tbuckley/cabot-search huggingface dataset:
Hyper‐IgE in the allergy clinic––when is it primary immunodeficiency?
Authors: Mark J. Ponsford, Adam Klocperk, Federica Pulvirenti, Virgil A. S. H. Dalm, Tomas Milota, Francesco Cinetto, Zita Chovancova, Manuel J. Rial, Anna Sediva, Jiri Litzman, Carlo Agostini, Martin van Hagen, Isabella Quinti, Stephen Jolles
Journal: Allergy (2018)

Abstract The 2017 International Union of Immunological Societies ( IUIS ) classification recognizes 3 hyper‐IgE syndromes ( HIES ), including the prototypic Job's syndrome (autosomal dominant STAT 3‐loss of function) and autosomal recessive PGM 3 and SPINK 5 syndromes. Early diagnosis of PID can direct life‐saving or transformational interventions; however, it remains challenging owing to the rarity of these conditions. This can result in diagnostic delay and worsen prognosis. Within increasing access to “clinical‐exome” testing, clinicians need to be aware of the implication and rationale for genetic testing, including the benefits and limitations of current therapies. Extreme elevation of serum IgE has been associated with a growing number of PID syndromes including the novel CARD 11 and ZNF 341 deficiencies. Variable elevations in IgE are associated with defects in innate, humoral, cellular and combined immunodeficiency syndromes. Barrier compromise can closely phenocopy these conditions. The aim of this article was to update readers on recent developments at this important interface between allergy and immunodeficiency, highlighting key clinical scenarios which should draw attention to possible immunodeficiency associated with extreme elevation of IgE, and outline initial laboratory assessment and management.
Adrenaline after cardiac arrest doubles risk of serious brain damage, finds trial
Authors: Nigel Hawkes
Journal: BMJ (2018)

A randomised trial of use of adrenaline in patients who have a cardiac arrest outside hospital leaves paramedics with a dilemma.

More patients were alive 30 days after their hearts had been restarted with adrenaline, but their chances of serious brain damage were almost doubled, show the findings, reported in the New England Journal of Medicine .1 The finding is likely to lead to a change in guidelines for treating cardiac arrest, though the trial’s lead author, Gavin Perkins of Warwick University, was reluctant to commit himself.

Speaking at a briefing at the Science Media Centre in London, Perkins said it would need a broader consideration of the findings by bodies such as the …
Brain Development and Heart Function after Systemic Single-Agent Chemotherapy in a Mouse Model of Childhood Leukemia Treatment
Authors: T. Leigh Spencer Noakes, Thomas S. Przybycien, Amanda Forwell, Connor Nicholls, Yu-Qing Zhou, Darci T. Butcher, Rosanna Weksberg, Sharon L. Guger, Brenda J. Spiegler, Russell J. Schachar, Johann Hitzler, Shinya Ito, Ellen van der Plas, Brian J. Nieman
Journal: Clinical Cancer Research (2018)

Chemotherapy for childhood acute lymphoblastic leukemia (ALL) can cause late-appearing side effects in survivors that affect multiple organs, including the heart and brain. However, the complex ALL treatment regimen makes it difficult to isolate the causes of these side effects and impossible to separate the contributions of individual chemotherapy agents by clinical observation. Using a mouse model, we therefore assessed each of eight representative, systemically-administered ALL chemotherapy agents for their impact on postnatal brain development and heart function.
micro<scp>RNA</scp>‐146a is linked to the production of IgE in mice but not in atopic dermatitis patients
Authors: Gemma Carreras‐Badosa, Toomas Runnel, Mario Plaas, Jaanika Kärner, Beate Rückert, Freddy Lättekivi, Sulev Kõks, Cezmi A. Akdis, Külli Kingo, Ana Rebane
Journal: Allergy (2018)

Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Comparative effectiveness of treatment options for plantar heel pain: a systematic review with network meta-analysis
Authors: Opeyemi O Babatunde, Amardeep Legha, Chris Littlewood, Linda S Chesterton, Martin J Thomas, Hylton B Menz, Danielle van der Windt, Edward Roddy
Journal: British Journal of Sports Medicine (2018)

Objective To evaluate the comparative effectiveness of current treatment options for plantar heel pain (PHP). Design Systematic review and network meta-analysis (NMA). Data sources Medline, EMBASE, CINAHL, AMED, PEDro, Cochrane Database, Web of Science and WHO Clinical Trials Platform were searched from their inception until January 2018. Study selection Randomised controlled trials (RCTs) of adults with PHP investigating common treatments (ie, corticosteroid injection, non-steroidal anti-inflammatory drugs, therapeutic exercise, orthoses and/or extracorporeal shockwave therapy (ESWT)) compared with each other or a no treatment, placebo/sham control. Data extraction and analysis Data were extracted and checked for accuracy and completeness by pairs of reviewers. Primary outcomes were pain and function. Comparative treatment effects were analysed by random effects NMA in the short term, medium term and long term. Relative ranking of treatments was assessed by surface under the cumulative ranking probabilities (0–100 scale). Results Thirty-one RCTs (total n=2450 patients) were included. There was no evidence of inconsistency detected between direct and indirect treatment comparisons in the networks, but sparse data led to frequently wide CIs. Available evidence does not suggest that any of the commonly used treatments for the management of PHP are better than any other, although corticosteroid injections, alone or in combination with exercise, and ESWT were ranked most likely to be effective for the management of short-term, medium-term and long-term pain or function; placebo/sham/control appeared least likely to be effective; and exercise appeared to only be beneficial for long-term pain or function. Conclusions Current evidence is equivocal regarding which treatment is the most effective for the management of PHP. Given limited understanding of long-term effects, there is need for large, methodologically robust multicentre RCTs investigating and directly comparing commonly used treatments for the management of PHP. PROSPERO registration number CRD42016046963.
Relationship between socioeconomic status (SES) and treatment in stage II prostate cancer.
Authors: Van T.H. Do, Hoang V. Tran, Jessica Gries, Peter T. Silberstein
Journal: Journal of Clinical Oncology (2014)

e17561 Background: This is the largest study to evaluate the relationship between SES and treatment choices in stage II Prostate cancer. Methods: The National Cancer Database (NCDB) contains data from more than 70% of all new cancers diagnosed in the United States. 1,198,323 patients diagnosed with stage II Prostate cancer between 2000 and 2011 were identified and analyzed. Proportions were compared using Chi-square test. Results: Patients older than 70 were less likely to receive surgical treatment (20.5%) compared to patients younger than 70 (54.0%) (p<0.001). Black and Hispanic were more likely to get no treatment (10.5%) than White patients (6.5%) (p< 0.001). Private insurance holder had higher rate of surgical treatment (57.7%) than Medicare (30.3%), Medicaid patients (34.6%). Uninsured patients (15%) were more likely to have no treatment than Medicaid (12%), Managed (5%) and Medicare patients (8%) (p<0.001). Conclusions: This study highlights significant disparities in treatment among different SES in Stage II Prostate cancer patients. Patients that received higher rate of surgical treatment were: White, younger, higher income, more education, and had private insurance. Patients that had higher rate of no treatment included Black, Hispanic, older age, lower income, less education, and no insurance (all of these differences had p<0.001) Surgical treatment No treatment Age (year) <70 424,749 (54.0%) 46,092 (5.9%) ≥70 84,298 (20.5%) 41,384 (10%) Race White 410,829 (43.9%) 60,535 (6.5%) Black 57,991 (35.1%) 17,300 (10.5%) Hispanic 19,293 (39.5%) 5,132 (10.5%) Education (%without HS deg) Lower value means more education 31%+ 52,041 (36.5%) 13,815 (9.7%) 12-30.9% 270,292 (41%) 46,813 (7.1%) <12% 161,498 (47.7%) 22,276 (6.7%) Income (per year) <$28,000 36,800 (34.4%) 11,332 (10.6%) $28,000-$48,999 255,257 (41.5%) 43,616 (7.1%) $49,000+ 191,819 (45.9%) 27,962 (6.7%) Insurance status Not insured 6,743 (41.2%) 2,375 (14.5%) Private/managed 299,629 (57.7%) 24,925 (4.8%) Medicaid 6,893 (34.6%) 2,413 (12.1%) Medicare 163,840 (30.3%) 40,904 (7.6%)
Early Regenerative Capacity in the Porcine Heart
Authors: Lei Ye, Giuseppe D’Agostino, Sze Jie Loo, Chen Xu Wang, Li Ping Su, Shi Hua Tan, Gui Zhen Tee, Chee Jian Pua, Edgar Macabe Pena, Redmond Belen Cheng, Way Cherng Chen, Desiree Abdurrachim, Janise Lalic, Ru San Tan, Teck Hock Lee, JianYi Zhang, Stuart Alexander Cook
Journal: Circulation (2018)

The adult mammalian heart has limited ability to repair itself after injury. Zebrafish, newts, and neonatal mice can regenerate cardiac tissue, largely by cardiac myocyte (CM) proliferation. It is unknown whether hearts of young large mammals can regenerate.We examined the regenerative capacity of the pig heart in neonatal animals (ages 2, 3, or 14 days postnatal) after myocardial infarction or sham procedure. Myocardial scar and left ventricular function were determined by cardiac magnetic resonance imaging and echocardiography. Bromodeoxyuridine pulse-chase labeling, histology, immunohistochemistry, and Western blotting were performed to study cell proliferation, sarcomere dynamics, and cytokinesis and to quantify myocardial fibrosis. RNA-sequencing was also performed.After myocardial infarction, there was early and sustained recovery of cardiac function and wall thickness in the absence of fibrosis in 2-day-old pigs. In contrast, older animals developed full-thickness myocardial scarring, thinned walls, and did not recover function. Genome-wide analyses of the infarct zone revealed a strong transcriptional signature of fibrosis in 14-day-old animals that was absent in 2-day-old pigs, which instead had enrichment for cytokinesis genes. In regenerating hearts of the younger animals, up to 10% of CMs in the border zone of the myocardial infarction showed evidence of DNA replication that was associated with markers of myocyte division and sarcomere disassembly.Hearts of large mammals have regenerative capacity, likely driven by cardiac myocyte division, but this potential is lost immediately after birth.
Down Syndrome Critical Region 1 Gene, <i>Rcan1</i> , Helps Maintain a More Fused Mitochondrial Network
Authors: Valentina Parra, Francisco Altamirano, Carolina P. Hernández-Fuentes, Dan Tong, Victoriia Kyrychenko, David Rotter, Zully Pedrozo, Joseph A. Hill, Verónica Eisner, Sergio Lavandero, Jay W. Schneider, Beverly A. Rothermel
Journal: Circulation Research (2018)

The regulator of calcineurin 1 (RCAN1) inhibits CN (calcineurin), a Ca2+-activated protein phosphatase important in cardiac remodeling. In humans, RCAN1 is located on chromosome 21 in proximity to the Down syndrome critical region. The hearts and brains of Rcan1 KO mice are more susceptible to damage from ischemia/reperfusion (I/R); however, the underlying cause is not known.Mitochondria are key mediators of I/R damage. The goal of these studies was to determine the impact of RCAN1 on mitochondrial dynamics and function.Using both neonatal and isolated adult cardiomyocytes, we show that, when RCAN1 is depleted, the mitochondrial network is more fragmented because of increased CN-dependent activation of the fission protein, DRP1 (dynamin-1-like). Mitochondria in RCAN1-depleted cardiomyocytes have reduced membrane potential, O2 consumption, and generation of reactive oxygen species, as well as a reduced capacity for mitochondrial Ca2+ uptake. RCAN1-depleted cardiomyocytes were more sensitive to I/R; however, pharmacological inhibition of CN, DRP1, or CAPN (calpains; Ca2+-activated proteases) restored protection, suggesting that in the absence of RCAN1, CAPN-mediated damage after I/R is greater because of a decrease in the capacity of mitochondria to buffer cytoplasmic Ca2+. Increasing RCAN1 levels by adenoviral infection was sufficient to enhance fusion and confer protection from I/R. To examine the impact of more modest, and biologically relevant, increases in RCAN1, we compared the mitochondrial network in induced pluripotent stem cells derived from individuals with Down syndrome to that of isogenic, disomic controls. Mitochondria were more fused, and O2 consumption was greater in the trisomic induced pluripotent stem cells; however, coupling efficiency and metabolic flexibility were compromised compared with disomic induced pluripotent stem cells. Depletion of RCAN1 from trisomic induced pluripotent stem cells was sufficient to normalize mitochondrial dynamics and function.RCAN1 helps maintain a more interconnected mitochondrial network, and maintaining appropriate RCAN1 levels is important to human health and disease.
A Gut Commensal-Produced Metabolite Mediates Colonization Resistance to Salmonella Infection
Authors: Amanda Jacobson, Lilian Lam, Manohary Rajendram, Fiona Tamburini, Jared Honeycutt, Trung Pham, Will Van Treuren, Kali Pruss, Stephen Russell Stabler, Kyler Lugo, Donna M. Bouley, Jose G. Vilches-Moure, Mark Smith, Justin L. Sonnenburg, Ami S. Bhatt, Kerwyn Casey Huang, Denise Monack
Journal: Cell Host & Microbe (2018)
Oncogenic hijacking of the stress response machinery in T cell acute lymphoblastic leukemia
Authors: Nikos Kourtis, Charalampos Lazaris, Kathryn Hockemeyer, Juan Carlos Balandrán, Alejandra R. Jimenez, Jasper Mullenders, Yixiao Gong, Thomas Trimarchi, Kamala Bhatt, Hai Hu, Liza Shrestha, Alberto Ambesi-Impiombato, Michelle Kelliher, Elisabeth Paietta, Gabriela Chiosis, Monica L. Guzman, Adolfo A. Ferrando, Aristotelis Tsirigos, Iannis Aifantis
Journal: Nature Medicine (2018)
Inflammatory Pathways Regulated by Tumor Necrosis Receptor–Associated Factor 1 Protect From Metabolic Consequences in Diet-Induced Obesity
Authors: Nathaly Anto Michel, Christian Colberg, Konrad Buscher, Björn Sommer, Akula Bala Pramod, Erik Ehinger, Bianca Dufner, Natalie Hoppe, Katharina Pfeiffer, Timoteo Marchini, Florian Willecke, Peter Stachon, Ingo Hilgendorf, Timo Heidt, Constantin von zur Muhlen, Dominik von Elverfeldt, Dietmar Pfeifer, Roland Schüle, Ulrich Kintscher, Sebastian Brachs, Klaus Ley, Christoph Bode, Andreas Zirlik, Dennis Wolf
Journal: Circulation Research (2018)

The coincidence of inflammation and metabolic derangements in obese adipose tissue has sparked the concept of met-inflammation. Previous observations, however, suggest that inflammatory pathways may not ultimately cause dysmetabolism.We have revisited the relationship between inflammation and metabolism by testing the role of TRAF (tumor necrosis receptor-associated factor)-1, an inhibitory adapter of inflammatory signaling of TNF (tumor necrosis factor)-α, IL (interleukin)-1β, and TLRs (toll-like receptors).Mice deficient for TRAF-1, which is expressed in obese adipocytes and adipose tissue lymphocytes, caused an expected hyperinflammatory phenotype in adipose tissue with enhanced adipokine and chemokine expression, increased leukocyte accumulation, and potentiated proinflammatory signaling in macrophages and adipocytes in a mouse model of diet-induced obesity. Unexpectedly, TRAF-1-/- mice were protected from metabolic derangements and adipocyte growth, failed to gain weight, and showed improved insulin resistance-an effect caused by increased lipid breakdown in adipocytes and UCP (uncoupling protein)-1-enabled thermogenesis. TRAF-1-dependent catabolic and proinflammatory cues were synergistically driven by β3-adrenergic and inflammatory signaling and required the presence of both TRAF-1-deficient adipocytes and macrophages. In human obesity, TRAF-1-dependent genes were upregulated.Enhancing TRAF-1-dependent inflammatory pathways in a gain-of-function approach protected from metabolic derangements in diet-induced obesity. These findings identify TRAF-1 as a regulator of dysmetabolism in mice and humans and question the pathogenic role of chronic inflammation in metabolism.
Community screening campaign for Strongyloides stercoralis among Latin American immigrants in Spain
Authors: B. Monge-Maillo, M. Navarro, E. Rodríguez, J.M. Ramos Rincón, S. Chamorro Tojeiro, S. Jiménez Sánchez, M.J. Casas del Corral, R. López-Vélez
Journal: Clinical Microbiology and Infection (2018)
Searching for Survivor-Specific Services at NCI-Designated Comprehensive Cancer Centers: A Qualitative Assessment
Authors: Betsy Rolland, Jordan Eschler
Journal: Journal of the National Comprehensive Cancer Network (2018)

Background: Cancer survivorship presents unique medical, psychosocial, and logistical challenges for survivors, their caregivers, and clinicians. NCI-designated Comprehensive Cancer Centers (CCCs) serve a unique role in the delivery of cancer care because they not only provide care but also serve as a model for community oncologists and clinics through the development and dissemination of standards of care. Survivors, their caregivers, and clinicians look to CCCs to provide information about how to navigate the transition from active to posttreatment care. However, there is wide variability in the types of resources CCCs make available on their websites. The goal of our assessment was to understand the types of posttreatment survivor-specific resources CCCs are providing on their website. Methods: We analyzed the websites of the 47 CCCs to evaluate survivor-specific resources around the 4 components of survivorship care described by the Institute of Medicine guidelines for survivorship care plans: surveillance, prevention, intervention, and coordination. Results: Of the 47 CCCs, 74.5% (n=35) had discoverable survivor-specific services on their websites. Despite our inclusive approach to coding, few websites contained extensive information targeted at survivors, their caregivers, or clinicians. Only the coordination and intervention elements were discussed by at least half of the CCCs. From the vantage point of cancer survivors, their lay caregivers, loved ones, or clinicians, there is limited information about survivor-specific services on the websites of the 47 CCCs. This dearth of information translates into substantial work for these groups to find the resources they may need. Conclusions: The CCCs have an opportunity to serve as information hubs and to lessen the amount of work associated with survivorship. As models of cancer care delivery, the CCCs can also set the standard for community oncologists and clinics for delivery of care that improves the quality of life for survivors.
Coding Errors in Survey Study of Best Practices for In-Hospital Cardiac Arrest
Authors: Paul S. Chan, Brahmajee K. Nallamothu
Journal: JAMA Cardiology (2018)

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Malignancies and lung transplantation.
Authors: David Perez Callejo, Elena Almagro, Bernard Gaston Doger de Speville, Miriam Huelves, Patricia Ibeas, Ana Lopez-Gonzalez, Magda Palka, Andrea Ruiz-Valdepeñas, Raphael Mohr, MariCruz Carreño, Rosalia Laporta, Mariano Provencio
Journal: Journal of Clinical Oncology (2012)

e12015 Background: Malignacies rank fourth on the leading causes of death in recipients of solid organ transplantation. High-dose immunosuppression, infections with oncogenic viruses and the pre-transplant risk, mainly due to tobacco, make these patients more susceptible for developing cancer. In the present study we reviewed a collective of 50 patients with lung transplantation (LT) and cancer. Methods: Retrospective study of 503 lung transplant patients, performed at the Hospital Universitario Puerta de Hierro during 1993 and 2012. We included the following variables: date of birth, reason and date of transplantation, date of diagnosis of malignancy, histology and response to treatment, date and cause of exitus. The contrasts between proportions were performed using Chi-square test and survival curves using the product-limit method of Kaplan-Meier. Results: The 503 included transplant patients developed a total of 55 post-transplant malignancies in 50 patients. Four patients presented tumors already previous to the transplantation. The main underlying pathologies of the patient collective are idiopathic pulmonary fibrosis (50%), emphysema (30%) and cystic fibrosis (14%). Histology of the 55 post-transplant tumors: 18 skin cancer, 12 lung cancer, 8 gastrointestinal cancer, 6 Non-Hodgkin Lymphomas, 2 bladder cancer, 2 myelodysplastic syndromes, 2 sarcomas and 5 others. The mean age of diagnosis of malignancies is at 59 years (18-68). The mean time from transplantation to tumor diagnosis amounts 4 years (1-15). Of the 21 patients (42%) that have died until data collection, cancer was death cause in 15 (30%) Conclusions: Relying on our data, the majority of malignancies are skin and lung cancer and lymphoproliferative syndromes, attributing complications that should be considered in lung transplantation.