bluuebunny/crossref_metadata_2025_split huggingface dataset:
Emergency Computed Tomography Predicts Caustic Esophageal Stricture Formation
Authors: Bruzzi Matthieu , Chirica Mircea , Resche-Rigon Matthieu , Corte Helene , Voron Thibault , Sarfati Emile , Zagdanski Anne-Marie , Cattan Pierre 
Published: March 2018

Background:
Endoscopy is the best predictor of stricture formation after caustic ingestion.

Objective:
Our aim was to compare the accuracy of emergency computed tomography (CT) and endoscopy in predicting risks of esophageal stricture.

Methods:
We describe a CT classification of esophageal caustic injuries: Grade I show normal esophagus; Grade IIa display internal enhancement of the esophageal mucosa and enhancement of the outer wall conferring a “target” aspect; Grade IIb present as a fine rim of external esophageal wall enhancement. In 152 patients (56 males, median age 45) who underwent esophageal preservation after caustic ingestion we compared the accuracy of the CT and endoscopic (Zargar) classifications in predicting esophageal stricture.

Results:
On endoscopy esophageal injuries were classified as grade 1 (n = 50; 33%), grade 2a (n = 11; 7%), grade 2b (n = 19; 13%), grade 3a (n = 14; 9%), and grade 3b (n = 58; 38%). On CT, 47 (31%) patients had grade I, 47 (31%) had grade IIa and 58 (38%) had grade IIb esophageal injuries. Fifty-six (37%) patients developed esophageal strictures. The risk of esophageal stricture formation was 0%, 17%, and 83%, for grade I, IIa, and IIb CT injuries and 0, 0, 28, 50, and 76% for endoscopic grade 1, 2a, 2b, and 3a and 3b injuries, respectively. ROC curve analysis at 120 days after ingestion showed that CT outperformed endoscopy in predicting stricture formation (AUC: 85.1 [95% CI, 74.9–95.3] vs 77.8 [95% CI, 66.5–89.0], P = 0.047) and did just as well as a combined CT-endoscopy algorithm (AUC: 85.8 [95% CI, 76.5–95.0] vs 85.1 [95% CI, 74.9–95.3], P = 0.73).

Conclusion:
Emergency CT outperforms endoscopy in predicting esophageal stricture formation after caustic ingestion. Emergency endoscopy evaluation after caustic ingestion is not indispensable.
Health hazards to wild birds and risk factors associated with anthropogenic food provisioning
Authors: Lawson Becki , Robinson Robert A. , Toms Mike P. , Risely Kate , MacDonald Susan , Cunningham Andrew A. 
Published: March 2018

Provision of supplementary food for wild birds at garden feeding stations is a common, large-scale and year-round practice in multiple countries including Great Britain (GB). While these additional dietary resources can benefit wildlife, there is a concomitant risk of disease transmission, particularly when birds repeatedly congregate in the same place at high densities and through interactions of species that would not normally associate in close proximity. Citizen science schemes recording garden birds are popular and can integrate disease surveillance with population monitoring, offering a unique opportunity to explore inter-relationships between supplementary feeding, disease epidemiology and population dynamics. Here, we present findings from a national surveillance programme in GB and note the dynamism of endemic and emerging diseases over a 25-year period, focusing on protozoal (finch trichomonosis), viral (Paridae pox) and bacterial (passerine salmonellosis) diseases with contrasting modes of transmission. We also examine the occurrence of mycotoxin contamination of food residues in bird feeders, which present both a direct and indirect (though immunosuppression) risk to wild bird health. Our results inform evidence-based mitigation strategies to minimize anthropogenically mediated health hazards, while maintaining the benefits of providing supplementary food for wild birds.
This article is part of the theme issue ‘Anthropogenic resource subsidies and host–parasite dynamics in wildlife’.
Consequences of resource supplementation for disease risk in a partially migratory population
Authors: Brown Leone M. , Hall Richard J. 
Published: March 2018

Anthropogenic landscape features such as urban parks and gardens, landfills and farmlands can provide novel, seasonally reliable food sources that impact wildlife ecology and distributions. In historically migratory species, food subsidies can cause individuals to forgo migration and form partially migratory or entirely sedentary populations, eroding a crucial benefit of migration: pathogen avoidance through seasonal abandonment of transmission sites and mortality of infected individuals during migration. Since many migratory taxa are declining, and wildlife populations in urban areas can harbour zoonotic pathogens, understanding the mechanisms by which anthropogenic resource subsidies influence infection dynamics and the persistence of migration is important for wildlife conservation and public health. We developed a mathematical model for a partially migratory population and a vector-borne pathogen transmitted at a shared breeding ground, where food subsidies increase the nonbreeding survival of residents. We found that higher resident nonbreeding survival increased infection prevalence in residents and migrants, and lowered the fraction of the population that migrated. The persistence of migration may be especially threatened if residency permits emergence of more virulent pathogens, if resource subsidies reduce costs of infection for residents, and if infection reduces individual migratory propensity.This article is part of the theme issue ‘Anthropogenic resource subsidies and host–parasite dynamics in wildlife’.
Assessing the direct and indirect effects of food provisioning and nutrient enrichment on wildlife infectious disease dynamics
Authors: Civitello David J. , Allman Brent E. , Morozumi Connor , Rohr Jason R. 
Published: March 2018

Anthropogenic resource supplementation can shape wildlife disease directly by altering the traits and densities of hosts and parasites or indirectly by stimulating prey, competitor or predator species. We first assess the direct epidemiological consequences of supplementation, highlighting the similarities and differences between food provisioning and two widespread forms of nutrient input: agricultural fertilization and aquatic nutrient enrichment. We then review an aquatic disease system and a general model to assess whether predator and competitor species can enhance or overturn the direct effects of enrichment. All forms of supplementation can directly affect epidemics by increasing host population size or altering parasite production within hosts, but food provisioning is most likely to aggregate hosts and increase parasite transmission. However, if predators or competitors increase in response to supplementation, they could alter resource-fuelled outbreaks in focal hosts. We recommend identifying the traits of hosts, parasites or interacting species that best predict epidemiological responses to supplementation and evaluating the relative importance of these direct and indirect mechanisms. Theory and experiments should examine the timing of behavioural, physiological and demographic changes for realistic, variable scenarios of supplementation. A more integrative view of resource supplementation and wildlife disease could yield broadly applicable disease management strategies.
This article is part of the theme issue ‘Anthropogenic resource subsidies and host–parasite dynamics in wildlife’.
High affinity Na+ transport by wheat HKT1;5 is blocked by K+
Authors: Xu Bo , Hrmova Maria , Gilliham Matthew 
Published: March 2018

AbstractThe wheat sodium transporters TmHKT1;5-A and TaHKT1;5-D are encoded by genes underlying major shoot Na+ exclusion loci Nax2 and Kna1 from Triticum monococcum (Tm) and Triticum aestivum (Ta), respectively. In contrast to HKT2 transporters that have been shown to exhibit high affinity K+-dependent Na+ transport, HKT1 proteins have, with one exception, only been shown to catalyse low affinity Na+ transport and no K+ transport. Here, using heterologous expression in Xenopus laevis oocytes we show that both TmHKT1;5-A and TaHKT1;5-D encode dual (high and low) affinity Na+-transporters with the high-affinity component being abolished when external K+ is in excess of external Na+. Based on 3-D structural modelling we propose that tighter binding of K+, compared to that of Na+ in the selectivity filter region by means of additional van der Waals forces, explains the K+ block at the molecular level. The low-affinity component for Na+ transport of TmHKT1;5-A had a lower Km than that of TaHKT1;5-D and was less sensitive to external K+. We propose that these properties underpin the improvements in shoot Na+-exclusion and crop plant salt tolerance following the introgression of TmHKT1;5-A into diverse wheat backgrounds.
Principles of Computer Numerical Controlled Machining Applied to Cranial Microsurgery
Authors: Ghanbari Leila , Rynes Mathew , Hu Jay Jia , Shulman Daniel Sousa , Johnson Gregory , Laroque Micheal , Shull Gabriella , Kodandaramaiah Suhasa B. 
Published: March 2018

ABSTRACTOver the last decade, a plethora of tools have been developed for neuroscientists to interface with the brain. Implementing these tools requires precise removal of sections of the skull to access the brain. These delicate cranial microsurgical procedures need to be performed on sub-millimeter thick bone without damaging the underlying tissue and therefore, require significant training. Automating some of these procedures would not only enable more precise microsurgical operations, but also democratize use of advanced neurotechnologies. Here, we describe the ‘Craniobot’, a cranial microsurgery platform that combines automated skull surface profiling with a computer numerical controlled (CNC) milling machine to perform a variety of cranial microsurgical procedures in mice. The Craniobot utilizes a low force contact sensor to profile the skull surface and uses this information to perform micrometer-scale precise milling operations within minutes. We have used the Craniobot to drill pilot holes to anchor cranial implants, perform skull thinning, and open small to large craniotomies. The Craniobot is built using off-the-shelf components for under $1000 and is controlled using open-source CNC programming software.
CRISPR-Tag: an Efficient DNA Tagging System in Living Cells
Authors: Chen Baohui , Zou Wei , Huang Bo 
Published: March 2018

Main textA lack of efficient tools to image non-repetitive genes in living cells has limited our ability to explore the functional impact of spatiotemporal dynamics of genes. Here, we addressed this issue by developing the CRISPR-Tag system as a new DNA tagging strategy to label protein-coding genes with high signal-to-noise ratio under wild-field fluorescence microscopy by using 1 to 4 highly active sgRNAs. The CRISPR-Tag, with minimal size of ∼ 250 bp, represents an easily and broadly applicable technique to study spatiotemporal organization of genomic elements in living cells.
Synaptic plasticity onto inhibitory neurons as a mechanism for ocular dominance plasticity
Authors: Bono Jacopo , Clopath Claudia 
Published: March 2018

AbstractOcular dominance plasticity is a well-documented phenomenon allowing us to study properties of cortical maturation. Understanding this maturation might be an important step towards unravelling how cortical circuits function. However, it is still not fully understood which mechanisms are responsible for the opening and closing of the critical period for ocular dominance and how changes in cortical responsiveness arise after visual deprivation. In this article, we present a theory of ocular dominance plasticity. Following recent experimental work, we propose a framework where a reduction in inhibition is necessary for ocular dominance plasticity in both juvenile and adult animals. In this framework, two ingredients are crucial to observe ocular dominance shifts: a sufficient level of inhibition as well as excitatory-to-inhibitory synaptic plasticity. In our model, the former is responsible for the opening of the critical period, while the latter limits the plasticity in adult animals. Finally, we also provide a possible explanation for the variability in ocular dominance shifts observed in individual neurons and for the counter-intuitive shifts towards the closed eye.
Neuronal signature of social novelty exploration in the VTA: implication for Autism Spectrum Disorder
Authors: Bariselli Sebastiano , Hörnberg Hanna , Prévost-Solié Clément , Musardo Stefano , Hatstatt-Burkle Laetitia , Scheiffele Peter , Bellone Camilla 
Published: March 2018

AbstractNovel stimuli attract our attention, promote exploratory behavior, and facilitate learning. Atypical habituation and aberrant novelty exploration have been related with the severity of Autism Spectrum Disorders (ASD) but the underlying neuronal circuits are unknown. Here, we report that dopamine (DA) neurons of the ventral tegmental area (VTA) promote the behavioral responses to novel social stimuli, support preference for social novelty, and mediate the reinforcing properties of novel social interaction. Social novelty exploration is associated with the insertion of calcium-permeable GluA2-lacking AMPA-type glutamate receptors at excitatory synapses on VTA DA neurons. These novelty-dependent synaptic adaptations only persist upon repeated exposure to social stimuli and sustain social interaction. Global or DA neuron-specific inactivation of the ASD risk gene Neuroligin3 alters both social novelty exploration and the reinforcing properties of social stimuli. These behavioral deficits are accompanied by an aberrant expression of non-canonical GluA2-lacking AMPA-receptors at excitatory synapses on VTA DA neurons and an occlusion of novelty-induced synaptic plasticity. Altogether, these findings causally link impaired novelty exploration in an ASD mouse model to VTA DA circuit dysfunction.
clusterExperiment and RSEC: A Bioconductor package and framework for clustering of single-cell and other large gene expression datasets
Authors: Risso Davide , Purvis Liam , Fletcher Russell , Das Diya , Ngai John , Dudoit Sandrine , Purdom Elizabeth 
Published: March 2018

AbstractClustering of genes and/or samples is a common task in gene expression analysis. The goals in clustering can vary, but an important scenario is that of finding biologically meaningful subtypes within the samples. This is an application that is particularly appropriate when there are large numbers of samples, as in many human disease studies. With the increasing popularity of single-cell transcriptome sequencing (RNA-Seq), many more controlled experiments on model organisms are similarly creating large gene expression datasets with the goal of detecting previously unknown heterogeneity within cells.It is common in the detection of novel subtypes to run many clustering algorithms, as well as rely on subsampling and ensemble methods to improve robustness. We introduce a Bioconductor R package, clusterExperiment, that implements a general and flexible strategy we entitle Resampling-based Sequential Ensemble Clustering (RSEC). RSEC enables the user to easily create multiple, competing clusterings of the data based on different techniques and associated tuning parameters, including easy integration of resampling and sequential clustering, and then provides methods for consolidating the multiple clusterings into a final consensus clustering. The package is modular and allows the user to separately apply the individual components of the RSEC procedure, i.e., apply multiple clustering algorithms, create a consensus clustering or choose tuning parameters, and merge clusters. Additionally, clusterExperimentprovides a variety of visualization tools for the clustering process, as well as methods for the identification of possible cluster signatures or biomarkers.The package clusterExperimentis publicly available through the Bioconductor Project, with a detailed manual (vignette) as well as well documented help pages for each function.
Evaluation of Whole Exome Sequencing as an Alternative of BeadChip and Whole Genome Sequencing in Human Population Genetic Analysis
Authors: Maróti Zoltán , Boldogkői Zsolt , Tombácz Dóra , Snyder Michael , Kalmár Tibor 
Published: March 2018

ABSTRACTUnderstanding the underlying genetic structure of human populations is of fundamental interest to both biological and social sciences. Advances in high-throughput genotyping technology have markedly improved our understanding of global patterns of human genetic variation. The most widely used methods for collecting variant information at the DNA-level include whole genome sequencing, which continues to remain costly, and the more economical solution of array-based techniques, as these are capable of simultaneously genotyping a pre-selected set of variable DNA sites in the human genome. The largest publicly accessible set of human genomic sequence data available today originates from exome sequencing that comprises around 1.2% of the whole genome (approximately 30 million base pairs). In this study, we compared the application of the exome dataset to the array-based dataset and to the gold standard whole genome dataset using the same population genetic analysis methods. Our results draw attention to some of the inherent problems that arise from using pre-selected SNP sets for population genetic analysis. Additionally, we demonstrate that exome sequencing provides a better alternative to the array-based methods for population genetic analysis. In this study, we propose a strategy for unbiased variant collection from exome data and offer a bioinformatics protocol for proper data processing.
The landscape of incident disease risk for the biomarker GlycA and its mortality stratification in angiography patients
Authors: Kettunen Johannes , Ritchie Scott C. , Anufrieva Olga , Lyytikäinen Leo-Pekka , Hernesniemi Jussi , Karhunen Pekka J. , Kuukasjärvi Pekka , Laurikka Jari , Kähönen Mika , Lehtimäki Terho , Havulinna Aki S. , Salomaa Veikko , Männistö Satu , Ala-Korpela Mika , Perola Markus , Inouye Michael , Würtz Peter 
Published: March 2018

AbstractIntegration of systems-level biomolecular information with electronic health records has led to the discovery of robust blood-based biomarkers predictive of future health and disease. Of recent intense interest is the GlycA biomarker, a complex nuclear magnetic resonance (NMR) spectroscopy signal reflective of acute and chronic inflammation, which predicts long term risk of diverse outcomes including cardiovascular disease, type 2 diabetes, and all-cause mortality. To systematically explore the specificity of the disease burden indicated by GlycA we analysed the risk for 468 common incident hospitalization and mortality outcomes occurring during an 8-year follow-up of 11,861 adults from Finland. Our analyses of GlycA replicated known associations, identified associations with specific cardiovascular disease outcomes, and uncovered new associations with risk of alcoholic liver disease (meta-analysed hazard ratio 2.94 per 1-SD, P=5×10-6), chronic renal failure (HR=2.47, P=3×10-6), glomerular diseases (HR=1.95, P=1×10-6), chronic obstructive pulmonary disease (HR=1.58, P=3×10-5), inflammatory polyarthropathies (HR=1.46, P=4×10-8), and hypertension (HR=1.21, P=5×10-5). We further evaluated GlycA as a biomarker in secondary prevention of 12-year cardiovascular mortality in 900 angiography patients with suspected coronary artery disease. We observed hazard ratios of 4.87 and 5.00 for 12-year mortality in angiography patients in the fourth and fifth quintiles by GlycA levels demonstrating the prognostic potential of GlycA for identification of high mortality-risk individuals. Both GlycA and C-reactive protein had shared as well as independent contributions to mortality hazard, emphasising the importance of chronic inflammation in secondary prevention of cardiovascular disease.
Causal evidence for mnemonic metacognition in human precuneus
Authors: Ye Qun , Zou Futing , Lau Hakwan , Hu Yi , Kwok Sze Chai 
Published: March 2018

AbstractMetacognition is the capacity to introspectively monitor and control one’s own cognitive processes. Previous anatomical and functional neuroimaging findings implicated the important role of precuneus in metacognition processing, especially during mnemonic tasks. However, the issue of whether this medial parietal cortex is a domain-specific region that supports mnemonic metacognition remains controversial. Here, we focally disrupted this parietal area with repetitive transcranial magnetic stimulation in healthy participants of both sexes, seeking to ascertain its functional necessity for metacognition for memory versus perceptual decisions. Perturbing the precuneal activity impaired the metacognitive efficiency selectively in the memory judgment of temporal-order, but not in perceptual discrimination. Moreover, the correlation in individuals’ metacognitive efficiency between the domains disappeared when the precuneus was perturbed. Together with the previous finding that lesion to the anterior prefrontal cortex impairs perceptual but not mnemonic metacognition, we double dissociated the macro-anatomical underpinnings for the two kinds of metacognitive capacity in an interconnected network of brain regions.SIGNIFICANCE STATEMENTTheories on the neural basis of metacognition have thus far largely centered on the role of prefrontal cortex. Here we refined the theoretical framework through characterizing a unique precuneal involvement in mnemonic metacognition with a noninvasive but inferentially powerful method: transcranial magnetic stimulation. By quantifying meta-cognitive efficiency across two distinct domains (memory vs. perception) that are matched for stimulus characteristics, we reveal an instrumental – and highly selective – role of the precuneus in mnemonic metacognition. These causal evidence corroborate ample clinical reports that parietal lobe lesions often produce inaccurate self-reports of confidence in memory recollection and establish that the precuneus as a nexus for the introspective ability to evaluate the success of memory judgment in humans.
Elucidating the activation mechanisms for bifurcation of regulatory and effector T cell fates by multidimensional single cell analysis
Authors: Bradley Alla , Hashimoto Tetsuo , Ono Masahiro 
Published: March 2018

AbstractIn T cells, T cell receptor (TCR) signalling initiates downstream transcriptional mechanisms for T cell activation and differentiation. Foxp3-expressing regulatory T cells (Treg) require TCR signals for their suppressive function and maintenance in the periphery. It is, however, unclear how TCR signalling controls the transcriptional programme of Treg. Since most of studies identified the transcriptional features of Treg in comparison to naïve T cells, the relationship between Treg and non-naïve T cells including memory-phenotype T cells (Tmem) and effector T cells (Teff) is not well understood. Here we dissect the transcriptomes of various T cell subsets from independent datasets using the multidimensional analysis method Canonical Correspondence Analysis (CCA). We show that resting Treg share gene modules for activation with Tmem and Teff. Importantly, Tmem activate the distinct transcriptional modules for T cell activation, which are uniquely repressed in Treg. The activation signature of Treg is dependent on TCR signals, and is more actively operating in activated Treg. Furthermore, by analysing single cell RNA-seq data from tumour-infiltrating T cells, we revealed that FOXP3 expression occurs predominantly in activated T cells. Moreover, we identified FOXP3-driven and T follicular helper (Tfh)-like differentiation pathways in tumour microenvironments, and their bifurcation point, which is enriched with recently activated T cells. Collectively, our study reveals the activation mechanisms downstream of TCR signals for the bifurcation of Treg and Teff differentiation and their maturation processes.