bluuebunny/crossref_metadata_2025_split huggingface dataset:
Measuring hip muscle strength in patients with femoroacetabular impingement and other hip pathologies
Authors: Mayne E. , Memarzadeh A. , Raut P. , Arora A. , Khanduja V. 
Published: January 2017

ObjectivesThe aim of this study was to systematically review the literature on measurement of muscle strength in patients with femoroacetabular impingement (FAI) and other pathologies and to suggest guidelines to standardise protocols for future research in the field.MethodsThe Cochrane and PubMed libraries were searched for any publications using the terms ‘hip’, ‘muscle’, ‘strength’, and ‘measurement’ in the ‘Title, Abstract, Keywords’ field. A further search was performed using the terms ‘femoroacetabular’ or ‘impingement’. The search was limited to recent literature only.ResultsA total of 29 articles were reviewed to obtain information on a number of variables. These comprised the type of device used for measurement, rater standardisation, the type of movements tested, body positioning and comparative studies of muscle strength in FAI versus normal controls. The studies found that hip muscle strength is lower in patients with FAI; this is also true for the asymptomatic hip in patients with FAI.ConclusionsCurrent literature on this subject is limited and examines multiple variables. Our recommendations for achieving reproducible results include stabilising the patient, measuring isometric movements and maximising standardisation by using a single tester and familiarising the participants with the protocol. Further work must be done to demonstrate the reliability of any new testing method. Cite this article: E. Mayne, A. Memarzadeh, P. Raut, A. Arora, V. Khanduja. Measuring hip muscle strength in patients with femoroacetabular impingement and other hip pathologies: A systematic review. Bone Joint Res 2017;6:66–72. DOI: 10.1302/2046-3758.61.BJR-2016-0081.
Effects of early‐life exposure to THIP on brainstem neuronal excitability in the Mecp2‐null mouse model of Rett syndrome before and after drug withdrawal
Authors: Zhong Weiwei , Johnson Christopher M. , Cui Ningren , Oginsky Max F. , Wu Yang , Jiang Chun 
Published: January 2017

AbstractRett syndrome (RTT) is mostly caused by mutations of the X‐linked MECP2 gene. Although the causal neuronal mechanisms are still unclear, accumulating experimental evidence obtained from Mecp2−/Y mice suggests that imbalanced excitation/inhibition in central neurons plays a major role. Several approaches may help to rebalance the excitation/inhibition, including agonists of GABAA receptors (GABAAR). Indeed, our previous studies have shown that early‐life exposure of Mecp2‐null mice to the extrasynaptic GABAAR agonist THIP alleviates several RTT‐like symptoms including breathing disorders, motor dysfunction, social behaviors, and lifespan. However, how the chronic THIP affects the Mecp2−/Y mice at the cellular level remains elusive. Here, we show that the THIP exposure in early lives markedly alleviated hyperexcitability of two types of brainstem neurons in Mecp2−/Y mice. In neurons of the locus coeruleus (LC), known to be involved in breathing regulation, the hyperexcitability showed clear age‐dependence, which was associated with age‐dependent deterioration of the RTT‐like breathing irregularities. Both the neuronal hyperexcitability and the breathing disorders were relieved with early THIP treatment. In neurons of the mesencephalic trigeminal nucleus (Me5), both the neuronal hyperexcitability and the changes in intrinsic membrane properties were alleviated with the THIP treatment in Mecp2‐null mice. The effects of THIP on both LC and Me5 neuronal excitability remained 1 week after withdrawal. Persistent alleviation of breathing abnormalities in Mecp2−/Y mice was also observed a week after THIP withdrawal. These results suggest that early‐life exposure to THIP, a potential therapeutic medicine, appears capable of controlling neuronal hyperexcitability in Mecp2−/Y mice, which occurs in the absence of THIP in the recording solution, lasts at least 1 week after withdrawal, and may contribute to the RTT‐like symptom mitigation.
Intracellular oxygen tension limits muscle contraction‐induced change in muscle oxygen consumption under hypoxic conditions during Hb‐free perfusion
Authors: Takakura Hisashi , Ojino Minoru , Jue Thomas , Yamada Tatsuya , Furuichi Yasuro , Hashimoto Takeshi , Iwase Satoshi , Masuda Kazumi 
Published: January 2017

AbstractUnder acute hypoxic conditions, the muscle oxygen uptake (mO2) during exercise is reduced by the restriction in oxygen‐supplied volume to the mitochondria within the peripheral tissue. This suggests the existence of a factor restricting the mO2 under hypoxic conditions at the peripheral tissue level. Therefore, this study set out to test the hypothesis that the restriction in mO2 is regulated by the net decrease in intracellular oxygen tension equilibrated with myoglobin oxygen saturation (∆PmbO2) during muscle contraction under hypoxic conditions. The hindlimb of male Wistar rats (8 weeks old, n = 5) was perfused with hemoglobin‐free Krebs–Henseleit buffer equilibrated with three different fractions of O2 gas: 95.0%O2, 71.3%O2, and 47.5%O2. The deoxygenated myoglobin (Mb) kinetics during muscle contraction were measured under each oxygen condition with a near‐infrared spectroscopy. The ∆[deoxy‐Mb] kinetics were converted to oxygen saturation of myoglobin (SmbO2), and the PmbO2 was then calculated based on the SmbO2 and the O2 dissociation curve of the Mb. The SmbO2 and PmbO2 at rest decreased with the decrease in O2 supply, and the muscle contraction caused a further decrease in SmbO2 and PmbO2 under all O2 conditions. The net increase in mO2 from the muscle contraction (∆mO2) gradually decreased as the ∆PmbO2 decreased during muscle contraction. The results of this study suggest that ΔPmbO2 is a key determinant of the ΔmO2.
Roflumilast and aquaporin‐2 regulation in rat renal inner medullary collecting duct
Authors: Umejiego Ezigbobiara N. , Wang Yanhua , Knepper Mark A. , Chou Chung‐Lin 
Published: January 2017

AbstractRoflumilast is a cyclic nucleotide phosphodiesterase inhibitor that is FDA‐approved for treatment of chronic obstructive pulmonary disease. With a view toward possible use for treatment of patients with X‐linked nephrogenic diabetes insipidus (NDI) due to hemizygous mutations in the V2 vasopressin receptor, this study sought to determine the effect of roflumilast on aquaporin‐2 (AQP2) phosphorylation, AQP2 trafficking, and water permeability in the rat inner medullary collecting duct (IMCD). In the presence of the vasopressin analog dDAVP (0.1 nmol/L), both roflumilast and its active metabolite roflumilast N‐oxide (RNO) significantly increased phosphorylation at S256, S264, and S269, and decreased phosphorylation at S261 (immunoblotting) in IMCD suspensions in a dose‐dependent manner (3–3000 nmol/L). Another commonly used phosphodiesterase inhibitor, IBMX, affected phosphorylation only at the highest concentration in this range. However, neither roflumilast nor RNO had an effect on AQP2 phosphorylation in the absence of vasopressin. Furthermore, roflumilast alone did not increase AQP2 trafficking to the plasma membrane (immunofluorescence) or increase water permeability in freshly microdissected perfused IMCD segments. We conclude that roflumilast can be used to enhance vasopressin's action on AQP2 activity in the renal collecting duct, but has no detectable effect in the absence of vasopressin. These findings suggest that roflumilast may not have a beneficial effect in X‐linked NDI, but could find useful application in acquired NDI.
Barycentric Jacobi Spectral Method for Numerical Solutions of the Generalized Burgers-Huxley Equation
Authors: Pindza Edson , Owolabi M. K. , Patidar K.C. 
Published: January 2017

Abstract
Numerical solutions of nonlinear partial differential equations, such as the generalized and extended Burgers-Huxley equations which combine effects of advection, diffusion, dispersion and nonlinear transfer are considered in this paper. Such system can be divided into linear and nonlinear parts, which allow the use of two numerical approaches. Barycentric Jacobi spectral (BJS) method is employed for the spatial discretization, the resulting nonlinear system of ordinary differential equation is advanced with a fourth-order exponential time differencing predictor corrector. Comparative numerical results for the values of options are presented. The proposed method is very elegant from the computational point of view. Numerical computations for a wide variety of problems, show that the present method offers better accuracy and efficiency in comparison with other previous methods. Moreover the method can be applied to a wide class of nonlinear partial differential equations.
Development and Organization of the Evolutionarily Conserved Three-Layered Olfactory Cortex
Authors: Klingler Esther 
Published: January 2017

AbstractThe olfactory cortex is part of the mammalian cerebral cortex together with the neocortex and the hippocampus. It receives direct input from the olfactory bulbs and participates in odor discrimination, association, and learning (Bekkers and Suzuki, 2013). It is thought to be an evolutionarily conserved paleocortex, which shares common characteristics with the three-layered general cortex of reptiles (Aboitiz et al., 2002). The olfactory cortex has been studied as a “simple model” to address sensory processing, though little is known about its precise cell origin, diversity, and identity. While the development and the cellular diversity of the six-layered neocortex are increasingly understood, the olfactory cortex remains poorly documented in these aspects. Here is a review of current knowledge of the development and organization of the olfactory cortex, keeping the analogy with those of the neocortex. The comparison of olfactory cortex and neocortex will allow the opening of evolutionary perspectives on cortical development.
Genome-Wide Analysis of lncRNA and mRNA Expression During Differentiation of Abdominal Preadipocytes in the Chicken
Authors: Zhang Tao , Zhang Xiangqian , Han Kunpeng , Zhang Genxi , Wang Jinyu , Xie Kaizhou , Xue Qian 
Published: January 2017

Abstract
Long noncoding RNAs (lncRNAs) regulate adipogenesis and other processes associated with metabolic tissue development and function. However, little is known about the function and profile of lncRNAs during preadipocyte differentiation in the chicken (Gallus gallus). Herein, lncRNA and mRNA expression in preadipocytes at different stages of differentiation were analyzed using RNA sequencing. A total of 1,300,074,528 clean reads and 27,023 novel lncRNAs were obtained from 12 samples. The number of genes (1336 lncRNAs and 1759 mRNAs; 3095 in total) differentially expressed across various stages declined as differentiation progressed. Differentially expressed genes were found to be involved in several pathways related to preadipocyte differentiation that have been extensively studied, including glycerolipid metabolism, and the mammalian target of rapamycin, peroxisome proliferator-activated receptor, and mitogen-activated protein kinase signaling pathways. To our knowledge, some pathways are being reported for the first time, including the propanoate metabolism, fatty acid metabolism, and oxidative phosphorylation pathways. Furthermore, 3095 differentially expressed genes were clustered into eight clusters, and their expression patterns were determined through K-means clustering. Genes involved in the K2 cluster likely play important roles in preadipocyte differentiation. Six stage-specific modules related to A0 (day 0), A2 (day 2), and A6 (day 6) stages were identified, using weighted coexpression network analysis. Nine central, highly connected .genes in stage-specific modules were subsequently identified, including XLOC_068731, XLOC_022661, XLOC_045161, XLOC_070302, CHD6, LLGL1, NEURL1B, KLHL38, and ACTR6. This study provides a valuable resource for further study of chicken lncRNA and facilitates a better understanding of preadipocyte differentiation in the chicken
Predicted Residual Error Sum of Squares of Mixed Models: An Application for Genomic Prediction
Authors: Xu Shizhong 
Published: January 2017

AbstractGenomic prediction is a statistical method to predict phenotypes of polygenic traits using high-throughput genomic data. Most diseases and behaviors in humans and animals are polygenic traits. The majority of agronomic traits in crops are also polygenic. Accurate prediction of these traits can help medical professionals diagnose acute diseases and breeders to increase food products, and therefore significantly contribute to human health and global food security. The best linear unbiased prediction (BLUP) is an important tool to analyze high-throughput genomic data for prediction. However, to judge the efficacy of the BLUP model with a particular set of predictors for a given trait, one has to provide an unbiased mechanism to evaluate the predictability. Cross-validation (CV) is an essential tool to achieve this goal, where a sample is partitioned into K parts of roughly equal size, one part is predicted using parameters estimated from the remaining K – 1 parts, and eventually every part is predicted using a sample excluding that part. Such a CV is called the K-fold CV. Unfortunately, CV presents a substantial increase in computational burden. We developed an alternative method, the HAT method, to replace CV. The new method corrects the estimated residual errors from the whole sample analysis using the leverage values of a hat matrix of the random effects to achieve the predicted residual errors. Properties of the HAT method were investigated using seven agronomic and 1000 metabolomic traits of an inbred rice population. Results showed that the HAT method is a very good approximation of the CV method. The method was also applied to 10 traits in 1495 hybrid rice with 1.6 million SNPs, and to human height of 6161 subjects with roughly 0.5 million SNPs of the Framingham heart study data. Predictabilities of the HAT and CV methods were all similar. The HAT method allows us to easily evaluate the predictabilities of genomic prediction for large numbers of traits in very large populations.
Genotype Calling from Population-Genomic Sequencing Data
Authors: Maruki Takahiro , Lynch Michael 
Published: January 2017

AbstractGenotype calling plays important roles in population-genomic studies, which have been greatly accelerated by sequencing technologies. To take full advantage of the resultant information, we have developed maximum-likelihood (ML) methods for calling genotypes from high-throughput sequencing data. As the statistical uncertainties associated with sequencing data depend on depths of coverage, we have developed two types of genotype callers. One approach is appropriate for low-coverage sequencing data, and incorporates population-level information on genotype frequencies and error rates pre-estimated by an ML method. Performance evaluation using computer simulations and human data shows that the proposed framework yields less biased estimates of allele frequencies and more accurate genotype calls than current widely used methods. Another type of genotype caller applies to high-coverage sequencing data, requires no prior genotype-frequency estimates, and makes no assumption on the number of alleles at a polymorphic site. Using computer simulations, we determine the depth of coverage necessary to accurately characterize polymorphisms using this second method. We applied the proposed method to high-coverage (mean 18×) sequencing data of 83 clones from a population of Daphnia pulex. The results show that the proposed method enables conservative and reasonably powerful detection of polymorphisms with arbitrary numbers of alleles. We have extended the proposed method to the analysis of genomic data for polyploid organisms, showing that calling accurate polyploid genotypes requires much higher coverage than diploid genotypes.
Fluctuating Selection in the Moran
Authors: Dean Antony M , Lehman Clarence , Yi Xiao 
Published: January 2017

Abstract
Contrary to classical population genetics theory, experiments demonstrate that fluctuating selection can protect a haploid polymorphism in the absence of frequency dependent effects on fitness. Using forward simulations with the Moran model, we confirm our analytical results showing that a fluctuating selection regime, with a mean selection coefficient of zero, promotes polymorphism. We find that increases in heterozygosity over neutral expectations are especially pronounced when fluctuations are rapid, mutation is weak, the population size is large, and the variance in selection is big. Lowering the frequency of fluctuations makes selection more directional, and so heterozygosity declines. We also show that fluctuating selection raises dn/ds ratios for polymorphism, not only by sweeping selected alleles into the population, but also by purging the neutral variants of selected alleles as they undergo repeated bottlenecks. Our analysis shows that randomly fluctuating selection increases the rate of evolution by increasing the probability of fixation. The impact is especially noticeable when the selection is strong and mutation is weak. Simulations show the increase in the rate of evolution declines as the rate of new mutations entering the population increases, an effect attributable to clonal interference. Intriguingly, fluctuating selection increases the dn/ds ratios for divergence more than for polymorphism, a pattern commonly seen in comparative genomics. Our model, which extends the classical neutral model of molecular evolution by incorporating random fluctuations in selection, accommodates a wide variety of observations, both neutral and selected, with economy.
Meiotic Crossing Over in Maize Knob Heterochromatin
Authors: Stack Stephen M , Shearer Lindsay A , Lohmiller Leslie , Anderson Lorinda K 
Published: January 2017

AbstractThere is ample evidence that crossing over is suppressed in heterochromatin associated with centromeres and nucleolus organizers (NORs). This...There is ample evidence that crossing over is suppressed in heterochromatin associated with centromeres and nucleolus organizers (NORs). This characteristic has been attributed to all heterochromatin, but the generalization may not be justified. To investigate the relationship of crossing over to heterochromatin that is not associated with centromeres or NORs, we used a combination of fluorescence in situ hybridization of the maize 180-bp knob repeat to show the locations of knob heterochromatin and fluorescent immunolocalization of MLH1 protein and AFD1 protein to show the locations of MLH1 foci on maize synaptonemal complexes (SCs, pachytene chromosomes). MLH1 foci correspond to the location of recombination nodules (RNs) that mark sites of crossing over. We found that MLH1 foci occur at similar frequencies per unit length of SC in interstitial knobs and in the 1 µm segments of SC in euchromatin immediately to either side of interstitial knobs. These results indicate not only that crossing over occurs within knob heterochromatin, but also that crossing over is not suppressed in the context of SC length in maize knobs. However, because there is more DNA per unit length of SC in knobs compared to euchromatin, crossing over is suppressed (but not eliminated) in knobs in the context of DNA length compared to adjacent euchromatin.
Chromatin Regulation by the NuA4 Acetyltransferase Complex Is Mediated by Essential Interactions Between Enhancer of Polycomb (Epl1) and Esa1
Authors: Searle Naomi E , Torres-Machorro Ana Lilia , Pillus Lorraine 
Published: January 2017

AbstractEnzymes that modify and remodel chromatin act in broadly conserved macromolecular complexes. One key modification is the dynamic acetylation of...Enzymes that modify and remodel chromatin act in broadly conserved macromolecular complexes. One key modification is the dynamic acetylation of histones and other chromatin proteins by opposing activities of acetyltransferase and deacetylase complexes. Among acetyltransferases, the NuA4 complex containing Tip60 or its Saccharomyces cerevisiae ortholog Esa1 is of particular significance because of its roles in crucial genomic processes including DNA damage repair and transcription. The catalytic subunit Esa1 is essential, as are five noncatalytic NuA4 subunits. We found that of the noncatalytic subunits, deletion of Enhancer of polycomb (Epl1), but not the others, can be bypassed by loss of a major deacetylase complex, a property shared by Esa1. Noncatalytic complex subunits can be critical for complex assembly, stability, genomic targeting, substrate specificity, and regulation. Understanding the essential role of Epl1 has been previously limited, a limitation now overcome by the discovery of its bypass suppression. Here, we present a comprehensive in vivo study of Epl1 using the powerful tool of suppression combined with transcriptional and mutational analyses. Our results highlight functional parallels between Epl1 and Esa1 and further illustrate that the structural role of Epl1 is important for promotion of Esa1 activity. This conclusion is strengthened by our dissection of Epl1 domains required in vivo for interaction with specific NuA4 subunits, histone acetylation, and chromatin targeting. These results provide new insights for the conserved, essential nature of Epl1 and its homologs, such as EPC1/2 in humans, which is frequently altered in cancers.
Histone H3K4 and H3K36 Methylation Independently Recruit the NuA3 Histone Acetyltransferase in Saccharomyces cerevisiae
Authors: Martin Benjamin J E , McBurney Kristina L , Maltby Vicki E , Jensen Kristoffer N , Brind’Amour Julie , Howe LeAnn J 
Published: January 2017

Abstract
Histone post-translational modifications (PTMs) alter chromatin structure by promoting the interaction of chromatin-modifying complexes with nucleosomes. The majority of chromatin-modifying complexes contain multiple domains that preferentially interact with modified histones, leading to speculation that these domains function in concert to target nucleosomes with distinct combinations of histone PTMs. In Saccharomyces cerevisiae, the NuA3 histone acetyltransferase complex contains three domains, the PHD finger in Yng1, the PWWP domain in Pdp3, and the YEATS domain in Taf14; which in vitro bind to H3K4 methylation, H3K36 methylation, and acetylated and crotonylated H3K9, respectively. While the in vitro binding has been well characterized, the relative in vivo contributions of these histone PTMs in targeting NuA3 is unknown. Here, through genome-wide colocalization and by mutational interrogation, we demonstrate that the PHD finger of Yng1, and the PWWP domain of Pdp3 independently target NuA3 to H3K4 and H3K36 methylated chromatin, respectively. In contrast, we find no evidence to support the YEATS domain of Taf14 functioning in NuA3 recruitment. Collectively our results suggest that the presence of multiple histone PTM binding domains within NuA3, rather than restricting it to nucleosomes containing distinct combinations of histone PTMs, can serve to increase the range of nucleosomes bound by the complex. Interestingly, however, the simple presence of NuA3 is insufficient to ensure acetylation of the associated nucleosomes, suggesting a secondary level of acetylation regulation that does not involve control of HAT-nucleosome interactions.