tbuckley/cabot-search huggingface dataset:
Chronic Obstructive Pulmonary Disease and Smoking Status — United States, 2017
Authors: Anne G. Wheaton, Yong Liu, Janet B. Croft, Brenna VanFrank, Thomas L. Croxton, Antonello Punturieri, Lisa Postow, Kurt J. Greenlund
Journal: MMWR Morbidity and Mortality Weekly Report (2019)

Cigarette smoking is the leading cause of chronic obstructive pulmonary disease (COPD) in the United States; however, an estimated one fourth of adults with COPD have never smoked (1). CDC analyzed state-specific Behavioral Risk Factor Surveillance System (BRFSS) data from 2017, which indicated that, overall among U.S. adults, 6.2% (age-adjusted) reported having been told by a health care professional that they had COPD. The age-adjusted prevalence of COPD was 15.2% among current cigarette smokers, 7.6% among former smokers, and 2.8% among adults who had never smoked. Higher prevalences of COPD were observed in southeastern and Appalachian states, regardless of smoking status of respondents. Whereas the strong positive correlation between state prevalence of COPD and state prevalence of current smoking was expected among current and former smokers, a similar relationship among adults who had never smoked suggests secondhand smoke exposure as a potential risk factor for COPD. Continued promotion of smoke-free environments might reduce COPD among both those who smoke and those who do not.
Linking the International Wheat Genome Sequencing Consortium bread wheat reference genome sequence to wheat genetic and phenomic data
Authors: Michael Alaux, Jane Rogers, Thomas Letellier, Raphaël Flores, Françoise Alfama, Cyril Pommier, Nacer Mohellibi, Sophie Durand, Erik Kimmel, Célia Michotey, Claire Guerche, Mikaël Loaec, Mathilde Lainé, Delphine Steinbach, Frédéric Choulet, Hélène Rimbert, Philippe Leroy, Nicolas Guilhot, Jérôme Salse, Catherine Feuillet, . International Wheat Genome Sequencing Consortium (iwgsc), Etienne Paux, Kellye Eversole, Anne-Francoise Adam-Blondon, Hadi Quesneville
Journal: Genome biology (2018)

The Wheat@URGI portal has been developed to provide the international community of researchers and breeders with access to the bread wheat reference genome sequence produced by the International Wheat Genome Sequencing Consortium. Genome browsers, BLAST, and InterMine tools have been established for in-depth exploration of the genome sequence together with additional linked datasets including physical maps, sequence variations, gene expression, and genetic and phenomic data from other international collaborative projects already stored in the GnpIS information system. The portal provides enhanced search and browser features that will facilitate the deployment of the latest genomics resources in wheat improvement.
Characterization of antibody and memory T-cell response in H7N9 survivors: a cross-sectional analysis
Authors: M.-J. Ma, X.-X. Wang, M.-N. Wu, X.-J. Wang, C.-J. Bao, H.-J. Zhang, Y. Yang, K. Xu, G.-L. Wang, M. Zhao, W. Cheng, W.-J. Chen, W.-H. Zhang, L.-Q. Fang, W.J. Liu, E.-F. Chen, W.-C. Cao
Journal: Clinical Microbiology and Infection (2019)
Pharmacological prophylaxis of venous thromboembolism in adult medical and surgical wards in the Gaza Strip: a multi-centre clinical audit
Authors: Yousef Abuowda, Mohammad Alswerki, Abdelrahman Alsheikh Ahmad, Maha Alfaqawi, Tayseer Afifi, Hasan Alyazouri, Abdelrahman Alqedra, Bettina Böttcher
Journal: The Lancet (2019)
IL-22 and its receptors are increased in human and experimental COPD and contribute to pathogenesis
Authors: Malcolm R. Starkey, Maximilian W. Plank, Paolo Casolari, Alberto Papi, Stelios Pavlidis, Yike Guo, Guy J.M. Cameron, Tatt Jhong Haw, Anthony Tam, Ma'en Obiedat, Chantal Donovan, Nicole G. Hansbro, Duc H. Nguyen, Prema Mono Nair, Richard Y. Kim, Jay C. Horvat, Gerard E. Kaiko, Scott K. Durum, Peter A. Wark, Don D. Sin, Gaetano Caramori, Ian M. Adcock, Paul S. Foster, Philip M. Hansbro
Journal: European Respiratory Journal (2019)

Chronic obstructive pulmonary disease (COPD) is the third leading cause of morbidity and death globally. The lack of effective treatments results from an incomplete understanding of the underlying mechanisms driving COPD pathogenesis.Interleukin (IL)-22 has been implicated in airway inflammation and is increased in COPD patients. However, its roles in the pathogenesis of COPD is poorly understood. Here, we investigated the role of IL-22 in human COPD and in cigarette smoke (CS)-induced experimental COPD.IL-22 and IL-22 receptor mRNA expression and protein levels were increased in COPD patients compared to healthy smoking or non-smoking controls. IL-22 and IL-22 receptor levels were increased in the lungs of mice with experimental COPD compared to controls and the cellular source of IL-22 included CD4+ T-helper cells, γδ T-cells, natural killer T-cells and group 3 innate lymphoid cells. CS-induced pulmonary neutrophils were reduced in IL-22-deficient (Il22-/-) mice. CS-induced airway remodelling and emphysema-like alveolar enlargement did not occur in Il22-/- mice. Il22-/- mice had improved lung function in terms of airway resistance, total lung capacity, inspiratory capacity, forced vital capacity and compliance.These data highlight important roles for IL-22 and its receptors in human COPD and CS-induced experimental COPD.
Abstract 5618: Statins Reduce Angiographical Restenosis As Well As De Novo Lesions Causing Unstable Angina in Japanese Patients Underwent Percutaneous Coronary Intervention
Authors: Ryusuke Tsunoda, Tomohiro Sakamoto, Sunao Kojima, Yasuhiro Ogata, Hisao Ogawa
Journal: Circulation (2008)

Background With the introduction of drug-eluting stents (DES), restenosis and target-vessel revascularization could be reduced to rates below 10%. After resolution of the restenosis issue, cardiova...
Abstract 18033: Whole Exome Sequencing Identifies Novel Candidate Genes in a Cohort of Patients with Idiopathic Pulmonary Arterial Hypertension
Authors: Roham T Zamanian, Maria Lyuksyutova, Patricia Angeles del Rosario, Robin Navarro, Vinicio De Jesus Perez
Journal: Circulation (2012)

Introduction: Idiopathic pulmonary arterial hypertension (IPAH) is a life-threatening disorder characterized by elevated pulmonary pressures and chronic right heart failure. Genetic studies have id...
Real-Time Functional Connectivity-Informed Neurofeedback of Amygdala-Frontal Pathways Reduces Anxiety
Authors: Zhiying Zhao, Shuxia Yao, Keshuang Li, Cornelia Sindermann, Feng Zhou, Weihua Zhao, Jianfu Li, Michael Lührs, Rainer Goebel, Keith M. Kendrick, Benjamin Becker
Journal: Psychotherapy and Psychosomatics (2019)

&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; Deficient emotion regulation and exaggerated anxiety represent a major transdiagnostic psychopathological marker. On the neural level these deficits have been closely linked to impaired, yet treatment-sensitive, prefrontal regulatory control over the amygdala. Gaining direct control over these pathways could therefore provide an innovative and promising intervention to regulate exaggerated anxiety. To this end the current proof-of-concept study evaluated the feasibility, functional relevance and maintenance of a novel connectivity-informed real-time fMRI neurofeedback training. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; In a randomized crossover sham-controlled design, 26 healthy subjects with high anxiety underwent real-time fMRI-guided neurofeedback training to enhance connectivity between the ventrolateral prefrontal cortex (vlPFC) and the amygdala (target pathway) during threat exposure. Maintenance of regulatory control was assessed after 3 days and in the absence of feedback. Training-induced changes in functional connectivity of the target pathway and anxiety ratings served as primary outcomes. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; Training of the target, yet not the sham control, pathway significantly increased amygdala-vlPFC connectivity and decreased levels of anxiety. Stronger connectivity increases were significantly associated with higher anxiety reduction on the group level. At the follow-up, volitional control over the target pathway was maintained in the absence of feedback. &lt;b&gt;&lt;i&gt;Conclusions:&lt;/i&gt;&lt;/b&gt; The present results demonstrate for the first time that successful self-regulation of amygdala-prefrontal top-down regulatory circuits may represent a novel intervention to control anxiety. As such, the present findings underscore both the critical contribution of amygdala-prefrontal circuits to emotion regulation and the therapeutic potential of connectivity-informed real-time neurofeedback.
PB1662 INTEGRATION OF GENOME‐WIDE ANALYSIS INTO CLINICAL DIAGNOSIS OF ACUTE LYMPHOBLASTIC LEUKEMIA: HOW MUCH CAN WE IMPROVE CYTOGENETIC TESTING?
Authors: M. Othman, J. Melo, I. Carreira, B. Grygalewicz, M. Silva, T. Liehr
Journal: HemaSphere (2019)

Background: Acute lymphoblastic leukemia (ALL) is a heterogeneous, aggressive disease, and most common in children. It is a leading cause of cancer death in young and adult, too. However, about 30% of pediatric and 50% of adult ALL patients still lack defined genetic hallmarks of biological and clinical significance. In addition, complex karyotype‐ALL (CX‐ALL) promoting a wide spectrum of diverse genetic alterations with striking genomic instability, are overall often neglected by research. Aims: The overall goal of this study was to characterize karyotypes and genetic content of 25 ALL cases and to rule out if one single molecular approach may be sufficient to detect genomic aberrations in these patients. Methods: ALL cases were retrospectively studied by multitude multicolor banding (mMCB), fluorescence in situ hybridization (FISH) using selected locus‐specific probes and array‐comparative genomic hybridization (aCGH). Results: Most strikingly, 13 of the studied 25 ALLs (∼55%) revealed abnormal karyotypes, applying mMCB: structural abnormalities were present in 12 and even numerical ones were identified in 2 cases. Overall, 123 copy number alterations (CNAs) were identified as loss (∼80%) or as gains (∼20%). Furthermore, highly complex karyotypes were detected by aCGH and mMCB in 4 out of the 13 aberrant cases. The latter four patients had either deletions or amplifications in genes involved in lymphoid development, cell cycle, Hematopoietic stem cells development and/or DNA repair ( IKZF1 , CDKN2A/B , PAX5 , BIRC3 , ATM , RB1, RUNX1 ), as shown by FISH, and also presented acquired marker chromosomes. Summary/Conclusion: Molecular approaches are suited to identify cryptic aberrations and potential target genes involved in leukemogenesis and progression of the disease. The present work demonstrated that aCGH is a highly efficient tool for detection of CNAs in ALL. However, while aCGH provide data on imbalanced genomic alterations, molecular cytogenetics additionally detects different leukemic subclones within one sample, as well as balanced translocations leading to tumor‐specific fusion genes. Thus, still no single approach is sufficient to comprehensively characterize all acquired aberrations in ALL.
AB1353-HPR PREVALENCE OF PAIN MEDICATIONS PRESCRIPTIONS IN PATIENTS WITH RA
Authors: Wilberto Rivero, Diana Buitrago-Garcia, Pedro Santos-Moreno, Fernando Rodriguez
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Pain is often disabling and can reduce the quality of life of a patient. Pain medications are drugs commonly prescribed for a variety of conditions one of them rheumatoid arthritis. The common molecules prescribed are paracetamol, nonsteroidal anti-inflammatory drugs (NSAIDs), and opioids. <h3>Objectives</h3> The goal of this study was to analyze the prevalence of pain medication prescription in patients with Rheumatoid Arthritis in a specialized center in Colombia. <h3>Methods</h3> We collected data from the medical charts in a specialized RA center conducted during 5 years, we performed a descriptive analysis, we collected sociodemographic information, DAS28, and the prevalence of prescription of analgesic medications divided in three groups non-opioid analgesics, opioid analgesics and NSAIDS. We calculated means, and standard deviations for continuous variables and categorical variables were presented as rates. We evaluated the relationship between DAS28 and the usage of pain medications. <h3>Results</h3> We reviewed the medical charts of 7076 patients diagnosed with rheumatoid arthritis, 82% were female and 17% were male. Median age was 60 years RIQ (51-69). The prevalence of usage of pain medications was 45%. Most of patients received paracetamol followed by a combination of paracetamol. See table 1. The prevalence of pain medications usage was not with associated disease activity. <h3>Conclusion</h3> As other studies have shown the prevalence of pain medications in patients with RA is high. The most prescribed medication was paracetamol or opioids, coinciding with other studies (1). This descriptive study is useful for further studies to develop in Colombia and Latin America. Additionally, it is important to consider other alternative therapies in order to approach in painful condition like RA. <h3>Disclosure of Interests</h3> Wilberto Rivero: None declared, Diana Buitrago-Garcia: None declared, Pedro Santos-Moreno Grant/research support from: Dr Santos has received research grants from Janssen, Abbvie and UCB, Speakers bureau: Dr Santos has received speaker fees from Sanofi, Lilly, Bristol, Pfizer, Abbvie, Janssen and UCB, Fernando Rodriguez: None declared
OP0188 PATHOGENICITY OF FUNCTIONAL AUTOANTIBODIES AGAINST AT1R IN A MOUSE MODEL OF SYSTEMIC SCLEROSIS
Authors: Junping Yin, Xiaoqing Wang, Xiaoyang Yue, Gabriela Riemekasten, Xinhua Yu, Frank Petersen
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Systemic sclerosis (SSc) is an autoimmune connective tissue disease featured by autoimmunity, fibrosis and vasculopathy. Although many autoantibodies have been detected in the sera of patients with SSc, it is not clear whether they play a role in the pathogenesis of disease. It has been reported that autoantibodies against the angiotensin-II receptor type 1 (AT1R) are present in the sera of SSc patients and are associated with several clinical symptoms of the disease, suggesting that these autoantibodies may act as pathogenic drivers. Recently, our group has developed a novel mouse model for SSc by immunizing mice with human AT1R (hAT1R). From this model we were able to generate functional monoclonal antibodies agonizing AT1R. <h3>Objectives</h3> In the current study, we aim to clarify, whether B cells and antibodies directed against AT1R are involved in the pathogenesis of experimental SSc <i>in vivo.</i> <h3>Methods</h3> To investigate the role of B cells in the hAT1R-induced mouse model of SSc, we immunized B-cell deficient mice with hAT1R. Nine weeks after the first immunization, mice were sacrificed and sera and tissues were collected for further evaluation. To investigate the pathogenicity of anti-AT1R antibodies in the disease, monoclonal autoantibodies against hAT1R were applied to the ear of C57Bl/6 mice by single or repetitive injection. Mice were sacrificed 24 hours or 14 days after the first injection for single and repeated application, respectively, and ear and lung tissues were collected for further evaluation. <h3>Results</h3> Compared to the wild type C57Bl/6 mice, hAT1R-immunized B-cell deficient mice were resistant against experimental SSc with regard to autoantibody production, inflammation in the lung and skin, and skin fibrosis. Furthermore, both single and repetitive injection of monoclonal antibodies against hAT1R induced inflammation in ears of mice. Despite this local effect, repetitive injection of anti-AT1R monoclonal antibodies provoked also inflammation in the lung of mice. <h3>Conclusion</h3> Our data demonstrate that i) B cells are indispensable for the pathogenesis of the hAT1R-induced mouse model for SSc and ii) monoclonal antibodies against hAT1R can induce inflammation in mice. Therefore, our results support a role of autoantibodies against AT1R in the pathogenesis of SSc. <h3>References</h3> [1] Yannick Allanore, et al. Nat Rev Dis Primers2015. [2] Gabriela Riemekasten, et al. Ann Rheum Dis2011. [3] Mike O. Becker, et al. Am J Respir Crit Care Med2014. <h3>Disclosure of Interests</h3> Junping Yin: None declared, Xiaoqing Wang: None declared, Xiaoyang Yue: None declared, Gabriela Riemekasten Consultant for: Chugai, F. Hoffmann-La Roche, Speakers bureau: Chugai, F. Hoffmann-La Roche, Xinhua Yu: None declared, Frank Petersen: None declared
FRI0608 ASSOCIATION BETWEEN INTERSTITIAL LUNG DISEASE AND RHEUMATIC DISEASE: IMPLICATIONS IN CLINICAL PRACTICE
Authors: Vera Ortiz-Santamaria, Noelí Reguart Oto, Pau Sendra de Dios, Noemí Busquets, Maria Pascual, Andrés Ponce, Xavier Surís, Yolanda Galea, Anna Mola, Marta Torrella, Julia Tarrega, Enric Barbeta
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> The relationship between interstitial lung disease (ILD) and rheumatic diseases is well known. Recently, a new clinical entity has been described that relates ILD with autoimmune findings, IPAF (Interstitial Pneumonia with Autoimmune Features), which allows identifying and condensing non-cataloged diseases with pulmonary and rheumatic involvement. <h3>Objectives</h3> Our aim is to establish which patients with ILD have a rheumatic disease, and which of them meet the IPAF criteria. We analyzed the role of nailfold capillaroscopy in these patients. <h3>Methods</h3> This is a prospective descriptive observational study. The observation period was 2 years (2016-2018), in a county university hospital. Patients diagnosed with ILD of unknown etiology, derived from Pneumology Service, were included. A medical history was obtained focused on autoimmune disease, rheumatological evaluation, rheumatological blood markers and nailfold capillaroscopy, in order to establish whether they had a concomitant rheumatic disease. <h3>Results</h3> Thirty patients with ILD were evaluated, with a mean age of 70,5 years (53 - 88). Of the 30 subjects, 12 (40%) had usual interstitial pneumonia (UIP), 11 (36.67%) had organizing pneumonia (OP) and 7 (23.33%) had nonspecific interstitial pneumonia (NSIP). Eleven (36,67%) of the 30 patients had an altered capillaroscopy, 6 of them (54,5%) had a rheumatic disease. In our sample, 5 cases meet diagnostic IPAF criteria, 4 OP and 1 UIP, three of them with altered capillaroscopy. <h3>Conclusion</h3> In our serie, one third of the patients were diagnosed with rheumatic disease associated with interstitial lung disease. Of the thirty evaluated patients, 36.67% had altered capillaroscopy, 54.5% presenting concomitant rheumatic disease. Following the IPAF classification criteria, we obtained 5 cases in our sample: four OP and one UIP, 3 of them with altered capillaroscopy. It is important to be aware of this association with a multidisciplinary approach for the adequate diagnosis and follow-up of these patients. <h3>Disclosure of Interests</h3> Vera Ortiz-Santamaria Speakers bureau: GSK, Roche, Pfizer, MSD, Noelí Reguart Oto: None declared, Pau Sendra de Dios: None declared, Noemí Busquets: None declared, Maria Pascual: None declared, Andrés Ponce Speakers bureau: Abbie, Roche, Pfizer, MSD, Xavier Surís Speakers bureau: Lilly, Pfizer, MSD, Yolanda Galea: None declared, Anna Mola: None declared, Marta Torrella: None declared, Julia Tarrega: None declared, Enric Barbeta Speakers bureau: GSK, Boehringer Ingelheim, Roche
Abstract 12443: Perivalvular Aortic Regurgitation and Clinical Outcome after TAVI : Role of the Delivery Approach - Insights from the France 2 Registry
Authors: Eric van Belle, Francis Juthier, Pierre Yves Litzler, Martine Gilard, Helene Eltchaninoff, Benard Iung, Carlo Banfi, Pascal Leprince, Jean Fajadet, Alain Leguerrier, Alain Prat, Marc Laskar, Emmanuel Teiger
Journal: Circulation (2012)

Background: Significant aortic regurgitation (AR) is observed in 15-20% post-TAVI. The potential interaction between delivery approach, AR and clinical outcome is ill defined. On one hand, non-femo...
Final Overall Survival of a Randomized Trial of Bevacizumab for Primary Treatment of Ovarian Cancer
Authors: Krishnansu S. Tewari, Robert A. Burger, Danielle Enserro, Barbara M. Norquist, Elizabeth M. Swisher, Mark F. Brady, Michael A. Bookman, Gini F. Fleming, Helen Huang, Howard D. Homesley, Jeffrey M. Fowler, Benjamin E. Greer, Matthew Boente, Sharon X. Liang, Chenglin Ye, Carlos Bais, Leslie M. Randall, John K. Chan, J. Stuart Ferriss, Robert L. Coleman, Carol Aghajanian, Thomas J. Herzog, Philip J. DiSaia, Larry J. Copeland, Robert S. Mannel, Michael J. Birrer, Bradley J. Monk
Journal: Journal of Clinical Oncology (2019)

PURPOSE We report the final, protocol-specified analysis of overall survival (OS) in GOG-0218, a phase III, randomized trial of bevacizumab in women with newly diagnosed ovarian, fallopian tube, or primary peritoneal carcinoma. METHODS A total of 1,873 women with incompletely resected stage III to IV disease were randomly assigned 1:1:1 to six 21-day cycles of intravenous carboplatin (area under the concentration v time curve 6) and paclitaxel (175 mg/m 2 ) versus chemotherapy plus concurrent bevacizumab (15 mg/kg, cycles 2 to 6) versus chemotherapy plus concurrent and maintenance bevacizumab (cycles 2 to 22). Inclusion criteria included a Gynecologic Oncology Group performance status of 0 to 2 and no history of clinically significant vascular events or evidence of intestinal obstruction. OS was analyzed in the intention-to-treat population. A total of 1,195 serum and/or tumor specimens were sequenced for BRCA1/2 and damaging mutations in homologous recombination repair (HRR) genes. Intratumoral microvessel density was studied using CD31 immunohistochemistry. RESULTS Median follow-up was 102.9 months. Relative to control (n = 625), for patients receiving bevacizumab-concurrent (n = 625), the hazard ratio (HR) of death was 1.06 (95% CI, 0.94 to 1.20); for bevacizumab-concurrent plus maintenance (n = 623), the HR was 0.96 (95% CI, 0.85 to 1.09). Disease-specific survival was not improved in any arm. No survival advantage was observed after censoring patients who received bevacizumab at crossover or as second line. Median OS for stage IV bevacizumab-concurrent plus maintenance was 42.8 v 32.6 months for stage IV control (HR, 0.75; 95% CI, 0.59 to 0.95). Relative to wild type, the HR for death for BRCA1/2 mutated carcinomas was 0.62 (95% CI, 0.52 to 0.73), and for non- BRCA1/2 HRR, the HR was 0.65 (95% CI, 0.51 to 0.85). BRCA1/2, HRR, and CD31 were not predictive of bevacizumab activity. CONCLUSION No survival differences were observed for patients who received bevacizumab compared with chemotherapy alone. Testing for BRCA1/2 mutations and homologous recombination deficiency is essential.