tbuckley/cabot-search huggingface dataset:
Validity of the qSOFA Score in Low- and Middle-Income Countries
Authors: Joseph M. Lewis, Marc Henrion, Jamie Rylance
Journal: JAMA (2018)

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Hepatocyte-Macrophage Acetoacetate Shuttle Protects against Tissue Fibrosis
Authors: Patrycja Puchalska, Shannon E. Martin, Xiaojing Huang, Justin E. Lengfeld, Bence Daniel, Mark J. Graham, Xianlin Han, Laszlo Nagy, Gary J. Patti, Peter A. Crawford
Journal: Cell Metabolism (2018)
Abstract 15810: Pcsk9, Thromboxane and Cardiovacular Events in Atrial Fibrillation
Authors: Daniele Pastori, Roberto Carnevale, Maria Santulli, Francesco Violi, Pasquale Pignatelli
Journal: Circulation (2017)

Introduction: Patients with atrial fibrillation (AF) display enhanced platelet activation but the underlying mechanism is still unclear. Hypothesis: We investigated 1) the association between solub...
INTENSIVE CARE MEDICINE IN THE DEVELOPING WORLD - REAL-TIME, TRANSCONTINENTAL TEACHING OF TRAINEE PHYSICIANS IN SOMALILAND USING A DEDICATED SOCIAL NETWORKING PORTAL: A NOVEL APPLICATION OF TELE CRITICAL CARE
Authors: J M Strachan, T P Hellyer, F R Ali, A Leather, A E Finlayson
Journal: Intensive Care Medicine (2011)
National plan is needed to tackle early childhood trauma, say MPs
Authors: Gareth Iacobucci
Journal: BMJ (2018)

The government should produce a new national strategy to tackle adversity and trauma in childhood an earlier stage so as to reduce the risk of ill health and social problems in later life, an influential group of MPs has urged.

The current provision of early intervention in England was “highly variable” and often undermined by inadequate funding, poor quality data collection, and insufficient focus on evidence, said the new report by the House of Commons Science and Technology Committee.1

The report identified examples of early intervention schemes that worked effectively but said that the lack of an overarching national strategy or an effective means of monitoring what local authorities were doing was hampering progress.

A clear …
Transforming health policy through machine learning
Authors: Hutan Ashrafian, Ara Darzi
Journal: PLoS Medicine (2018)

Machine learning (ML) is one of the most prominent applications of artificial intelligence (AI) technology and offers multiple routes to support the core objectives of health policy.These include 'creating the conditions that ensure good health' [1] and social care for an entire population through preventive strategies, protection from disease, promotion of healthy lifestyles, and population screening through knowledge capture (typically in the form of big data).Overall governance will offer a patient-centred approach with the consideration of patient advocacy and workforce and resource management [2] (Fig 1).Herein, we will break down the role of ML in each of these areas.The most prominent contribution of AI to health policy knowledge currently resides within the application of ML to large, population-level datasets such as those from medical imaging, electronic health records (EHRs), and whole-genome studies.This information can guide interventions for high-risk individuals.Current applications can outperform established risk scores to predict clinical outcomes.These include in-hospital mortality, 30-day unplanned readmission, prolonged length of stay, and final discharge diagnoses for patient populations numbering in the several hundred thousands [3].Here, the major limitation is access to large and high-quality population-level datasets with which to apply ML approaches.We feel that the unification of the United Kingdom National Health Service (NHS) dataset of over 66 Fig 1.The components of health policy.
As Blind as a Bat? Opsin Phylogenetics Illuminates the Evolution of Color Vision in Bats
Authors: Bruno F Simões, Nicole M Foley, Graham M Hughes, Huabin Zhao, Shuyi Zhang, Stephen J Rossiter, Emma C Teeling
Journal: Molecular Biology and Evolution (2018)

Through their unique use of sophisticated laryngeal echolocation bats are considered sensory specialists amongst mammals and represent an excellent model in which to explore sensory perception. Although several studies have shown that the evolution of vision is linked to ecological niche adaptation in other mammalian lineages, this has not yet been fully explored in bats. Recent molecular analysis of the opsin genes, which encode the photosensitive pigments underpinning color vision, have implicated high-duty cycle (HDC) echolocation and the adoption of cave roosting habits in the degeneration of color vision in bats. However, insufficient sampling of relevant taxa has hindered definitive testing of these hypotheses. To address this, novel sequence data was generated for the SWS1 and MWS/LWS opsin genes and combined with existing data to comprehensively sample species representing diverse echolocation types and niches (SWS1 n = 115; MWS/LWS n = 45). A combination of phylogenetic analysis, ancestral state reconstruction, and selective pressure analyses were used to reconstruct the evolution of these visual pigments in bats and revealed that although both genes are evolving under purifying selection in bats, MWS/LWS is highly conserved but SWS1 is highly variable. Spectral tuning analyses revealed that MWS/LWS opsin is tuned to a long wavelength, 555-560 nm in the bat ancestor and the majority of extant taxa. The presence of UV vision in bats is supported by our spectral tuning analysis, but phylogenetic analyses demonstrated that the SWS1 opsin gene has undergone pseudogenization in several lineages. We do not find support for a link between the evolution of HDC echolocation and the pseudogenization of the SWS1 gene in bats, instead we show the SWS1 opsin is functional in the HDC echolocator, Pteronotus parnellii. Pseudogenization of the SWS1 is correlated with cave roosting habits in the majority of pteropodid species. Together these results demonstrate that the loss of UV vision in bats is more widespread than was previously considered and further elucidate the role of ecological niche specialization in the evolution of vision in bats.
Overcoming Inertia to Improve Medication Use and Deprescribing
Authors: Michael A. Steinman, C. Seth Landefeld
Journal: JAMA (2018)

Inertia is a powerful force. Stopping or starting is difficult in health care as well as in other sciences. Ineffective or potentially harmful treatments are often not stopped, even years after they have been started, and effective treatments are too often not started at all.
Abstract 21327: <i>In vivo</i> Reduction of Mitochondrial Oxidative Stress Abolishes Arrhythmic Sudden Cardiac Death (SCD) in Non-Ischemic Heart Failure
Authors: Swati Dey, Deeptankar DeMazumder, Brian O'Rourke
Journal: Circulation (2017)

Intro: Reactive oxygen species (ROS) are central to SCD pathophysiology, but their effects depend on where and how ROS are generated. Insight into this has been limited by the lack of adequate experimental methods. Employing innovative approaches, we tested the hypothesis that elevated mitochondrial ROS (mROS) is a principal source of oxidative stress and in vivo reduction of mROS mitigates SCD in non-ischemic heart failure (HF). Methods: In a unique guinea pig model that mimics human non-ischemic HF with a high incidence of SCD, we performed a randomized 2x2 crossover study of vehicle (v) and MitoTEMPO therapies (vM/Mv). In the untreated HF model, we performed in vivo gene transfer with novel, genetically encoded ratiometric redox sensors targeted to the cytosol (cROS) or mitochondria of cardiomyocytes. In isolated left ventricular (LV) myocytes, we quantified ROS dynamics during field stimulation (1 Hz, 37°C) in the presence or absence of MitoTEMPO. Results: Over 4 weeks, 65% of the HF animals experienced SCD. MitoTEMPO therapy abolished SCD and LV dysfunction. Crossover to MitoTEMPO (vM) prevented SCD and improved LV function; the converse (Mv) worsened HF without increasing SCD for up to 5 weeks of follow up, suggesting distinct underlying mechanisms. EKG analysis revealed that MitoTEMPO therapy decreased PVC burden, reduced dispersion of repolarization and decreased QT variability in arrhythmogenic failing hearts. MitoTEMPO therapy also prevented many of the changes in expression proteome and phosphoproteome leading to contractile dysfunction, arrhythmia and SCD. In subcellular studies of LV myocytes, acute MitoTEMPO exposure strongly suppressed both mROS and cROS. Exogenous H 2 O 2 increased ROS in all intracellular compartments, but mROS scavenging was impaired more than cROS, consistent with downregulation of mitochondrial antioxidant enzymes. Conclusions: Mitochondria are a principal source of cellular oxidative stress in failing arrhythmogenic hearts, but also are the major sink of ROS. Impaired mROS scavenging cause failing hearts to become more vulnerable to demand-induced oxidative stress and promote arrhythmic SCD. Maintaining global redox balance by enhanced mROS scavenging may be an effective strategy for SCD therapy in HF.
Early childhood asthma: What are the questions?
Authors: M. Silverman, L. M. Taussig, F. Martinez, N. M. Wilson, M. Burr, S. Weiss, P. Jeffery, R. J. Martin, P. Holt, G. Larsen, J. Stocks, F. Marchal, R. Tepper, W. Busse, W. Castleman, P. Heymann, P. La Souef, J. Price, S. Pedersen
Journal: American Journal of Respiratory and Critical Care Medicine (1995)
ABC-03: A randomized phase II trial of cediranib (AZD2171) or placebo in combination with cisplatin/gemcitabine (CisGem) chemotherapy for patients (pts) with advanced biliary tract cancer (ABC).
Authors: Juan W. Valle, Harpreet Wasan, Mark Jitlal, Alison Catherine Backen, Daniel H. Palmer, Marian Duggan, David Cunningham, David Alan Anthoney, Philippa Corrie, Srinivasan Madhusudan, Anthony Maraveyas, Paul J. Ross, Justin S. Waters, William P. Steward, Charlotte Rees, Sandy Beare, Caroline Dive, John A. Bridgewater
Journal: Journal of Clinical Oncology (2014)

4002 Background: ABCs exhibit increased VEGF expression, correlating with metastatic disease. Combining cediranib (which inhibits VEGFR1, 2 and 3 tyrosine kinase and VEGF-induced signaling in endothelial cells) with CisGem may improve outcome. Methods: Pts with histo-/cytologically confirmed ABC, aged ≥18 yrs, ECOG PS 0-1 and adequate bone marrow, liver and renal function were randomized to receive Cis (25mg/m2) followed by Gem (1000mg/m2) on days 1 and 8 of a 21-day cycle (up to 8 cycles), plus either cediranib (20mg once daily [OD]) or placebo (OD), until disease progression (PD). Tumor assessment was performed 12-weekly until PD. The target hazard ratio (HR) for progression-free survival (PFS, primary endpoint) was 0.64, requiring 136 pts (for 92 PFS events, 80% power, alpha=0.2, two-sided, ITT analysis). Results: 124 pts were enrolled (62 per arm, Apr-11 to Sep-12, study closed early due to cessation of cediranib development). Pt characteristics (cediranib vs. placebo): median age 68.0 vs. 64.5 years; 45% vs. 55% female; 19% locally advanced and 81% metastatic vs. 13% and 87%; bile duct, gall bladder, ampulla (%): 61, 32, 6 vs. 63, 31, 6; prior adjuvant chemotherapy: 3% vs. 2%; ECOG PS 0, 1: 44, 56 vs. 45, 55%. The most common grade 3-4 non-haematological adverse events (AEs) were hypertension, diarrhea and fatigue; 50% and 45% of cediranib and placebo pts experienced grade 3-4 haematological AEs, predominantly neutropenia (40 vs. 39%). Response rate (RECIST, in evaluable pts): cediranib (23/55 [43%] vs. placebo 10/53 [19%], p=0.01. With a median follow-up of 11.9 mo, PFS was not different (median (95%-CI)): 7.7 (6.3 – 9.3) vs. 7.4 (5.7 – 8.6) mo, HR (80% CI) 0.99 (0.78 – 1.26), p=0.95; with a trend for longer OS in the cediranib arm, median (95% CI): 14.1 (10.2 – 16.0) vs. 11.9 (9.2 – 13.4) mo, HR (95% CI) 0.76 (0.50 – 1.14), p=0.19. ELISA was performed for 15 potential plasma biomarkers of which Angiopoietin-2 (HR 0.65 (0.44 to 0.97) p=0.006) and Fibroblast Growth Factor-b (HR 0.83 (0.68 to 1.00) p=0.009) were the most significant. Conclusions: Cediranib appears to improve response rate but not PFS; effect on OS may warrant further studies. Clinical trial information: NCT00939848.
What Chinese Medicine Can Do for Liver Cancer?
Authors: Feiyu Chen, Ning Wang, Yibin Feng
Journal: Liver Cancer (2018)

Liver cancer is an international problem, especially in Asian countries. It is because that most liver cancers are already late stage when they are diagnosed, and also most liver cancers have various previous chronic liver diseases induced by alcoholic, virus, and steatosis, etc. In recent years, laboratory and clinical studies focusing on liver cancer by Chinese medicine has been extensively studied. What Chinese medicine treatment formalities can be used in liver cancer? How Chinese medicine can be employed in treatment of liver cancer? What Chinese medicine can contribute to liver cancer? To answer these questions in this chapter, we will review and discuss treatment of liver cancer from Chinese medicine's perspective with scientific evidences as following three parts: (1) Chinese medicine as the source of discovering new treatment for liver cancer, (2) Chinese medicine as a complementary treatment of liver cancer, and (3) to discuss future research and application of Chinese medicine in liver cancer treatment.
Reduced Intensity Conditioned Sibling Transplantation Versus No Transplant in Intermediate or High Risk Acute Myeloid Leukemia: A Prospective Multi-Center Study in Patients 50-70 Years in First Complete Remission and with at Least One Potential Sibling Donor (ClinTrialGov 00342316)
Authors: Mats Brune, Thomas L. Kiss, Elisabeth Wallhult, Harald Anderson, Robert Delage, Jürgen Finke, Josee Hebert, Martin Höglund, Ain Kaare, Vladimir Lazarevic, Malin Nicklasson, Kari Remes, David Ritchie, Mitchell Sabloff, Ruth Spearing, Alexandros Spyridonidis, Jeffrey Szer, Per Ljungman
Journal: Blood (2018)
Immunological and clinical effects of low-dose interleukin-2 across 11 autoimmune diseases in a single, open clinical trial
Authors: Michelle Rosenzwajg, Roberta Lorenzon, Patrice Cacoub, Hang Phuong Pham, Fabien Pitoiset, Karim El Soufi, Claire RIbet, Claude Bernard, Selim Aractingi, Beatrice Banneville, Laurent Beaugerie, Francis Berenbaum, Julien Champey, Olivier Chazouilleres, Christophe Corpechot, Bruno Fautrel, Arsène Mekinian, Elodie Regnier, David Saadoun, Joe-Elie Salem, Jérémie Sellam, Philippe Seksik, Anne Daguenel-Nguyen, Valérie Doppler, Jéremie Mariau, Eric Vicaut, David Klatzmann
Journal: Annals of the Rheumatic Diseases (2018)

Objective Regulatory T cells (Tregs) prevent autoimmunity and control inflammation. Consequently, any autoimmune or inflammatory disease reveals a Treg insufficiency. As low-dose interleukin-2 (ld-IL2) expands and activates Tregs, it has a broad therapeutic potential. Aim We aimed to assess this potential and select diseases for further clinical development by cross-investigating the effects of ld-IL2 in a single clinical trial treating patients with 1 of 11 autoimmune diseases. Methods We performed a prospective, open-label, phase I–IIa study in 46 patients with a mild to moderate form of either rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, psoriasis, Behcet’s disease, granulomatosis with polyangiitis, Takayasu’s disease, Crohn’s disease, ulcerative colitis, autoimmune hepatitis and sclerosing cholangitis. They all received ld-IL2 (1 million IU/day) for 5 days, followed by fortnightly injections for 6 months. Patients were evaluated by deep immunomonitoring and clinical evaluation. Results ld-IL2 was well tolerated whatever the disease and the concomitant treatments. Thorough supervised and unsupervised immunomonitoring demonstrated specific Treg expansion and activation in all patients, without effector T cell activation. Indication of potential clinical efficacy was observed. Conclusion The dose of IL-2 and treatment scheme used selectively activate and expand Tregs and are safe across different diseases and concomitant treatments. This and preliminary indications of clinical efficacy should licence the launch of phase II efficacy trial of ld-IL2 in various autoimmune and inflammatory diseases. Trial registration number NCT01988506 .
Tumor-derived Autoantibodies Identify Malignant Pulmonary Nodules
Authors: Kristin J. Lastwika, Julia Kargl, Yuzheng Zhang, Xiaodong Zhu, Edward Lo, David Shelley, Jon J. Ladd, Wei Wu, Paul Kinahan, Sudhakar N. J. Pipavath, Timothy W. Randolph, Melissa Shipley, Paul D. Lampe, A. McGarry Houghton
Journal: American Journal of Respiratory and Critical Care Medicine (2018)

Rationale: Screening for non–small cell lung cancer is associated with earlier diagnosis and reduced mortality but also increased harm caused by invasive follow-up of benign pulmonary nodules. Lung tumorigenesis activates the immune system, components of which could serve as tumor-specific biomarkers.Objectives: To profile tumor-derived autoantibodies as peripheral biomarkers of malignant pulmonary nodules.Methods: High-density protein arrays were used to define the specificity of autoantibodies isolated from B cells of 10 resected lung tumors. These tumor-derived autoantibodies were also examined as free or complexed to antigen in the plasma of the same 10 patients and matched benign nodule control subjects. Promising autoantibodies were further analyzed in an independent cohort of 250 nodule-positive patients.Measurements and Main Results: Thirteen tumor B-cell–derived autoantibodies isolated ex vivo showed greater than or equal to 50% sensitivity and greater than or equal to 70% specificity for lung cancer. In plasma, 11 of 13 autoantibodies were present both complexed to and free from antigen. In the larger validation cohort, 5 of 13 tumor-derived autoantibodies remained significantly elevated in cancers. A combination of four of these autoantibodies could detect malignant nodules with an area under the curve of 0.74 and had an area under the curve of 0.78 in a subcohort of indeterminate (8–20 mm in the longest diameter) pulmonary nodules.Conclusions: Our novel pipeline identifies tumor-derived autoantibodies that could effectively serve as blood biomarkers for malignant pulmonary nodule diagnosis. This approach has future implications for both a cost-effective and noninvasive approach to determine nodule malignancy for widespread low-dose computed tomography screening.
Abstract 10550: Comparing a Mobile ECG Device With Holter Monitoring for Patients With Palpitations in an Urgent Care Setting: A Preliminary Study
Authors: Hersh V Goel, Joseph S Alpert, Mazen H Shaheen, Trevor A Jones, David P Skinner
Journal: Circulation (2018)

Introduction: The rapid uptake of mobile devices has given rise to smartphone-based ambulatory electrocardiographic monitoring (AEM). This cutting-edge category of AEM’s leverages the powerful proc...
Abstract 13751: Vascular Endothelial Growth Factor-C Levels and Cardiovascular and All-cause Mortality in Patients With Suspected Coronary Artery Disease: From the ANOX Study
Authors: Hiromichi Wada, Masahiro Suzuki, Morihiro Matsuda, Yoichi Ajiro, Tsuyoshi Shinozaki, Satoru Sakagami, Kazuya Yonezawa, Masatoshi Shimizu, Junichi Funada, Takashi Takenaka, Yukiko Morita, Toshihiro Nakamura, Kazuteru Fujimoto, Hiromi Matsubara, Toru Kato, Takashi Unoki, Daisuke Takagi, Shuichi Ura, Kyohma Wada, Moritake Iguchi, Nobutoyo Masunaga, Mitsuru Ishii, Akira Shimatsu, Kazuhiko Kotani, Noriko Satoh-Asahara, Mitsuru Abe, Masaharu Akao, Koji Hasegawa
Journal: Circulation (2017)

Background: Recent studies suggest that lymphatic system plays an important role in cholesterol metabolism and coronary artery disease (CAD). However, the relationship between vascular endothelial ...
Opioid-induced constipation in patients with cancer pain in Japan (OIC-J study): Patients’ self-assessment of the symptoms and the impact
Authors: T. Noriyuki, H. Imai, S. Fumita, T. Harada, M. Gamoh, Y. Akashi, H. Sato, Y. Kizawa, A. Tokoro
Journal: Annals of Oncology (2018)
Prostaglandin E<sub>2</sub> decrease in induced sputum of hypersensitive asthmatics during oral challenge with aspirin
Authors: Lucyna Mastalerz, Katarzyna E. Tyrak, Maria Ignacak, Ewa Konduracka, Filip Mejza, Adam Ćmiel, Michał Buczek, Adrianna Kot, Krzysztof Oleś, Marek Sanak
Journal: Allergy (2018)

Abstract Background A special regulatory role for prostaglandin E 2 ( PGE 2 ) has been postulated in nonsteroidal anti‐inflammatory drug ( NSAID )–exacerbated respiratory disease ( NERD ). Objective To investigate the effect of systemic aspirin (acetylsalicylic acid) administration on airway PGE 2 biosynthesis in induced sputum supernatant ( ISS ) among subjects with NERD or aspirin‐tolerant asthma with chronic rhinosinusitis with nasal polyposis ( ATA ‐ CRS w NP ), as well as healthy controls ( HC ). Methods Induced sputum ( IS ) was collected from patients with NERD (n = 26), ATA ‐ CRS w NP (n = 17), and HC (n = 21) at baseline and after aspirin challenge. Sputum differential cell count and IS supernatant ( ISS ) levels of prostanoids, PGE 2 , 8‐iso‐ PGE 2 , tetranor‐ PGE ‐M, 8‐iso‐ PGF 2 α, and leukotriene C 4 , D 4 , and E 4 , were determined using mass spectrometry. Urinary excretion of LTE 4 was measured by ELISA . Results NERD subjects had elevated sputum eosinophilic count as compared to ATA ‐ CRS w NP and HC (median NERD 9.1%, ATA ‐ CRS w NP 2.1%, and HC 0.4%; P &lt; 0.01). Baseline ISS levels of PGE 2 were higher in asthmatics as compared to HC at baseline ( NERD vs HC P = 0.04, ATA ‐ CRS w NP vs HC P &lt; 0.05). Post‐challenge ISS levels of PGE 2 compared to baseline significantly decreased in NERD and HC ( P &lt; 0.01 and P = 0.01), but not in ATA ‐ CRS w NP . In NERD , a similar decrease in PGE 2 as in HC resulted from 2.8 times lower dose of aspirin. Conclusion Aspirin‐precipitated bronchoconstriction is associated with a decrease in airway PGE 2 biosynthesis. These results support the mechanism of PGE 2 biosynthesis inhibition as a trigger for bronchoconstriction in NERD .