tbuckley/cabot-search huggingface dataset:
P1.05-014 Stemness Gene Expression Profile of Tumorspheres from Non-Small Cell Lung Cancer
Authors: Alejandro Herreros Pomares, Silvia Calabuig Fariñas, Ester Munera Maravilla, Ana Blasco, Aminta Isabel Martinez, Eva García Del Olmo, Eloisa Jantus-Lewintre, Carlos Camps
Journal: Journal of Thoracic Oncology (2017)
Bone marrow stem cell therapy partially ameliorates pathological consequences in livers of mice expressing mutant human α1‐antitrypsin
Authors: Prakash Baligar, Veena Kochat, Shailendra K. Arindkar, Zaffar Equbal, Snehashish Mukherjee, Swati Patel, Perumal Nagarajan, Sujata Mohanty, Jeffrey H. Teckman, Asok Mukhopadhyay
Journal: Hepatology (2017)

Alpha‐1‐antitrypsin (AAT) deficiency (AATD) is a genetic disease, caused by mutation of the AAT gene. Accumulation of mutated AAT protein aggregates in hepatocytes leads to endoplasmic reticulum stress, resulting in impairment of liver functions and, in some cases, hepatocellular carcinoma, whereas decline of AAT levels in sera is responsible for pulmonary emphysema. In advanced liver disease, the only option for treatment is liver transplantation, whereas AAT replacement therapy is therapeutic for emphysema. Given that hepatocytes are the primary affected cells in AATD, we investigated whether transplantation of bone marrow (BM)‐derived stem cells in transgenic mice expressing human AATZ (the Z variant of AAT) confers any competitive advantages compared to host cells that could lead to pathological improvement. Mouse BM progenitors and human mesenchymal stem cells (MSCs) appeared to contribute in replacement of 40% and 13% host hepatocytes, respectively. Transplantation of cells resulted in decline of globule‐containing hepatocytes, improvement in proliferation of globule‐devoid hepatocytes from the host‐derived hepatocytes, and apparently, donor‐derived cells. Further analyses revealed that transplantation partially improves liver pathology as reflected by inflammatory response, fibrosis, and apoptotic death of hepatocytes. Cell therapy was also found to improve liver glycogen storage and sera glucose level in mice expressing human AATZ mice. These overall improvements in liver pathology were not restricted to transplantation of mouse BM cells. Preliminary results also showed that following transplantation of human BM‐derived MSCs, globule‐containing hepatocytes declined and donor‐derived cells expressed human AAT protein. Conclusion : These results suggest that BM stem cell transplantation may be a promising therapy for AATD‐related liver disease. (H epatology 2017;65:1319‐1335).
The Diaphragm Acts as a Brake during Expiration to Prevent Lung Collapse
Authors: Mariangela Pellegrini, Göran Hedenstierna, Agneta Roneus, Monica Segelsjö, Anders Larsson, Gaetano Perchiazzi
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

The diaphragm is the major inspiratory muscle and is assumed to relax during expiration. However, electrical postinspiratory activity has been observed. Whether there is an expiratory diaphragmatic contraction that preserves lung patency has yet to be explored.We hypothesized the occurrence of an expiratory diaphragmatic contraction directed at stabilizing peripheral airways and preventing or reducing cyclic expiratory lung collapse.Mild acute respiratory distress syndrome was induced in 10 anesthetized, spontaneously breathing pigs. Lung volume was decreased by lowering end-expiratory airway pressure in a stepwise manner. We recorded the diaphragmatic electric activity during expiration, dynamic computed tomographic scans, and respiratory mechanics. In five pigs, the same protocol was repeated during mechanical ventilation after muscle paralysis.Diaphragmatic electric activity during expiration increased by decreasing end-expiratory lung volume during spontaneous breathing. This enhanced the diaphragm muscle force, to a greater extent with lower lung volume, indicating a diaphragmatic electromechanical coupling during spontaneous expiration. In turn, the resulting diaphragmatic contraction delayed and reduced the expiratory collapse and increased lung aeration compared with mechanical ventilation with muscle paralysis and absence of diaphragmatic activity.The diaphragm is an important regulator of expiration. Its expiratory activity seems to preserve lung volume and to protect against lung collapse. The loss of diaphragmatic expiratory contraction during mechanical ventilation and muscle paralysis may be a contributing factor to unsuccessful respiratory support.
Endothelial-to-mesenchymal transition contributes to endothelial dysfunction and dermal fibrosis in systemic sclerosis
Authors: Mirko Manetti, Eloisa Romano, Irene Rosa, Serena Guiducci, Silvia Bellando-Randone, Amato De Paulis, Lidia Ibba-Manneschi, Marco Matucci-Cerinic
Journal: Annals of the Rheumatic Diseases (2017)

Objective Systemic sclerosis (SSc) features multiorgan fibrosis orchestrated predominantly by activated myofibroblasts. Endothelial-to-mesenchymal transition (EndoMT) is a transdifferentiation by which endothelial cells (ECs) lose their specific morphology/markers and acquire myofibroblast-like features. Here, we determined the possible contribution of EndoMT to the pathogenesis of dermal fibrosis in SSc and two mouse models. Methods Skin sections were immunostained for endothelial CD31 or vascular endothelial (VE)-cadherin in combination with α-smooth muscle actin (α-SMA) myofibroblast marker. Dermal microvascular ECs (dMVECs) were prepared from SSc and healthy skin (SSc-dMVECs and H-dMVECs). H-dMVECs were treated with transforming growth factor-β1 (TGFβ1) or SSc and healthy sera. Endothelial/mesenchymal markers were assessed by real-time PCR, immunoblotting and immunofluorescence. Cell contractile phenotype was assayed by collagen gel contraction. Results Cells in intermediate stages of EndoMT were identified in dermal vessels of either patients with SSc or bleomycin-induced and urokinase-type plasminogen activator receptor (uPAR)-deficient mouse models. At variance with H-dMVECs, SSc-dMVECs exhibited a spindle-shaped appearance, co-expression of lower levels of CD31 and VE-cadherin with myofibroblast markers (α-SMA+ stress fibres, S100A4 and type I collagen), constitutive nuclear localisation of the EndoMT driver Snail1 and an ability to effectively contract collagen gels. Treatment of H-dMVECs either with SSc sera or TGFβ1 resulted in the acquisition of a myofibroblast-like morphology and contractile phenotype and downregulation of endothelial markers in parallel with the induction of mesenchymal markers. Matrix metalloproteinase-12-dependent uPAR cleavage was implicated in the induction of EndoMT by SSc sera. Conclusions In SSc, EndoMT may be a crucial event linking endothelial dysfunction and development of dermal fibrosis.
Using Multiparametric Flow Cytometry to Analysis the Immunophenotypic Abnormalities of Bone Marrow Cells in Patients with MDS-RAEB.
Authors: Jing Huang, Xin Du, Suxia Geng, Maohua Zhou, Jianyu Weng, Suijing Wu, Rong Guo, Zesheng Lu, Miaorong She
Journal: Blood (2009)
MA10.06 Centrality Definition in Non-Small Cell Lung Cancer. Predictor For Occult Mediastinal Lymph Node Involvment
Authors: David Sanchez-Lorente, Lucía Milla, Angela Guirao, Rudith Guzman, Marc Boada, Josep Maria Gimferrer, Guillermina Sanchez, Laureano Molins
Journal: Journal of Thoracic Oncology (2017)
A Novel Mechanism for Imatinib Mesylate (STI571) Resistance in CML Cells: Contribution of TC-PTP to Modulating Signals Down-Stream from the BCR-ABL Fusion Protein.
Authors: Takatsune Shimizu, Yoshitaka Miyakawa, Satoshi Iwata, Akiko Kuribara, Tony Tiganis, Chikao Morimoto, Yasuo Ikeda, Masahiro Kizaki
Journal: Blood (2004)
P2.03b-027 Circulating Free DNA (cfDNA) Analysis from Patients with Advanced Lung Adenocarcinoma
Authors: Maria Gabriela Fernandes, José Costa, Joana Reis, Vanessa Santos, Conceição Moura, Henrique Queiroga, Adriana Magalhães, António Morais, José Machado, Venceslau Hespanhol
Journal: Journal of Thoracic Oncology (2017)
Activation of Palliative Cares by hospital oncologists: first results of a survey conducted by Rete Oncologica del Piemonte e della Valle d'Aosta
Authors: I. Alabiso, A. Ballari, E. Brignardello, G. Numico, E. Sperti, A. Cristofano, E. Russi, C. Oliva, M. Mistrangelo, M. Levis, M. Gallo, G. Di Costanzo, O. Bertetto
Journal: Annals of Oncology (2016)
MA08.07 Prospective Sequential Counts of Total CTC or cKIT+CTC in Advanced NSCLC with 1st Line Chemotherapy (POLICE)
Authors: Xu-Chao Zhang, Zhen Wang, Yan-Ming Deng, Wei-Bang Guo, Jin -Ji Yang, Hong-Hong Yan, Qing Zhou, Binchao Wang, Wei-Neng Feng, Huajun Chen, Hai-Yan Tu, Li Zhang, Xiaoqing Liu, Qing-Feng Zou, Yi Long Wu
Journal: Journal of Thoracic Oncology (2017)
Remote ischemic conditioning provides humoural cross-species cardioprotection through glycine receptor activation
Authors: Juan José Alburquerque-Béjar, Ignasi Barba, Laura Valls-Lacalle, Marisol Ruiz-Meana, Michela Pecoraro, Antonio Rodríguez-Sinovas, David García-Dorado
Journal: Cardiovascular Research (2016)

Remote ischaemic conditioning (RIC) releases a humoural factor able to exert cross-species cardioprotection when plasma dialysate is applied to isolated hearts. However, the exact chemical nature of this factor is currently unknown.RIC (4 × 5min femoral occlusion/5min reperfusion) was applied to 10 male pigs, and blood was taken before and after the manoeuvre. Discriminant analysis of 1H-NMR spectra (n = 10-12) obtained from plasma dialysates (12-14 kDa cut-off) allowed to demonstrate a different metabolic profile between control and postRIC samples, with lactate (2.671 ± 0.294 vs. 3.666 ± 0.291 μmol/mL, P = 0.020), succinate (0.062 ± 0.005 vs. 0.082 ± 0.008 μmol/mL, P = 0.035) and glycine (0.055 ± 0.009 vs. 0.471 ± 0.151 μmol/mL, P = 0.015) being the main responsible for such differences. Plasma dialysates were then given to isolated mice hearts submitted to global ischaemia (35 min) and reperfusion (60 min), for 30 min before ischaemia or during the first 15 min of reflow. Infarct size was significantly reduced when postRIC dialysate was applied before ischaemia as compared with hearts pretreated with control dialysate (44.81 ± 3.22 vs. 55.55 ± 2.53%, P = 0.012, n = 12). Blockade of glycine receptors with strychnine 10 μM inhibited the protective effect caused by pretreatment with postRIC dialysate (52.76 ± 6.94 vs. 51.92 ± 5.78%, P-NS, n = 5), whereas pretreatment with glycine 3 mmol/L, but not succinate 100 μmol/L, mimicked RIC protection (41.90 ± 4.50% in glycine-treated vs. 61.51 ± 5.16 and 64.73 ± 4.47% in succinate-treated and control hearts, respectively, P < 0.05, n = 4-7).RIC releases glycine and exerts cross-species cardioprotection against infarction through glycine receptor activation.
OA07.05 Prognostic Impact of Pleural Lavage Cytology (PLC): Significance of PLC after Lung Resection
Authors: Shinya Katsumata, Junji Yoshida, Genichiro Ishii, Keigo Sekihara, Tomohiro Miyoshi, Keiju Aokage, Tomoyuki Hishida, Masahiro Tsuboi
Journal: Journal of Thoracic Oncology (2017)
P1.07-005 A Retrospective Study of Sequential Chemoradiotherapy for LD-SCLC Patients in Whom Concurrent Therapy is Not Indicated
Authors: Sayaka Ohara, Shintaro Kanda, Keiko Goto, Hideaki Shiraishi, Hitomi Okuma, Kota Itahashi, Yasushi Goto, Hidehito Horinouchi, Yutaka Fujiwara, Hiroshi Nokihara, Yoshinori Ito, Noboru Yamamoto, Kazuhiro Usui, Yuichiro Ohe
Journal: Journal of Thoracic Oncology (2017)
P3.03-014 Tumor Subtype-Specific Cells-Of-Origin of Malignant Pleural Mesothelioma
Authors: Hilda De Vries, Ji-Ying Song, Tadamoto Isogai, Metello Innocenti, Iris De Rink, Rajith Bhaskaran, Oscar Krijgsman, Anton Berns
Journal: Journal of Thoracic Oncology (2017)
Serum Level of Interleukin-10 Correlates Well with the Activity of Chronic Graft-Versus-Host Disease and the Responsiveness to Corticosteroid Treatment.
Authors: Su-Peng Yeh, Chang-Fang Chiu, Yu-Min Liao, Wen-Jyi Lo, Yu-Ching Liaw, Chiao-Lin Lin, Jan-Gowth Chang, Chung-Tsen Hsueh
Journal: Blood (2004)
P2.03a-040 Safety and Efficacy of Nab-Paclitaxel for 2nd Line Treatment of Elderly Patients with Stage IV Non-Small Cell Lung Cancer
Authors: Jared Weiss, Thomas Stinchcombe, Allison Deal, Liza Villaruz, Jeffrey Crane, Howard West, Carrie Lee, James Stevenson, William Irvin, Mark Socinski, Nathan Pennell
Journal: Journal of Thoracic Oncology (2017)
P1.02-073 Characterizing the Genomes of Lung Adenocarcinomas from Never Smokers Reveals SHPRH as a Novel Candidate Tumor Suppressor Gene
Authors: Tanya De Silva, Victor Martinez, Kelsie Thu, Daniel Lu, Min Oh, Stephen Lam, Wan Lam, Harold Varmus, William Lockwood
Journal: Journal of Thoracic Oncology (2017)
CRISPR/Cas9 Editing of the Mutant Huntingtin Allele In Vitro and In Vivo
Authors: Alex Mas Monteys, Shauna A. Ebanks, Megan S. Keiser, Beverly L. Davidson
Journal: Molecular Therapy (2017)

Huntington disease (HD) is a fatal dominantly inherited neurodegenerative disorder caused by CAG repeat expansion (>36 repeats) within the first exon of the huntingtin gene. Although mutant huntingtin (mHTT) is ubiquitously expressed, the brain shows robust and early degeneration. Current RNA interference-based approaches for lowering mHTT expression have been efficacious in mouse models, but basal mutant protein levels are still detected. To fully mitigate expression from the mutant allele, we hypothesize that allele-specific genome editing can occur via prevalent promoter-resident SNPs in heterozygosity with the mutant allele. Here, we identified SNPs that either cause or destroy PAM motifs critical for CRISPR-selective editing of one allele versus the other in cells from HD patients and in a transgenic HD model harboring the human allele.
Relationship Between Normalization of Negative T Waves on Exercise ECG and Residual Myocardial Viability in Patients With Previous Myocardial lnfarction and no Post-Infarction Angina
Authors: Ryuichi Ajisaka, Shigeyuki Watanabe, Takeshi Masuoka, Takayoshi Yamanouchi, Takumi Saitoh, Masahiro Toyama, Tohru Takeda, Yuji ltai, Yasuro Sugishita
Journal: Circulation (1998)
Frequency of Molecular and PET/CT Complete Remissions in Patients with Multiple Myeloma after Autologous Followed by Reduced-Intensity Allogeneic Stem Cell Transplants.
Authors: Ping Zhou, Hugo Castro-Malaspina, Esperanza B. Papadopoulos, James W. Young, Kenneth Miller, Neeta Pandit-Taskar, Daniel A. Filippa, Martin Fleisher, Raymond L. Comenzo
Journal: Blood (2004)
From Microscale Devices to 3D Printing
Authors: Anton V. Borovjagin, Brenda M. Ogle, Joel L. Berry, Jianyi Zhang
Journal: Circulation Research (2017)

Current strategies for engineering cardiovascular cells and tissues have yielded a variety of sophisticated tools for studying disease mechanisms, for development of drug therapies, and for fabrication of tissue equivalents that may have application in future clinical use. These efforts are motivated by the need to extend traditional 2-dimensional (2D) cell culture systems into 3D to more accurately replicate in vivo cell and tissue function of cardiovascular structures. Developments in microscale devices and bioprinted 3D tissues are beginning to supplant traditional 2D cell cultures and preclinical animal studies that have historically been the standard for drug and tissue development. These new approaches lend themselves to patient-specific diagnostics, therapeutics, and tissue regeneration. The emergence of these technologies also carries technical challenges to be met before traditional cell culture and animal testing become obsolete. Successful development and validation of 3D human tissue constructs will provide powerful new paradigms for more cost effective and timely translation of cardiovascular tissue equivalents.
Diagnostic Value of Minor Salivary Glands Biopsy in Systemic Amyloidosis
Authors: Giacinto La Verde, Maria Paola Bianchi, Giusy Antolino, Giulia Galassi, Francescaromana Festuccia, Giorgio Bandiera, Armando Bartolazzi, Paolo Menè, Agostino Tafuri
Journal: Blood (2015)
Prognostic Value of the ‘Monosomal Karyotype’ Entity in Elderly Patients with AML: a GOELAMS Study of 186 Patients with Unfavourable Cytogenetic Abnormalities.
Authors: Aurore Perrot, Isabelle Luquet, Arnaud Pigneux, Francine Mugneret, Jacques Delaunay, Jean-Luc Harousseau, Francis Witz, Carole Barin, Jean-Yves Cahn, Philippe Guardiola, Chantal Himberlin, Christian Recher, Norbert Vey, Bruno Lioure, Olivier Tournilhac, Nathalie Fegueux, Christian Berthou, Martine Escoffre-Barbe, Marie-Christine Béné, Norbert Ifrah
Journal: Blood (2009)
P1.02-076 DNA Methylation Profiling Unravels a TGF-β Hyperresponse in Tumor Associated Fibroblasts from Lung Cancer Patients
Authors: Rafael Ikemori, Miguel Vizoso, Marta Puig, Anna Labernardie, Marta Gabasa, Xavier Trepat, Noemi Reguart, Manel Esteller, Jordi Alcaraz
Journal: Journal of Thoracic Oncology (2017)
P177 High prevalence of unrecognised asthma in children with sickle cell disease
Authors: M Akthar, G Ruiz, S Chakravorty, C Bossley, D Rees, A Gupta
Journal: Thorax (2016)

<h3>Background</h3> Sickle Cell Disease (SCD) affects about 1 in 1,900 children born in the UK. Respiratory morbidity affects children as well as adults with SCD and the burden may have been underestimated in the past. The published literature suggests that asthma, airway hyper-reactivity and sleep disordered breathing (SDB) are common in children with SCD. Furthermore asthma and SDB have been reported to be associated with acute chest syndrome (ACS) and vaso-occlusive crises (VOC). Children with SCD are increasingly referred to our respiratory clinic in a tertiary paediatric centre in the UK. We did an analysis of a sample of these children to gain some preliminary insights into the problem. <h3>Method</h3> A retrospective observational study was carried out using data from children with SCD who had been referred to our tertiary paediatric respiratory clinic between 1<sup>st</sup> September 2009 and 31<sup>st</sup> August 2014. Data was collected from electronic patient records and electronic investigation results. <h3>Results</h3> 54 patient records were evaluated. The mean age of the children was 11 years and 54% were male. The most common reason for referral was low oxygen saturation on pulse oximetry (23/54). Surprisingly, asthma and wheeze were uncommon reasons for referrals comprising only 7/54 (Figure 1). However, of all the patients 48% were discovered to have asthma and 52% had SDB. In those patients who underwent lung function testing an abnormal result was reported in 60% (25/42). In addition 71% of children who had a sleep study had an abnormal result (35/49). No association between ACS or VOC events in those patients with asthma or SDB was noted but this could have been due to the small numbers. <h3>Conclusion</h3> In this sample of children with SCD referred mainly because of low oxygen saturation, the high proportion with an abnormal sleep study and SDB might have been expected. However, the relative paucity of reported wheeze and exercise intolerance despite large numbers with abnormal lung physiology suggested that conditions such as asthma may be unrecognised in these patients.
Molecular Responses to Dasatinib and Nilotinib in Patients with Chronic Myeloid Leukemia in Chronic Phase (CML-CP).
Authors: Alfonso QuintαsCardama, Hagop Kantarjian, Franziska Michor, Adam Olshen, Mithat Gonen, Dan Jones, Mary Beth Rios, Susan O’Brien, Jorge Cortes
Journal: Blood (2008)
Effects of Multisite Biventricular Pacing in Patients with Heart Failure and Intraventricular Conduction Delay
Authors: Serge Cazeau, Christophe Leclercq, Thomas Lavergne, Stuart Walker, Chetan Varma, Cecilia Linde, Stéphane Garrigue, Lukas Kappenberger, Guy A. Haywood, Massimo Santini, Christophe Bailleul, Philippe Mabo, Arnaud Lazarus, Philippe Ritter, Terry Levy, William McKenna, Jean-Claude Daubert
Journal: New England Journal of Medicine (2001)

One third of patients with chronic heart failure have electrocardiographic evidence of a major intraventricular conduction delay, which may worsen left ventricular systolic dysfunction through asynchronous ventricular contraction. Uncontrolled studies suggest that multisite biventricular pacing improves hemodynamics and well-being by reducing ventricular asynchrony. We assessed the clinical efficacy and safety of this new therapy.
Aberrant Subcellular Localization of Azurophil Granule Proteins in Myeloid Leukemia Favors Peptide Antigen Presentation on MHC-I and Susceptibility to Killing by Cytotoxic T Lymphocytes.
Authors: Gheath Alatrash, Yoko Ono, Sijie Lu, Anna Sergeeva, Changqing Wang, Eric Wieder, Jeffrey J. Molldrem
Journal: Blood (2007)
A novel kindred with inherited STAT2 deficiency and severe viral illness
Authors: Leen Moens, Lien Van Eyck, Dirk Jochmans, Tania Mitera, Glynis Frans, Xavier Bossuyt, Patrick Matthys, Johan Neyts, Michael Ciancanelli, Shen-Ying Zhang, Rik Gijsbers, Jean-Laurent Casanova, Stephanie Boisson-Dupuis, Isabelle Meyts, Adrian Liston
Journal: Journal of Allergy and Clinical Immunology (2017)
Mechanisms of Discrepancy Between CD33 Expression and Gemtuzumab Ozogamicin-Induced Cytotoxicity in Leukemia Cells.
Authors: Yasushi Takamatsu, Shiro Jimi, Nanako Toyota, Shuuji Hara, Yuka Yoshimura, Junji Suzumiya, Kazuo Tamura
Journal: Blood (2009)
A Proof-of-Concept for Epigenetic Therapy of Tissue Fibrosis: Inhibition of Liver Fibrosis Progression by 3-Deazaneplanocin A
Authors: Müjdat Zeybel, Saimir Luli, Laura Sabater, Timothy Hardy, Fiona Oakley, Jack Leslie, Agata Page, Eva Moran Salvador, Victoria Sharkey, Hidekazu Tsukamoto, David C.K. Chu, Uma Sharan Singh, Mirco Ponzoni, Patrizia Perri, Daniela Di Paolo, Edgar J. Mendivil, Jelena Mann, Derek A. Mann
Journal: Molecular Therapy (2017)

The progression of fibrosis in chronic liver disease is dependent upon hepatic stellate cells (HSCs) transdifferentiating to a myofibroblast-like phenotype. This pivotal process is controlled by enzymes that regulate histone methylation and chromatin structure, which may be targets for developing anti-fibrotics. There is limited pre-clinical experimental support for the potential to therapeutically manipulate epigenetic regulators in fibrosis. In order to learn if epigenetic treatment can halt the progression of pre-established liver fibrosis, we treated mice with the histone methyltransferase inhibitor 3-deazaneplanocin A (DZNep) in a naked form or by selectively targeting HSC-derived myofibroblasts via an antibody-liposome-DZNep targeting vehicle. We discovered that DZNep treatment inhibited multiple histone methylation modifications, indicative of a broader specificity than previously reported. This broad epigenetic repression was associated with the suppression of fibrosis progression as assessed both histologically and biochemically. The anti-fibrotic effect of DZNep was reproduced when the drug was selectively targeted to HSC-derived myofibroblasts. Therefore, the in vivo modulation of HSC histone methylation is sufficient to halt progression of fibrosis in the context of continuous liver damage. This discovery and our novel HSC-targeting vehicle, which avoids the unwanted effects of epigenetic drugs on parenchymal liver cells, represents an important proof-of-concept for epigenetic treatment of liver fibrosis.
Consumer Preferences and Online Comparison Tools Used to Select a Surgeon
Authors: Justin B. Ziemba, Mohamad E. Allaf, Dalal Haldeman
Journal: JAMA Surgery (2017)

The public reporting of physician quality is mandated by the US federal government and made accessible through the website Physician Compare. 1 However, Physician Compare is only 1 of several online resources that provide physician ratings to consumers. 2Despite the widespread availability of this information, little is known about how consumers use it to make decisions regarding health care, particularly when selecting a surgeon.
P1.02-063 Mutation Profiling by Targeted Next-Generation Sequencing of an Unselected NSCLC Cohort
Authors: Linnea La Fleur, Elin Falk-Sorqvist, Patrik Smeds, Magnus Sundstrom, Johanna Mattsson, Eva Brandén, Hirsh Koyi, Johan Isaksson, Hans Brunnström, Martin Sandelin, Kristina Lamberg, Per Landelius, Mats Nilsson, Patrick Micke, Lotte Moens, Johan Botling
Journal: Journal of Thoracic Oncology (2017)