bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adherence to coronary artery disease secondary prevention medicines: exploring modifiable barriers
Authors: Khatib Rani , Marshall Kay , Silcock Jon , Forrest Claire , Hall Alistair S 
Published: July 2019

BackgroundNon-adherence to secondary prevention medicines (SPMs) among patients with coronary artery disease (CAD) remains a challenge in clinical practice. This study attempted to identify actual and potential modifiable barriers to adherence that can be addressed in cardiology clinical practice.MethodsThis was a cross-sectional, postal survey-based study of the medicines-taking experience of patients with CAD treated at a secondary/tertiary care centre. All participants had been on SPM for ≥3 months.ResultsIn total, 696 eligible patients were sent the survey and 503 responded (72.3%). The median age was 70 years, and 403 (80.1%) were male; the mediannumber of individual daily dosesof all medicines was 6. The rate of non-adherence to at least one SPM was 43.5% (n=219), but 53.3% of reported non-adherence was to only one SPM. Statins contributed to 66.7% and aspirin to 61.7% of overall non-adherence identified by the Single Question (SQ) tool. In 30.8% of non-adherent patients (n=65), this was at least partly intentional. Barriers included forgetfulness (84.9%; n=186), worry that medicines will do more harm than good (33.8%; n=74), feeling hassled about medicines taking (18.7%; n=41), feeling worse when taking medicines (14.2%; n=31) and not being convinced of the benefit of medicines (9.1%; n=20). In a multivariate analysis, modifiable factors associated with overall non-adherence included being prescribed aspirin (OR: 2.22; 95% CI: 1.18 to 4.17), havingspecific concernabout SPM (OR: 1.12; 95% CI: 1.07 to 1.18) and issues with repeat prescriptions (OR: 2.48; 95% CI: 1.26 to 4.90). Different factors were often associated with intentional versus unintentional non-adherence.ConclusionsUsing appropriate self-report tools, patients share actual and potential modifiable barriers to adherence that can be addressed in clinical practice. Non-adherence behaviour was selective. Most non-adherence was driven by forgetfulness, concern about the harm caused by SPM and practical barriers.
Evaluation of foramsulfuron for poverty oat grass [Danthonia spicata (L.) P. Beauv. ex Roem. & Schult.] and rough bentgrass (Agrostis scabra Willd.) management in lowbush blueberry (Vaccinium angustifolium Ait.)
Authors: White Scott N. , Zhang Linshan 
Published: July 2019

The susceptibility of poverty oat grass and rough bentgrass to foramsulfuron was assessed in greenhouse and field experiments. A dose response study was conducted in a greenhouse with treatments consisting of 0, 4.4, 8.8, 17.5, 35, 70, 140, and 280 g foramsulfuron ha−1. Field experiments were conducted using a similar dose response and also included industry standard fluazifop-P-butyl and sethoxydim applications. Foramsulfuron application rates of 4.04 ± 0.73 and 6.6 ± 1.3 g a.i. ha−1 reduced poverty oat grass biomass by 50% in the greenhouse. In contrast, 4.4 g a.i. ha−1 foramsulfuron caused >70% reduction in rough bentgrass biomass in the greenhouse. In the field, 280 g a.i. ha−1 of foramsulfuron was required to reduce poverty oat grass total and flowering tuft density and >35 g a.i. ha−1 (registered foramsulfuron rate) was required to reduce flowering tuft inflorescence number by 50%. In contrast, rough bentgrass was injured by 4.4 and 8.8 g a.i. ha−1 of foramsulfuron and total and flowering tuft density and flowering tuft inflorescence number were reduced by all other foramsulfuron rates evaluated. Foramsulfuron application rates of 13.1 ± 2.4, 10.3 ± 1.2, and 5.4 ± 0.9 g a.i. ha−1 reduced rough bentgrass total tuft density, flowering tuft density, and tuft inflorescence number, respectively, by 50%. Lowbush blueberry growers can consider foramsulfuron for postemergence management of rough bentgrass, but additional research is required to identify new herbicides for postemergence poverty oat grass management.
CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC
Authors: Becker Jeffrey H. , Gao Yandi , Soucheray Margaret , Pulido Ines , Kikuchi Eiki , Rodríguez María L. , Gandhi Rutu , Lafuente-Sanchis Aranzazu , Aupí Miguel , Alcácer Fernández-Coronado Javier , Martín-Martorell Paloma , Cremades Antonio , Galbis-Caravajal José M. , Alcácer Javier , Christensen Camilla L. , Simms Patricia , Hess Ashley , Asahina Hajime , Kahle Michael P. , Al-Shahrour Fatima , Borgia Jeffrey A. , Lahoz Agustín , Insa Amelia , Juan Oscar , Jänne Pasi A. , Wong Kwok-Kin , Carretero Julian , Shimamura Takeshi 
Published: July 2019

Abstract

Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutation, who progressed on EGFR inhibitors, demonstrated increased CXCR7 expression. These data suggest that CXCR7 inhibition could considerably delay and prevent the emergence of acquired EGFR TKI resistance in EGFR-mutant NSCLC.

Significance:
Increased expression of the chemokine receptor CXCR7 constitutes a mechanism of resistance to EGFR TKI in patients with non–small cell lung cancer through reactivation of ERK signaling.
Notas sobre Public spectacles of violence: sensational cinema and journalism in early twentieth-century Mexico and Brazil, de Rielle Navitski
Authors: Di Giacomo Carolina Azevedo 
Published: July 2019

Esta resenha trata do livro Public spectacles of violence: sensational cinema and journalism in early twentieth-century Mexico and Brazil, de Rielle Navitski, que discute diferentes formas de espetacularização da violência no cinema silencioso dos dois países.
O elemento inconsciente na literatura e na filosofia (1921)
Authors: Cornford Fracis 
Published: July 2019

Tradução em português de:
CORNFORD, Francis M. (1950). “The Unconscious Element in Literature and Philosophy (1921)”, In: The Unwritten Philosophy and Other Essays, edited by W. K. C. Guthrie, Cambridge: Cambridge University Press, pp. 1-13.
Quantitative Myocardial Perfusion in Fabry Disease
Authors: Knott Kristopher D. , Augusto Joao B. , Nordin Sabrina , Kozor Rebecca , Camaioni Claudia , Xue Hui , Hughes Rebecca K. , Manisty Charlotte , Brown Louise A.E. , Kellman Peter , Ramaswami Uma , Hughes Derralyn , Plein Sven , Moon James C. 
Published: July 2019

Background:
Fabry disease (FD) is an X-linked lysosomal storage disease resulting in tissue accumulation of sphingolipids. Key myocardial processes that lead to adverse outcomes in FD include storage, hypertrophy, inflammation, and fibrosis. These are quantifiable by multiparametric cardiovascular magnetic resonance. Recent developments in cardiovascular magnetic resonance perfusion mapping allow rapid in-line perfusion quantification permitting broader clinical application, including the assessment of microvascular dysfunction. We hypothesized that microvascular dysfunction in FD would be associated with storage, fibrosis, and edema.

Methods:
A prospective, observational study of 44 FD patients (49 years, 43% male, 24 [55%] with left ventricular hypertrophy [LVH]) and 27 healthy controls with multiparametric cardiovascular magnetic resonance including vasodilator stress perfusion mapping. Myocardial blood flow (MBF) was measured and its associations with other processes investigated.

Results:

Compared with LVH− FD, LVH+ FD had higher left ventricular ejection fraction (73% versus 68%), more late gadolinium enhancement (85% versus 15%), and a lower stress MBF (1.76 versus 2.36 mL/g per minute). The reduction in stress MBF was more pronounced in the subendocardium than subepicardium. LVH− FD had lower stress MBF than controls (2.36 versus 3.00 mL/g per minute;
P
=0.002). Across all FD, late gadolinium enhancement and low native T1 were independently associated with reduced stress MBF. On a per-segment basis, stress MBF was independently associated with wall thickness, T2, extracellular volume fraction, and late gadolinium enhancement.

Conclusions:
FD patients have reduced perfusion, particularly in the subendocardium with greater reductions with LVH, storage, edema, and scar. Perfusion is reduced even without LVH suggesting it is an early disease marker.
Multi‐Site Coronary Vein Sampling Study on Cardiac Troponin T Degradation in Non–ST‐Segment–Elevation Myocardial Infarction: Toward a More Specific Cardiac Troponin T Assay
Authors: Damen Sander A. J. , Vroemen Wim H. M. , Brouwer Marc A. , Mezger Stephanie T. P. , Suryapranata Harry , van Royen Niels , Bekers Otto , Meex Steven J. R. , Wodzig Will K. W. H. , Verheugt Freek W. A. , de Boer Douwe , Cramer G. Etienne , Mingels Alma M. A. 
Published: July 2019

Background

Cardiac troponin T (
cTnT
) is seen in many other conditions besides myocardial infarction, and recent studies demonstrated distinct forms of
cTnT
. At present, the in vivo formation of these different
cTnT
forms is incompletely understood. We therefore performed a study on the composition of
cTnT
during the course of myocardial infarction, including coronary venous system sampling, close to its site of release.

Methods and Results

Baseline samples were obtained from multiple coronary venous system locations, and a peripheral artery and vein in 71 non–
ST
‐segment–elevation myocardial infarction patients. Additionally, peripheral blood was drawn at 6‐ and 12‐hours postcatheterization.
cTnT
concentrations were measured using the high‐sensitivity‐
cTnT
immunoassay. The
cTnT
composition was determined via gel filtration chromatography and Western blotting in an early and late presenting patient. High‐sensitivity ‐
cTnT
concentrations were 28% higher in the coronary venous system than peripherally (n=71,
P
<0.001). Coronary venous system samples demonstrated
cT
n T‐I‐C complex, free intact
cTnT
, and 29
kD
a and 15 to 18
kD
a
cTnT
fragments, all in higher concentrations than in simultaneously obtained peripheral samples. While
cT
n T‐I‐C complex proportionally decreased, and disappeared over time, 15 to 18
kD
a
cTnT
fragments increased. Moreover,
cT
n T‐I‐C complex was more prominent in the early than in the late presenting patient.

Conclusions

This explorative study in non–
ST
‐segment–elevation myocardial infarction shows that
cTnT
is released from cardiomyocytes as a combination of
cT
n T‐I‐C complex, free intact
cTnT
, and multiple
cTnT
fragments indicating intracellular
cTnT
degradation. Over time, the
cT
n T‐I‐C complex disappeared because of in vivo degradation. These insights might serve as a stepping stone toward a high‐sensitivity‐
cTnT
immunoassay more specific for myocardial infarction.
Causation in Securities and Financial Product Disclosure Cases: An Analysis and Critique
Authors: Saunders Benjamin B 
Published: July 2019

AbstractThis article critically examines the approach adopted by the courts to causation in securities and financial product disclosure cases, where a plaintiff alleges loss as a result of defective disclosure by a product issuer. The article argues that the reliance approach should be rejected as the sole approach to causation in securities and financial product disclosure cases. The article gives two principal arguments in support of this claim. Firstly, the reliance approach, by insisting that causation may only be established by proving reliance on the disclosure document, implicitly assumes a ‘rational choice’ approach to investor decision-making which, as demonstrated by a significant body of behavioural research, does not accurately reflect the reality of investor decision-making. Secondly, the reliance approach sits at odds with other developments in securities cases and misleading and deceptive conduct jurisprudence. I argue that the courts should recognise that causation may potentially be demonstrated in a variety of ways other than reliance on the disclosure document, including reliance on sources such as communications from financial advisers, newspapers, online sources, briefings, investor roadshows, social media and other marketing practices.
Echocardiographic association of epicardial fat with carotid intima–media thickness in patients with type 2 diabetes
Authors: Yafei Saeed , Elsewy Fathy , Youssef Eman , Ayman Mohamed , Elshafei Mohamed , Abayazeed Rasha 
Published: July 2019

Background:Epicardial fat is recognized as active endocrine organ and as emerging risk factor for cardio-metabolic diseases. The aim of this study was to explore the relationship between epicardial fat and carotid intima–media thickness in type 2 diabetes patients.Methods:Epicardial fat thickness was measured in 76 type 2 diabetes patients without clinical atherosclerotic cardiovascular disease and 30 age- and sex-matched controls. In addition to laboratory tests, all patients underwent transthoracic echocardiography for epicardial fat thickness and ultrasonographic examination of carotid intima–media thickness.Results:Patients with diabetes had higher epicardial fat thickness and carotid intima–media thickness than those of the controls (6.23 ± 1.27 mm vs 4.6 ± 1.03 mm, p < 0.001 and 0.77 ± 0.150 mm vs 0.58 ± 0.08 mm, p < 0.001, respectively). Epicardial fat thickness was correlated significantly with age, duration of type 2 diabetes, body mass index, waist circumference, HbA1c, carotid intima–media thickness, Homeostasis Model Assessment Index for insulin resistance and lipid profile in the type 2 diabetic patients. Stepwise regression analysis showed that carotid intima–media thickness, duration of diabetes, triglyceride and body mass index were the independent predictors of epicardial fat thickness, with carotid intima–media thickness the most important predictor ( β = 3.078, t = 4.058, p < 0.001). Receiver operating characteristic curve analysis was done and cut-off high-risk epicardial fat thickness value of 6.1 mm was determined with a sensitivity and specificity of 71.4% and 72%, respectively.Conclusion:Patients with type 2 diabetes have higher carotid intima–media thickness and epicardial fat thickness. Epicardial fat thickness was found to be a strong predictor of subclinical atherosclerosis.
Endovascular treatment of intracranial ‘blister’ and dissecting aneurysms
Authors: Kaschner Marius G , Kraus Bastian , Petridis Athanasios , Turowski Bernd 
Published: July 2019

Introduction Blister and dissecting aneurysms may have a different pathological background but they are commonly defined by instability of the vessel wall and bear a high risk of fatal rupture and rerupture. Lack of aneurysm sack makes treatment challenging. Purpose The purpose of this study was to assess the safety and feasibility of endovascular treatment of intracranial blister and dissecting aneurysms. Methods We retrospectively analysed all patients with ruptured and unruptured blister and dissecting aneurysms treated endovascularly between 2004–2018. Procedural details, complications, morbidity/mortality, clinical favourable outcome (modified Rankin Scale ≤2) and aneurysm occlusion rates were assessed. Results Thirty-four patients with endovascular treatment of 35 aneurysms (26 dissecting aneurysms and 9 blister aneurysms) were included. Five aneurysms were treated by parent vessel occlusion, and 30 aneurysms were treated by vessel reconstruction using stent monotherapy ( n = 9), stent-assisted coiling ( n = 7), flow diverting stents ( n = 13) and coiling + Onyx embolization ( n = 1). No aneurysm rebleeding and no procedure-related major complications or deaths occurred. There were five deaths in consequence of initial subarachnoid haemorrhage. Complete occlusion (79.2%) was detected in 19/24 aneurysms available for angiographic follow-up, and aneurysm recurrence in 2/24 (8.3%). The modified Rankin Scale ≤2 rate at mean follow-up of 15.1 months was 64.7%. Conclusion Treatment of blister and dissecting aneurysms developed from coil embolization to flow diversion with multiple stents to the usage of flow diverting stents. Results using modern flow diverting stents encourage us to effectively treat this aneurysm entity endovascularly by vessel reconstruction. Therefore, we recommend preference of vessel reconstructive techniques to parent vessel occlusion.
Strenuous occupational physical activity: Potential association with esophageal squamous cell carcinoma risk
Authors: Shah Idrees Ayoub , Bhat Gulzar Ahmad , Rafiq Rumaisa , Nissa Najma , Muzaffar Mansha , Rasool Malik Tariq , Lone Mohd Maqbool , Lone Ghulam Nabi , Boffetta Paolo , Dar Nazir Ahmad 
Published: July 2019

Objective: The impact of recreational physical activity (RPA) on cancer risk has been extensively studied. However, the association of occupational physical activity (OPA), which differs in dose and intensity from RPA, with different cancers including esophageal squamous cell carcinoma (ESCC), has received less attention. Materials and methods: We conducted a hospital-based case–control study in Kashmir, India, majorly a rural population, to evaluate the association of OPA with ESCC risk. Histopathologically confirmed 703 ESCC cases and 1664 controls, individually matched to the respective cases for age, sex and district of residence, were recruited. Main outcome measures: Information on type, duration and intensity of physical activity was obtained in face-to-face interviews with participants using a structured questionnaire. Conditional logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs). Body mass index was unable to be accounted for in the analysis. Results: A high level of OPA was associated with increased ESCC risk (OR = 2.17, 95% CI; 1.41–3.32), compared to subjects with moderate OPA. The association with ESCC risk was stronger in strenuous workers (OR = 3.64, 95% CI; 2.13–6.20). The association of strenuous OPA with ESCC risk persisted only in subjects that were involved in strenuous activities for equal to or greater than five days/week. Conclusions: Our study suggests a possible association of strenuous OPA with ESCC risk. Although our results were adjusted for multiple factors, including indicators of socioeconomic status, more replicative occupational epidemiological studies are needed to rule out any residual confounding.
Transcriptional profiling of human intestinal plasma cells reveals effector functions beyond antibody production
Authors: Snir Omri , Kanduri Chakravarthi , Lundin Knut E A , Sandve Geir Kjetil , Sollid Ludvig M 
Published: July 2019

BackgroundPlasma cells (PCs) are terminally differentiated B‐lymphocytes producing antibodies. In coeliac disease (CeD) there is increased density of PCs in the small‐intestinal lesion. Many of these PCs produce disease‐specific autoantibodies targeting transglutaminase 2 (TG2).ObjectiveThe plasmacytosis of CeD motivated us to study the transcriptional programme of PCs from coeliac gut lesions.MethodsRNA‐seq was performed on the PCs of CeD patients and disease controls, being specific or non‐specific for TG2.ResultsBeing antibody‐producing cells, 67% of the PCs’ transcript was aligned to immunoglobulin genes. Strikingly, genes encoding ligands and receptors of chemokines and cytokines were abundant. Higher transcript levels of genes associated with cell activation and immune responses were observed in PCs of CeD patients compared to controls. TG2‐specific compared to non‐TG2 specific PCs expressed increased levels of CXCR3, CXCL10 and interleukin‐15; factors that have been implicated in the pathogenesis of CeD yet with production attributed to other cells than PCs. The presence of transcripts of HLA class II and T‐cell co‐stimulatory molecules suggests that PCs may serve as antigen‐presenting cells for CD4 + helper T cells.ConclusionsOur findings shed new light on the biology of intestinal PCs, implicating functions that go beyond the production of immunoglobulins.
Prevention of progression of pulmonary hypertension by the Nur77 agonist 6-mercaptopurine: role of BMP signalling
Authors: Kurakula Kondababu , Sun Xiao-Qing , Happé Chris , da Silva Goncalves Bos Denielli , Szulcek Robert , Schalij Ingrid , Wiesmeijer Karien C. , Lodder Kirsten , Tu Ly , Guignabert Christophe , de Vries Carlie J.M. , de Man Frances S. , Vonk Noordegraaf Anton , ten Dijke Peter , Goumans Marie-José , Bogaard Harm Jan 
Published: July 2019

Pulmonary arterial hypertension (PAH) is a progressive fatal disease characterised by abnormal remodelling of pulmonary vessels, leading to increased vascular resistance and right ventricle failure. This abnormal vascular remodelling is associated with endothelial cell dysfunction, increased proliferation of smooth muscle cells, inflammation and impaired bone morphogenetic protein (BMP) signalling. Orphan nuclear receptor Nur77 is a key regulator of proliferation and inflammation in vascular cells, but its role in impaired BMP signalling and vascular remodelling in PAH is unknown.We hypothesised that activation of Nur77 by 6-mercaptopurine (6-MP) would improve PAH by inhibiting endothelial cell dysfunction and vascular remodelling.Nur77 expression is decreased in cultured pulmonary microvascular endothelial cells (MVECs) and lungs of PAH patients. Nur77 significantly increased BMP signalling and strongly decreased proliferation and inflammation in MVECs. In addition, conditioned medium from PAH MVECs overexpressing Nur77 inhibited the growth of healthy smooth muscle cells. Pharmacological activation of Nur77 by 6-MP markedly restored MVEC function by normalising proliferation, inflammation and BMP signalling. Finally, 6-MP prevented and reversed abnormal vascular remodelling and right ventricle hypertrophy in the Sugen/hypoxia rat model of severe angioproliferative PAH.Our data demonstrate that Nur77 is a critical modulator in PAH by inhibiting vascular remodelling and increasing BMP signalling, and activation of Nur77 could be a promising option for the treatment of PAH.
The lncRNA UCA1 promotes proliferation, migration, immune escape and inhibits apoptosis in gastric cancer by sponging anti-tumor miRNAs
Authors: Wang Chao-Jie , Zhu Chun-Chao , Xu Jia , Wang Ming , Zhao Wen-Yi , Liu Qiang , Zhao Gang , Zhang Zi-Zhen 
Published: July 2019

Abstract
Background
UCA1 is a long non-coding RNA which was found overexpressed in various human cancers including gastric cancer (GC). It is identified that UCA1 promotes GC cells proliferation, migration and invasion, however, the role of UCA1 during the processes of immune escape is still not unclear.

Methods
We collected 40 paired GC and non-tumor tissue samples. The level of UCA1 in GC and control tissue samples were determined by in situ hybridization and qRT-PCR. Cell viability was determined by MTT assay. GC cells’ migration capacities were examined by transwell assay. To understand the roles of UCA1 during immune escape, wildtype or UCA1 KO GC cells co-cultured with peripheral blood mononuclear cells or cytokine-induced killer cells in vitro. Mouse model was used to examine the function of UCA1 in vivo.

Results
UCA1 promoted GC cells proliferation and migration, and inhibit apoptosis. UCA1 repressed miR-26a/b, miR-193a and miR-214 expression through direct interaction and then up-regulated the expression of PDL1. UCA1-KO GC cells could induce a higher IFNγ expression when co-cultured with peripheral blood mononuclear cells (PBMCs), and have a lower survival rate when co-cultured with cytokine-induced killer (CIK) cells in vitro. UCA1-KO GC cells formed smaller tumors, had higher miR-26a, −26b, −193a and − 214 level, reduced cell proliferation and increased apoptosis in xenograft mouse model.

Conclusions
UCA1 overexpression protected PDL1 expression from the repression of miRNAs and contributed to the GC cells immune escape. UCA1 could serve as a potential novel therapeutic target for GC treatment.