bluuebunny/crossref_metadata_2025_split huggingface dataset:
Survey on the Adherence to the 2009 NASPGHAN‐ESPGHAN Gastroesophageal Reflux Guidelines by Brazilian Paediatricians
Authors: Vieira Sarah Cristina Fontes , Gurgel Flavia Matos , Leão Maria Zuleide , Costa‐Silva Tiê Emídio , Barreto Ikaro Daniel de Carvalho , Martins‐Filho Paulo Ricardo Saquete , Vieira Mário César , Gurgel Ricardo Queiroz 
Published: February 2018

ABSTRACTObjective:The aim of the study was to evaluate the management of gastroesophageal reflux in children among Brazilian pediatricians and adherence to the 2009 North American Society of Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN), and European Society of Gastroenterology, Hepatology, and Nutrition (ESPGHAN) Guideline in Brazil.Methods:An observational cross‐sectional study was conducted, applying a standard questionnaire with 12 questions about gastroesophageal reflux (GER) and gastroesophageal reflux disease (GERD) management in infants, children, and adolescents to the pediatricians during the 37th Brazilian Pediatrics Congress in October, 2015. Adherence to the 2009 NASPGHAN‐ESPGHAN Guideline was verified through analyses of interviewees’ answers. Pediatricians’ demographic and professional characteristics were screened.Results:A total of 390 Brazilian pediatricians answered the questionnaire. None showed complete adherence to Guideline recommendations. GERD diagnosis by history alone was reported by 67%, irrespective of the child's age. The mean score for diagnostic adherence to the guidelines was 0.94 ± 0.86 (range 0–4). Working in public health services (P = 0.026) was the only variable retained as a significant predictor of poor adherence for GER/GERD diagnosis after multivariate logistic regression analysis. No significant statistical differences were found between Brazilian regions on total score (P = 0.774). Proton pump inhibitors were prescribed by 28.4% of the pediatricians independent of child's age, and 59% use proton pump inhibitors to treat babies with unexplained crying and/or distressed behavior.Conclusions:2009 NASPGHAN‐ESPGHAN Guideline recommendations had poor adherence by Brazilian pediatricians. Studies evaluating the reasons for the poor adherence to NASPGHAN/ESPGHAN guidelines are urgently needed.
Impact of Relational Coordination on Nurse Job Satisfaction, Work Engagement and Burnout
Authors: Havens Donna Sullivan , Gittell Jody Hoffer , Vasey Joseph 
Published: February 2018

AIM
To explore how relational coordination, known to enhance quality and efficiency outcomes for patients and hospitals, impacts direct care nurse outcomes such as burnout, work engagement, and job satisfaction, addressing the “Quadruple Aim,” to improve the experience of providing care.

BACKGROUND
Hospitals are complex organizations in which multiple providers work interdependently, under conditions of uncertainty and time constraints, to deliver safe quality care despite differences in specialization, training, and status. Relational coordination—communicating and relating for the purpose of task integration—is known to improve quality, safety, and efficiency under these conditions, but less is known about its impact on the well-being of direct care providers themselves.

METHODS
Surveys measuring relational coordination among nurses and other types of providers as well as job-related outcomes in 5 acute care community hospitals were completed by direct care RNs.

RESULTS
Relational coordination was significantly related to increased job satisfaction, increased work engagement, and reduced burnout.

CONCLUSIONS
Relational coordination contributes to the well-being of direct care nurses, addressing the Quadruple Aim by improving the experience of providing care.
Psychological Stress and Mitochondria: A Conceptual Framework
Authors: Picard Martin , McEwen Bruce S. 
Published: February 2018

ABSTRACT

Background
The integration of biological, psychological, and social factors in medicine has benefited from increasingly precise stress response biomarkers. Mitochondria, a subcellular organelle with its own genome, produce the energy required for life and generate signals that enable stress adaptation. An emerging concept proposes that mitochondria sense, integrate, and transduce psychosocial and behavioral factors into cellular and molecular modifications. Mitochondrial signaling might in turn contribute to the biological embedding of psychological states.

Methods
A narrative literature review was conducted to evaluate evidence supporting this model implicating mitochondria in the stress response, and its implementation in behavioral and psychosomatic medicine.

Results
Chronically, psychological stress induces metabolic and neuroendocrine mediators that cause structural and functional recalibrations of mitochondria, which constitutes mitochondrial allostatic load. Clinically, primary mitochondrial defects affect the brain, the endocrine system, and the immune systems that play a role in psychosomatic processes, suggesting a shared underlying mechanistic basis. Mitochondrial function and dysfunction also contribute to systemic physiological regulation through the release of mitokines and other metabolites. At the cellular level, mitochondrial signaling influences gene expression and epigenetic modifications, and modulates the rate of cellular aging.

Conclusions
This evidence suggests that mitochondrial allostatic load represents a potential subcellular mechanism for transducing psychosocial experiences and the resulting emotional responses—both adverse and positive—into clinically meaningful biological and physiological changes. The associated article in this issue of Psychosomatic Medicine presents a systematic review of the effects of psychological stress on mitochondria. Integrating mitochondria into biobehavioral and psychosomatic research opens new possibilities to investigate how psychosocial factors influence human health and well-being across the life-span.
Uncomplicated 90Y Selective Internal Radio Therapy in a Patient With Hepatocellular Carcinoma After Arterial and Portal Vein Embolizations
Authors: van der Pol Jochem , de Vos-Geelen Judith , Bucerius Jan , Mitea Cristina , van der Leij Christiaan 
Published: February 2018

Abstract
Selective internal radio therapy (SIRT) with 90Y-glass microspheres was performed in a cirrhotic patient with hepatocellular carcinoma (Barcelona Clinic Liver Cancer stage C) after arterial coil embolization for treatment of intratumoral hemorrhage and planned preoperative right portal vein embolization. Three technetium 99mTc macro-albumin-aggregate injections were needed to optimize intralesional uptake without extrahepatic deposition. The consecutive SIRT treatment was uncomplicated with a remarkable result.
Metabolic Changes in Central Poststroke Pain Following Thalamic Intracerebral Hemorrhage
Authors: Kim Na Young , Lee Sang Chul , An Young-sil , Shin Ji-Cheol , Kim Yong Wook 
Published: February 2018

Purpose
Central poststroke pain (CPSP) is one of the most refractory neuropathic pains following stroke. Injury in the spinothalamic pathway appears crucial for the development of CPSP, but changes in activity in multiple brain regions may also be related. We investigated brain metabolic changes in patients with CPSP following thalamic intracerebral hemorrhage (ICH).

Methods
Forty-three patients with thalamic ICH were examined. Overall brain metabolism was measured with 18F-FDG PET. Images were analyzed with statistical parametric mapping (SPM12). Patients with CPSP (n = 20) were compared with patients without CPSP (n = 23). In addition, the association between regional brain metabolism and the severity of CPSP was investigated.

Results
In comparison to patients in the non-CPSP group, the CPSP group exhibited significant hypometabolism in the ipsilesional precentral, postcentral gyri, and the contralesional cuneus (P
uncorrected < 0.001), whereas significant hypermetabolism was found in the medial dorsal nucleus of the contralesional thalamus (P
uncorrected < 0.001). In addition, brain metabolism in the ipsilesional Crus I and Crus II of the cerebellum was positively correlated to pain intensity ratings (P
uncorrected < 0.001).

Conclusion
Our findings suggested that an altered state of resting brain metabolism in various brain regions related to sensory processing and cognitive functioning may be involved in the underlying mechanism of CPSP following thalamic ICH.
Safety and Efficacy of Rituximab: Experience of a Single Multiple Sclerosis Center
Authors: Alldredge Brett , Jordan Allison , Imitola Jaime , Racke Michael K. 
Published: February 2018

Objectives
Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system. B cells play an important pathogenic role in MS. Rituximab (RTX), a B-cell depleting drug, has been used to treat MS and neuromyelitis optica (NMO). Patient characteristics, safety, and efficacy measures are reviewed to ascertain the therapeutic benefit and safety of RTX in a real-world setting with long-term follow-up.

Methods
This is a retrospective chart review of patients who received RTX at The Ohio State University's MS clinic from January 2005 to October 2016.

Results
Of the 64 patient charts reviewed, 23 had a relapsing remitting MS, 17 had primary progressive MS (PPMS), and 24 had NMO. In the relapsing remitting MS cohort, there was an annual relapse rate of 0.005 and 87% were reported as clinically stable at the end of the chart review period. In the primary progressive MS cohort, 47% were reported as clinically stable at the end of the chart review period. In the NMO cohort, there was an annual relapse rate of 0.0074 and 79% were reported as clinically stable at the end of the chart review period. A total of 29 infusion reactions were reported in 21 patients. None were serious and only 1 patient elected to stop RTX due to an adverse event.

Conclusions
Rituximab demonstrated good tolerability and efficacy in cases of both relapsing and progressive forms of MS and NMO.
Molecular determinants of Yellow Fever Virus pathogenicity in Syrian Golden Hamsters: one mutation away from virulence
Authors: Klitting Raphaëlle , Roth Laura , Rey Félix A. , de Lamballerie Xavier 
Published: February 2018

ABSTRACTYellow fever virus (Flavivirusgenus) is an arthropod-borne pathogen which can infect humans, causing a severe viscerotropic disease with a high mortality rate. Adapted viral strains allow the reproduction of yellow fever disease in hamsters with features similar to the human disease. Here, we used the Infectious Subgenomic Amplicons reverse genetics method to produce an equivalent to the hamster-virulent strain, Yellow FeverAp7, by introducing a set of 4 synonymous and 6 non-synonymous mutations into a single subgenomic amplicon, derived from the sequence of theAsibistrain. The resulting strain, Yellow FeverAp7M, induced a disease similar to that described forAp7in terms of symptoms, weight evolution, viral loads in the liver and lethality. Using the same methodology, we produced mutant strains derived from eitherAp7MorAsibiviruses and investigated the role of each ofAp7Mnon-synonymous mutations in itsin vivophenotype. This allowed identifying key components of the virulence mechanism in hamsters. InAp7Mvirus, the reversion of either E/Q27H or E/D155A mutations, led to an important reduction of both virulence andin vivoreplicative fitness. In addition, the introduction of the single D155AAp7Mmutation within the E protein of theAsibivirus was sufficient to drastically modify its phenotype in hamsters towards both a greater replication efficiency and virulence. Finally, inspection of theAsibistrain E protein structure combined toin vivotesting revealed the importance of an exposed α-helix in domain I, containing residues 154 and 155, forAp7Mvirulence in hamsters.
Next generation CRISPR/Cas9 transcriptional activation inDrosophilausing flySAM
Authors: Jia Yu , Xu Rong-Gang , Ren Xingjie , Ewen-Campen Ben , Rajakumar Rajendhran , Zirin Jonathan , Yang-Zhou Donghui , Zhu Ruibao , Wang Fang , Mao Decai , Peng Ping , Qiao Huan-Huan , Wang Xia , Liu Lu-Ping , Xu Bowen , Ji Jun-Yuan , Liu Qingfei , Sun Jin , Perrimon Norbert , Ni Jian-Quan 
Published: February 2018

AbstractCRISPR/Cas9-based transcriptional activation (CRISPRa) has recently emerged as a powerful and scalable technique for systematic over-expression genetic analysis inDrosophila melanogaster.We present flySAM, a potent new tool forin vivoCRISPRa, which offers a major improvement over existing strategies in terms of effectiveness, scalability, and ease-of-use. flySAM outperforms existingin vivoCRISPRa strategies, and approximates phenotypes obtained using traditional Gal4-UAS over-expression. Further, because flySAM typically only requires a single sgRNA, it dramatically improves scalability. We use flySAM to demonstrate multiplexed CRISPRa, which has not been previously shownin vivo.In addition, we have simplified the experimental usage of flySAM by creating a single vector encoding both the UAS:Cas9-activator and the sgRNA, allowing for inducible CRISPRa in a single genetic cross. flySAM will thus replace previous CRISPRa strategies as the basis of our growing genome-wide transgenic over-expression resource, TRiP-OE.
A Gender-Dependent Molecular Switch of Inflammation via MyD88/Estrogen Receptor-alpha Interaction
Authors: El Sabeh Rana , Bonnet Mélanie , Le Corf Katy , Lang Kevin , Kfoury Alain , Badran Bassam , Hussein Nader , Virard François , Treilleux Isabelle , Le Romancer Muriel , Lebecque Serge , Manié Serge , Coste Isabelle , Renno Toufic 
Published: February 2018

AbstractMost Toll-like receptors and IL-1/IL-18 receptors activate a signaling cascade via the adaptor molecule MyD88, resulting in NF-κB activation and inflammatory cytokine and chemokine production. Females are less susceptible than males to inflammatory conditions, presumably due to protection by estrogen. Here we show that MyD88 interacts with a methylated, cytoplasmic form of estrogen receptor-alpha (methER-α). This interaction is required for NF-κB transcriptional activity and pro-inflammatory cytokine production, and is dissociated by estrogen. Importantly, we show a strong gender segregation in gametogenic reproductive organs, with MyD88/methER-α interactions found in testicular tissues and in ovarian tissues from menopausal women, but not in ovaries from women age 49 and less -suggesting a role for estrogen in disrupting this complex in situ. Collectively, our results indicate that the formation of MyD88/methER-α complexes during inflammatory signaling and their disruption by estrogen may represent a mechanism that contributes to gender bias in inflammatory responses.
Cross-type Biomedical Named Entity Recognition with Deep Multi-Task Learning
Authors: Wang Xuan , Zhang Yu , Ren Xiang , Zhang Yuhao , Zitnik Marinka , Shang Jingbo , Langlotz Curtis , Han Jiawei 
Published: February 2018

AbstractMotivationState-of-the-art biomedical named entity recognition (BioNER) systems often require handcrafted features specific to each entity type, such as genes, chemicals and diseases. Although recent studies explored using neural network models for BioNER to free experts from manual feature engineering, the performance remains limited by the available training data for each entity type.ResultsWe propose a multi-task learning framework for BioNER to collectively use the training data of different types of entities and improve the performance on each of them. In experiments on 15 benchmark BioNER datasets, our multi-task model achieves substantially better performance compared with state-of-the-art BioNER systems and baseline neural sequence labeling models. Further analysis shows that the large performance gains come from sharing character- and word-level information among relevant biomedical entities across differently labeled corpora.AvailabilityOur source code is available athttps://github.com/yuzhimanhua/lm-lstm-crf.Contactxwang174@illinois.edu,xiangren@usc.edu.
Exploratory re-encoding of Yellow Fever Virus genome: new insights for the design of live-attenuated viruses
Authors: Klitting R. , Riziki T. , Moureau G. , Piorkowski G. , Gould E. A. , de Lamballerie X. 
Published: February 2018

AbstractVirus attenuation by genome re-encoding is a pioneering approach for generating effective live-attenuated vaccine candidates. Its core principle is to introduce a large number of synonymous substitutions into the viral genome to produce stable attenuation of the targeted virus. Introduction of large numbers of mutations has also been shown to maintain stability of the attenuated phenotype by lowering the risk of reversion and recombination of re-encoded genomes. Identifying mutations with low fitness cost is pivotal as this increases the number that can be introduced and generates more stable and attenuated viruses. Here, we sought to identify mutations with low deleterious impact on thein vivoreplication and virulence of yellow fever virus (YFV). Following comparative bioinformatic analyses of flaviviral genomes, we categorized synonymous transition mutations according to their impact on CpG/UpA composition and secondary RNA structures. We then designed 17 re-encoded viruses with 100-400 synonymous mutations in the NS2A-to-NS4B coding region of YFVAsibiandAp7M(hamster-adapted) genomes. Each virus contained a panel of synonymous mutations designed according to the above categorisation criteria. The replication and fitness characteristics of parent and re-encoded viruses were comparedin vitrousing cell culture competition experiments.In vivolaboratory hamster models were also used to compare relative virulence and immunogenicity characteristics. Most of the re-encoded strains showed no decrease in replicative fitnessin vitro. However, they showed reduced virulence and, in some instances, decreased replicative fitnessin vivo. Importantly, the most attenuated of the re-encoded strains induced robust, protective immunity in hamsters following challenge withAp7M, a virulent virus. Overall, the introduction of transitions with no or a marginal increase in the number of CpG/UpA dinucleotides had the mildest impact on YFV replication and virulencein vivo. Thus, this strategy can be incorporated in procedures for the finely tuned creation of substantially re-encoded viral genomes.
Ethical Shades of Gray: Questionable Research Practices in Health Professions Education
Authors: Artino Anthony R. , Driessen Erik W. , Maggio Lauren A. 
Published: February 2018

AbstractPurposeTo maintain scientific integrity and engender public confidence, research must be conducted responsibly. Whereas scientific misconduct, like data fabrication, is clearly irresponsible and unethical, other behaviors—often referred to as questionable research practices (QRPs)—exploit the ethical shades of gray that color acceptable practice. This study aimed to measure the frequency of self-reported QRPs in a diverse, international sample of health professions education (HPE) researchers.MethodIn 2017, the authors conducted an anonymous, cross-sectional survey study. The web-based survey contained 43 QRP items that asked respondents to rate how often they had engaged in various forms of scientific misconduct. The items were adapted from two previously published surveys.ResultsIn total, 590 HPE researchers took the survey. The mean age was 46 years (SD=11.6), and the majority of participants were from the United States (26.4%), Europe (23.2%), and Canada (15.3%). The three most frequently reported QRPs were adding authors to a paper who did not qualify for authorship (60.6%), citing articles that were not read (49.5%), and selectively citing papers to please editors or reviewers (49.4%). Additionally, respondents reported misrepresenting a participant’s words (6.7%), plagiarizing (5.5%), inappropriately modifying results (5.3%), deleting data without disclosure (3.4%), and fabricating data (2.4%). Overall, 533 (90.3%) respondents reported at least one QRP.ConclusionsNotwithstanding the methodological limitations of survey research, these findings indicate that a substantial proportion of HPE researchers report a range of QRPs. In light of these results, reforms are needed to improve the credibility and integrity of the HPE research enterprise.“Researchers should practice research responsibly. Unfortunately, some do not.” –Nicholas H. Steneck, 20061
KLF6 and STAT3 co-occupy regulatory DNA and functionally synergize to promote axon growth in CNS neurons
Authors: Wang Zimei , Mehra Vatsal , Simpson Matthew.T. , Maunze Brian , Holan Lyndsey , Eastwood Erik , Blackmore Murray G. , Venkatesh Ishwariya 
Published: February 2018

ABSTRACTMembers of the KLF family of transcription factors can exert both positive and negative effects on axon regeneration in the central nervous system, but the underlying mechanisms are unclear. KLF6 and −7 share nearly identical DNA binding domains and stand out as the only known growth-promoting family members. Here we confirm that similar to KLF7, expression of KLF6 declines during postnatal cortical development and that forced re-expression of KLF6 in corticospinal tract neurons of adult female mice enhances axon regeneration after cervical spinal injury. Unlike KLF7, however, these effects were achieved with wildtype KLF6, as opposed constitutively active mutants, thus simplifying the interpretation of mechanistic studies. To clarify the molecular basis of growth promotion, RNA sequencing identified 454 genes whose expression changed upon forced KLF6 expression in cortical neurons. Network analysis of these genes revealed sub-networks of downregulated genes that were highly enriched for synaptic functions, and sub-networks of upregulated genes with functions relevant to axon extension including cytoskeleton remodeling, lipid synthesis and transport, and bioenergetics. The promoter regions of KLF6-sensitive genes showed enrichment for the binding sequence of STAT3, a previously identified regeneration-associated gene. Notably, co-expression of constitutively active STAT3 along with KLF6 in cortical neurons produced synergistic increases in neurite length. Finally, genome-wide ATAC-seq footprinting detected frequent co-binding by the two factors in pro-growth gene networks, indicating co-occupancy as an underlying mechanism for the observed synergy. These findings advance understanding of KLF-stimulated axon growth and indicate functional synergy of KLF6 transcriptional effects with those of STAT3.SIGNIFICANCE STATEMENTThe failure of axon regeneration in the CNS limits recovery from damage and disease. These findings show the transcription factor KLF6 to be a potent promoter of axon growth after spinal injury, and more importantly clarify the underlying transcriptional changes. In addition, bioinformatics analysis predicted a functional interaction between KLF6 and a second transcription factor, STAT3, and genome-wide footprinting confirmed frequent co-occupancy. Co-expression of the two factors yielded synergistic elevation of neurite growth in primary neurons. These data point the way toward novel transcriptional interventions to promote CNS regeneration.