tbuckley/cabot-search huggingface dataset:
Radioactive Jewelry as Cause of Cutaneous Tumor
Authors: Marvin N. Winer
Journal: JAMA (1968)

<h3>To the Editor:—</h3> A common dermatologic complaint is an eruption beneath the ring finger. This is usually attributed to an accumulation of alkali soaps and detergents and is diagnosed as an irritative type of contact dermatitis. In April 1967, Simon and Harley<sup>1</sup>reported the cases of a husband and wife who wore gold wedding rings, and subsequently a radiodermatitis developed. Dr. Richard Leone presented a similar case at the Central States Dermatologic Society in Buffalo on May 25, 1968. The following case report is therefore the third we know of, and is complicated by the development of a squamous cell carcinoma which required amputation of the ring finger. <h3>Report of a Case:—</h3> A 50-year-old white man complained of a lesion involving the left ring finger. Over a period of 30 years, the patient had worn three different rings. A cameo ring, which he had purchased in December 1935, was worn
Herbert Davis Donald Hugh Garrow Glaslyn J Griffiths Douglas Abeysinghe Gunawardena Gerald Rookledge Holtby John Archibald Orr Cyril Rabbs Abdul Rashid Anne Patricia Roberts Norman Edward Winstone
Authors: E. North
Journal: BMJ (2001)

King's College and Charing Cross 1942; FRCS), died from oesophageal cancer on
Overexpression of uridine diphospho glucuronosyltransferase 2B17 in high-risk chronic lymphocytic leukemia
Authors: Michaela Gruber, Judith Bellemare, Gregor Hoermann, Andreas Gleiss, Edit Porpaczy, Martin Bilban, Trang Le, Sonja Zehetmayer, Christine Mannhalter, Alexander Gaiger, Medhat Shehata, Karin Fleiss, Cathrin Skrabs, Éric Lévesque, Katrina Vanura, Chantal Guillemette, Ulrich Jaeger
Journal: Blood (2012)
NATRIURETIC PEPTIDES ARE ASSOCIATED WITH LEFT VENTRICULAR FILLING PRESSURE IN MI PATIENTS WITH NEAR NORMAL EJECTION FRACTION
Authors: Mads J. Andersen, John Bro-Jeppesen, Mads Ersboll, Jacob Møller, Christian Hassager, Lars Kober, Jens Goetze, Finn Gustafsson
Journal: Journal of the American College of Cardiology (2014)
Rheumatoid arthritis: a psychiatric assessment
Authors: A J D Macdonald
Journal: BMJ (1981)

and the astute pathologist (I)r D Eakins) noted that the lymph node attached to the gall bladder showcd classical sarcoid.When she Xwas admitted on that occasion hcr x-ray film showed infiltrative changes and her EGG showed first-degree heart block xwith dropped beats and left bundle-branch block.''hus there was definite active sarcoidosis at the age of 88 years, though not actually "acute sarcoidosis" as rcported by Dr Brown and his colleagues.In our study of sarcoid heart disease' we now have over 200 cases reported to us, 67 with necropsy confirmation.Over 80 of these are from East Anglia (necropsy proof in 28).We still feel that this high local prevalence might be due to our known interest and would ask that any further possible cases in the United Kingdom should be reported to us.
Univentricular heart of right ventricular type with double or common inlet.
Authors: B R Keeton, F J Macartney, S Hunter, C Mortera, P Rees, E A Shinebourne, M Tynan, J L Wilkinson, R H Anderson
Journal: Circulation (1979)

Seventeen cases are described in which both atria connect directly to a chamber with right ventricular characteristics. The atria connected through separate atrioventricular valves in six hearts and a common valve in 11. All hearts had a posterior rudimentary chamber. The septum which separated it from the main chamber was directed to the crux of the heart. Ten hearts were from patients with atrial situs solitus and seven from patients with atrial situs ambigous. Arterial connections were concordant in three cases, had a double outlet from the main ventricular chamber in nine and single outlet of the heart in five. The patent artery always arose from the main chamber, with pulmonary atresia in three and aortic atresia in two. This and other studies indicate that double inlet atrioventricular connection does not predict the morphology of the main chamber. Although usually associated with a main chamber of left ventricular type, it may also be associated with a main chamber having right ventricular characteristics. Both types should be considered as univentricular hearts; the posterior chamber in hearts of right ventricular type are analogous to the anterior chamber in univentricular hearts of left ventricular type and are a rudimentary chamber rather than a hypoplastic ventricle. In the right ventricular form of univentricular heart, the trabecular zone of the rudimentary chamber is of left ventricular type.
Identification of Pax5 as a Target of MTA1 in B-Cell Lymphomas
Authors: Seetharaman Balasenthil, Anupama E. Gururaj, Amjad H. Talukder, Rozita Bagheri-Yarmand, Ty Arrington, Brian J. Haas, John C. Braisted, Insun Kim, Norman H. Lee, Rakesh Kumar
Journal: Cancer Research (2007)

Previously, we have shown that metastasis-associated protein 1 (MTA1) overexpression in transgenic mice was accompanied by high incidence of spontaneous B-cell lymphomas including diffuse large B-cell lymphomas (DLBCL). To understand the molecular basis of lymphoma in MTA1-transgenic (MTA1-TG) mice, we wished to identify a putative MTA1 target with a causal role in B-cell lymphogenesis. Using chromatin immunoprecipitation assays, we identified paired box gene 5 (Pax5), a molecule previously implicated in B-cell lymphogenesis, as a potential downstream effector of MTA1. Lymphomas from MTA1-TG mice also showed up-regulation of Pax5. We also found that MTA1 acetylated on Lys(626) interacted with p300 histone acetyltransferase, and that acetylated MTA1 was recruited to the Pax5 promoter to stimulate Pax5 transcription. Global gene profiling identified down-regulation of a set of genes, including those downstream of Pax5 and directly implicated in the B-cell lymphogenesis. Significance of these murine studies was established by evidence showing a widespread up-regulation of both MTA1 and Pax5 in DLBCL from humans. These observations provide in vivo genetic evidence for a role of MTA1 in lymphomagenesis.
Reversal of Endothelial Nitric Oxide Synthase Uncoupling and Up-Regulation of Endothelial Nitric Oxide Synthase Expression Lowers Blood Pressure in Hypertensive Rats
Authors: Huige Li, Klaus Witte, Michael August, Isolde Brausch, Ute Gödtel-Armbrust, Alice Habermeier, Ellen I. Closs, Mathias Oelze, Thomas Münzel, Ulrich Förstermann
Journal: Journal of the American College of Cardiology (2006)
Abstract 1053: Interplay of YB-1 and IL-6 in the acquisition of EMT-like characteristics
Authors: Barbara Castellana, Trond Aasen, Santiago Ramón y Cajal
Journal: Cancer Research (2014)

Abstract An important step towards tumor progression and metastasis is the activation of the epithelial-mesenchymal transition (EMT) program. This complex process confers cancer cells traits such as enhanced motility, invasiveness and resistance to therapy. EMT can be triggered by the convergence of intrinsic factors and signals from the tumor microenvironment, such as aberrant expression of cytokines. Recently, the multifunctional oncoprotein YB-1 has been shown to play an important role in malignant tumors facilitating many of the “hallmarks of cancer” proposed by Hanahan and Weinberg. In this project we focused on the alliance between YB-1 and the cytokine IL-6, which has been implicated in tumor-cell metastasis and is a well known EMT inducer. Overexpression or direct addition of IL-6 up-regulates and activates YB-1 in the epithelial breast cancer cell line MCF7, leading to an upregulation of mesenchymal markers (Snail1, N-cadherin), increased cell migration and invasion, as well as morphological changes associated with an EMT-like phenotype. Conversely, in the mesenchymal-like breast cancer cell line MDA-MB-231, RNAi-mediated downregulation of YB-1 resulted in decreased IL-6 expression and an increase in epithelial-like cell characteristics. Our results describe a novel interplay whereby IL-6 regulates YB-1 and vice versa creating a positive feed-forward loop driving EMT during breast cancer progression. In the future we aim to delineate the exact signalling pathways linking IL-6 and YB-1, and how they converge to orchestrate important processes such as growth, invasion and metastasis. The understanding of this interplay will set the stage for new combinatorial treatments of aggressive breast cancers. Acronyms: EMT, epithelial to mesenchymal transition; YB-1, Ybox binding protein-1; IL-6 , Interleukin-6. Citation Format: Barbara Castellana, Trond Aasen, Santiago Ramón y Cajal. Interplay of YB-1 and IL-6 in the acquisition of EMT-like characteristics. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1053. doi:10.1158/1538-7445.AM2014-1053
Galectin-3 deficiency prevents concanavalin A-induced hepatitis in mice
Authors: Vladislav Volarevic, Marija Milovanovic, Biljana Ljujic, Nada Pejnovic, Nebojsa Arsenijevic, Ulf Nilsson, Hakon Leffler, Miodrag L. Lukic
Journal: Hepatology (2011)

We used concanavalin A (Con A)-induced liver injury to study the role of galectin-3 (Gal-3) in the induction of inflammatory pathology and hepatocellular damage. We tested susceptibility to Con A-induced hepatitis in galectin-3-deficient (Gal-3(-/-)) mice and analyzed the effects of pretreatment with a selective inhibitor of Gal-3 (TD139) in wild-type (WT) C57BL/6 mice, as evaluated by a liver enzyme test, quantitative histology, mononuclear cell (MNC) infiltration, cytokine production, intracellular staining of immune cells, and percentage of apoptotic MNCs in the liver. Gal-3(-/-) mice were less sensitive to Con A-induced hepatitis and had a significantly lower number of activated lymphoid and dendritic cells (DCs) in the liver. The level of tumor necrosis factor alpha (TNFα), interferon gamma (IFNγ), and interleukin (IL)-17 and -4 in the sera and the number of TNFα-, IFNγ-, and IL-17- and -4-producing cluster of differentiation (CD)4(+) cells as well as IL-12-producing CD11c(+) DCs were lower, whereas the number of IL-10-producing CD4(+) T cells and F4/80(+) macrophages were significantly higher in livers of Gal-3(-/-) mice. Significantly higher percentages of late apoptotic Annexin V(+) propidium-idodide(+) liver-infiltrating MNCs and splenocytes were observed in Gal-3(-/-) mice, compared to WT mice. Pretreatment of WT C57BL/6 mice with TD139 led to the attenuation of liver injury and milder infiltration of IFNγ- and IL-17- and -4-producing CD4(+) T cells, as well as an increase in the total number of IL-10-producing CD4(+) T cells and F4/80(+) CD206(+) alternatively activated macrophages and prevented the apoptosis of liver-infiltrating MNCs.Gal-3 plays an important proinflammatory role in Con A-induced hepatitis by promoting the activation of T lymphocytes and natural killer T cells, maturation of DCs, secretion of proinflammatory cytokines, down-regulation of M2 macrophage polarization, and apoptosis of MNCs in the liver.
Infectious Diseases of Humans: Dynamics and Control
Authors: Joel E. Cohen
Journal: JAMA (1992)

This long and important book summarizes the results of nearly a decade and a half of collaboration between two of the world's best analysts of infectious diseases and alludes to related work by many others. The authors are Roy M. Anderson, FRS, of Imperial College, University of London, and Robert M. May, FRS and Foreign Member of the US National Academy of Sciences, of the University of Oxford. The authors write, "The primary aim of this book is to show how simple mathematical models of the transmission of infectious agents within human communities can help to interpret observed epidemiological trends, to guide the collection of data towards further understanding, and to design programmes for the control of infection and disease. Our major goal is further understanding of the interplay between the variables that determine the course of infection within an individual, and the variables that control the pattern of infection
Abstract 5240: Differential anticancer drug response by high-dimensional protein monitoring.
Authors: Satoshi S. Nishizuka, Kazushige Ishida, Go Wakabayashi
Journal: Cancer Research (2013)

Abstract Cellular signal transduction responses to drugs are not always identical; rather, they depend on concentration, administration method, and time after administration. To monitor drug-induced signaling, we produced “reverse-phase” protein arrays (RPPAs) using cell lysates from three anticancer drugs (5FU, CIS, CPT), two administration methods (sustained, Sus; temporal, Tem), and three concentrations (High, Medium, Low) of drug administration over a 24-hour period. The combination of drug types, concentrations, and administration methods collectively yielded 18 unique drug administration conditions. Each RPPA was individually probed with 37 primary antibodies from our antibody panel; these antibodies recognize the proteins involved in genotoxic stress response. The quantitative readout was then analyzed to see if there was: (i) a general trend in protein dynamics in response to each drug condition; and (ii) significance in those proteins that exhibited similar dynamics. We first classified 666 time-course protein dynamics. About 38% of the protein dynamics showed an increasing trend, whereas about 32% showed a decreasing trend. Proteins exhibited earlier peaks when stimulated by Low or Medium concentrations for all drugs, while proteins exhibited later peaks when stimulated by High concentrations. Clustering analysis of protein dynamics induced by drugs revealed that each dynamic class included proteins of diverse functions. Hence, it is unlikely for cells to respond to particular drugs in a defined pattern. Subsequently, to clarify whether any functional associations are prioritized in drug responses, we evaluated the similarities between the protein dynamics by distance correlation (DC, which is known to have a higher value the tighter the association), to see if any pair of protein dynamics demonstrated a geometric similarity associated with its known interaction. It appeared that apoptosis-related proteins tended to show high DC to other proteins when anticancer drugs were administrated at high enough concentrations to induce apoptosis. We also found that structural cell proteins, such as keratins, showed high DC to apoptosis-related proteins, and confirmed that when these two functional protein groups interact, what results is degradation in the progression of drug-induced apoptosis.These observations indicate that high-dimensional drug response protein dynamic monitoring by RPPAs may offer a unique opportunity to find drug-specific general dynamic trends and potentially novel protein interactions unique to drug administrative conditions such as dose. Citation Format: Satoshi S. Nishizuka, Kazushige Ishida, Go Wakabayashi. Differential anticancer drug response by high-dimensional protein monitoring. [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 5240. doi:10.1158/1538-7445.AM2013-5240
Crosstalk between the Estrogen Receptor and the HER Tyrosine Kinase Receptor Family: Molecular Mechanism and Clinical Implications for Endocrine Therapy Resistance
Authors: Grazia Arpino, Lisa Wiechmann, C. Kent Osborne, Rachel Schiff
Journal: Endocrine Reviews (2008)

Breast cancer evolution and tumor progression are governed by the complex interactions between steroid receptor [estrogen receptor (ER) and progesterone receptor] and growth factor receptor signaling. In recent years, the field of cancer therapy has witnessed the emergence of multiple strategies targeting these specific cancer pathways and key molecules (ER and growth factor receptors) to arrest tumor growth and achieve tumor eradication; treatment success, however, has varied and both de novo (up front) and acquired resistance have proven a challenge. Recent studies of ER biology have revealed new insights into ER action in breast cancer and have highlighted the role of an intimate crosstalk between the ER and HER family signaling pathways as a fundamental contributor to the development of resistance to endocrine therapies against the ER pathway. The aim of this review article is to summarize the current knowledge on mechanisms of resistance of breast cancer cells to endocrine therapies due to the crosstalk between the ER and the HER growth factor receptor signaling pathways and to explore new available therapeutic strategies that could prolong duration of response and circumvent endocrine resistant tumor growth.
Strength of Study Evidence Examined by the FDA in Premarket Approval of Cardiovascular Devices
Authors: Sanket S. Dhruva
Journal: JAMA (2009)

<h3>Context</h3>Medical devices are common in clinical practice and have important effects on morbidity and mortality, yet there has not been a systematic examination of evidence used by the US Food and Drug Administration (FDA) for device approval.<h3>Objectives</h3>To study premarket approval (PMA)—the most stringent FDA review process—of cardiovascular devices and to characterize the type and strength of evidence on which it is based.<h3>Data Sources and Study Selection</h3>Systematic review of 123 summaries of safety and effectiveness data for 78 PMAs for high-risk cardiovascular devices that received PMA between January 2000 and December 2007.<h3>Data Extraction</h3>Examination of the methodological characteristics considered essential to minimize confounding and bias, as well as the primary end points of the 123 studies supporting the PMAs.<h3>Results</h3>Thirty-three of 123 studies (27%) used to support recent FDA approval of cardiovascular devices were randomized and 17 of 123 (14%) were blinded. Fifty-one of 78 PMAs (65%) were based on a single study. One hundred eleven of 213 primary end points (52%) were compared with controls and 34 of 111 controls (31%) were retrospective. One hundred eighty-seven of 213 primary end points (88%) were surrogate measures and 122 of 157 (78%) had a discrepancy between the number of patients enrolled in the study and the number analyzed.<h3>Conclusion</h3>Premarket approval of cardiovascular devices by the FDA is often based on studies that lack adequate strength and may be prone to bias.
Analysis of histocompatibility requirements for proliferative and helper T cell activity. T cell populations depleted of alloreactive cells by negative selection.
Authors: W W Shih, P C Matzinger, S L Swain, R W Dutton
Journal: The Journal of Experimental Medicine (1980)

T cell populations were prepared from donors immunized with hapten-carrier conjugates and were depleted of alloreactive cells by negative selection. This was accomplished by injection of the cells into H-2-disparate irradiated recipients and recovery from the thoracic duct after 18-40 h. The genetic requirements for the proliferative and helper activity of these populations was determined. The proliferative response to antigen presented on adherent, Thy-1-negative cells was determined, and a requirement for syngeneic antigen-presenting cells (APC) was demonstrated. The same T cells were assayed for their ability to give help to hapten primed B cells. It was shown that there was a requirement for syngeneic APC and for linked recognition of hapten and carrier determinants on the same molecule by the B cell and T cell. There was no requirement for the B cell to be H-2 compatible with the T cell. The requirement for linked recognition was taken as evidence that the responses in allogeneic combinations were not a result of positive allogeneic effects. Precisely comparable restrictions were found with positively selected cells.
Food Hypersensitivity in Patients with Pollen Allergy
Authors: Nils E. Eriksson, Hans Formgren, Eivor Svenonius
Journal: Allergy (1982)

Six hundred patients with pollen allergy answered a questionnaire about food hypersensitivity. Hypersensitivity to various nuts, fruits and roots was reported more often by patients with birch pollen allergy (70%) than by patients without birch pollen allergy (19%). The stronger the skin test reaction to birch pollen, the higher was the incidence of food hypersensitivity. A negative correlation was found between grass pollen allergy and food hypersensitivity. In the diagnosis of springtime hayfever, the presence of hypersensitivity to nuts, fruits and roots supports a diagnosis of birch pollen allergy.
Eosinophilic apoptosis in sinus mucosa: Relationship to tissue eosinophilia and its resolution in allergic sinusitis
Authors: Guo-Kang Fan, Takashi Itoh, Masashi Imanaka, Shigeharu Fujieda, Hiroshi Takenaka
Journal: Journal of Allergy and Clinical Immunology (2000)

<h2>Abstract</h2> <b>Background:</b> Apoptosis, which is regulated by both cell survival and death signals, is important for the swift clearance of unwanted cells. <b>Objective:</b> We sought to elucidate whether eosinophilic apoptosis is associated with tissue eosinophilia and to determine its resolution in allergic sinusitis (AS). <b>Methods:</b> Numbers of eosinophils, numbers of IL-5<sup>+</sup> cells, and the apoptosis index of eosinophils were calculated in the submucosa (both superficial and deep layers) of patients with AS by using histochemical methods before and after prednisolone treatment. Patients without AS were used for control groups. Anti-EG2 antibody was used to identify eosinophils. IL-5, Fas, or Bax expression of eosinophils was evaluated to elucidate the role of the factors affecting eosinophilic apoptosis. <b>Results:</b> EG2 and IL-5<sup>+</sup> cells were abundant in the submucosa of patients with AS, especially in the superficial layer. About 50% to 60% of the IL-5–producing cells were eosinophils. Apoptotic eosinophils were less numerous in the superficial layer than the deep layer in these diseases. After prednisolone treatment, an induction of eosinophilic apoptosis was accompanied by a significant decrease in the number of EG2<sup>+</sup> and IL-5<sup>+</sup> cells. No remarkable difference was observed in the Fas or Bax expression of eosinophils after prednisolone treatment. <b>Conclusion:</b> Autocrine secretion of IL-5 from eosinophils may be one reason why eosinophilic disease is difficult to manage. Induction of eosinophilic apoptosis is critical for reversing tissue eosinophilia in patients with AS. (J Allergy Clin Immunol 2000;106:551-8.)