tbuckley/cabot-search huggingface dataset:
Cardiac incidentaloma during endoscopic ultrasound: cardiac myxoma with Gamna–Gandy bodies
Authors: Paula Fazendas, Pedro Marques, Francisco Tortosa, Ricardo Tinto, Cláudia Reis, Carlos Cotrim, Helder Pereira
Journal: Endoscopy (2014)

A 63-year-old female patient underwent endoscopic ultrasonography (EUS) for a gastric subepithelial lesion previously identified during upper endoscopy. A linear echoendoscope (Olympus UCT140AL5; Olympus, Tokyo, Japan) was used and no subepithelial lesion was found. However, a systematic evaluation revealed a 2-cm mass in the left atrium ([Fig. 1]). A transesophageal echocardiogram (TEE) confirmed the presence of a sessile mass, which was adherent to the upper third of the interatrial septum in the left atrium, with a heterogeneous appearance and a slight multilobulated contour (area 3.9 cm2, dimensions 2.4 × 1.94 cm) ([Fig. 2]).
BOOKS IN REVIEW 1990
Authors: E. J. SEIFTER
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article BOOKS IN REVIEW 1990 Get access ERIC J. SEIFTER ERIC J. SEIFTER Book Review Editor,Johns Hopkins UniversityBaltimore, MD 21201 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 3, 6 February 1991, Pages 208–209, https://doi.org/10.1093/jnci/83.3.208 Published: 06 February 1991
Chronic lymphocytic leukemia: 2013 update on diagnosis, risk stratification and treatment
Authors: Michael Hallek
Journal: American Journal of Hematology (2013)

Chronic lymphocytic leukemia (CLL) is the commonest leukemia in western countries. The disease typically occurs in elderly patients and has a highly variable clinical course. Leukemic transformation is initiated by specific genomic alterations that impair apoptosis of clonal B-cells.The diagnosis is established by blood counts, blood smears, and immunophenotyping of circulating B-lymphocytes, which identify a clonal B-cell population carrying the CD5 antigen as well as B-cell markers.Two prognostic staging systems exist, the Rai and Binet staging systems, which are established by physical examination and blood counts. Various biological and genetic markers also have prognostic value. Deletions of the short arm of chromosome 17 (del(17p)) predict resistance to most available therapies.Patients with active or symptomatic disease or with advanced Binet or Rai stages require therapy. For physical fit patients, chemoimmunotherapy with fludarabine, cyclophosphamide and rituximab represents the current standard therapy. For unfit patients, treatment with an anti-CD20 antibody plus a milder chemotherapy (chlorambucil) is currently established as standard treatment. At relapse, the initial treatment may be repeated, if the treatment-free interval exceeds two years. If the disease relapses earlier, alternative therapies such as bendamustine alone or with rituximab, alemtuzumab, lenalidomide, or ofatumumab should be used. Patients with a del(17p) or TP53 should be considered for an allogeneic SCT.Several new agents (e.g., ibrutinib, obinutuzumab) hold the potential to change standard of CLL treatment in the next 6-12 months. Therefore, CLL patients should be included into current clinical trials whenever possible.
Treatment of Incapacitated Euthyroid Cardiac Patients by Producing Hypothyroidism with Radioactive Iodine
Authors: Herrman L. Blumgart, A. Stone Freedberg, George S. Kurland
Journal: New England Journal of Medicine (1951)

THE purpose of this communication is to summarize our experience since November, 1947, in treating 37 patients with chronic heart disease by lessening the cardiac work through inducing hypothyroidism with radioactive iodine (I131).1 2 3 Our efforts have proceeded in four main directions: the clinical appraisal of the therapeutic value of the procedure; study of possible deleterious radiation effects; establishment of criteria for the proper selection of patients; and investigation and control of the secondary consequences of the hypothyroid state. Although final conclusions concerning these problems must await the results obtained over many years in various clinics, it may be helpful . . .
OP0226 Human Mast Cells Engulf and Store Exogenous IL-17A
Authors: T. Noordenbos, J.E. Paramarta, I.C. Blijdorp, L.J. van Mens, J. Stap, R.A. Hoebe, E. Mul, N.G. Yeremenko, D.L. Baeten
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> IL-17A plays an important role in rheumatic diseases, like rheumatoid arthritis and spondyloarthritis. Direct analysis of inflamed synovial tissue revealed an abundant presence of IL-17A-positive mast cells. <h3>Objectives</h3> As mast cells are not known to produce IL-17A in mice, we aimed to investigate the mechanism of IL-17A expression by human mast cells. <h3>Methods</h3> IL-17A, IL-17F and RORC mRNA and protein expression was assessed ex vivo and after PMA/ionomycine stimulation in primary human mast cells sorted from tonsils. Internalization of exogenous IL-17A was assessed by Western blot, imagestream, live imaging and confocal microscopy. <h3>Results</h3> Immunohistochemistry and western blot analysis confirmed the presence of IL-17A protein in primary human mast cells. In contrast to T cells, however, mast cells did not express RORC protein, the exclusive transcriptional factor controlling IL-17A expression. Accordingly, <i>IL17A</i>, <i>IL17F</i>, and <i>RORC</i> gene expression was readily detectable in sorted T lymphocytes but not in mast cells, even after ex vivo stimulation. Given the discrepancy between the presence of IL-17A protein and absence of its transcriptional machinery, we investigated the uptake of GFP-fused or 6xhistidin-tagged recombinant IL-17A. Imagestream and Western blot indicated that both primary mast cells and the LAD2 mast cell line engulf and store exogenous IL-17A. Live imaging and confocal microscopy revealed that internalized IL-17A is stored in endocytic vesicles and that this uptake can be blocked by inhibiting receptor-mediated endocytosis. <h3>Conclusions</h3> Human mast cells do not produce IL-17A but engulf and store exogenous IL-17A from the inflamed milieu. Molecular pathways of IL-17A uptake and eventually release are under investigation. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2566
Abstract PL03-02: Microenvironment survival signals for disseminated cancer cells
Authors: Joan Massagué
Journal: Cancer Research (2011)

Abstract To form metastases, circulating cancer cells that egress into a distant parenchyma must be able to survive in the newly invaded microenvironment. Identifying these survival mechanisms may provide therapeutic strategies for the eradication of disseminated disease and the prevention of metastasis. In breast cancer, where relapse develops in an organ-specific manner, we have identified metastasis progression genes that prime cancer cells for extravasation into specific organs, as well as genes that mediate overt metastatic colonization. However, the survival of newly extravasated cells depends on a distinct set of genes and pathways. SRC primes breast cancer cells for survival in the bone marrow by potentiating AKT activation by CXCL12 and IGF1, cytokines that are abundant in the marrow. Recent work revealed how bone metastatic seeds may be preselected in the primary tumor. In the lungs, VCAM1- and tenascin-C support the survival of micrometastatic cancer cells. The mechanisms involve interactions with tumor-infiltrating leukocytes and an extracellular matrix niche. Inhibition of SRC, VCAM1 and tenascin-C suppresses experimental micrometastases and the growth of aggressive lesions. 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 PL03-02. doi:10.1158/1538-7445.AM2011-PL03-02
F-18 FDG PET/CT Findings of Primary Sinonasal Hemangiopericytoma
Authors: Mustafa Aras, Fuat Dede, Tunc Ones, Beste Melek Atasoy, Sabahat Inanir, Tanju Yusuf Erdil, Halil Turgut Turoglu
Journal: Clinical Nuclear Medicine (2011)

Hemangiopericytoma is an unusual tumor that arises from vascular smooth muscle cells. It is mainly experienced in 4th to 5th decades of life and soft-tissue masses are frequently located in lower extremity, pelvis, and retroperitoneum. A 29-year-old man presented with a mass lesion in the right nasal cavity associated with shortness of breath as a result of nasal obstruction. An incisional biopsy was reported as sinonasal type hemangiopericytoma. The initial staging F-18 flourodeoxyglucose PET/CT successfully demonstrated severe hypermetabolism in the primary tumor location and mild-to-moderate hypermetabolism in the right upper jugular lymph node.
Abstract 5129: Mapping the activity of oncogenic signaling networks with phospho-specific Liquid Tissue® mass spectrometry
Authors: Todd A. Hembrough, Sheeno Thyparambil, Wei-Li Liao, David Krizman, Marlene Darfler, Kathleen Bengali, Joe Abdo, Jon Burrows
Journal: Cancer Research (2011)

Abstract Many of the current targeted therapies in oncology target the activity of either receptor tyrosine kinases (Her2, EGFR, IGF1R, cMet, FGFR, PGDFR) or cytoplasmic tyrosine kinases (cSrc, AurA, PI3K, MEK, Raf, Akt). The current slate of clinically useful diagnostic tests measure target expression either directly by immunohistochemistry or indirectly by extrapolation from the level of gene or mRNA expression/amplification. These assays are limited by lack of quantitation, and no assay can directly assess the activation state of the signaling pathway components. The lack of information regarding target activation and downstream signal transduction can be overcome using the Liquid Tissue®-SRM technology platform. This approach enables relative and absolute quantification of multiple proteins and their phosphorylation status directly in formalin fixed tissue. In order to fill this diagnostic ‘gap’ we have used this platform to develop a quantitative multiplexed phospho-target assay format which measures the specific phosphorylation state of many clinically relevant oncogenic kinases (EGFR, cMet, Her3, Erk, cSrc, Mek, Akt, p70S6K) directly in FFPE tumor tissue. This phosphopeptide multiplex assay was initially preclinically validated on the A431 tumor cell line which harbors an amplification of the EGFR gene. These cells were stimulated with a dose range of EGF (50-200ng/ml) or in a time course study (EGF 50ng/ml for 5-30min). Confluent, EGF stimulated cells were then formalin fixed, subjected to Liquid Tissue® processing, and then phospho-enriched using TiO2 magnetic beads. The resulting enriched phosphopeptides were then analyzed by mass spectrometry. This method demonstrated the feasibility, and reproducibility of this method for quantitating EGFR pY1197, EGFRpT693, AKT pS473, p-p70S6K pS447, ERK pT202/pY204. We extended this study by performing phosphoenrichment and mass spectrometric analysis of human tumor xenografts, primary human tumor NSCLC explants and clinical trial tissue from EGFR inhibitor treated NSCLC and colorectal cancer patients. In each case we were able to enrich and measure the phosphorylation of a large set of important oncogenic kinases. Our intention is to develop this diagnostic tool to provide a multiplex assay format in formalin fixed tissue that can be applied from preclinical to clinical studies that will impact both targeted drug development and patient stratification needs in this era of personalized healthcare. 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 5129. doi:10.1158/1538-7445.AM2011-5129
Emergence of chikungunya fever on the French side of Saint Martin island, October to December 2013
Authors: S Cassadou, S Boucau, M Petit-Sinturel, P Huc, I Leparc-Goffart, M Ledrans
Journal: Eurosurveillance (2014)

On 18 November 2013, five residents of Saint Martin presented with severe joint pain after an acute episode of dengue-like fever. Epidemiological, laboratory and entomological investigations provided evidence of the first autochthonous transmission of chikungunya virus in the Americas. The event indicates a risk of epidemics in America and Europe through substantial passenger traffic to and from continental France. We describe detection and confirmation of the first six cases and results of the first weeks of surveillance.
LEFT VENTRICULAR LONGITUDINAL DYSFUNCTION ASSESSED BY LONGITUDINAL FRACTIONAL SHORTENING: A CLINICAL TWO-DIMENSIONAL ECHOCARDIOGRAPHIC STUDY
Authors: Yuya Adachi, Tetsuro Ohta, Kimiko Hiroe, Kouji Matsuda, Masaki Takeda, Seiji Okada, Kazuaki Tanabe
Journal: Journal of the American College of Cardiology (2016)
AB0131 NAMPT/VISFATIN in osteoarthritis: An adipokine involved in the communication between cartilage and bone
Authors: M.-C. Laiguillon, C. Bougault, S. Priam, M. Gosset, Z. Mladenovic, A. Pigenet, C. Jacques, X. Houard, F. Berenbaum, J. Sellam
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> It has been recently demonstrated that a pro-inflammatory adipokine called visfatin can be produced by chondrocytes in osteoarthritis (OA). Visfatin is also known as nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the salvage pathway of nicotinamide adenine dinucleotide (NAD) biosynthesis from nicotinamide. Interestingly, this pathway is involved in cytokine production such as TNFα. Recently, it has been suggested that the pathophysiology of OA may rely, at least in part, on the release of soluble mediators coming from chondrocytes and acting on bone cells. To date, the action of Nampt/visfatin on osteoblasts remains unknown. <h3>Objectives</h3> We aimed i) to investigate whether Nampt/visfatin could be responsible for osteoblast activation and ii) assess the role of the enzymatic activity in this osteoblast activation. <h3>Methods</h3> Osteoblasts were obtained by enzymatic digestion of calvaria from Swiss mice and cultured for 3 weeks. Cells were then stimulated with a recombinant Nampt/visfatinfor 24 hours. In order to evaluate the part of the enzymatic activity in the cell stimulation, a 4 hours pre-treatment of osteoblasts with APO866 (10nM), a specific competitive inhibitor of Nampt activity,was performed. The effects on IL-6, Kc (i.e. murine IL-8), IL-1β, MCP-1 and SDF-1 expression and on IL-6 and Kc release were assessed by quantitative PCR and enzyme-linked immunosorbent assay (ELISA), respectively. <h3>Results</h3> 5 μg/mL Nampt/visfatin (considered as the optimal concentration according to a dose-response experiment) significantly induced the expression of IL-6, Kc/IL-8, IL-1β, MCP-1 and SDF-1 mRNA (n=4) (Table). The release of IL-6 and Kc proteins was also increased by Nampt/visfatin (104 and 142-fold, respectively; n=4). The inhibition of Nampt/visfatinactivity by APO866 decreased this response at mRNA level (up to 73% of inhibition, see Table) as well as at protein level (38±25% and 42±17% of inhibition for IL-6 and Kc proteins release, respectively). APO866 alone had no effect on osteoblasts activation. The effect of Nampt/visfatin was selective since it did not significantly induce VEGF or TGFβ. <h3>Conclusions</h3> We demonstrate that Nampt/visfatinactivates osteoblasts partly through its enzymatic activity which is thus involved in the pro-inflammatory cytokine effect of visfatin. This study suggests that Nampt/visfatin could be part of the cytokine network involved in the communication between cartilage and bone in OA. <h3>Disclosure of Interest</h3> None Declared
Analgetic Drugs
Authors: Leroy D. Vandam
Journal: New England Journal of Medicine (1972)

"Pleasure is oft a visitant: but pain clings cruelly to us." [Keats, Endymion].TREATMENT of pain constitutes a large part of the physician's practice, and the most favorable results come from healing of the disease or eradication of the source of pain. Even when this is possible, symptomatic relief may be needed initially. Furthermore, many diseases causing pain cannot be treated specifically, and symptomatic treatment of the pain with analgetics becomes essential. Analgetics are by definition compounds that relieve pain on systemic administration without affecting consciousness. For a variety of therapeutic and legal reasons, these drugs fit loosely into two . . .
Abstract P2-06-03: A Polymorphic AAAG Repeat in the Estrogen Receptor-Related-Gamma Gene May Represent a Breast Cancer Predisposition Biomarker
Authors: HR Garner, JF McCormick, L-S Li, LJ McIver, VJ Bubb, AC George, DA Boothman, JP Quinn, C. Galindo
Journal: Cancer Research (2010)

Abstract Background: There is a strong genetic component to breast cancer, which is the most common neoplasm in women; however current risk markers are few, accounting for less than 10% of breast cancer cases. This means that the majority of familial breast cancers remain unexplained. Our laboratory has studied microsatellite polymorphisms for many years, and we developed techniques to assay these understudied regions of the genome en masse and individually via shot-gun methods to rapidly identify those that are likely to be polymorphic and therefore potentially contribute to phenotype. Material and Methods: Using these novel approaches, we identified a polymorphic AAAG microsatellite repeat in the estrogen-related receptor gamma (ERR-γ) that is expanded in -10% of the general population. We genotyped over 300 individuals and found a longer allelic version (13+ repeat copies) in 14.3% of breast cancer patients, compared to only 4.8% in cancer-free individuals. We computationally identified 22 transcription factors that could bind directly to this AAAG repeat and the surrounding region. We hypothesized that the AAAG-containing region might serve as a promoter for ERR-y. Results: We found a statistically significant number of breast cancer patients with the expanded AAAG allele, and preliminary experiments confirm that the AAAG-containing region of ERR-γ does indeed drive reporter gene expression in estrogen receptor positive (ER+) MCF-7 breast cancer cells. This was not the case for the ER-breast cancer cells (MDA-MB-231) we also examined. Our initial assessments also revealed that SKBR-3 breast cancer cells are naturally heterozygotic for the long and short allelic versions of the AAAG repeat. Our ongoing studies involve knockdown of transcription factors in MCF-7 cells that abrogate the endogenous expression of ERR-γ. Discussion: The role of microsatellites in cancer is well defined for colon cancer, but few studies have been conducted to examine the contribution of these simple sequence repeats in breast cancer. We discovered a polymorphic AAAG repeat in the ERR-γ gene, and our studies indicate that a longer version of this repeat is more prevalent in the genomes of breast cancer patients. Based on our assessment, this allele carries a 2.98 relative risk for the development of breast cancer. The higher incidence of this putative biomarker in breast cancer patients may be a result of altered ERR-γ expression, as the AAAG-containing sequence can drive reporter expression. If the frequency of this potentially predictive marker is sustained in a larger population, and the mechanism by which it confers the cancer phenotype can be identified, it may contribute substantially as a biomarker offering surveillance, prophylactic surgery, and chemoprevention options to patients. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P2-06-03.
PTH-111 Changes in Mri Enetrography in Crohn’S Patients Treated with Adalimumab
Authors: A Bajwa, S Vijayan, A Haynes, P Hawker, R Sinha
Journal: Gut (2013)

<h3>Introduction</h3> MRI enterography has become the gold standard radiological assessment for Crohn’s disease. The radiological response of Crohn’s disease following mono therapy with Adalimumab is not clearly documented. The aim of this study was to compare pre and post treatment MRI enterograms in Crohn’s patients on treatment with Adlumimab monotherapy <h3>Methods</h3> 24 consecutive Crohn’s patients being treated with Adalimumab monotherapy according to NICE guidelines. Median age was 37.5years (range 21–66). Pre treatment MRI enterograms were compared with enterograms at a median of 6 months after commencement of treatment. MRI parameters compared were bowel thickness (BT), enhancement ration (ER), diffusion value (DV) and the apparent diffusion coefficient (ADC). Post treatment enterograms were compared with 24 control subjects without inflammatory bowel disease. Changes in these parameters were further correlated with changes in biochemistry (FBC, CRP and Albumin) <h3>Results</h3> Significant improvements in all MRI parameters were noted with treatment (Mean changes: BT 2.0, p = &lt; 0.001; ER –0.32, p = &lt; 0.0001;DV –111.09, p = &lt; 0.0001, ADC 0.18, p = &lt; 0.0001). There was a trend to an improvement in biochemical parameters, none of which were statistically significant. Changes in biochemical parameters did not correlate with MRI changes. On comparison with control MRI enterograms, ER was the only parameter not significantly deleterious in Crohn’s patients indicating ongoing inflammation <h3>Conclusion</h3> Marked radiological improvement is apparent 6 months into Adalimumab monotherapy for Crohn’s disease. However, significant features of inflammation persist indicating mucosal healing has not been achieved in this treatment period. <h3>Disclosure of Interest</h3> None Declared.
Isolation of a Microtatobiote from Patients with Hemolytic-Uremic Syndrome and Thrombotic Thrombocytopenic Purpura and from Mites in the United States
Authors: Norma E. Mettler
Journal: New England Journal of Medicine (1969)

An organism provisionally classified as a microtatobiote, order of rickettsiales, family of bartonellaceae, was isolated from two patients with hemolytic-uremic syndrome (HUS) and from another with thrombotic-thrombocytopenic purpura. The same organism was recovered from mites collected in the bedroom of one of the children with HUS. The organism was seen in blood smears from the patients. Primary isolation was accomplished in vitro on blood-containing mediums and in vivo in guinea pigs. The organism was adapted to suckling mice. A complement-fixation (CF) system using experimental serums and infected mouse brain as a source of antigen was obtained. The four strains isolated were indistinguishable by morphology and by the CF test. Inoculation of infected mouse brain into rhesus monkeys reproduced a mild disease with anemia, thrombocytopenia and leukocytosis. The findings support the view that there is an etiologic relation between the agent isolated and the disease in the cases reported.