bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predicting Pain Levels Following Vaginal Reconstructive Surgery: Who Is at Highest Risk?
Authors: Shatkin-Margolis Abigail , Crisp Catrina C. , Morrison Christopher , Pauls Rachel N. 
Published: February 2018

Objectives
An ability to anticipate individuals at increased risk of postoperative pain would improve coordination of care and patient satisfaction. We sought to describe predictive factors of postoperative pain following vaginal reconstructive surgery.

Methods
This institutional review board–approved, retrospective study used previously collected data from research performed at 1 center from 2009 to 2015. Eligible trials enrolled subjects undergoing vaginal reconstructive surgery for pelvic organ prolapse. All studies used a validated visual analog scale (VAS) for pain on postoperative day 1. Other information collected included pain medication use, medical and surgical history, and demographics. Linear regression analyses, multiple regression analyses, Mann-Whitney U, and Kruskal-Wallis tests were used to analyze the relationship between VAS scores and other variables.

Results
Six studies were analyzed with a total of 364 patients. The median age was 60 years (interquartile range, 16 years), and the median pain score on postoperative day 1 was 35 mm on a 100-mm VAS. Patients younger than 60 years (P < 0.001), those who used tobacco (P = 0.014), those who used pain medication prior to surgery (P = 0.007), and those who did not have a concomitant midurethral sling (P = 0.018) had significantly higher pain scores postoperatively. A trend was also noted with operating times greater than 210 minutes (P = 0.057) and preexisting history of depression (P = 0.065). Multiple regression was performed, and age, depression, tobacco use, and concomitant sling were found to be independent factors predictive of postoperative pain scores.

Conclusions
Age, depression, tobacco use, and concomitant midurethral sling are significant independent factors predictive of postoperative pain following vaginal reconstructive surgery.
Optic Nerve Head and Macular Optical Coherence Tomography Measurements in Papilledema Compared With Pseudopapilledema
Authors: Aghsaei Fard Masoud , Okhravi Sara , Moghimi Sasan , Subramanian Prem S. 
Published: February 2018

Background:
To compare macular and optic nerve head optical coherence tomography (OCT) measurements in mild to moderate papilledema and pseudopapilledema.

Methods:
One hundred nineteen eyes of 61 patients with mild to moderate papilledema, 84 eyes of 48 patients with pseudopapilledema, and 60 eyes of 60 healthy normal individuals were enrolled in this cross-sectional study. Using Spectralis SD-OCT, macular scans with macular ganglion cell–inner plexiform layer (GCIPL) and macular retinal nerve fiber layer (RNFL) segmentation were performed and divided into 2 regions (inner and outer, with a diameter of 3 and 6 mm, respectively); in addition, Bruch membrane opening (BMO) area and peripapillary RNFL thickness were obtained.

Results:
BMO area was similar in papilledema (1.83 ± 0.34 mm2), pseudopapilledema (1.85 ± 0.37 mm2), and controls (1.85 ± 0.32 mm2). Average inner region macular GCIPL thickness in the papilledema, pseudopapilledema, and control groups was 87.2 ± 14.4 μm, 90.8 ± 6.1 μm, and 91.2 ± 9.8 μm, respectively (P > 0.05). Outer temporal region macular GCIPL was significantly thinner in the papilledema group compared with control group (P = 0.01). By contrast, outer inferior and outer nasal macular RNFL sectors were significantly thicker in the papilledema group compared with control groups (P = 0.01 and P < 0.01, respectively). Those measures were not different between pseudopapilledema and control eyes.

Conclusions:
In papilledema eyes, outer temporal region macular GCIPL thickness decreased and outer inferior and outer nasal macular RNFL sectors thickness increased compared with the control group. These changes were not observed in the pseudopapilledema group.
The effects of haploid selection on Y chromosome evolution in two closely related dioecious plants
Authors: Sandler George , Beaudry Felix E.G. , Barrett Spencer C.H. , Wright Stephen I. 
Published: February 2018

AbstractThe evolution of sex chromosomes is usually considered to be driven by sexually antagonistic selection in the diploid phase. However, selection during the haploid gametic phase of the lifecycle has recently received theoretical attention as possibly playing a central role in sex chromosome evolution, especially in plants where gene expression in the haploid phase is extensive. In particular, male-specific haploid selection might favour the linkage of pollen beneficial alleles to male sex determining regions on incipient Y chromosomes. This linkage might then allow such alleles to further specialise for the haploid phase. Purifying haploid selection is also expected to slow the degeneration of Y-linked genes expressed in the haploid phase. Here, we examine the evolution of gene expression in flower buds and pollen of two species ofRumexto test for signatures of haploid selection acting during plant sex chromosome evolution. We find that genes with high ancestral pollen expression bias occur more often on sex chromosomes than autosomes and that genes on the Y chromosome are more likely to become enriched for pollen expression bias. We also find that genes with low expression in pollen are more likely to be lost from the Y chromosome. Our results suggest that sex-specific haploid selection during the gametophytic stage of the lifecycle may be a major contributor to several features of plant sex chromosome evolution.
Dissociable contributions of the amygdala to the immediate and delayed effects of emotional arousal on memory
Authors: Schümann Dirk , Sommer Tobias 
Published: February 2018

AbstractEmotionally arousal enhances memory encoding and consolidation leading to better immediate and delayed memory. Although the central noradrenergic system and the amygdala play critical roles in both effects of emotional arousal, we have recently shown that these effects are at least partly independent of each other, suggesting distinct underlying neural mechanisms. Here we aim to dissociate the neural substrates of both effects in 70 female participants using an emotional memory paradigm to investigate how neural activity, as measured by fMRI, and a polymorphism in the α2B-noradrenoceptor vary for these effects. To also test whether the immediate and delayed effects of emotional arousal on memory are stable traits, we invited back participants who were a part of a large-scale behavioral memory study about 3.5 years ago. We replicated the low correlation of the immediate and delayed emotional enhancement of memory across participants (r = 0.16) and observed, moreover, that only the delayed effect was, to some degree, stable over time (r = 0.23). Bilateral amygdala activity, as well as its coupling with the visual cortex and the fusiform gyrus, was related to the preferential encoding of emotional stimuli, which is consistent with affect-biased attention. Moreover, the adrenoceptor genotype modulated the bilateral amygdala activity associated with this effect. The left amygdala and its coupling with the hippocampus was specifically associated with the more efficient consolidation of emotional stimuli, which is consistent with amygdalar modulation of hippocampal consolidation.
Reading Profiles in Multi-site Data with Missingness
Authors: Eckert Mark A. , Vaden Kenneth I. , Gebregziabher Mulugeta ,   Dyslexia Data Consortium
Published: February 2018

AbstractChildren with reading disability exhibit varied deficits in reading and cognitive abilities that contribute to their reading comprehension problems. Some children exhibit primary deficits in phonological processing, while others can exhibit deficits in oral language and executive functions that affect comprehension. This behavioral heterogeneity is problematic when missing data prevent the characterization of different reading profiles, which often occurs in retrospective data sharing initiatives without coordinated data collection. Here we show that reading profiles can be reliably identified based on Random Forest classification of incomplete behavioral datasets, after the missForest method is used to multiply impute missing values. Results from simulation analyses showed that reading profiles could be accurately classified across degrees of missingness (e.g., ~5% classification error for 30% missingness across the sample). The application of missForest to a real multi-site dataset (n = 924) showed that reading disability profiles significantly and consistently differed in reading and cognitive abilities for cases with and without missing data. The results of validation analyses indicated that the reading profiles (cases with and without missing data) exhibited significant differences for an independent set of behavioral variables that were not used to classify reading profiles. Together, the results show how multiple imputation can be applied to the classification of cases with missing data and can increase the integrity of results from multi-site open access datasets.
FERONIA’s sensing of cell wall pectin activates ROP GTPase signaling in Arabidopsis
Authors: Lin Wenwei , Tang Wenxin , Anderson Charles T. , Yang Zhenbiao 
Published: February 2018

ABSTRACTPlant cells need to monitor the cell wall dynamic to control the wall homeostasis required for a myriad of processes in plants, but the mechanisms underpinning cell wall sensing and signaling in regulating these processes remain largely elusive. Here, we demonstrate that receptor-like kinase FERONIA senses the cell wall pectin polymer to directly activate the ROP6 GTPase signaling pathway that regulates the formation of the cell shape in the Arabidopsis leaf epidermis. The extracellular malectin domain of FER directly interacts with de-methylesterified pectin in vivo and in vitro. Both loss-of-FER mutations and defects in the pectin biosynthesis and de-methylesterification caused changes in pavement cell shape and ROP6 signaling. FER is required for the activation of ROP6 by de-methylesterified pectin, and physically and genetically interacts with the ROP6 activator, RopGEF14. Thus, our findings elucidate a cell wall sensing and signaling mechanism that connects the cell wall to cellular morphogenesis via the cell surface receptor FER.
High affinity interactions and signal transduction between Aβ oligomers and TREM2
Authors: Lessard Christian B. , Malnik Samuel L. , Zhou Yingyue , Ladd Thomas B. , Cruz Pedro E. , Ran Yong , Chakrabaty Paramita , Mahan Thomas E. , Holtzman David M. , Ulrich Jason D , Colonna Marco , Golde Todd E. 
Published: February 2018

ABSTRACTRare coding variant in the Triggering receptor expressed on myeloid cells 2 (TREM2) are associated with increased risk for Alzheimer’s disease (AD), but how they confer this risk remains uncertain. We assessed binding of TREM2, AD associated TREM2 variants to various forms of Aβ and APOE in multiple assays. TREM2 interacts directly with various forms of Aβ, with highest affinity interactions observed between TREM2 and soluble Aβ42 oligomers. We confirm the previous interaction between APOE3 and APOE4 and TREM2. High affinity binding of TREM2 to Aβ oligomers is characterized by very slow dissociation. Pre-incubation with Aβ is shown to block the interaction of APOE. In cellular assays, AD-associated variants of TREM2 reduced the amount of Aβ42 internalized, and in NFAT assay the R47H variant decreased NFAT signaling activity in response to Aβ42. These studies demonstrate i) a high affinity interaction between TREM2 and Aβ oligomers that can block interaction with another ligand and ii) that AD-associated TREM2 variants bind Aβ with equivalent affinity but show loss of function in terms of signaling and Aβ internalization.
A systematic approach for identifying shared mechanisms in epilepsy and its comorbidities
Authors: Hoyt Charles Tapley , Domingo-Fernández Daniel , Balzer Nora , Güldenpfennig Anka , Hofmann-Apitius Martin 
Published: February 2018

AbstractCross-sectional epidemiological studies have shown that the incidence of several nervous system diseases is more frequent in epilepsy patients than in the general population. Some comorbidities (e.g., Alzheimer’s disease and Parkinson’s disease) are also risk factors for the development of seizures; suggesting they may share pathophysiological mechanisms with epilepsy.A literature-based approach was used to identify gene overlap between epilepsy and its comorbidities as a proxy for a shared genetic basis for disease, or genetic pleiotropy, as a first effort to identify shared mechanisms. While the results identified neurological disorders as the group of diseases with the highest gene overlap, this analysis was insufficient for identifying putative common mechanisms shared across epilepsy and its comorbidities. This motivated the use of a dedicated literature mining and knowledge assembly approach in which a cause-and-effect model of epilepsy was captured with Biological Expression Language.After enriching the knowledge assembly with information surrounding epilepsy, its risk factors, its comorbidities, and antiepileptic drugs, a novel comparative mechanism enrichment approach was used to propose several downstream effectors (including the GABA receptor, GABAergic pathways, etc.) that could explain the therapeutic effects carbamazepine in both the contexts of epilepsy and AD.We have made the Epilepsy Knowledge Assembly available at https://www.scai.fraunhofer.de/content/dam/scai/de/downloads/bioinformatik/epilepsy.bel and queryable through NeuroMMSig at http://neurommsig.scai.fraunhofer.de. The source code used for analysis and tutorials for reproduction are available on GitHub at https://github.com/cthoyt/epicom.
Simultaneous detection of DNA and RNA virus species involved in bovine respiratory disease by PCR-free rapid tagmentation-based library preparation and MinION nanopore sequencing
Authors: McCabe Matthew S. , Cormican Paul , Johnston Dayle , Earley Bernadette 
Published: February 2018

AbstactThe Oxford Nanopore MinION Mk1B is a portable 90 g device that sequences DNA directly at 450 bases/second generating sequence reads in excess of 400 kb. Recent improvements in error rate and speed of library preparation mean that this device has considerable potential for rapid molecular bovine pathogen diagnostics. We tested the MinION for rapid untargeted detection of viral pathogens associated with bovine respiratory disease (BRD), an economically important disease often involving primary infection of the lung by one or more of a number of DNA and/or RNA viruses. We combined three foetal lung cell cultures which were infected with either Bovine Respiratory Syncytial Virus (BRSV), Bovine Herpes Virus 1 (BoHV1) or Bovine Parainfluenza Virus 3 (BPI-3). BoHV1 is a DNA virus and BPI-3 and BRSV are RNA viruses. The cell cultures were treated with DNase and RNase to deplete bovine nucleic acid prior to viral nucleic acid extraction and double-stranded cDNA synthesis. Sequencing libraries were generated by PCR-free tagmentation in under 10 minutes and loaded onto a MinION sequencer. Approximately 7,000 sequencing reads were generated and analysed using high-throughput local BLAST against the NCBI nr/nt database. The top BLAST hit for 2,937 of these reads was identified as a virus. Of these, 2,926 (99.6%) were correctly identified either as BoHV1, BRSV or BPI-3.
CTD-dependent and - independent mechanisms govern co-transcriptional capping of Pol II transcripts
Authors: Gonzalez Melvin Noe , Sato Shigeo , Tomomori-Sato Chieri , Conaway Joan W. , Conaway Ronald C. 
Published: February 2018

AbstractCo-transcriptional capping of RNA polymerase II (Pol II) transcripts by capping enzyme proceeds orders of magnitude more efficiently than capping of free RNA. Previous studies brought to light a role for the phosphorylated Pol II CTD in activation of co-transcriptional capping; however, CTD phosphorylation alone could not account for the observed magnitude of activation. Here, we exploit a defined Pol II transcription system that supports both CTD phosphorylation and robust activation of capping to dissect the mechanism of co-transcriptional capping. Taken together, our findings identify a novel CTD-independent, but Pol II-mediated, mechanism that functions in parallel with CTD-dependent processes to ensure optimal capping, and they support a “tethering” model for the mechanism of activation.
Tandem tyrosine residues in the EPEC multicargo chaperone CesT support differential type III effector translocation and early host colonization
Authors: Runte Cameron , Jain Umang , Getz Landon J. , Secord Sabrina , Kuwae Asaomi , Abe Akio , LeBlanc Jason J. , Stadnyk Andrew W. , Kaper James B. , Hansen Anne-Marie , Thomas Nikhil A. 
Published: February 2018

AbstractEnteropathogenic Escherichia coli (EPEC) are worldwide human enteric pathogens inflicting significant morbidity and causing large economic losses. A type 3 secretion system (T3SS) is critical for EPEC intestinal colonization, and injection of effectors into host cells contributes to cellular subversion and innate immune evasion. Here, we demonstrate that two strictly conserved C-terminal tyrosine residues, Y152 and Y153, within the multicargo T3SS chaperone CesT serve differential roles in regulating effector secretion in EPEC. Conservative substitution of both tyrosine residues to phenylalanine attenuated EPEC type 3 effector injection into host cells, and significantly limited Tir effector mediated intimate adherence, a key feature of attaching and effacing pathogenesis. Whereas CesT Y153 supported normal levels of Tir translocation, CesT Y152 was strictly required for the effector NleA to be expressed and subsequently translocated into host cells during infection. Other effectors were observed to be dependent on CesT Y152 for maximal translocation efficiency. Unexpectedly, EPEC expressing a CesT Y152, Y153F variant exhibited significantly enhanced effector translocation of many CesT-interacting effectors, further implicating Y152 in CesT functionality. A mouse infection model of EPEC intestinal disease using Citrobacter rodentium revealed that CesT tyrosine substitution variants displayed delayed colonization and were more rapidly cleared from the intestine. These data demonstrate genetically separable functions for strictly conserved tandem tyrosine residues within CesT. Tyrosine 152 of CesT is implicated in NleA expression, providing functional relevance for localized amino acid conservation. Therefore, CesT via its novel C-terminal domain, has relevant roles beyond typical T3SC that interact and stabilize effector proteins.
Spinal stretch reflexes exploit musculoskeletal redundancy to support postural hand control
Authors: Weiler Jeffrey , Gribble Paul L , Pruszynski J. Andrew 
Published: February 2018

AbstractMotor behaviour is most efficiently controlled by only correcting disturbances or deviations that influence task success. It is currently thought that such sophisticated control is computed within a transcortical feedback pathway. Here we show that even the fastest spinal feedback pathway can produce corrective responses that adhere to this control scheme. We first applied small mechanical perturbations that flexed the elbow joint – stretching the triceps muscle – and simultaneously flexed or extended the wrist joint, displacing the hand various distances away from a central target. We then changed the arm’s orientation and applied the same joint perturbations, which reversed the mapping between joint motion and hand displacement. In all cases, we found that the triceps’ spinal stretch reflex was tuned to the hand’s displacement relative to the target, and not how the triceps muscle was stretched. Our findings reveal that the fastest spinal feedback pathway is capable of integrating and modulating feedback from multiple muscles to produce efficient corrective responses, forcing a re-evaluation of the how the nervous system derives the sophisticated control laws that support natural motor behaviour.
Inhibition and late errors in the antisaccade task: Influence of task design
Authors: Aponte Eduardo A. , Tschan Dominic G. , Stephan Klaas E. , Heinzle Jakob 
Published: February 2018

AbstractIn the antisaccade task, subjects are instructed to saccade in the opposite direction of a peripheral visual cue (PVC). Importantly, several psychiatric disorders are associated with increased error rates in this paradigm. Despite this observation, there is no consensus about the mechanism behind antisaccade errors: while often explained as inhibition failures, some studies have suggested that errors are caused by deficits in the ability to initiate voluntary saccades. Using a computational model, we recently showed that under some conditions high latency or late errors can be explained by a race process between voluntary pro- and antisaccades. A limitation of our findings is that in our previous experiment the PVC signaled the trial type, whereas in most studies, subjects are informed about the trial type before the PVC is presented. We refer to these task designs as asynchronous (AC) and synchronous cues (SC) conditions. Here, we investigated to which extent differences in design affect the type and frequency of errors in the antisaccade task. Twenty-four subjects participated in mixed blocks of pro- and antisaccade trials in both conditions. Our results demonstrate that error rates were highly correlated across task designs and a non-negligible fraction of them were classified as late errors in both conditions. In summary, our findings indicate that errors in the AC task are the result of both inhibition failures and inaccurate voluntary action initiation.
A comprehensive assessment of benign genetic variability for neurodegenerative disorders
Authors: Guerreiro Rita , Sassi Celeste , Raphael Gibbs Jesse , Edsall Connor , Hernandez Dena , Brown Kristelle , Lupton Michelle K , Parkinnen Laura , Ansorge Olaf , Hodges Angela , Ryten Mina ,   for the UK Brain Expression Consortium, Tienari Pentti J. , Van Deerlin Vivanna M. , Trojanowski John Q , Morgan Kevin , Powell John , Singleton Andrew , Hardy John , Bras Jose 
Published: February 2018

1AbstractOver the last few years, as more and more sequencing studies have been performed, it has become apparent that the identification of pathogenic mutations is, more often than not, a complex issue. Here, with a focus on neurodegenerative diseases, we have performed a survey of coding genetic variability that is unlikely to be pathogenic.We have performed whole-exome sequencing in 478 samples derived from several brain banks in the United Kingdom and the United States of America. Samples were included when subjects were, at death, over 60 years of age, had no signs of neurological disease and were subjected to a neuropathological examination, which revealed no evidence of neurodegeneration. This information will be valuable to studies of genetic variability as a causal factor for neurodegenerative syndromes. We envisage it will be particularly relevant for diagnostic laboratories as a filter step to the results being produced by either genome-wide or gene-panel sequencing. We have made this data publicly available at www.alzforum.org/exomes/hex.