bluuebunny/crossref_metadata_2025_split huggingface dataset:
Barriers to and enablers of diabetic retinopathy screening attendance: a systematic review of published and grey literature
Authors: Graham‐Rowe E. , Lorencatto F. , Lawrenson J. G. , Burr J. M. , Grimshaw J. M. , Ivers N. M. , Presseau J. , Vale L. , Peto T. , Bunce C. , J Francis J. 
Published: May 2018

AbstractAimsTo identify and synthesize studies reporting modifiable barriers/enablers associated with retinopathy screening attendance in people with Type 1 or Type 2 diabetes, and to identify those most likely to influence attendance.MethodsWe searched MEDLINE, EMBASE, PsycINFO, Cochrane Library and the ‘grey literature’ for quantitative and qualitative studies to February 2017. Data (i.e. participant quotations, interpretive summaries, survey results) reporting barriers/enablers were extracted and deductively coded into domains from the Theoretical Domains Framework; with domains representing categories of theoretical barriers/enablers proposed to mediate behaviour change. Inductive thematic analysis was conducted within domains to describe the role each domain plays in facilitating or hindering screening attendance. Domains that were more frequently coded and for which more themes were generated were judged more likely to influence attendance.ResultsSixty‐nine primary studies were included. We identified six theoretical domains [‘environmental context and resources’ (75% of included studies), ‘social influences’ (51%), ‘knowledge’ (51%), ‘memory, attention, decision processes’ (50%), ‘beliefs about consequences’ (38%) and ‘emotions’ (33%)] as the key mediators of diabetic retinopathy screening attendance. Examples of barriers populating these domains included inaccurate diabetic registers and confusion between routine eye care and retinopathy screening. Recommendations by healthcare professionals and community‐level media coverage acted as enablers.ConclusionsAcross a variety of contexts, we found common barriers to and enablers of retinopathy screening that could be targeted in interventions aiming to increase screening attendance.
P465L‐PPARγ mutation confers partial resistance to the hypolipidaemic action of fibrates
Authors: Rodriguez‐Cuenca Sergio , Carobbio Stefania , Barceló‐Coblijn Gwendolyn , Prieur Xavier , Relat Joana , Amat Ramon , Campbell Mark , Dias Ana Rita , Bahri Myriam , Gray Sarah L. , Vidal‐Puig Antonio 
Published: May 2018

AimsFamilial partial lipodystrophic syndrome 3 (FPLD3) is associated with mutations in the transcription factor PPARγ. One of these mutations, the P467L, confers a dominant negative effect. We and others have previously investigated the pathophysiology associated with this mutation using a humanized mouse model that recapitulates most of the clinical symptoms observed in patients who have been phenotyped under different experimental conditions. One of the key clinical manifestations observed, both in humans and mouse models, is the ectopic accumulation of fat in the liver. With this study we aim to dissect the molecular mechanisms that contribute to the excessive accumulation of lipids in the liver and characterize the negative effect of this PPARγ mutation on the activity of PPARα in vivo when activated by fibrates.Material and MethodsP465L‐PPAR mutant and wild‐type mice were divided into 8 experimental groups, 4 different conditions per genotype. Briefly, mice were fed a chow diet or a high‐fat diet (HFD 45% Kcal from fat) for a period of 28 days and treated with WY14643 or vehicle for five days before culling. At the end of the experiment, tissues and plasma were collected. We performed extensive gene expression, fatty acid composition and histological analysis in the livers. The serum collected was used to measure several metabolites and to perform basic lipoprotein profile.ResultsP465L mice showed increased levels of insulin and free fatty acids (FFA) as well as increased liver steatosis. They also exhibit decreased levels of very low density lipoproteins (VLDL) when fed an HFD. We also provide evidence of impaired expression of a number of well‐established PPARα target genes in the P465L mutant livers.ConclusionOur data demonstrate that P465L confers partial resistance to the hypolipidemic action of fibrates. These results show that the fatty liver phenotype observed in P465L mutant mice is not only the consequence of dysfunctional adipose tissue, but also involves defective liver metabolism. All in all, the deleterious effects of P465L‐PPARγ mutation may be magnified by their collateral negative effect on PPARα function.
Left atrial compression and right ventricular outflow tract diameter on echocardiography are independently associated with exercise capacity in patients with large hiatal hernia
Authors: Naoum Christopher , Kritharides Leonard , Falk Gregory L. , Martin David , Yiannikas John 
Published: May 2018

IntroductionLarge hiatal hernia (HH) is often associated with left atrial (LA) compression, anteroposterior cardiac compression (manifesting as reduced right ventricular outflow tract (RVOT) diameter), and left ventricular (LV) compression (manifesting as systolic paradoxical outward motion (LV‐PM) of the posterobasal LV segment). Exercise impairment, also common in this population, improves following HH surgery. We aimed to identify echocardiographic parameters independently associated with exercise impairment due to HH‐mediated cardiogenic compression.MethodsPatients with a large HH (>30% intra‐thoracic stomach, n = 163) referred for cardiac evaluation were included. Echocardiographic parameters were retrospectively analyzed in relation to HH‐related LA compression severity and the presence of LV‐PM. Echocardiographic parameters independently associated with exercise capacity were identified by multivariable analysis.ResultsMean baseline metabolic equivalents were reduced (70 ± 28% predicted). Moderate–severe LA compression and LV‐PM were present in 91 of 163 (56%) and 65 of 162 (40%) patients, respectively. Patients with moderate–severe LA compression and LV‐PM had decreased LA and LV dimensions. Moderate–severe LA compression was also associated with reduced RVOT diameter while LV‐PM predicted a greater reduction in LV volumes. LA compression and RVOT diameter were independently associated with baseline exercise capacity and increased following HH surgery performed in a subgroup (n = 72, LA diameter: 14 ± 5 vs 20 ± 4 mm/m2; RVOT diameter: 17 ± 3 vs 19 ± 3 mm/m2, P < .001 for both). Conversely, LV‐PM was not independently associated with exercise capacity.ConclusionHiatal hernia‐related cardiac compression reduces LA and RVOT dimensions. These parameters are independently associated with baseline exercise capacity and improve following HH surgery. LV‐PM is associated with decreased LV volumes but not exercise capacity in this population.
Can cardiovascular MRI be used to more definitively characterize cardiac masses initially identified using echocardiography?
Authors: Rathi Vikas K. , Czajka Anna T. , Thompson Diane V. , Doyle Mark , Tewatia Tarun , Yamrozik June , Williams Ronald B. , Biederman Robert W. W. 
Published: May 2018

In diagnosing cardiac and paracardiac masses, cardiac MRI (CMR) has gained acceptance as the gold standard. CMR has been observed to be superior to echocardiography in characterizing soft‐tissue structures and, specifically, in classifying cardiac masses. The aim of our study was to evaluate the association between mortality and cardiac or paracardiac masses initially identified by echocardiography (ECHO) and confirmed by CMR. Between January 2002 and August 2007, a total of 158 patients underwent both ECHO and CMR for the evaluation of cardiac masses that were equivocal or undefined by ECHO. The primary study endpoints were 5‐year all‐cause mortality and 5‐year cardiac mortality. Causes of death as of April 1, 2015 were obtained from medical records or the National Death Index. Patients were analyzed according to mass type determined by CMR using the Kruskal–Wallis test, Kaplan–Meier curves, and the log‐rank test. Over a mean duration of follow‐up of 10.4 ± 2.9 years (range: 0.01–12 years) post‐CMR, the overall all‐cause mortality rate was 25.9% (41/158). Median age at death was 76 years and there were 21 females (51.2%). Mortality rates in the different classifications of cardiac masses by CMR were as follows: 20% (1/5) in patients with a Nondiagnostic CMR; 20% (1/5) in Other Diagnoses; 17.9% (7/39) in No Masses (includes Normal Anatomical Variants); 16.7% (3/18) in Benign Masses; 23.8% (15/63) in Fat; 50% (5/10) in Thrombus; and 61.5% (8/13) in Malignant Mass. The mean survival time in patients with No Mass (n = 39) was not significantly longer than patients with any type of cardiac mass (n = 114) (P = .16). No significant difference was found in age at death between patients when grouped by CMR classification (P = .40). However, among CMR‐confirmed masses, there were some significant differences by mass classification type (P = .006). During the follow‐up period, 26% (41/158) of patients died and 22% (9/41) of the deaths were cardiovascular related; there was no significant difference in mean survival times with respect to cause of mortality (P = .23). In patients with cardiac masses, dually confirmed by ECHO and CMR, significant differences in survival time were observed based upon CMR classified type of mass while CMR was instrumental in obviating invasive biopsy.
Interactions between insulin and diet on striatal dopamine uptake kinetics in rodent brain slices
Authors: Patel Jyoti C. , Stouffer Melissa A. , Mancini Maria , Nicholson Charles , Carr Kenneth D. , Rice Margaret E. 
Published: May 2018

AbstractDiet influences dopamine transmission in motor‐ and reward‐related basal ganglia circuitry. In part, this reflects diet‐dependent regulation of circulating and brain insulin levels. Activation of striatal insulin receptors amplifies axonal dopamine release in brain slices, and regulates food preference in vivo. The effect of insulin on dopamine release is indirect, and requires striatal cholinergic interneurons that express insulin receptors. However, insulin also acts directly on dopamine axons to increase dopamine uptake by promoting dopamine transporter (DAT) surface expression, counteracting enhanced dopamine release. Here, we determined the functional consequences of acute insulin exposure and chronic diet‐induced changes in insulin on DAT activity after evoked dopamine release in striatal slices from adult ad‐libitum fed (AL) rats and mice, and food‐restricted (FR) or high‐fat/high‐sugar obesogenic (OB) diet rats. Uptake kinetics were assessed by fitting evoked dopamine transients to the Michaelis‐Menten equation and extracting Cpeak and Vmax. Insulin (30 nm) increased both parameters in the caudate putamen and nucleus accumbens core of AL rats in an insulin receptor‐ and PI3‐kinase‐dependent manner. A pure effect of insulin on uptake was unmasked using mice lacking striatal acetylcholine, in which increased Vmax caused a decrease in Cpeak. Diet also influenced Vmax, which was lower in FR vs. AL. The effects of insulin on Cpeak and Vmax were amplified by FR but blunted by OB, consistent with opposite consequences of these diets on insulin levels and insulin receptor sensitivity. Overall, these data reveal acute and chronic effects of insulin and diet on dopamine release and uptake that will influence brain reward pathways.
Behavioural state‐specific neurons in the mouse medulla involved in sleep‐wake switching
Authors: Sakai Kazuya 
Published: May 2018

AbstractThe medullary reticular formation (RF) is involved in the maintenance of several vital physiological functions and level of vigilance. In this study, in nonanesthetised, head‐fixed mice, I examined the role of medullary RF neurons in the control of sleep‐wake states, that is, wakefulness (W), slow‐wave sleep (SWS) and paradoxical (or rapid eye movement) sleep (PS). I showed, for the first time, that the mouse medullary RF contains presumed SWS‐promoting, SWS‐on neurons that remain silent during W, display a sharp increase in discharge rate at sleep onset, and discharge tonically and selectively during SWS. In addition, I showed the presence in the medullary RF of both PS‐on and PS‐off neurons, which, respectively, commence discharging or cease firing selectively just prior to, and during, PS. PS‐off neurons were located in the raphe nuclei and ventral medulla, while PS‐on neurons were found in both the lateral part of the ventral gigantocellular reticular nucleus and the raphe nuclei, as were SWS‐on neurons. PS‐off and SWS‐on neurons appear to play an important role in both the W‐SWS and SWS‐PS switches, while PS‐on and PS‐off neurons play an important role in the PS‐W switch. The present findings on the trends in spike activity at the transitions from SWS to PS and from PS to W are in line with the reciprocal interaction hypothesis according to which PS occurs as a result of the cessation of discharge of PS‐off neurons, while PS ends as a result of the start of discharge of PS‐off neurons.
Molecular and cellular characterization of nicotinic acetylcholine receptor subtypes in the arcuate nucleus of the mouse hypothalamus
Authors: Calarco Cali A. , Li Zhiying , Taylor Seth R. , Lee Somin , Zhou Wenliang , Friedman Jeffrey M. , Mineur Yann S. , Gotti Cecilia , Picciotto Marina R. 
Published: May 2018

AbstractNicotine, acting through nicotinic acetylcholine receptors (nAChRs), increases the firing rate of both orexigenic agouti‐related peptide (AgRP) and anorexigenic pro‐opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARC), yet nicotine and other nAChR agonists decrease food intake in mice. Viral‐mediated knockdown of the β4 nAChR subunit in all neuronal cell types in the ARC prevents the nicotinic agonist cytisine from decreasing food intake, but it is not known whether the β4 subunit is selectively expressed in anorexigenic neurons or how other nAChR subtypes are distributed in this nucleus. Using translating ribosome affinity purification (TRAP) on ARC tissue from mice with ribosomes tagged in either AgRP or POMC cells, we examined nAChR subunit mRNA levels using real‐time PCR. Both AgRP and POMC cells express a comparable panel of nAChR subunits with differences in α7 mRNA levels and a trend for difference in α4 levels, but no differences in β4 expression. Immunoprecipitation of assembled nAChRs revealed that the β4 subunit forms assembled channels with α3, β2 and α4, but not other subunits found in the ARC. Finally, using cell type‐selective, virally delivered small hairpin RNAs targeting either the β4 or α7 subunit, we examined the contribution of each subunit in either AgRP or POMC cells to the behavioural response to nicotine, refining the understanding of nicotinic regulation of this feeding circuit. These experiments identify a more complex set of nAChRs expressed in ARC than in other hypothalamic regions. Thus, the ARC appears to be a particular target of nicotinic modulation.
Resolving ambiguities in SUDEP classification
Authors: Devinsky Orrin , Bundock Elizabeth , Hesdorffer Dale , Donner Elizabeth , Moseley Brian , Cihan Esma , Hussain Fizza , Friedman Daniel 
Published: May 2018

SummaryObjectiveTo examine the consistency of applying the Nashef et al (2012) criteria to classify sudden unexpected death in epilepsy (SUDEP).MethodsWe reviewed cases from the North American SUDEP Registry (n = 250) and Medical Examiner Offices (n = 1301: 698 Maryland, 457 New York City, 146 San Diego). Two epileptologists with expertise in SUDEP and epilepsy‐related mortality independently reviewed medical records, scene investigation, autopsy, and toxicology and assigned a SUDEP class.ResultsMajor areas of disagreement arose between adjudicators concerned differentiating (1) Definite SUDEP Plus Comorbidity from Possible SUDEP and (2) Resuscitated (Near) SUDEP from SUDEP. In many cases, distinguishing between contributing and competing causes of death when trying to classify Definite SUDEP Plus Comorbidity versus Possible SUDEP is ambiguous and relies on judgement. Similarly, determining if an intervention was lifesaving or not (Resuscitated SUDEP or Not SUDEP), or if resuscitation merely delayed SUDEP (Resuscitated SUDEP or SUDEP) is often a judgement call and can differ between experienced adjudicators. Given these persisting ambiguities, we propose more explicit criteria for distinguishing these categories.SignificanceAccurate and consistent classification of cause of death among individuals with epilepsy remains a dire public health concern. SUDEP is likely underestimated in national health statistics. Greater standardization of criteria among epilepsy researchers, medical examiners, and epidemiologists to determine cause and classify death will lead to more accurate tracking of SUDEP and other epilepsy‐related mortalities.
Overexpression of Tet3 in donor cells enhances goat somatic cell nuclear transfer efficiency
Authors: Han Chengquan , Deng Ruizhi , Mao Tingchao , Luo Yan , Wei Biao , Meng Peng , Zhao Lu , Zhang Qing , Quan Fusheng , Liu Jun , Zhang Yong 
Published: May 2018

Ten–eleven translocation 3 (TET3) mediates active DNA demethylation of paternal genomes during mouse embryonic development. However, the mechanism of DNA demethylation in goat embryos remains unknown. In addition, aberrant DNA methylation reprogramming prevalently occurs in embryos cloned by somatic cell nuclear transfer (SCNT). In this study, we reported that TET3 is a key factor in DNA demethylation in goat pre‐implantation embryos. Knockdown of Tet3 hindered DNA demethylation at the two‐ to four‐cell stage in goat embryos and decreased Nanog expression in blastocysts. Overexpression of Tet3 in somatic cells can initiate DNA demethylation, reduce 5‐methylcytosine level, increase 5‐hydroxymethylcytosine level and promote the expression of key pluripotency genes. After SCNT, overexpression of Tet3 in donor cells corrected abnormal DNA hypermethylation of cloned embryos and significantly enhanced in vitro and in vivo developmental rate (P < 0.05). We conclude that overexpression of Tet3 in donor cells significantly improves goat SCNT efficiency.
Factors regulating carbon sinks in mangrove ecosystems
Authors: Li Shi‐Bo , Chen Po‐Hung , Huang Jih‐Sheng , Hsueh Mei‐Li , Hsieh Li‐Yung , Lee Chen‐Lu , Lin Hsing‐Juh 
Published: May 2018

AbstractMangroves are recognized as one of the richest carbon storage systems. However, the factors regulating carbon sinks in mangrove ecosystems are still unclear, particularly in the subtropical mangroves. The biomass, production, litterfall, detrital export and decomposition of the dominant mangrove vegetation in subtropical (Kandelia obovata) and tropical (Avicennia marina) Taiwan were quantified from October 2011 to July 2014 to construct the carbon budgets. Despite the different tree species, a principal component analysis revealed the site or environmental conditions had a greater influence than the tree species on the carbon processes. For both species, the net production (NP) rates ranged from 10.86 to 27.64 Mg C ha−1 year−1 and were higher than the global average rate due to the high tree density. While most of the litterfall remained on the ground, a high percentage (72%–91%) of the ground litter decomposed within 1 year and fluxed out of the mangroves. However, human activities might cause a carbon flux into the mangroves and a lower NP rate. The rates of the organic carbon export and soil heterotrophic respiration were greater than the global mean values and those at other locations. Only a small percentage (3%–12%) of the NP was stored in the sediment. The carbon burial rates were much lower than the global average rate due to their faster decomposition, indicating that decomposition played a critical role in determining the burial rate in the sediment. The summation of the organic and inorganic carbon fluxes and soil heterotrophic respiration well exceeded the amount of litter decomposition, indicating an additional source of organic carbon that was unaccounted for by decomposition in the sediment. Sediment‐stable isotope analyses further suggest that the trapping of organic matter from upstream rivers or adjacent waters contributed more to the mangrove carbon sinks than the actual production of the mangrove trees.
Challenges to representing the population from new forms of consumer data
Authors: Lansley Guy , Cheshire James 
Published: May 2018

AbstractA large share of human activity is now routinely captured and stored by commercial organisations as consumer data. These new forms of data have provided many new and exciting opportunities for understanding population trends at fine spatial scales. In many settings, they have reduced our dependence on theory and traditional modelling approaches and fundamentally changed how geographers approach producing representations of the population. However, consumer data are typically created for commercial benefit and do not have academic standard data quality controls, and so, in repurposing the data for social research, we encounter inherent issues of veracity. Without an understanding of uncertainty, social scientists can risk overstretching consumer datasets beyond the specific populations or phenomena they directly pertain to. Moreover, the technical characteristics of large and complex datasets also make it challenging to generate valid information efficiently. Therefore, this paper reviews the major challenges to harnessing consumer data to produce valid spatial representations of the population at large.
Managing paediatric bleeding disorder patients undergoing surgical procedures: Leveraging the electronic medical record
Authors: Tarango C. , Dahale D. , Dodson N. , Otte A. , Schoettker P. J. 
Published: May 2018

IntroductionIndividuals with bleeding disorders have a high risk of bleeding complications with surgical procedures. Careful planning and management of peri‐operative treatment is vital for their safety. Yet, inter‐provider communication and communication between patients/families and providers is not reliable.AimOur haemophilia treatment centre (HTC) created a care gap report that used the electronic medical record to inform our team when patients with bleeding disorders were scheduled for procedures.MethodsAn electronic medical record‐based patient registry was linked to the hospital’s surgical schedule and a report was run daily by HTC staff for the upcoming 14 days. We determined the number of surgeries scheduled for patients with a bleeding disorder without the knowledge of the HTC, identified by the care gap report during the 6 months prior to and 2 years after implementing the report.ResultsHad the report been in effect 6 months prior, the majority of surgery cases would have been detected and planned for an average of 10 days prior to the procedure. Following implementation, the report identified 62 of 225 surgeries on patients with known bleeding disorders where the HTC did not have prior communication from the patient/family or surgical team.ConclusionThis surgery care gap report provides the date and time of procedures on bleeding disorder patients without relying on contact from patients/families or the surgical team. Its use has resulted in an improved peri‐operative process for patients with bleeding disorders undergoing surgical procedures and potentially prevented surgery cancellations.