tbuckley/cabot-search huggingface dataset:
Assisted Reproductive Technology Surveillance — United States, 2014
Authors: Saswati Sunderam, Dmitry M. Kissin, Sara B. Crawford, Suzanne G. Folger, Denise J. Jamieson, Lee Warner, Wanda D. Barfield
Journal: MMWR Surveillance Summaries (2017)

Since the first U.S. infant conceived with assisted reproductive technology (ART) was born in 1981, both the use of ART and the number of fertility clinics providing ART services have increased steadily in the United States. ART includes fertility treatments in which eggs or embryos are handled in the laboratory (i.e., in vitro fertilization [IVF] and related procedures). Women who undergo ART procedures are more likely than women who conceive naturally to deliver multiple-birth infants. Multiple births pose substantial risks to both mothers and infants, including obstetric complications, preterm delivery, and low birthweight infants. This report provides state-specific information for the United States (including the District of Columbia and Puerto Rico) on ART procedures performed in 2014 and compares birth outcomes that occurred in 2014 (resulting from ART procedures performed in 2013 and 2014) with outcomes for all infants born in the United States in 2014.
Optical Radiomic Signatures Derived from Optical Coherence Tomography Images Improve Identification of Melanoma
Authors: Zahra Turani, Emad Fatemizadeh, Tatiana Blumetti, Steven Daveluy, Ana Flavia Moraes, Wei Chen, Darius Mehregan, Peter E. Andersen, Mohammadreza Nasiriavanaki
Journal: Cancer Research (2019)

Abstract The current gold standard for clinical diagnosis of melanoma is excisional biopsy and histopathologic analysis. Approximately 15–30 benign lesions are biopsied to diagnose each melanoma. In addition, biopsies are invasive and result in pain, anxiety, scarring, and disfigurement of patients, which can add additional burden to the health care system. Among several imaging techniques developed to enhance melanoma diagnosis, optical coherence tomography (OCT), with its high-resolution and intermediate penetration depth, can potentially provide required diagnostic information noninvasively. Here, we present an image analysis algorithm, “optical properties extraction (OPE),” which improves the specificity and sensitivity of OCT by identifying unique optical radiomic signatures pertinent to melanoma detection. We evaluated the performance of the algorithm using several tissue-mimicking phantoms and then tested the OPE algorithm on 69 human subjects. Our data show that benign nevi and melanoma can be differentiated with 97% sensitivity and 98% specificity. These findings suggest that the adoption of OPE algorithm in the clinic can lead to improvements in melanoma diagnosis and patient experience. Significance: This study describes a noninvasive, safe, simple-to-implement, and accurate method for the detection and differentiation of malignant melanoma versus benign nevi.
Evidence-Based Medicine and the American Thoracic Society Clinical Practice Guidelines
Authors: Ross C. Schumacher, Oanh Kieu Nguyen, Kaivalya Deshpande, Anil N. Makam
Journal: JAMA Internal Medicine (2019)

This study assesses whether American Thoracic Society clinical practice guidelines are substantiated by high-quality evidence and can be used to promote evidence-based medicine.
Response of high-risk MDS to azacitidine and lenalidomide is impacted by baseline and acquired mutations in a cluster of three inositide-specific genes
Authors: Matilde Y. Follo, Andrea Pellagatti, Richard N. Armstrong, Stefano Ratti, Sara Mongiorgi, Sara De Fanti, Maria Teresa Bochicchio, Domenico Russo, Marco Gobbi, Maurizio Miglino, Sarah Parisi, Giovanni Martinelli, Michele Cavo, Donata Luiselli, James A. McCubrey, Pann-Ghill Suh, Lucia Manzoli, Jacqueline Boultwood, Carlo Finelli, Lucio Cocco
Journal: Leukemia (2019)

Specific myeloid-related and inositide-specific gene mutations can be linked to myelodysplastic syndromes (MDS) pathogenesis and therapy. Here, 44 higher-risk MDS patients were treated with azacitidine and lenalidomide and mutations analyses were performed at baseline and during the therapy. Results were then correlated to clinical outcome, overall survival (OS), leukemia-free-survival (LFS) and response to therapy. Collectively, 34/44 patients were considered evaluable for response, with an overall response rate of 76.25% (26/34 cases): 17 patients showed a durable response, 9 patients early lost response and 8 patients never responded. The most frequently mutated genes were ASXL1, TET2, RUNX1, and SRSF2. All patients early losing response, as well as cases never responding, acquired the same 3 point mutations during therapy, affecting respectively PIK3CD (D133E), AKT3 (D280G), and PLCG2 (Q548R) genes, that regulate cell proliferation and differentiation. Moreover, Kaplan–Meier analyses revealed that this mutated cluster was significantly associated with a shorter OS, LFS, and duration of response. All in all, a common mutated cluster affecting 3 inositide-specific genes is significantly associated with loss of response to azacitidine and lenalidomide therapy in higher risk MDS. Further studies are warranted to confirm these data and to further analyze the functional role of this 3-gene cluster.
Differentiation block in FLT3 mutant AML by inactivation of C/EBPalpha function by phosphorylation
Authors: D. Basseres, H. S. Radomska, Y. Yamamoto, D. W. Sternberg, N. Lokker, C. Sullivan, N. A. Giese, S. Schnittger, S. Bohlander, W. Hiddemann, D. G. ry Gilliland, D. G. Tenen
Journal: Blood (2003)
COSMOS-E: Guidance on conducting systematic reviews and meta-analyses of observational studies of etiology
Authors: Olaf M. Dekkers, Jan P. Vandenbroucke, Myriam Cevallos, Andrew G. Renehan, Douglas G. Altman, Matthias Egger
Journal: PLoS Medicine (2019)

Background To our knowledge, no publication providing overarching guidance on the conduct of systematic reviews of observational studies of etiology exists. Methods and findings Conducting Systematic Reviews and Meta-Analyses of Observational Studies of Etiology (COSMOS-E) provides guidance on all steps in systematic reviews of observational studies of etiology, from shaping the research question, defining exposure and outcomes, to assessing the risk of bias and statistical analysis. The writing group included researchers experienced in meta-analyses and observational studies of etiology. Standard peer-review was performed. While the structure of systematic reviews of observational studies on etiology may be similar to that for systematic reviews of randomised controlled trials, there are specific tasks within each component that differ. Examples include assessment for confounding, selection bias, and information bias. In systematic reviews of observational studies of etiology, combining studies in meta-analysis may lead to more precise estimates, but such greater precision does not automatically remedy potential bias. Thorough exploration of sources of heterogeneity is key when assessing the validity of estimates and causality. Conclusion As many reviews of observational studies on etiology are being performed, this document may provide researchers with guidance on how to conduct and analyse such reviews.
Genetic relatedness of ceftriaxone-resistant and high-level azithromycin resistant Neisseria gonorrhoeae cases, United Kingdom and Australia, February to April 2018
Authors: Amy V Jennison, David Whiley, Monica M Lahra, Rikki M Graham, Michelle J Cole, Gwenda Hughes, Helen Fifer, Monique Andersson, Anne Edwards, David Eyre
Journal: Eurosurveillance (2019)

Between February and April 2018, three ceftriaxone-resistant and high-level azithromycin-resistant Neisseria gonorrhoeae cases were identified; one in the United Kingdom and two in Australia. Whole genome sequencing was used to show that the isolates from these cases belong to a single gonococcal clone, which we name the A2543 clone.
UEG Week 2013 highlights: putting endoscopy into perspective
Authors: Ioannis Papanikolaou, Peter Siersema
Journal: Endoscopy (2013)

The 21st United European Gastroenterology (UEG) Week was held in Berlin in October 2013 and presented the opportunity for those interested in gastrointestinal endoscopy to learn of recent developments and research trends from all over the world. This report highlights oral presentations of the most important and exciting topics in gastrointestinal endoscopy and reviews them in the context of current knowledge.
Abstract IA20: Targeting DNA repair in cancer therapy
Authors: Alan D. D'Andrea
Journal: Clinical Cancer Research (2018)

Abstract Human cancer cells have genomic instability resulting from germline or acquired defects in DNA repair. One DNA repair pathway—the Fanconi anemia/BRCA pathway (D'Andrea A. N Engl J Med 2010;362:1909)—is defective in many human cancers, including breast, ovarian, and pancreatic neoplasms. Disruption of the FA/BRCA pathway results in the characteristic chromosome instability and radiation/crosslinker hypersensitivity of these tumors. In general, loss of one DNA repair pathway often leads to hyperdependence on another pathway for tumor cell survival. This hyperdependence offers a unique opportunity for the development of anticancer therapeutics. For instance, FA/BRCA pathway-deficient tumors are hyperdependent on base excision repair (BER) and, accordingly, these tumors are hypersensitive to single-agent treatment with PARP1 inhibitors, which block BER, or with ATM inhibitors. Our research program is focused on profiling the FA/BRCA pathway and the other five major DNA repair pathways in tumor cells (Kennedy RD, D'Andrea A. J Clin Oncol 2006;24:3799, 2006). Each DNA repair pathway has a characteristic biomarker and repairs a specific type of DNA lesion. By profiling these pathways in primary tumor samples with activation-specific antibodies to DNA repair proteins, we have been able (1) to predict the sensitivity of tumors to conventional chemotherapy and radiation; (2) to subset tumors for their sensitivity to novel classes of DNA repair inhibitors, (i.e., PARP1, Chk1, ATM, and proteasome inhibitors); and (3) to screen for new small-molecule inhibitors of other DNA repair pathways. This combination of novel DNA repair inhibitors, conventional DNA-damaging agents, and DNA repair biomarkers offers new opportunities for developing more effective anticancer therapy. In my presentation, I will also discuss novel approaches to sensitizing triple negative breast cancers (TNBCs) and ovarian tumors (OCs) to PARP1 inhibitors. We have previously shown that exposure of these tumors to either a CDK inhibitor or a proteasome inhibitor can block homologous recombination (HR) repair and thereby sensitize the tumor cells to PARP1 inhibitor. The CDK inhibitor/PARP1 inhibitor combination has been examined in orthotopic primary TNBC and OC xenograft models. Finally, we have identified an additional PARP1-dependent DNA repair mechanism in TNBCs and OCs. This pathway is driven by a novel alternative end-joining polymerase, POLθ. These tumors are hypersensitive to inhibitors of this new pathway, suggesting a new target for DNA repair therapies. Citation Format: Alan D. D'Andrea. Targeting DNA repair in cancer therapy [abstract]. In: Proceedings of the AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(1_Suppl):Abstract nr IA20.
EPB41L5 Mediates TGFβ-Induced Metastasis of Gastric Cancer
Authors: Mi-Hyeon Jeong, Soo-Yeon Park, Seung-Hyun Lee, JaeSung Seo, Jung-Yoon Yoo, Seung-Ho Park, Mi Jeong Kim, SooYeon Lee, Subhin Jang, Hyo-Kyoung Choi, Jae Eun Lee, Su-Jin Shin, Kyung-Chul Choi, Jae-Ho Cheong, Ho-Geun Yoon
Journal: Clinical Cancer Research (2019)

Because of disease heterogeneity, limited studies on effective chemotherapies and therapeutic agents for advanced gastric cancer are available. Erythrocyte membrane protein band 4.1-like 5 (EPB41L5) has critical roles in renal and breast cancer metastasis. However, its role in metastatic gastric cancer remains unknown.The specimens of 78 gastric cancer patients were analyzed by oligonucleotide microarray and survival analysis. In vitro experiments and metastatic mice models were used to assess the effects of EPB41L5 on gastric cancer metastasis.Gastric cancer patients with high EPB41L5 levels had poor prognosis and low survival rate. Further, TGFβ1-induced EPB41L5 expression promoted gastric cancer cell migration and invasion by Smad-dependent TGFβ signaling. Phospho-Smad3 recruitment to the EPB41L5 promoter was significantly inhibited by a TGFβ inhibitor. EPB41L5 overexpression increased lung metastasis of gastric cancer cells in nude mice, which was completely reversed by anti-EPB41L5 monoclonal antibody treatment. Importantly, p120-catenin knockdown abolished EPB41L5-enhanced gastric cancer cell metastasis. Anti-EPB41L5 monoclonal antibody treatment blocked the association of EPB41L5 with p120-catenin.TGFβ/EPB41L5/p120-catenin axis regulates gastric cancer cell metastasis, and EPB41L5 is a promising therapeutic target for advanced gastric cancer.
A Clinical Model of Progression to Multiple Myeloma in Solitary Plasmacytoma
Authors: Elisabet E. Manasanch, Catherine M. Claussen, Wenli Dong, Hans C. Lee, Sheeba K. Thomas, Krina K. Patel, Valerie K Reed, Bouthaina S. Dabaja, Sarah Milgrom, Chelsea C Pinnix, Simrit Parmar, Qaiser Bashir, Muzaffar H. Qazilbash, Behrang Amini, Alexanian Raymond, Robert Z. Orlowski, Lei Feng, Donna M. Weber
Journal: Blood (2017)
Medical encounters (including injury and illness) at mass community-based endurance sports events: an international consensus statement on definitions and methods of data recording and reporting
Authors: Martin Schwellnus, Courtney Kipps, William O Roberts, Jonathan A Drezner, Pierre D’Hemecourt, Chris Troyanos, Dina Christina Janse van Rensburg, Jannelene Killops, Jill Borresen, Mark Harrast, Paolo E Adami, Stéphane Bermon, Xavier Bigard, Sergio Migliorini, Esme Jordaan, Mats Borjesson
Journal: British Journal of Sports Medicine (2019)

Mass participation endurance sports events are popular but a large number of participants are older and may be at risk of medical complications during events. Medical encounters (defined fully in the statement) include those traditionally considered 'musculoskeletal' (eg, strains) and those due to 'illness' (eg, cardiac, respiratory, endocrine). The rate of sudden death during mass endurance events (running, cycling and triathlon) is between 0.4 and 3.3 per 100 000 entrants. The rate of other serious medical encounters (eg, exertional heat stroke, hyponatraemia) is rarely reported; in runners it can be up to 100 times higher than that of sudden death, that is, between 16 and 155 per 100 000 race entrants. This consensus statement has two goals. It (1) defines terms for injury and illness-related medical encounters, severity and timing of medical encounters, and diagnostic categories of medical encounters, and (2) describes the methods for recording data at mass participation endurance sports events and reporting results to authorities and for publication. This unifying consensus statement will allow data from various events to be compared and aggregated. This will inform athlete/patient management, and thus make endurance events safer.
P112 Studying cellular senescence in human lymph node stromal cells during the earliest phases of rheumatoid arthritis
Authors: TA De Jong, AL Timmerman, JF Semmelink, JS Hähnlein, LG van Baarsen
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Career situation of first and presenting author</h3> Student for a master or a PhD. <h3>Introduction</h3> Cellular senescence is a state of proliferation arrest of cells. The persistence and accumulation of senescent cells has been implicated in the pathogenesis of age-related diseases. Ageing is an important risk factor of rheumatoid arthritis (RA), a prototypic autoimmune disease in which loss of immune tolerance and systemic autoimmunity precedes clinical onset of disease. Through their intimate contact with lymphocytes, lymph node stromal cells (LNSCs) are important regulators of peripheral tolerance. Therefore, malfunctioning senescent LNSCs may potentially lead to defective peripheral tolerance and the development of systemic autoimmune disease. <h3>Objectives</h3> To determine the extent of cellular senescence of LNSCs during early phases of systemic autoimmunity. <h3>Methods</h3> We included individuals with arthralgia without any evidence of arthritis who were positive for IgM rheumatoid factor (IgM-RF) and/or anti-citrullinated protein antibodies (ACPA; RA-risk group), early arthritis patients (ACR/EULAR 2010 criteria; disease duration &lt;1 year) and seronegative healthy controls. All study subjects underwent ultrasound-guided inguinal lymph node biopsy. LNSCs were cultured from freshly collected lymph node needle biopsies and passages 0–9 were used for experiments. Flow cytometry, qPCR and microscopy were used to measure cell size, granularity, senescence-associated gene expression levels, telomere attrition and senescence-associated β-galactosidase (SA β-gal) activity. <h3>Results</h3> Preliminary flow cytometry data shows that the cell size of LNSCs from RA patients (n=11) and RA-risk individuals (n=7) is increased compared with healthy LNSCs (n=7), while granularity was specifically increased in LNSCs from RA patients (n=9). Initial SA β-gal stainings indicate higher activity in LNSCs from RA-risk (n=3) and RA patients (n=4) compared with healthy controls (n=2), however this data needs to be carefully interpreted and more donors should be analysed. Expression levels of senescence-associated genes significantly increased over culture passages and significantly higher p21 and p53 levels were observed in passage 9 LNSCs from RA patients compared with healthy controls (n=6 per group). <h3>Conclusions</h3> These preliminary findings provide a rationale for studying cellular senescence in LNSCs in more detail during different phases of RA and to investigate the consequence of senescent LNSCs on immune cell responses upon their interaction. <h3>Disclosure of Interest</h3> None declared.
The Future of Registries in the Era of Real-world Evidence for Medical Devices
Authors: Rachael L. Fleurence, Kathleen Blake, Jeffrey Shuren
Journal: JAMA Cardiology (2019)

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Tobacco Product Use Among Adults — United States, 2017
Authors: Teresa W. Wang, Kat Asman, Andrea S. Gentzke, Karen A. Cullen, Enver Holder-Hayes, Carolyn Reyes-Guzman, Ahmed Jamal, Linda Neff, Brian A. King
Journal: MMWR Morbidity and Mortality Weekly Report (2018)

In 2017, approximately 47 million (one in five) U.S. adults currently used any tobacco product, and an estimated 14% of adults were current cigarette smokers, down from 15.5% in 2016. Among current tobacco product users, approximately 87% (41 million) smoked combustible tobacco products, and 19% (9 million) used two or more tobacco products.
P134/O32 Selective expansion of a thymic-derived and functionally competent regulatory T cell population by low-dose IL-2 therapy in patients with refractory SLE
Authors: JY Humrich, C von Spee-Mayer, E Siegert, M Bertolo, A Rose, D Abdirama, P Enghard, B Stuhlmüller, F Hiepe, T Alexander, E Feist, A Radbruch, G-R Burmester, G Riemekasten
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Career situation of first and presenting author</h3> Instructor. <h3>Objectives</h3> An acquired deficiency of interleukin-2 (IL-2) and related defects in regulatory T cell (Treg) homeostasis play a crucial role in the pathogenesis of SLE. Here, we report the responses of Treg and other lymphocyte subsets to low-dose IL-2 therapy observed during an open-label, uncontrolled, dose adaption, phase 1/2a single-center clinical trial in patients with active and refractory SLE. <h3>Methods</h3> 12 patients with active and refractory SLE (SLEDAI ≥6) were treated at our site with a low-dose IL-2 regimen consisting of four separate treatment cycles each with daily subcutaneous injections of recombinant human IL-2 (aldesleukin) at single daily doses of either 0.75, 1.5 or 3.0 million IU for five consecutive days. Cells from peripheral blood were analyzed by flow cytometry before and one day after each treatment cycle. <h3>Results</h3> All patients showed highly significant cycle- and dose-dependent increases in the proportions and absolute numbers of CD3+CD4+FoxP3+CD127 lo Treg and of CD25hi expressing cells among Treg. By contrast, we observed no relevant changes in the absolute numbers of CD3+CD4+FoxP3 conventional T cells (Tcon), of CD3+CD8+ T cells, of CD3+CD56+NK T cells and of CD3-CD56+NK cells. The IL-2 expanded Treg population displayed a preserved suppressive capacity and expressed high levels of the Treg-associated molecules Helios, CD39 and CD137. In addition, we noted robust and dose-dependent increases in the proportions of Treg expressing the proliferation marker Ki67. Although significant increases in the proportions of Ki67 +cells among Tcon and also among other lymphocyte subsets were observed at the end of each treatment cycle, the calculated ratio between Ki67+ Treg and Ki67+ Tcon continuously increased and was significantly higher at the end of the treatment phase, suggesting a preferential targeting of the Treg population. <h3>Conclusions</h3> Low-dose IL-2 therapy promotes the selective expansion of a functionally competent and thymic-derived Treg population in patients with refractory SLE. This study also provides novel insights into the pharmacodynamics and the broad biologic effects of low-dose IL-2 therapy. <h3>Disclosure of Interest</h3> J. Humrich Consultant for: ILTOO Pharma, C. von Spee-Mayer: None declared, E. Siegert: None declared, M. Bertolo: None declared, A. Rose: None declared, D. Abdirama: None declared, P. Enghard: None declared, B. Stuhlmüller: None declared, F. Hiepe: None declared, T. Alexander: None declared, E. Feist: None declared, A. Radbruch: None declared, G.-R. Burmester: None declared, G. Riemekasten Consultant for: ILTOO Pharma.