bluuebunny/crossref_metadata_2025_split huggingface dataset:
The ‘Collective Voice that Could Change the World’: A Qualitative Interpretive Meta-Synthesis of Arts-Based Programming for Adults Experiencing Homelessness
Authors: Murphy Erin R , Alexander Amanda S 
Published: November 2019

AbstractHomelessness is a global phenomenon that contributes to and exacerbates social exclusion and marginalisation. The objective of this study is to generate a rich description of the experience of participating in arts-based programming as told by adults experiencing homelessness using a qualitative interpretive meta-synthesis. The synthesis includes eight studies, using direct quotes provided by fifty-three individuals in Canada, the USA and Australia. Synthesis of the eight studies results in three themes that describe the experience of participating in arts-based programming across geographic locations and art mediums: ‘arts as healing’, ‘arts as advocacy’ and ‘arts as self-empowerment’. While social workers, homelessness service providers, arts-based educators and researchers may be intuitively aware of the power of the arts, the synergistic findings of these eight articles indicate its influence among marginally housed populations. Implications and opportunities for future research are discussed.
Dexterous Object Manipulation Requires Context-Dependent Sensorimotor Cortical Interactions in Humans
Authors: Parikh Pranav J , Fine Justin M , Santello Marco 
Published: November 2019

Abstract
Dexterous object manipulation is a hallmark of human evolution and a critical skill for everyday activities. A previous work has used a grasping context that predominantly elicits memory-based control of digit forces by constraining where the object should be grasped. For this “constrained” grasping context, the primary motor cortex (M1) is involved in storage and retrieval of digit forces used in previous manipulations. In contrast, when choice of digit contact points is allowed (“unconstrained” grasping), behavioral studies revealed that forces are adjusted, on a trial-to-trial basis, as a function of digit position. This suggests a role of online feedback of digit position for force control. However, despite the ubiquitous nature of unconstrained hand–object interactions in activities of daily living, the underlying neural mechanisms are unknown. Using noninvasive brain stimulation, we found the role of primary motor cortex (M1) and somatosensory cortex (S1) to be sensitive to grasping context. In constrained grasping, M1 but not S1 is involved in storing and retrieving learned digit forces and position. In contrast, in unconstrained grasping, M1 and S1 are involved in modulating digit forces to position. Our findings suggest that the relative contribution of memory and online feedback modulates sensorimotor cortical interactions for dexterous manipulation.
Relationship between soluble urokinase-type plasminogen activator receptor and serum biomarkers of endothelial activation in patients with idiopathic nephrotic syndrome
Authors: Roca Neus , Jatem Elias , Martín María Luisa , Muñoz Marina , Molina Maria , Martínez Cristina , Segarra Alfons 
Published: November 2019

Abstract

Background
Serum levels of soluble urokinase-type plasminogen activator receptor (suPAR) are high in some patients with idiopathic nephrotic syndrome (INS). Given that suPAR constitutes a predictor of vascular disease and has been associated with endothelial dysfunction, we hypothesized that suPAR levels are related to endothelial activation or dysfunction in INS patients. The aims of this study were to evaluate the relationship between serum concentrations of endothelial biomarkers and suPAR in patients with different histological patterns of INS and healthy controls, and to determine the demographic, clinical and biochemical characteristics of INS patients that influence suPAR serum levels.

Methods
This observational, cross-sectional study included patients with INS, diagnosed with minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS) or membranous nephropathy (MN) by renal biopsy. Patient demographic, clinical and biochemical characteristics were recorded and blood samples were obtained at the time of diagnosis. Measurements of suPAR and endothelial molecules via serum levels were performed using Enzyme-Linked ImmunoSorbent Assay kits.

Results
Patients with nephrotic syndrome (n = 152) caused by FSGS, MCD or MN had increased circulating levels of endothelial markers. suPAR levels positively correlated with age and the serum levels of almost all endothelial markers. Generally, endothelial cell molecules positively correlated with each other. suPAR levels were not associated with the histopathological pattern of INS.

Conclusions
In patients with INS secondary to FSGS, MCD and NM, circulating levels of suPAR are independent of the primary renal disease, and significantly associated with age, glomerular filtration rate and the levels of various endothelial markers.
Imbalanced turnover of collagen type III is associated with disease progression and mortality in high-risk chronic kidney disease patients
Authors: Genovese Federica , Rasmussen Daniel Guldager Kring , Karsdal Morten A , Jesky Mark , Ferro Charles , Fenton Anthony , Cockwell Paul 
Published: November 2019

Abstract

Background
Tubulointerstitial fibrosis is a major pathological feature in chronic kidney disease (CKD) and collagen type III (COL3) is a major component of the renal fibrotic scar. We hypothesized that a dysregulated turnover of COL3 is an important determinant of CKD progression. We assessed the relationship between fragments reflecting active formation (PRO-C3) and degradation (C3M) of COL3 and CKD disease progression and mortality in a prospective cohort of CKD patients.

Methods
We measured PRO-C3 and C3M in urine (uPRO-C3 and uC3M) and serum (sPRO-C3 and sC3M) of 500 patients from the Renal Impairment in Secondary Care study. Disease progression was defined as a decline in estimated glomerular filtration rate &gt;30% or the start of renal replacement therapy within 12 and 30 months.

Results
Levels of uC3M/creatinine decreased, whereas levels of uPRO-C3/creatinine and sPRO-C3 increased with increasing CKD stage. uC3M/creatinine was inversely and independently associated with disease progression by 12 months {odds ratio [OR] 0.39 [95% confidence interval (CI) 0.18–0.83]; P = 0.01 per doubling of uC3M/creatinine} with development of end-stage renal disease [hazard ratio (HR) 0.70 (95% CI 0.50–0.97); P = 0.03 per doubling of uC3M/creatinine]. sPRO-C3 at baseline was independently associated with increased mortality [HR 1.93 (95% CI 1.21–3.1); P = 0.006 per doubling of sPRO-C3] and disease progression by 30 months [OR 2.16 (95% CI 1.21–3.84); P = 0.009 per doubling of sPRO-C3].

Conclusions
Dynamic products of COL3 formation and degradation were independently associated with CKD progression and mortality and may represent an opportunity to link pathological processes with targeted treatments against fibrosis.
Nitric oxide modulates cardiomyocyte pH control through a biphasic effect on sodium/hydrogen exchanger-1
Authors: Richards Mark A , Simon Jillian N , Ma Ruichong , Loonat Aminah A , Crabtree Mark J , Paterson David J , Fahlman Richard P , Casadei Barbara , Fliegel Larry , Swietach Pawel 
Published: November 2019

Abstract

Aims
When activated, Na+/H+ exchanger-1 (NHE1) produces some of the largest ionic fluxes in the heart. NHE1-dependent H+ extrusion and Na+ entry strongly modulate cardiac physiology through the direct effects of pH on proteins and by influencing intracellular Ca2+ handling. To attain an appropriate level of activation, cardiac NHE1 must respond to myocyte-derived cues. Among physiologically important cues is nitric oxide (NO), which regulates a myriad of cardiac functions, but its actions on NHE1 are unclear.

Methods and results
NHE1 activity was measured using pH-sensitive cSNARF1 fluorescence after acid-loading adult ventricular myocytes by an ammonium prepulse solution manoeuvre. NO signalling was manipulated by knockout of its major constitutive synthase nNOS, adenoviral nNOS gene delivery, nNOS inhibition, and application of NO-donors. NHE1 flux was found to be activated by low [NO], but inhibited at high [NO]. These responses involved cGMP-dependent signalling, rather than S-nitros(yl)ation. Stronger cGMP signals, that can inhibit phosphodiesterase enzymes, allowed [cAMP] to rise, as demonstrated by a FRET-based sensor. Inferring from the actions of membrane-permeant analogues, cGMP was determined to activate NHE1, whereas cAMP was inhibitory, which explains the biphasic regulation by NO. Activation of NHE1-dependent Na+ influx by low [NO] also increased the frequency of spontaneous Ca2+ waves, whereas high [NO] suppressed these aberrant forms of Ca2+ signalling.

Conclusions
Physiological levels of NO stimulation increase NHE1 activity, which boosts pH control during acid-disturbances and results in Na+-driven cellular Ca2+ loading. These responses are positively inotropic but also increase the likelihood of aberrant Ca2+ signals, and hence arrhythmia. Stronger NO signals inhibit NHE1, leading to a reversal of the aforementioned effects, ostensibly as a potential cardioprotective intervention to curtail NHE1 overdrive.
The independent and incremental value of ultrasound carotid plaque length to predict the presence and severity of coronary artery disease: analysis from the carotid plaque length prospective registry
Authors: Tang Wendong , Shen Xiaxian , Li Hailing , Bai Yuan , Zhang Bili , Guo Zhifu , Wu Hong , Li Pan , Zhao Xianxian 
Published: November 2019

Abstract

Aims
Data regarding the relationship between carotid plaque length (CPL) and coronary artery disease (CAD) are lacking. This study aimed to assess the predictive value of CPL for the severity of CAD.

Methods and results
We prospectively enrolled 2149 consecutive patients who underwent both first coronary angiography and carotid ultrasonography with measurements of intima-media thickness (IMT), plaque score (PS), and CPL. In total, 1408 (65.5%) patients had CAD (defined as stenosis ≥50%), and 741 (34.5%) patients had no CAD. Patients with CAD had longer maximal CPL than those without CAD (P &lt; 0.001). The severity of CAD, measured by the Gensini score (GS), was closely correlated with max-CPL (rs = 0.560), followed by PS (rs = 0.486) and mean-IMT (rs = 0.292). Multivariate analysis revealed that max-CPL remained independently associated with CAD and high-GS after adjustment for traditional risk factors (TRF). Max-CPL, compared with PS or mean-IMT, had significantly higher discrimination value for predicting high-GS [area under the curve (AUC) 0.819 vs. 0.769 vs. 0.634, P &lt; 0.001]. At a cut-off value for the max-CPL of 6.3 mm, the sensitivity and negative predictive value for high-GS were 84.6% and 89.1%, respectively. Furthermore, the addition of max-CPL significantly improved the discrimination (AUC 0.832 vs. 0.720, P &lt; 0.001) and reclassification (net reclassification improvement = 0.431, P &lt; 0.001) over TRF for high-GS.

Conclusion
Ultrasound max-CPL provides independent and incremental predictive value for the clinical severity of CAD over TRF and seems a simple useful marker in CAD risk stratification.
Risk of gastrointestinal bleeding associated with oral anticoagulation and non-steroidal anti-inflammatory drugs in patients with atrial fibrillation: a nationwide study
Authors: Olsen Anne-Marie Schjerning , McGettigan Patricia , Gerds Thomas Alexander , Fosbøl Emil Loldrup , Olesen Jonas Bjerring , Sindet-Pedersen Caroline , Staerk Laila , Lock Hansen Morten , Pallisgaard Jannik Langtved , Køber Lars , Torp-Pedersen Christian , Gislason Gunnar Hilmar , Lamberts Morten 
Published: November 2019

Abstract

Aims
Non-vitamin K antagonist oral anticoagulants (NOACs) are displacing vitamin K antagonists (VKAs) for stroke prophylaxis in patients with atrial fibrillation (AF). Concomitant use of non-steroidal anti-inflammatory drugs (NSAIDs) could increase gastrointestinal bleeding (GIB) risks among these patients. The aim of this study was to examine the risk of GIB among Danish AF patients taking oral anticoagulants (OACs) and NSAIDs.

Methods and results
Using nationwide administrative registries, we determined concomitant NSAID use among anticoagulant-naïve patients with AF initiating OACs between August 2011 and June 2017. We calculated short-term absolute risks differences and hazard ratios (HRs) for GIB based on multiple adjusted cause-specific Cox regressions with time-dependent NSAID treatment. Among 41 183 patients [median age 70 years (interquartile range 64–78); 55% men], 21% of patients on NOACs and 18% on VKA were co-prescribed NSAIDs. The differences in absolute risk [95% confidence interval (CI)] of GIB within 14 days of commencing concomitant NSAID therapy (vs. no concomitant NSAID therapy) were 0.10% (0.04–0.18%) for NOACs and 0.13% (0.03–0.24%) for VKA. NOACs overall were associated with less GIB than VKA [HR 0.77 (95% CI 0.69–0.85)]. Compared with OACs alone, concomitant NSAIDs doubled the GIB risk associated with NOACs overall [HR 2.01 (95% CI 1.40–2.61)] and with VKA [HR 1.95 (95% CI 1.21–2.69)].

Conclusion
Among this nationwide AF population taking OACs, concomitant NSAID therapy increased the short-term absolute risk of GIB. Non-vitamin K antagonist oral anticoagulants alone were associated with lower GIB risks than VKA but concomitant NSAIDs abolished this advantage. The findings align with post hoc analyses from randomized studies. Physicians should exercise appropriate caution when prescribing NSAIDs for patients with AF taking NOACs or VKA.
Cabins, castles, and constant hearts: rhythm control therapy in patients with atrial fibrillation
Authors: Willems Stephan , Meyer Christian , de Bono Joseph , Brandes Axel , Eckardt Lars , Elvan Arif , van Gelder Isabelle , Goette Andreas , Gulizia Michele , Haegeli Laurent , Heidbuchel Hein , Haeusler Karl Georg , Kautzner Josef , Mont Lluis , Ng G Andre , Szumowski Lukasz , Themistoclakis Sakis , Wegscheider Karl , Kirchhof Paulus 
Published: November 2019

Abstract
Recent innovations have the potential to improve rhythm control therapy in patients with atrial fibrillation (AF). Controlled trials provide new evidence on the effectiveness and safety of rhythm control therapy, particularly in patients with AF and heart failure. This review summarizes evidence supporting the use of rhythm control therapy in patients with AF for different outcomes, discusses implications for indications, and highlights remaining clinical gaps in evidence. Rhythm control therapy improves symptoms and quality of life in patients with symptomatic AF and can be safely delivered in elderly patients with comorbidities (mean age 70 years, 3–7% complications at 1 year). Atrial fibrillation ablation maintains sinus rhythm more effectively than antiarrhythmic drug therapy, but recurrent AF remains common, highlighting the need for better patient selection (precision medicine). Antiarrhythmic drugs remain effective after AF ablation, underpinning the synergistic mechanisms of action of AF ablation and antiarrhythmic drugs. Atrial fibrillation ablation appears to improve left ventricular function in a subset of patients with AF and heart failure. Data on the prognostic effect of rhythm control therapy are heterogeneous without a clear signal for either benefit or harm. Rhythm control therapy has acceptable safety and improves quality of life in patients with symptomatic AF, including in elderly populations with stroke risk factors. There is a clinical need to better stratify patients for rhythm control therapy. Further studies are needed to determine whether rhythm control therapy, and particularly AF ablation, improves left ventricular function and reduces AF-related complications.
The impact of mechanical oesophageal deviation on posterior wall pulmonary vein reconnection
Authors: Iwasawa Jin , Koruth Jacob S , Mittnacht Alexander J , Tran Van N , Palaniswamy Chandrasekar , Sharma Dinesh , Bhardwaj Rahul , Naniwadekar Aditi , Joshi Kamal , Sofi Aamir , Syros Georgios , Choudry Subbarao , Miller Marc A , Dukkipati Srinivas R , Reddy Vivek Y 
Published: November 2019

Abstract

Aims
During atrial fibrillation ablation, oesophageal heating typically prompts reduction or termination of radiofrequency energy delivery. We previously demonstrated oesophageal temperature rises are associated with posterior left atrial pulmonary vein reconnection (PVR) during redo procedures. In this study, we assessed whether mechanical oesophageal deviation (MED) during an index procedure minimizes posterior wall PVRs during redo procedures.

Methods and results
Patients in whom we performed a first-ever procedure followed by a clinically driven redo procedure were divided based on both the use of MED for oesophageal protection and the ablation catheter employed (force or non-force sensing) in the first procedure. The PVR sites were compared between MED using a force-sensing catheter (MEDForce), or no MED with a non-force (ControlNoForce) or force (ControlForce) sensing catheter. Despite similar clinical characteristics, the MEDForce redo procedure rate (9.2%, 26/282 patients) was significantly less than the ControlNoForce (17.2%, 126/734 patients; P = 0.002) and ControlForce (17.5%, 20/114 patients; P = 0.024) groups. During the redo procedure, the posterior PVR rate with MEDForce (2%, 1/50 PV pairs) was significantly less than with either ControlNoForce (17.7%, 44/249 PV pairs; P = 0.004) or ControlForce (22.5%, 9/40 PV pairs; P = 0.003), or aggregate Controls (18.3%, 53/289 PV pairs; P = 0.006). However, the anterior PVR rate with MEDForce (8%, 4/50 PV pairs) was not significantly different than Controls (aggregate Controls—3.5%, 10/289 PV pairs, P = 0.136; ControlNoForce—2.4%, 6/249 PV pairs, P = 0.067; ControlForce—10%, 4/40 PV pairs, P = 1.0).

Conclusion
Oesophageal deviation improves the durability of the posterior wall ablation lesion set during AF ablation.
Desmoglein-2 mutations in propeptide cleavage-site causes arrhythmogenic right ventricular cardiomyopathy/dysplasia by impairing extracellular 1-dependent desmosomal interactions upon cellular stress
Authors: Vite Alexia , Gandjbakhch Estelle , Hery Tiphaine , Fressart Veronique , Gary Francoise , Simon Francoise , Varnous Shaida , Hidden Lucet Francoise , Charron Philippe , Villard Eric 
Published: November 2019

AbstractAimsDesmoglein-2 (DSG2) mutations, which encode a heart-specific cadherin crucial for desmosomal adhesion, are frequent in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D). DSG2 mutations have been associated with higher risk of biventricular involvement. Among DSG2 mutations, mutations of the inhibitory propeptide consensus cleavage-site (Arg-X-Arg/Lys-Arg), are particularly frequent. In the present work, we explored the functional consequences of DSG2 propeptide cleavage site mutations p.Arg49His, p.Arg46Trp, and p.Arg46Gln on localization, adhesive properties, and desmosome incorporation of DSG2.Methods and resultsWe studied the expression of mutant-DSG2 in human heart and in epithelial and cardiac cellular models expressing wild-type or mutant (p.Arg49His, p.Arg46Trp, and p.Arg46Gln) proDSG2-GFP fusion proteins. The consequences of the p.Arg46Trp mutation on DSG2 adhesiveness were studied by surface plasmon resonance. Incorporation of mutant p.Arg46Trp DSG2 into desmosomes was studied under low-calcium culture conditions and cyclic mechanical stress. We demonstrated in human heart and cellular models that all three mutations prevented N-terminal propeptide cleavage, but did not modify intercellular junction targeting. Surface plasmon resonance experiments showed a propeptide-dependent loss of interaction between the cadherin N-terminal extracellular 1 (EC1) domains. Additionally, proDSG2 mutant proteins were abnormally incorporated into desmosomes under low-calcium culture conditions or following mechanical stress. This was accompanied by an epidermal growth factor receptor-dependent internalization of proDSG2, suggesting increased turnover of unprocessed proDSG2.ConclusionOur results strongly suggest weakened desmosomal adhesiveness due to abnormal incorporation of uncleaved mutant proDSG2 in cellular stress conditions. These results provide new insights into desmosomal cadherin regulation and ARVC/D pathophysiology, in particular, the potential role of mechanical stress on desmosomal dysfunction.
Does poor mental health explain socio-demographic gradients in breast cancer screening uptake? A population-based study
Authors: Ross Emma , Maguire Aideen , Donnelly Michael , Mairs Adrian , Hall Clare , O’Reilly Dermot 
Published: November 2019

Abstract

Background
Research from the USA indicates disparities in breast cancer screening uptake for women with poor mental health. However, no attempt has been made to examine the contribution of poor mental health to socio-demographic variations in breast screening uptake. The current study aims to examine the impact of self-reported chronic poor mental health on attendance at breast screening in the UK, and to what extent this explains socio-demographic inequalities in screening uptake.

Methods
Breast screening records were linked to 2011 Census records within the Northern Ireland Longitudinal Study. This identified a cohort of 57 328 women who were followed through one 3-year screening cycle of the National Health Service Breast Screening Programme. Information on mental health status, in addition to other individual and household-level attributes, was derived from the 2011 Census. Logistic regression was employed to calculate odds ratios (ORs) and 95% confidence intervals (CIs) of attendance at screening.

Results
10.7% of women in the cohort reported poor mental health, and in fully adjusted analyses, these individuals were 23% less likely to attend breast screening (OR 0.77; 95% CI 0.73–0.82). Although poor mental health was a strong predictor of screening uptake, it did not explain the observed inequalities in uptake by socio-economic status, marital status, or area of residence.

Conclusions
This study provides novel evidence of inequalities in breast screening uptake for women with chronic poor mental health in the UK. Targeted interventions are necessary to ensure equitable screening access and to enhance overall mortality benefit.
Age, gut location and diet impact the gut microbiome of a tropical herbivorous surgeonfish
Authors: Parata Lara , Nielsen Shaun , Xing Xing , Thomas Torsten , Egan Suhelen , Vergés Adriana 
Published: November 2019

Abstract
Herbivorous fishes play important ecological roles in coral reefs by consuming algae that can otherwise outcompete corals, but we know little about the gut microbiota that facilitates this process. This study focussed on the gut microbiota of an ecologically important coral reef fish, the convict surgeonfish Acanthurus triostegus. We sought to understand how the microbiome of this species varies along its gastrointestinal tract and how it varies between juvenile and adult fish. Further, we examined if the bacteria associated with the diet consumed by juveniles contributes to the gut microbiota. 16S rRNA gene amplicon sequencing showed that bacterial communities associated with the midgut and hindgut regions were distinct between adults and juveniles, however, no significant differences were seen for gut wall samples. The microbiota associated with the epilithic algal food source was similar to that of the juvenile midgut and gut wall but differed from the microbiome of the hindgut. A core bacterial community including members of taxa Epulopiscium and Brevinemataceae was observed across all gastrointestinal and diet samples, suggesting that these bacterial symbionts can be acquired by juvenile convict surgeonfish horizontally via their diet and then are retained into adulthood.