studies. However, despite the effectiveness of ischemic preconditioning and preconditioning mimetics for protecting ischemic myocardium, there are no preconditioning-based therapies that are routinely used in clinical medicine at the current time. Part of the problem is the need to administer therapy prior to the known ischemic event. Other issues are that percutaneous coronary intervention technology has advanced so far (with the development of stents and drug-eluting stents) that ischemic preconditioning or preconditioning mimetics have not been needed in most interventional cases. Recent clinical trials such as AMISTAD I and II (Acute Myocardial Infarction STudy of ADenosine) suggest that some preconditioning mimetics may reduce myocardial infarct size when given along with reperfusion or, as in the IONA trial, have benefit on clinical events when administered chronically in patients with known coronary artery disease. It is possible that some of the benefit described for adenosine in the AMISTAD 1 and 2 trials represents a manifestation of the recently described postconditioning phenomenon. It is probable that postconditioning – in which reperfusion is interrupted with brief coronary occlusions and reperfusion sequences – is more likely than preconditioning to be feasible as a clinical application to patients undergoing percutaneous coronary intervention for acute myocardial infarction.
Survey of a Methadone Maintenance Treatment Program
Authors: MARVIN E. PERKINS, HARRIET I. BLOCH
Journal: American Journal of Psychiatry (1970)

Four interrelated studies of heroin addicts applying to a methadone maintenance program elicited data on the "typical" patient admitted to the program, a comparison between addicts who were admitted and those who were not accepted to it, and variables associated with discharge from the program as well as those associated with continued drug use. The authors feel the results may aid in refining selection criteria for this kind of program.
Delayed hypersensitivity reaction to heparin
Authors: B.F. O'DONNELL, C.Y. TAN
Journal: British Journal of Dermatology (1993)

Journal Article Delayed hypersensitivity reaction to heparin Get access B.F. O'DONNELL, B.F. O'DONNELL The Skin Hospital, 35 George Road, Edgbaston. Birmingham B15 1PR. U.K. B.F.O'Donnell, St John's Institute of Dermatology, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH. U.K. Search for other works by this author on: Oxford Academic Google Scholar C.Y. TAN C.Y. TAN The Skin Hospital, 35 George Road, Edgbaston. Birmingham B15 1PR. U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 129, Issue 5, 1 November 1993, Pages 634–636, https://doi.org/10.1111/j.1365-2133.1993.tb00502.x Published: 01 November 1993 Article history Accepted: 10 May 1993 Published: 01 November 1993
Asthma Exacerbations after Glucocorticoid Withdrawal Reflects T Cell Recruitment to the Airway
Authors: Mario Castro, Sharon R. Bloch, Michelle V. Jenkerson, Steve DeMartino, Daniel L. Hamilos, Rebecca B. Cochran, Xueping E. Liang Zhang, Haochuan Wang, Joseph P. Bradley, Kenneth B. Schechtman, Michael J. Holtzman
Journal: American Journal of Respiratory and Critical Care Medicine (2004)

We reasoned that a prospective assessment of glucocorticoid withdrawal in subjects with asthma would provide insight into the basis for flares of the disease. We therefore enrolled 25 subjects with moderate persistent asthma and treated them for 30 days with inhaled fluticasone propionate (1,760 μg/day) followed by a withdrawal period that lasted until peak expiratory airflow decreased by 25% and FEV1 by 15% or 6 weeks elapsed. After glucocorticoid withdrawal, 13 of 25 subjects reached the target, whereas 12 subjects did not. The number of eosinophils in bronchial biopsies was increased by glucocorticoid withdrawal in both groups, but increases in airway T cells were found in only those with exacerbation. T-cell accumulation was a reflection of similar increases in both CD4+ and CD8+ T cells and was accompanied by increased expression of chemokine CCL5 (regulated upon activation, normal T cell expressed and secreted) in the airway epithelium without activation of the transcription factor nuclear factor-κB. The pattern of glucocorticoid-sensitive inflammation during an asthma exacerbation is more reminiscent of an antiviral response than an eosinophil-predominant response to allergen and implies an independent role for airway T cells in mediating asthma flares and in determining glucocorticoid efficacy in the treatment of this disease.
Putting the vasoactive effects of COX-2-derived prostanoids into clinical perspective
Authors: F. Krotz
Journal: Cardiovascular Research (2008)

Ever since the recognition that the selective inhibitor of cyclooxygenase (COX)-2, rofecoxib, increases the risk for adverse cardiovascular events, enormous attention has been given to the mechanisms underlying these adverse vascular effects of the coxibs.1,2 Many recent studies that have investigated the biological consequences of COX-2 inhibition in the vasculature have focussed either on the prothrombotic side effects of decreased endothelial prostacyclin production during selective COX-2 blockade3,4 or on detrimental effects of such an intervention on atherosclerosis.5,6 Although such studies have greatly broadened our understanding of the pathophysiological roles of COX-2-mediated prostanoid production in vascular biology, the important vasodilatory functions of COX-2-derived prostanoids have been somewhat eclipsed by them.

Foudi et al. presents data that address the topic of detrimental vascular effects of COX-2 inhibition from this different, yet important, point of view.7 They show in isolated human internal mammary arteries (IMA) that under conditions of acute septic inflammation, which is induced by simultaneous administration of interleukin-1β (IL-1β) and lipopolysaccharide (LPS), COX-2 is upregulated and produces prostacyclin and prostaglandin E2 (PGE2) rather than thromboxane A2 (TxA2). COX-2 expression is shown to be enhanced not only in the intima, but also in the smooth muscle cell-containing media of the vasculature. When vasoconstriction is induced by norepinephrine in the IMA preparations, COX-2 inhibition leads … 

Corresponding author. Tel: +49 89 5160 2111; fax: +49 89 5160 2410. E-mail address : florian.kroetz{at}med.uni-muenchen.de
Drug Treatment of Huntington's Chorea
Authors: R. Ll. Lyon
Journal: BMJ (1962)

The cases of two patients who bear a superficial resemblance to Huntington's chorea are described.The reasons against the condition being hereditary are explained and the importance of a diagnosis of non- hereditarv chronic adult chorea is stressed.I am indebted to those medical colleagues and the district registrars of births and deaths who made the ancestry of these patients so clear.
Lineage Relationship of Gleason Patterns in Gleason Score 7 Prostate Cancer
Authors: Irina V. Kovtun, John C. Cheville, Stephen J. Murphy, Sarah H. Johnson, Shabnam Zarei, Farhad Kosari, William R Sukov, R. Jeffrey Karnes, George Vasmatzis
Journal: Cancer Research (2013)

Gleason score 7 (GS7) prostate cancer [tumors with both Gleason patterns 3 (GP3) and 4 (GP4)] portends a significantly more aggressive tumor than Gleason score 6 (GS6). It is, therefore, critical to understand the molecular relationship of adjacent GP3 and GP4 tumor cell populations and relate molecular abnormalities to disease progression. To decipher molecular relatedness, we used laser capture microdissection (LCM) and whole-genome amplification (WGA) to separately collect and amplify DNA from adjacent GP3 and GP4 cell populations from 14 cases of GS7 prostate cancer. We then carried out massively parallel mate-pair next generation sequencing (NGS) to examine the landscape of large chromosomal alterations. We identified four to 115 DNA breakpoints in GP3 and 17 to 480 in GP4. Our findings indicate that while GP3 and GP4 from the same tumor each possess unique breakpoints, they also share identical ones, indicating a common origin. Approximately 300 chromosomal breakpoints were localized to the regions affected in at least two tumors, whereas more than 3,000 were unique within the set of 14 tumors. TMPRSS2-ERG was the most recurrent rearrangement present in eight cases, in both GP3 and GP4. PTEN rearrangements were found in five of eight TMPRSS2-ERG fusion-positive cases in both GP3 and GP4. Hierarchical clustering analysis revealed that GP3 has greater breakpoint similarity to its partner GP4 compared with GP3 from different patients. We show evidence that LCM, WGA, and NGS of adjacent tumor regions provide an important tool in deciphering lineage relationships and discovering chromosomal alterations associated with tumor progression.
Interleukin-18 Regulates Acute Graft-Versus-Host Disease by Enhancing Fas-mediated Donor T Cell Apoptosis
Authors: Pavan Reddy, Takanori Teshima, Mark Kukuruga, Rainer Ordemann, Chen Liu, Kathy Lowler, James L.M. Ferrara
Journal: The Journal of Experimental Medicine (2001)

Interleukin (IL)-18 is a recently discovered cytokine that modulates both T helper type 1 (Th1) and Th2 responses. IL-18 is elevated during acute graft-versus-host disease (GVHD). We investigated the role of IL-18 in this disorder using a well characterized murine bone marrow transplantation (BMT) model (B6 → B6D2F1). Surprisingly, blockade of IL-18 accelerated acute GVHD-related mortality. In contrast, administration of IL-18 reduced serum tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS) levels, decreased intestinal histopathology, and resulted in significantly improved survival (75 vs. 15%, P &amp;lt; 0.001). Administration of IL-18 attenuated early donor T cell expansion and was associated with increased Fas expression and greater apoptosis of donor T cells. The administration of IL-18 no longer protected BMT recipients from GVHD when Fas deficient (lpr) mice were used as donors. IL-18 also lost its ability to protect against acute GVHD when interferon (IFN)-γ knockout mice were used as donors. Together, these results demonstrate that IL-18 regulates acute GVHD by inducing enhanced Fas-mediated apoptosis of donor T cells early after BMT, and donor IFN-γ is critical for this protective effect.
Polymorphic variation in surfactant protein B is associated with COPD exacerbations
Authors: M. G. Foreman, D. L. DeMeo, C. P. Hersh, V. J. Carey, V. S. Fan, J. J. Reilly, S. D. Shapiro, E. K. Silverman
Journal: European Respiratory Journal (2008)

Exacerbations of chronic obstructive pulmonary disease (COPD) reduce quality of life and increase mortality. Genetic variation might explain the substantial variability seen in exacerbation frequency among COPD subjects with similar lung function. Polymorphisms in five candidate genes, previously associated with COPD susceptibility, were analysed in order to determine whether they demonstrated association with COPD exacerbations. A total of 88 single nucleotide polymorphisms (SNPs) in the genes microsomal epoxide hydrolase (<i>EPHX1</i>), transforming growth factor, beta-1 (<i>TGFB1</i>), serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 2 (<i>SERPINE2</i>), glutathione S-transferase pi (<i>GSTP1</i>) and surfactant protein B (<i>SFTPB</i>) were genotyped in 389 non-Hispanic white participants in the National Emphysema Treatment Trial. Exacerbations were defined as COPD-related emergency room visits or hospitalisations using the Centers for Medicare and Medicaid Services claims data. One or more exacerbations were experienced by 216 (56%) subjects during the study period. An <i>SFTPB</i> promoter polymorphism, rs3024791, was associated with COPD exacerbations. Logistic regression models, analysing a binary outcome of presence or absence of exacerbations, confirmed the association of rs3024791 with COPD exacerbations. Negative binomial regression models demonstrated association of multiple <i>SFTPB</i> SNPs (rs2118177, rs2304566, rs1130866 and rs3024791) with exacerbation rates. Polymorphisms in <i>EPHX1</i>, <i>GSTP1</i>, <i>TGFB1</i> and <i>SERPINE2</i> did not demonstrate association with COPD exacerbations. In conclusion, genetic variation in surfactant protein B is associated with chronic obstructive pulmonary disease susceptibility and exacerbation frequency.
Emergence of the Drug-Resistant Phenotype in Tumor Subpopulations: A Hybrid Model
Authors: S. Michelson, D. Slate
Journal: JNCI Journal of the National Cancer Institute (1989)

A mathematical model is proposed that describes the emergence of drug resistance in a tumor cell population. The model is termed a hybrid in the sense that the population-wide dynamics are described by a stochastic birth-death-migration model with transition probabilities dependent on the deterministic distribution of drug within the average cell. In the model, the probability that a cell dies is proportional to the concentration of drug within the target site in the cell. The micropharmacology describing the distribution of drug within the average cell is described by a standard well-mixed compartment model. Possible mechanisms that can confer drug resistance on a cell are described: decreased drug uptake, increased drug efflux, intracellular metabolism or inactivation, or both, of a drug, and a change in the level or sensitivity of a target. The biologic mechanisms underlying resistance and potential strategies for overcoming it are discussed within the context of our model. Results from a numerical simulation are presented as verification of the initial theory.
DOUBLE-BLIND STUDY OF IVERMECTIN AND DIETHYLCARBAMAZINE IN AFRICAN ONCHOCERCIASIS PATIENTS WITH OCULAR INVOLVEMENT
Authors: Michel Lariviere, Mohammed Aziz, Daniel Weimann, Jacques Ginoux, Philippe Gaxotte, Pierre Vingtain, Bernadette Beauvais, Francis Derouin, Hartwig Schulz-Key, Didier Basset, Claudine Sarfati
Journal: The Lancet (1985)
Active Immunization Against the Vascular Endothelial Growth Factor Receptor flk1 Inhibits Tumor Angiogenesis and Metastasis
Authors: Yiwen Li, Mei-Nai Wang, Hongli Li, Karen D. King, Rajiv Bassi, Haijun Sun, Angel Santiago, Andrea T. Hooper, Peter Bohlen, Daniel J. Hicklin
Journal: The Journal of Experimental Medicine (2002)

The vascular endothelial growth factor (VEGF) receptor fetal liver kinase 1 (flk1; VEGFR-2, KDR) is an endothelial cell–specific receptor tyrosine kinase that mediates physiological and pathological angiogenesis. We hypothesized that an active immunotherapy approach targeting flk1 may inhibit tumor angiogenesis and metastasis. To test this hypothesis, we first evaluated whether immune responses to flk1 could be elicited in mice by immunization with dendritic cells pulsed with a soluble flk1 protein (DC-flk1). This immunization generated flk1-specific neutralizing antibody and CD8+ cytotoxic T cell responses, breaking tolerance to self-flk1 antigen. Tumor-induced angiogenesis was suppressed in immunized mice as measured in an alginate bead assay. Development of pulmonary metastases was strongly inhibited in DC-flk1–immunized mice challenged with B16 melanoma or Lewis lung carcinoma cells. DC-flk1 immunization also significantly prolonged the survival of mice challenged with Lewis lung tumors. Thus, an active immunization strategy that targets an angiogenesis-related antigen on endothelium can inhibit angiogenesis and may be a useful approach for treating angiogenesis-related diseases.
An immunoglobulin Cκ-reactive single chain antibody fusion protein induces tolerance through receptor editing in a normal polyclonal immune system
Authors: Djemel Ait-Azzouzene, Laurent Verkoczy, Jorieke Peters, Amanda Gavin, Patrick Skog, José Luis Vela, David Nemazee
Journal: The Journal of Experimental Medicine (2005)

Understanding immune tolerance mechanisms is a major goal of immunology research, but mechanistic studies have generally required the use of mouse models carrying untargeted or targeted antigen receptor transgenes, which distort lymphocyte development and therefore preclude analysis of a truly normal immune system. Here we demonstrate an advance in in vivo analysis of immune tolerance that overcomes these shortcomings. We show that custom superantigens generated by single chain antibody technology permit the study of tolerance in a normal, polyclonal immune system. In the present study we generated a membrane-tethered anti-Igκ–reactive single chain antibody chimeric gene and expressed it as a transgene in mice. B cell tolerance was directly characterized in the transgenic mice and in radiation bone marrow chimeras in which ligand-bearing mice served as recipients of nontransgenic cells. We find that the ubiquitously expressed, Igκ-reactive ligand induces efficient B cell tolerance primarily or exclusively by receptor editing. We also demonstrate the unique advantages of our model in the genetic and cellular analysis of immune tolerance.
Intracoronary Bone Marrow Mononuclear Cells After Myocardial Infarction—Reply
Authors: Jay H. Traverse, Timothy D. Henry, Carl J. Pepine
Journal: JAMA (2012)

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LATE CARDIAC ABNORMALITIES AFTER ANTHRACYCLINE THERAPY IN ASYMPTOMATIC ADULT SURVIVORS OF CHILDHOOD CANCER: LONG-TERM FOLLOW-UP STUDY FROM THE MEMORIAL SLOAN-KETTERING CANCER CENTER
Authors: Jennifer E. Liu, Jayant Raikhelkar, Kevin Oeffinger, Emily Zabor, Roberto Adsuar, Emily Tonorezos, Richard Steingart
Journal: Journal of the American College of Cardiology (2011)
Cell Surface Tetraspanin Tspan8 Contributes to Molecular Pathways of Exosome-Induced Endothelial Cell Activation
Authors: Irina Nazarenko, Sanyukta Rana, Alexandra Baumann, Jessica McAlear, Andrea Hellwig, Michael Trendelenburg, Günter Lochnit, Klaus T. Preissner, Margot Zöller
Journal: Cancer Research (2010)

Tumor-derived exosomes containing the tetraspanin Tspan8 can efficiently induce angiogenesis in tumors and tumor-free tissues. However, little information exists on exosome-endothelial cell (EC) interactions or the proangiogenic role of tetraspanins, which are a constitutive component of exosomes. In this study, we used a rat adenocarcinoma model (AS-Tspan8) to explore the effects of exosomal Tspan8 on angiogenesis. Tspan8 contributed to a selective recruitment of proteins and mRNA into exosomes, including CD106 and CD49d, which were implicated in exosome-EC binding and EC internalization. We found that EC internalized Tspan8-CD49d complex-containing exosomes. Exosome uptake induced vascular endothelial growth factor (VEGF)-independent regulation of several angiogenesis-related genes, including von Willebrand factor, Tspan8, chemokines CXCL5 and MIF, chemokine receptor CCR1, and, together with VEGF, VEGF receptor 2. EC uptake of Tspan8-CD49d complex-containing exosomes was accompanied by enhanced EC proliferation, migration, sprouting, and maturation of EC progenitors. Unraveling these new pathways of exosome-initiated EC regulation could provide new options for therapeutic interference with tumor-induced angiogenesis.
Identification of <i>Carboxypeptidase of Glutamate Like-B</i> as a Candidate Suppressor in Cell Growth and Metastasis in Human Hepatocellular Carcinoma
Authors: Pingping Zhang, David Wai Chan, YiYi Zhu, Jin Jun Li, Irene Oi-Lin Ng, Dafang Wan, Jianren Gu
Journal: Clinical Cancer Research (2006)

Abstract Purpose: We have previously done large-scale cDNA transfection screening on human hepatocellular carcinoma (HCC) cells and have identified 3,806 cDNA genes that possess the ability of either stimulating or inhibiting cell growth. In this study, we characterized one of these growth suppressor genes, carboxypeptidase of glutamate like-B (CPGL-B), in HCC. Experimental Design: Semiquantitative reverse-transcription PCR was used to examine the expression levels of CPGL-B. The cellular localization and functions of CPGL-B were investigated by enforced expression of CPGL-B in HCC cells. Results: From our previous cDNA transfection screening, we identified a gene named CPGL and its isoform, CPGL-B. With computational analysis, CPGL was located at chromosome 18q22.3 and was a homologue of peptidase family M20. CPGL was expressed in all adult and fetal tissues, whereas its isoform, CPGL-B, lacking exons 3 and 4, was expressed in all fetal tissues but only in liver and placenta of adult tissues. In HCC, CPGL-B was frequently underexpressed (35 of 90, 38.9%) in tumorous tissues compared with the corresponding nontumorous livers. Intriguingly, the underexpression was significantly associated with the presence of venous invasion (P = 0.018) and tumor microsatellite formation (P = 0.004). Stable transfection of CPGL-B in SMMC7721 HCC cells showed significant inhibition in cell viability, colony formation, cell invasion, and tumor formation in nude mice. CPGL-B also down-regulated CXCR3, matrix metalloproteinase 11, and CD44s, which are involved in cell growth and cell migration. Conclusions: These findings suggest that the frequent underexpression of CPGL-B may be associated with cell growth and metastasis of HCC.