tbuckley/cabot-search huggingface dataset:
S73 Viruses associated with community-acquired pneumonia in children – a large prospective study in the post-prevenar 13 era
Authors: AS Wort, M Gale, K Devine, AJ Simpson, AD Sails, DA Spencer, MF Thomas, M Brodlie
Journal: Thorax (2016)

<h3>Introduction and objectives</h3> Community-acquired pneumonia (CAP) is a common childhood illness and frequent reason for hospital admission. CAP may be caused by bacteria or viruses. Many studies have relied on administrative records that typically provide poor quality retrospective aetiological data. We have performed a large prospective study to investigate the aetiology of CAP in the ‘post-Prevenar 13 era’. We wished to describe the current epidemiology of viral CAP and compare this with data from studies that used similar methodology in the same population in 2009–2011 (post-Prevenar 7) and 2001–2002 (pre-Prevenar 7). <h3>Methods</h3> Children aged under 16 years admitted to a large paediatric centre, between January 2015 and June 2016, with a chest radiograph meeting WHO criteria were eligible. Following informed consent nasopharyngeal aspirate, nasal swab, sputum or endotracheal secretions were collected. Influenza A and B, Human Rhinovirus, Human Metapneumovirus, Adenovirus, Parainfluenza 1 – 4 and Respiratory Syncytial Virus (RSV) were tested using real-time PCR assays. Comparisons were made using appropriate non-parametric tests. <h3>Results</h3> A total of 148 children were recruited, median age 2.7 years, IQR 1.5–5.3. Samples from 63 participants (43%) were positive for a virus and 7 cases had co-infection with 2 viruses. Children that tested positive for a virus were significantly younger (median 2.1 years, IQR 1.2–3.2, versus 3.7 years, IQR 1.9–6.9, p = 0.0005). When compared with previous studies there was no significant change in the virus detection rate. The breakdown of individual viruses is shown in the table, no significant changes were identified apart from a reduction in RSV. <h3>Conclusions</h3> These results represent the most comprehensive data available on viruses associated with CAP in children in the UK in the ‘post-Prevenar 13 era’. They confirm that there has not been a significant shift in the viruses associated with children requiring admission to hospital. Our results also suggest that the introduction of the live attenuated intranasal influenza vaccine to children, which began in 2013, is yet to have a significant effect on the frequency of influenza detected in children with CAP. Future surveys will be important for ongoing evaluation of the viral aetiology of CAP. <h3>Reference</h3> Elemraid MA, <i>et al</i>. Aetiology of paediatric pneumonia after the introduction of pneumococcal conjugate vaccine.<i>Eur Respir J</i> 2013;<b>42</b>(6):1595–603.
P3.02b-015 Impact of Metastatic Status on the Prognosis of Patients Treated with First Generation EGFR-TKIs
Authors: Yoshihiko Taniguchi, Akihiro Tamiya, Kanako Katayama, Tsunehiro Tanaka, Kenji Nakahama, Nobuhiko Saijo, Yoko Naoki, Masaki Kanazu, Naoki Omachi, Kyoichi Okishio, Takahiko Kasai, Shinji Atagi
Journal: Journal of Thoracic Oncology (2017)
P3.02b-073 A Phase II, Liquid Biopsy Study Using Digital PCR in EGFR Mutated, Lung Cancer Patients Treated with Afatinib (WJOG 8114LTR)
Authors: Hiroaki Akamatsu, Yasuhiro Koh, Satoshi Morita, Daichi Fujimoto, Isamu Okamoto, Akihiro Bessho, Koichi Azuma, Kazuhiko Nakagawa, Nobuyuki Yamamoto
Journal: Journal of Thoracic Oncology (2017)
Successful implementation of the nationwide Danish CancerBiobank.
Authors: E. V. Høgdall, B. Bjerregaard
Journal: Journal of Clinical Oncology (2011)

e21066 Background: A donation from the Danish Ministry of Health and Prevention made it possible to implement the Danish CancerBiobank (DCB). The objective of the DCB is nationally to collect blood and tissues optimal for translational research from patients with primary cancer. Methods: The infrastructure was established through the Departments of Pathology and Departments of Clinical Biochemistry at six University hospitals in Denmark. Each university hospital is responsible for the local departments in their region. All departments agreed on national technical recommendations. A national on-line database was established to registry information such as pre-analytical factors, laboratory procedures and verification of the diagnosis of the colleted tissues. The database is linked to the national pathology register (www.patobank.dk) and the data can be combined with Danish clinical databases and other registers relevant for research. A draft for a quality assurance handbook has been accepted and a homepage designed (www.cancerbiobank.dk). Results: The establishment of the DCB started in 2008 and from January 2010 five of the six University hospitals used the database for registration. I 2010 biological materials from 5.281 patients have been collected, a total of 3.900 blood samples and 3.315 tissue samples equivalent to a coverage of 25 % of all patients with cancer diagnosed in the hospitals. From 740 tissue samples a corresponding blood sample was collected. In 88 % of all tissue samples collected, pathological verification of diagnosis was performed. Today DCB is responsible for collecting biological materials for 22 research projects, corresponding to 17 % of materials collected in DCB. Conclusions: The DCB is unique nationally and internationally, due to: 1) National recommendations for handling of blood and tissues; 2) Centralized nationwide data registration; 3) Correlation between information on blood and tissue for the single patient; 4) Connection to the final diagnosis through Patobanken; and 5) Connection to the nationwide clinical databases and other national registries. The criteria of success for DCB will be translational research projects of clinical importance for the treatment of cancer patients.
Epigenetic Regulation of Hematopoietic Stem and Progenitor Cells By the Eset Histone Methyltranferas
Authors: Shuhei Koide, Keiyo Takubo, Motohiko Oshima, Satoru Miyagi, Hirotaka Matsui, Hiroshi Kimura, Changshan Wang, George R Wendt, Shogo Yabata, Yoichi Shinkai, Toshio Suda, Atsushi Iwama
Journal: Blood (2014)
P3.02c-001 Phase I Study of Salazosulfapyridine Targeting Cancer Stem Cells in Combination with CDDP and Pemetrexed for Chemo-Naïve Advanced Non-Sq NSCLC
Authors: Kohei Otsubo, Kaname Nosaki, Chiyo K. Imamura, Hiroaki Ogata, Akitaka Fujita, Shinya Sakata, Fumihiko Hirai, Gouji Toyokawa, Eiji Iwama, Taishi Harada, Takashi Seto, Mitsuhiro Takenoyama, Takeshi Ozeki, Taisei Mushiroda, Mieko Inada, Junji Kishimoto, Osamu Nagano, Hideyuki Saya, Yoichi Nakanishi, Isamu Okamoto
Journal: Journal of Thoracic Oncology (2017)
3rd Asia-Pacific Primary Liver Cancer Expert Meeting
Authors: Sheng-Long Ye Shanghai, Kwang-Hyub Han Seoul, Masatoshi Kudo Osaka
Journal: Liver Cancer (2012)

Apolipoprotein E (ApoE) plays an important role in regulating the lipid and lipoprotein metabolism.We investigated whether the ApoE genotype could determine the disease outcome in hepatitis B virus (HBV) infected individuals to verify the association with the occurrence of hepatocellular carcinoma (HCC) in patients with chronic liver diseases of various etiologies.This hospital based case-control study enrolled 183 subjects (47 healthy controls, 50 HBV-originated liver cirrhosis, and 86 HCC).ApoE genotypes were determined with an ApoE genotyping kit, using the PCR method.Serum ApoE levels were measured with an ELISA kit.We identified that the ApoE genotype was associated with the progression to liver cirrhosis in chronic HBV carriers.Being an ApoE4 carrier was associated with a lower probability of developing liver cirrhosis.No influence of ApoE genotypes on the susceptibility to the occurrence of HCC was found.The serum ApoE measurements revealed a significantly higher level of ApoE in patients with liver cirrhosis than those in the healthy controls, but we observed no significant difference in the serum ApoE levels, with regard to the ApoE genotype.This study indicates that ApoE genotypes may be a part of the genetic variation underlying the susceptibility of individuals to disease progression of chronic HBV infection.
P2.02-039 Intercalated EGFR and Chemotherapy in Locally Advanced NSCLC with EGFR Mutations: Data on 5 Patients and Clinical Study
Authors: Frank Griesinger, Julia Roeper, Anne Lueers, Markus Falk, Cora Hallas, Markus Tiemann
Journal: Journal of Thoracic Oncology (2017)
P41 A prospective cohort study to measure in-vivo changes in lung glucose metabolism in patients with sscl-ild using fdg-pet
Authors: HS Garthwaite, V Holmes, T Mikolasch, G Azzopardi, CP Denton, AM Groves, JC Porter
Journal: Thorax (2016)

<h3>Background</h3> Systemic sclerosis (SScl) is a chronic inflammatory autoimmune rheumatic disease with a UK prevalence of 2–10 per 100,000. It is a heterogenous disease characterised by varying degrees of dermal and organ fibrosis. Interstitial lung disease (ILD) occurs in 60–80% of patients and ranges from mild, clinically trivial disease to extensive fibrosis that results in respiratory failure and premature death. Therapeutic options include cyclophosphamide, mycophenylate mofetil and rituximab. Clinical decisions are complex and decisions to treat or not have historically been based on radiology and lung function tests, neither of which (at a single time point) give a dynamic view of disease progression. Novel biomarkers are urgently needed to predict disease activity, progression and response to treatment in patients with SScl-ILD. <h3>Aims</h3> To investigate the potential of 18Fluoro-deoxyglucose Positron Emission Tomography (FDG-PET)/CT to act as a prognostic and response biomarker in patients with SScl-ILD. <h3>Methods</h3> 35 SScl-ILD patients were prospectively recruited for 18F-FDG-PET/CT. Patients were screened for lung involvement using clinical assessment, chest X-ray and pulmonary function testing (PFT). Those with confirmed SScl-ILD underwent combined high resolution CT scan (HRCT)/PET scanning. The imaging signal and clinical findings were correlated with the need for, and response to, therapy. Follow up was with clinical assessment, PFT and when a change in treatment was indicated, repeat imaging. <h3>Results</h3> The overall maximum pulmonary uptake of 18F-FDG (SUVmax), the minimum pulmonary uptake or background-lung-activity (SUVmin) and target-to-background (SUVmax/SUVmin) ratio (TBR) were quantified using routine region-of-interest analysis. Kaplan-Meir analysis was used to identify associations with disease progression and response to treatment <h3>Conclusions</h3> We have shown that high pulmonary uptake of 18F-FDG is associated with disease activity and progression in patients with SScl-ILD. These PET findings can be used to give additional information, supplemental to PFTs, which may then aid clinical treatment decisions.
P2.02-056 FGFR Gene Mutation is an Independent Prognostic Factor in Squamous Non-Small Cell Lung Cancer, and Associated with Lymph Node Metastasis
Authors: Li Jingjing, Yan Shi, Pan Yaqi, Liu Zheng, Qin Tan, Yang Yue, Woodward Emma, Wu Nan
Journal: Journal of Thoracic Oncology (2017)
P168 Safety and tolerability of nintedanib in patients with idiopathic pulmonary fibrosis (IPF): one-year data from post-marketing surveillance in the united states
Authors: T Maher, I Noth, A Allinger, M Kaul, CS Conoscenti, D Oelberg
Journal: Thorax (2016)

<h3>Introduction</h3> In the two replicate, 52-week, placebo-controlled INPULSIS® trials, nintedanib 150 mg twice daily significantly reduced the annual rate of decline in forced vital capacity compared with placebo and had a side-effect profile that was manageable for most patients. After the US approval of nintedanib for the treatment of IPF in October 2014, post-marketing surveillance was initiated to obtain additional information on the safety and tolerability of nintedanib in the real-world clinical setting. <h3>Methods</h3> Data were collected from the drug safety database from the time of drug launch (15 October 2014) to 23 October 2015. Data on adverse events in patients treated with nintedanib were collected both via proactive patient communications, as part of a patient support programme, and by the spontaneous reporting system. Adverse events were coded according to preferred terms in the Medical Dictionary for Regulatory Activities. Serious adverse events were defined according to International Conference on Harmonisation criteria as adverse events that were fatal or life threatening, required or prolonged hospitalisation, were associated with a congenital anomaly, or resulted in a disability. <h3>Results</h3> In the period from drug launch to 23 October 2015, 6,758 patients were treated with nintedanib, with duration of exposure 6 to 390 days (median 113 days). This analysis will present 1-year adverse event data collected both via proactive patient communications, as part of a patient support programme, and by the spontaneous reporting system. Previously reported data collected from drug launch up to 31 May 2015, from 3,838 patients, were consistent with the safety profile described in the product label. In this dataset and as observed in the Phase III trials, the most frequently reported adverse events with nintedanib were gastrointestinal in nature and non-serious in severity. <h3>Conclusion</h3> Data from post-marketing surveillance in the US are consistent with the safety profile of nintedanib as described in the label. Treatment with nintedanib in the real-world clinical setting appears to have an acceptable safety and tolerability profile, with no new safety concerns identified.
P2.01-075 Prognostic Value of Angiogenesis and Cell Adhesion Biomarkers in Non-small Cell Lung Cancer
Authors: Kostas Syrigos, Kyriaki Soldatou, Dimitra Grapsa, Dimitrios Sfairopoulos, Andriani Charpidou, Rodoula Trigidou, Antigoni Mitselou
Journal: Journal of Thoracic Oncology (2017)
SMCHD1 mutations associated with a rare muscular dystrophy can also cause isolated arhinia and Bosma arhinia microphthalmia syndrome
Authors: Natalie D Shaw, Harrison Brand, Zachary A Kupchinsky, Hemant Bengani, Lacey Plummer, Takako I Jones, Serkan Erdin, Kathleen A Williamson, Joe Rainger, Alexei Stortchevoi, Kaitlin Samocha, Benjamin B Currall, Donncha S Dunican, Ryan L Collins, Jason R Willer, Angela Lek, Monkol Lek, Malik Nassan, Shahrin Pereira, Tammy Kammin, Diane Lucente, Alexandra Silva, Catarina M Seabra, Colby Chiang, Yu An, Morad Ansari, Jacqueline K Rainger, Shelagh Joss, Jill Clayton Smith, Margaret F Lippincott, Sylvia S Singh, Nirav Patel, Jenny W Jing, Jennifer R Law, Nalton Ferraro, Alain Verloes, Anita Rauch, Katharina Steindl, Markus Zweier, Ianina Scheer, Daisuke Sato, Nobuhiko Okamoto, Christina Jacobsen, Jeanie Tryggestad, Steven Chernausek, Lisa A Schimmenti, Benjamin Brasseur, Claudia Cesaretti, Jose E García-Ortiz, Tatiana Pineda Buitrago, Orlando Perez Silva, Jodi D Hoffman, Wolfgang Mühlbauer, Klaus W Ruprecht, Bart L Loeys, Masato Shino, Angela M Kaindl, Chie-Hee Cho, Cynthia C Morton, Richard R Meehan, Veronica van Heyningen, Eric C Liao, Ravikumar Balasubramanian, Janet E Hall, Stephanie B Seminara, Daniel Macarthur, Steven A Moore, Koh-ichiro Yoshiura, James F Gusella, Joseph A Marsh, John M Graham, Angela E Lin, Nicholas Katsanis, Peter L Jones, William F Crowley, Erica E Davis, David R FitzPatrick, Michael E Talkowski
Journal: Nature Genetics (2017)
A Thrombin Inhibitor, but Not a Factor Xa Inhibitor, DU-176b, Aggravates Tissue Factor-Induced Hypercoagulation in Rats.
Authors: Yoshiyuki Morishima, Toshio Fukuda, Naoki Tsuji, Yuko Honda, Chikako Matsumoto, Taketoshi Furugohri, Toshiro Shibano
Journal: Blood (2005)
P2.02-030 Consolidation Chemotherapy Following Concurrent Chemoradiation for Stage III Non-Small Cell Lung Cancer: A Brazilian Multicentric Cohort
Authors: Vladmir Cordeiro De Lima, Clarissa Baldotto, Carlos Barrios, Eldsamira Sobrinho, Mauro Zukin, Clarissa Mathias, Facundo Zaffaroni, Rodrigo Nery, Gabriel Madeira, Alex Amadio, Guilherme Geib, Juliano Coelho, Maria Fernanda Simões, Gilberto De Castro
Journal: Journal of Thoracic Oncology (2017)
Prolonged Survival with Low Incidence of CNS Relapse and Late Toxicities in a Retrospective Series of 278 Young Patients with High-Risk (aa-IPI 2–3) Diffuse Large B-Cell Lymphoma Treated with Intensified Chemotherapy with or without Rituximab At Diagnosis
Authors: Annalisa Chiappella, Alessia Castellino, Maria Giuseppina Cabras, Anna Marina Liberati, Andrea Evangelista, Chiara Bottelli, Flavia Salvi, Andrea Rossi, Vincenzo Pavone, Maura Nicolosi, Guido Parvis, Anna Tonso, Fausto Rossini, Clara Pecoraro, Delia Rota-Scalabrini, Stefano Luminari, Pasqualina De Masi, Sonia Perticone, Nicola Cascavilla, Roberto Freilone, Umberto Vitolo
Journal: Blood (2011)
New Fine Structure within the Adult Hematopoietic Stem Cell Compartment Revealed by Longterm Analysis of Mice Repopulated with Single Cells or Their In Vitro Generated Clonal Progeny.
Authors: Brad Dykstra, David Kent, Lindsay McCaffrey, Kristin Lyons, Merete Kristiansen, Melisa Hamilton, Connie Eaves
Journal: Blood (2005)
Mitochondrial DNA haplogroups and ageing mechanisms in osteoarthritis
Authors: Ana M Valdes, Mary B Goldring
Journal: Annals of the Rheumatic Diseases (2017)

Osteoarthritis (OA) is the most common form of arthritis affecting more than 12% of people over the age of 60.1 Although late-onset articular cartilage degeneration is common and age is one of the most important risk factors for the disease, the relationship between old age and OA is not fully understood.2 In the past it was believed that the link with age was due to ‘wear and tear’ of articular cartilage by continuous mechanical stress; we now know, however, that OA involves an active response to injury comprising remodelling of articular cartilage and subchondral bone, in addition to synovial inflammation and damage to other joint structures such as ligaments and menisci.3

Biological ageing is a complex process and it is now widely accepted that ageing starts with molecular damage, leading to cell, tissue and, ultimately, organ dysfunction.4 Extensive evidence from animal models and in vitro studies indicates that mitochondria contribute to specific aspects of the ageing process, including cellular senescence, chronic inflammation and the age-dependent decline in stem cell activity.5

Perhaps the best known and most long-standing hypothesis to explain ageing is the free radical theory that proposes a central role for the mitochondrion as the principal source of intracellular reactive oxygen species (ROS) leading to mitochondrial DNA (mtDNA) mutations.4 ,5 Somatic (acquired) mtDNA mutations and their association with the decline in mitochondrial function during ageing are well described, but these observations do not necessarily imply a causal relationship between mitochondrial dysfunction and human ageing. The maternally inherited mtDNA sequences encode the key proteins involved in energy production, although the relevance of high sequence variability of mtDNA had been considered of little functional relevance. Latorre-Pellicer and coauthors showed recently …
Novel Pharmacological Agents Differentially Modulate Cytokine Release On CLL B-Cell-Stromal Cell Co-Culture: Implications for Stromal Rescue of CLL B-Cells From Chemotherapy
Authors: Connie Lesnick, Asish K Ghosh, Betsy R. LaPlant, Wei Ding, Neil E. Kay, Tait D. Shanafelt
Journal: Blood (2012)
Constitutive high expression of protein arginine methyltransferase 1 in asthmatic airway smooth muscle cells is caused by reduced microRNA-19a expression and leads to enhanced remodeling
Authors: Qingzhu Sun, Li Liu, Hui Wang, Jyotshna Mandal, Petra Khan, Katrin E. Hostettler, Daiana Stolz, Michael Tamm, Antonio Molino, Didier Lardinois, Shemin Lu, Michael Roth
Journal: Journal of Allergy and Clinical Immunology (2017)
Mode of Action of Catecholamines on Contraction Mechanism in Relation to Action Potential
Authors: Toyomi Sano, Fumio Suzuki
Journal: Circulation (1971)

1) Catecholamines induced shortening of plateau and total duration of action potential and increase of contraction and shortening of the time to peak tension and of the total duration of contraction of the rabbit ventricular muscle. Some parallelism was found between the electrical and mechanical changes. 2) The findings suggest the following: isoproterenol utilizes chiefly the extracellular calcium for its inotropic action. Norepinephrine shows an inotropic action by mobilizing in addition the intracellular calcium, and the contraction by this action is depressed by potassium. Both have little relation with sodium in their inotropic action.
MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis
Authors: Bishuang Cai, Edward B. Thorp, Amanda C. Doran, Brian E. Sansbury, Mat J.A.P. Daemen, Bernhard Dorweiler, Matthew Spite, Gabrielle Fredman, Ira Tabas
Journal: Journal of Clinical Investigation (2017)

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective resolution. In human carotid plaques, MerTK cleavage correlated with plaque necrosis and the presence of ischemic symptoms. Moreover, in fat-fed LDL receptor-deficient (Ldlr-/-) mice whose myeloid cells expressed a cleavage-resistant variant of MerTK, atherosclerotic lesions exhibited higher macrophage MerTK, lower levels of the cleavage product soluble Mer, improved efferocytosis, smaller necrotic cores, thicker fibrous caps, and increased ratio of proresolving versus proinflammatory lipid mediators. These findings provide a plausible molecular-cellular mechanism that contributes to defective efferocytosis, plaque necrosis, and impaired resolution during the progression of atherosclerosis.
P1.01-002 Environmental Tobacco Smoke Exposure and EGFR Mutations/ALK Translocation in Never Smokers. A Multicenter Study in Spanish Never-Smokers
Authors: Mónica Pérez-Ríos, Alberto Ruano-Ravina, Maruxa Zapata, María Torres-Durán, Virginia Leiro-Fernández, Isaura Parente-Lamelas, Iria Vidal-García, Olalla Castro-Añón, Margarita Amenedo, Mariano Provencio-Pulla, Antonio Golpe Gómez, Rosirys Guzmán-Taveras, María José Mejuto-Martí, Ángeles Rodríguez, Juan Barros-Dios
Journal: Journal of Thoracic Oncology (2017)