bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determinants of translation ambiguity
Authors: Degani Tamar , Prior Anat , Eddington Chelsea M. , Arêas da Luz Fontes Ana B. , Tokowicz Natasha 
Published: January 2016

Abstract
Ambiguity in translation is highly prevalent, and has consequences for second-language learning and for bilingual lexical processing. To better understand this phenomenon, the current study compared the determinants of translation ambiguity across four sets of translation norms from English to Spanish, Dutch, German and Hebrew. The number of translations an English word received was correlated across these different languages, and was also correlated with the number of senses the word has in English, demonstrating that translation ambiguity is partially determined by within-language semantic ambiguity. For semantically-ambiguous English words, the probability of the different translations in Spanish and Hebrew was predicted by the meaning-dominance structure in English, beyond the influence of other lexical and semantic factors, for bilinguals translating from their L1, and translating from their L2. These findings are consistent with models postulating direct access to meaning from L2 words for moderately-proficient bilinguals.
An exploratory study using an openEHR 2-level modeling approach to represent common data elements
Authors: Lin Ching-Heng , Fann Yang-Cheng , Liou Der-Ming 
Published: January 2016

Abstract
Background and Objective In order to facilitate clinical research across multiple institutions, data harmonization is a critical requirement. Common data elements (CDEs) collect data uniformly, allowing data interoperability between research studies. However, structural limitations have hindered the application of CDEs. An advanced modeling structure is needed to rectify such limitations. The openEHR 2-level modeling approach has been widely implemented in the medical informatics domain. The aim of our study is to explore the feasibility of applying an openEHR approach to model the CDE concept.
Materials and Methods Using the National Institute of Neurological Disorders and Stroke General CDEs as material, we developed a semiautomatic mapping tool to assist domain experts mapping CDEs to existing openEHR archetypes in order to evaluate their coverage and to allow further analysis. In addition, we modeled a set of CDEs using the openEHR approach to evaluate the ability of archetypes to structurally represent any type of CDE content.
Results Among 184 CDEs, 28% (51) of the archetypes could be directly used to represent CDEs, while 53% (98) of the archetypes required further development (extension or specialization). A comprehensive comparison between CDEs and openEHR archetypes was conducted based on the lessons learnt from the practical modeling.
Discussion CDEs and archetypes have dissimilar modeling approaches, but the data structure of both models are essentially similar. This study proposes to develop a comprehensive structure to model CDE concepts instead of improving the structure of CED.
Conclusion The findings from this research show that the openEHR archetype has structural coverage for the CDEs, namely the openEHR archetype is able to represent the CDEs and meet the functional expectations of the CDEs. This work can be used as a reference when improving CDE structure using an advanced modeling approach.
Self-monitoring practices, attitudes, and needs of individuals with bipolar disorder: implications for the design of technologies to manage mental health
Authors: Murnane Elizabeth L , Cosley Dan , Chang Pamara , Guha Shion , Frank Ellen , Gay Geri , Matthews Mark 
Published: January 2016

Objective To understand self-monitoring strategies used independently of clinical treatment by individuals with bipolar disorder (BD), in order to recommend technology design principles to support mental health management.Materials and Methods Participants with BD (N = 552) were recruited through the Depression and Bipolar Support Alliance, the International Bipolar Foundation, and WeSearchTogether.org to complete a survey of closed- and open-ended questions. In this study, we focus on descriptive results and qualitative analyses.Results Individuals reported primarily self-monitoring items related to their bipolar disorder (mood, sleep, finances, exercise, and social interactions), with an increasing trend towards the use of digital tracking methods observed. Most participants reported having positive experiences with technology-based tracking because it enables self-reflection and agency regarding health management and also enhances lines of communication with treatment teams. Reported challenges stem from poor usability or difficulty interpreting self-tracked data.Discussion Two major implications for technology-based self-monitoring emerged from our results. First, technologies can be designed to be more condition-oriented, intuitive, and proactive. Second, more automated forms of digital symptom tracking and intervention are desired, and our results suggest the feasibility of detecting and predicting emotional states from patterns of technology usage. However, we also uncovered tension points, namely that technology designed to support mental health can also be a disruptor.Conclusion This study provides increased understanding of self-monitoring practices, attitudes, and needs of individuals with bipolar disorder. This knowledge bears implications for clinical researchers and practitioners seeking insight into how individuals independently self-manage their condition as well as for researchers designing monitoring technologies to support mental health management.
Using the electronic health record for assessment of health insurance in community health centers
Authors: Hatch Brigit , Tillotson Carrie , Angier Heather , Marino Miguel , Hoopes Megan , Huguet Nathalie , DeVoe Jennifer 
Published: January 2016

Abstract
Objective To demonstrate use of the electronic health record (EHR) for health insurance surveillance and identify factors associated with lack of coverage.
Materials and Methods Using EHR data, we conducted a retrospective, longitudinal cohort study of adult patients ( n  = 279 654) within a national network of community health centers during a 2-year period (2012–2013).
Results Factors associated with higher odds of being uninsured (vs Medicaid-insured) included: male gender, age &gt;25 years, Hispanic ethnicity, income above the federal poverty level, and rural residence ( P  &lt; .01 for all). Among patients with no insurance at their initial visit ( n  = 114 000), 50% remained uninsured for every subsequent visit.
Discussion During the 2 years prior to 2014, many patients utilizing community health centers were unable to maintain stable health insurance coverage.
Conclusion As patients gain access to health insurance under the Affordable Care Act, the EHR provides a novel approach to help track coverage and support vulnerable patients in gaining and maintaining coverage.
Satellite accretion in action: a tidally disrupting dwarf spheroidal around the nearby spiral galaxy NGC 253
Authors: Romanowsky Aaron J. , Martínez-Delgado David , Martin Nicolas F. , Morales Gustavo , Jennings Zachary G. , GaBany R. Jay , Brodie Jean P. , Grebel Eva K. , Schedler Johannes , Sidonio Michael 
Published: January 2016

Abstract
We report the discovery of NGC 253-dw2, a dwarf spheroidal (dSph) galaxy candidate undergoing tidal disruption around a nearby spiral galaxy, NGC 253 in the Sculptor group: the first such event identified beyond the Local Group. The dwarf was found using small-aperture amateur telescopes, and followed up with Suprime-Cam on the 8 m Subaru Telescope in order to resolve its brightest stars. Using g- and Rc-band photometry, we detect a red giant branch consistent with an old, metal-poor stellar population at a distance of ∼3.5 Mpc. From the distribution of likely member stars, we infer a highly elongated shape with a semimajor axis half-light radius of (2 ± 0.4) kpc. Star counts also yield a luminosity estimate of ∼2 × 106 L⊙,V (MV ∼ −10.7). The morphological properties of NGC 253-dw2 mark it as distinct from normal dSphs and imply ongoing disruption at a projected distance of ∼50 kpc from the main galaxy. Our observations support the hierarchical paradigm wherein massive galaxies continuously accrete less massive ones, and provide a new case study for dSph infall and dissolution dynamics. We also note the continued efficacy of small telescopes for making big discoveries.
Mitochondrial DNA
Authors: Schäfer Simon T. , Franken Lars , Adamzik Michael , Schumak Beatrix , Scherag André , Engler Andrea , Schönborn Niels , Walden Jennifer , Koch Susanne , Baba Hideo A. , Steinmann Jörg , Westendorf Astrid M. , Fandrey Joachim , Bieber Thomas , Kurts Christian , Frede Stilla , Peters Jürgen , Limmer Andreas 
Published: January 2016

AbstractAbstract
Mitochondrial DNA (mtDNA) serum concentrations of the mitochondrial genes D-Loop and adenosine triphosphatase 6 were determined (quantitative polymerase chain reaction) in 165 septic patients and 50 healthy volunteers. Furthermore, cytotoxic T-cell activity was analyzed in wild-type and TLR9 knockout mice, with/without previous mtDNA administration, followed by injection of an ovalbumin-expressing adenoviral vector. It was found that mtDNA concentration is increased in sepsis and, besides inflammatory effects, has powerful immunosuppressive effects and can evoke immunosuppression on its own.

Background
Critically ill patients are at high risk to suffer from sepsis, even in the absence of an initial infectious source, but the molecular mechanisms for their increased sepsis susceptibility, including a suppressed immune system, remain unclear. Although microbes and pathogen-associated molecular pattern are accepted inducers of sepsis and septic immunosuppression, the role of endogenous Toll-like receptor (TLR) ligands, such as mitochondrial DNA (mtDNA), in altering the immune response is unknown.

Methods
Mitochondrial DNA serum concentrations of the mitochondrial genes D-Loop and adenosine triphosphatase 6 were determined (quantitative polymerase chain reaction) in 165 septic patients and 50 healthy volunteers. Furthermore, cytotoxic T-cell activity was analyzed in wild-type and TLR9 knockout mice, with/without previous mtDNA administration, followed by injection of an ovalbumin-expressing adenoviral vector.

Results
Mitochondrial DNA serum concentrations were increased in septic patients (adenosine triphosphatase 6, 123-fold; D-Loop, 76-fold, P < 0.0001) compared with volunteers. Furthermore, a single mtDNA injection caused profound, TLR9-dependent immunosuppression of adaptive T-cell cytotoxicity in wild-type but not in TLR9 knockout mice and evoked various immunosuppressive mechanisms including the destruction of the splenic microstructure, deletion of cross-presenting dendritic cells, and up-regulation of programmed cell death ligand 1 and indoleamine 2,3-dioxygenase. Several of these findings in mice were mirrored in septic patients, and mtDNA concentrations were associated with an increased 30-day mortality.

Conclusions
The findings of this study imply that mtDNA, an endogenous danger associated molecular pattern, is a hitherto unknown inducer of septic immunoparalysis and one possible link between initial inflammation and subsequent immunosuppression in critically ill patients.
Resolvin D1 Inhibits Mechanical Hypersensitivity in Sciatica by Modulating the Expression of Nuclear Factor-κB, Phospho-extracellular Signal–regulated Kinase, and Pro- and Antiinflammatory Cytokines in the Spinal Cord and Dorsal Root Ganglion
Authors: Liu Zhi-hua , Miao Gui-shen , Wang Jun-nan , Yang Cong-xian , Fu Zhi-jian , Sun Tao 
Published: January 2016

AbstractAbstract
Nucleus pulposus induced a significant inflammatory response in dorsal root ganglia. Resolvin significantly suppressed this inflammatory response and reduced mechanical allodynia for up to 3 weeks. The data suggest that resolvins might serve as novel therapeutic agents for the treatment of neuropathic pain.

Background
Accumulating evidence indicates that spinal inflammatory and immune responses play an important role in the process of radicular pain caused by intervertebral disk herniation. Resolvin D1 (RvD1) has been shown to have potent antiinflammatory and antinociceptive effects. The current study was undertaken to investigate the analgesic effect of RvD1 and its underlying mechanism in rat models of noncompressive lumbar disk herniation.

Methods
Rat models of noncompressive lumber disk herniation were established, and mechanical thresholds were evaluated using the von Frey test during an observation period of 21 days (n = 8/group). Intrathecal injection of vehicle or RvD1 (10 or 100 ng) was performed for three successive postoperative days. On day 7, the ipsilateral spinal dorsal horns and L5 dorsal root ganglions (DRGs) were removed to assess the expressions of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-10, and transforming growth factor-β1 (TGF-β1) and the activation of nuclear factor-κB (NF-κB)/p65 and phospho-extracellular signal–regulated kinase (p-ERK) signaling (n = 30/group).

Results
The application of nucleus pulposus to L5 DRG induced prolonged mechanical allodynia, inhibited the production of IL-10 and TGF-β1, and up-regulated the expression of TNF-α, IL-1β, NF-κB/p65, and p-ERK in the spinal dorsal horns and DRGs. Intrathecal injection of RvD1 showed a potent analgesic effect, inhibited the up-regulation of TNF-α and IL-1β, increased the release of IL-10 and TGF-β1, and attenuated the expression of NF-κB/p65 and p-ERK in a dose-dependent manner.

Conclusions
The current study showed that RvD1 might alleviate neuropathic pain via regulating inflammatory mediators and NF-κB/p65 and p-ERK pathways. Its antiinflammatory and proresolution properties may offer novel therapeutic approaches for the management of neuropathic pain.
Propofol-induced Inhibition of Catecholamine Release Is Reversed by Maintaining Calcium Influx
Authors: Han Liping , Fuqua Stephen , Li Quanlin , Zhu Liyu , Hao Xiaoyan , Li Aiping , Gupta Sangeeta , Sandhu Ravinder , Lonart György , Sugita Shuzo 
Published: January 2016

AbstractAbstract
Clinically relevant concentrations of propofol (10 to 30 μM) indeed inhibited the depolarization (by K+)-dependent norepinephrine release in cultured PC12 cells (which are derived from rat adrenal chromaffin cells) and synaptosomes. Unexpectedly, the same propofol concentrations that inhibited depolarization-dependent norepinephrine release increased ionomycin (a Ca2+ ionophore)-triggered catecholamine release in a Ca2+-dependent manner. The Ca2+-dependent propofol-induced increase in ionomycin-triggered catecholamine release was abolished in the presence of the Ca2+ chelator, EGTA.

Background
Propofol (2,6-diisopropylphenol) is one of the most frequently used anesthetic agents. One of the main side effects of propofol is to reduce blood pressure, which is thought to occur by inhibiting the release of catecholamines from sympathetic neurons. Here, the authors hypothesized that propofol-induced hypotension is not simply the result of suppression of the release mechanisms for catecholamines.

Methods
The authors simultaneously compared the effects of propofol on the release of norepinephrine triggered by high K+-induced depolarization, as well as ionomycin, by using neuroendocrine PC12 cells and synaptosomes. Ionomycin, a Ca2+ ionophore, directly induces Ca2+ influx, thus bypassing the effect of ion channel modulation by propofol.

Results
Propofol decreased depolarization (high K+)-triggered norepinephrine release, whereas it increased ionomycin-triggered release from both PC12 cells and synaptosomes. The propofol (30 μM)-induced increase in norepinephrine release triggered by ionomycin was dependent on both the presence and the concentration of extracellular Ca2+ (0.3 to 10 mM; n = 6). The enhancement of norepinephrine release by propofol was observed in all tested concentrations of ionomycin (0.1 to 5 μM; n = 6).

Conclusions
Propofol at clinically relevant concentrations promotes the catecholamine release as long as Ca2+ influx is supported. This unexpected finding will allow for a better understanding in preventing propofol-induced hypotension.
Classically Activated Macrophages Protect against Lipopolysaccharide-induced Acute Lung Injury by Expressing Amphiregulin in Mice
Authors: Xu Younian , Meng Chen , Liu Guilin , Yang Dong , Fu Lisha , Zhang Min , Zhang Zhao , Xia Huimin , Yao Shanglong , Zhang Shihai 
Published: January 2016

AbstractAbstract
Amphiregulin was expressed in alveolar macrophages after acute lung injury. Exogenous amphiregulin protected, whereas amphiregulin antibodies exacerbated lung injury. The results are consistent with the notion up-regulation of amphiregulin in activated alveolar macrophages can exert a protective effect on the lung tissue in a model of acute lung injury.
Supplemental Digital Content is available in the text.

Background
Alveolar macrophages (AMs) activated into M1 phenotype are involved in the development of lipopolysaccharide-induced acute lung injury (ALI). However, whether AMs express amphiregulin and what roles amphiregulin plays in lipopolysaccharide-induced ALI remain poorly understood.

Methods
Acute lung injury was induced by intratracheal instillation of lipopolysaccharide in male C57BL/6 mice. Lung injury scores, level of protein, and level of neutrophils in bronchial alveolar lavage fluid of lipopolysaccharide-induced ALI mice were compared with those in mice challenged with recombinant exogenous amphiregulin and antiamphiregulin antibody. Amphiregulin expression in macrophages and neutrophils in bronchial alveolar lavage fluid of lipopolysaccharide-induced ALI mice was determined by using immunofluorescence technique and further detected in M0, M1, and M2 phenotypes of both peritoneal macrophages and AMs. The effect of amphiregulin on apoptosis of MLE12 cells and activation of epithelial growth factor receptor-AKT pathway were, respectively, examined by using flow cytometry and western blotting.

Results
Alveolar macrophages were found to highly express amphiregulin in ALI mice. Amphiregulin neutralization aggravated, whereas recombinant exogenous amphiregulin attenuated lipopolysaccharide-induced ALI in mice (n = 6). In cultured AMs and peritoneal macrophages, amphiregulin was mainly generated by M1, rather than M0 or M2 phenotype (n = 5). Apoptosis ratio of lipopolysaccharide-challenged MLE12 cells was significantly reduced by recombinant exogenous amphiregulin from 16.60 ± 1.82 to 9.47 ± 1.67% (n = 5) but significantly increased from 17.45 ± 1.13 to 21.67 ± 1.10% (n = 5) after stimulation with supernatant of M1-polarized AM media conditioned with amphiregulin-neutrolizing antibody. Western blotting revealed that amphiregulin activated epithelial growth factor receptor and AKT in the lung tissues and MLE12 cells (n = 5).

Conclusions
Different from the common notion that classically activated AMs have just a detrimental effect on the lung tissues, the results of this study showed that classically activated AMs also exerted a protective effect on the lung tissues by producing high-level amphiregulin in lipopolysaccharide-induced ALI.
Anesthesia-induced Suppression of Human Dorsal Anterior Insula Responsivity at Loss of Volitional Behavioral Response
Authors: Warnaby Catherine Elizabeth , Seretny Marta , Ní Mhuircheartaigh Roísín , Rogers Richard , Jbabdi Saad , Sleigh Jamie , Tracey Irene 
Published: January 2016

AbstractAbstract
Simultaneous electroencephalography and functional magnetic resonance imaging in 15 healthy volunteers undergoing ultraslow induction of propofol anesthesia identified suppression of stimulus-evoked activity in the right dorsal anterior insula cortex coincident with reduced functional connectivity with frontoparietal regions at loss of responsiveness. The dorsal anterior insula cortex is a potential cortical gate underlying loss of responsiveness that might mediate subsequent loss of functional connectivity and information integration at deeper levels of anesthesia.

Background
It has been postulated that a small cortical region could be responsible for the loss of behavioral responsiveness (LOBR) during general anesthesia. The authors hypothesize that any brain region demonstrating reduced activation to multisensory external stimuli around LOBR represents a key cortical gate underlying this transition. Furthermore, the authors hypothesize that this localized suppression is associated with breakdown in frontoparietal communication.

Methods
During both simultaneous electroencephalography and functional magnetic resonance imaging (FMRI) and electroencephalography data acquisition, 15 healthy volunteers experienced an ultraslow induction with propofol anesthesia while a paradigm of multisensory stimulation (i.e., auditory tones, words, and noxious pain stimuli) was presented. The authors performed separate analyses to identify changes in (1) stimulus-evoked activity, (2) functional connectivity, and (3) frontoparietal synchrony associated with LOBR.

Results
By using an FMRI conjunction analysis, the authors demonstrated that stimulus-evoked activity was suppressed in the right dorsal anterior insula cortex (dAIC) to all sensory modalities around LOBR. Furthermore, the authors found that the dAIC had reduced functional connectivity with the frontoparietal regions, specifically the dorsolateral prefrontal cortex and inferior parietal lobule, after LOBR. Finally, reductions in the electroencephalography power synchrony between electrodes located in these frontoparietal regions were observed in the same subjects after LOBR.

Conclusions
The authors conclude that the dAIC is a potential cortical gate responsible for LOBR. Suppression of dAIC activity around LOBR was associated with disruption in the frontoparietal networks that was measurable using both electroencephalography synchrony and FMRI connectivity analyses.