bluuebunny/crossref_metadata_2025_split huggingface dataset:
A combination of sexual and ecological divergence contributes to rearrangement spread during initial stages of speciation
Authors: Kozak Genevieve M. , Wadsworth Crista B. , Kahne Shoshanna C. , Bogdanowicz Steven M. , Harrison Richard G. , Coates Brad S. , Dopman Erik B. 
Published: January 2017

AbstractChromosomal rearrangements between sympatric species often contain multiple loci contributing to assortative mating, local adaptation and hybrid sterility. When and how these associations arise during the process of speciation remains a subject of debate. Here, we address the relative roles of local adaptation and assortative mating on the dynamics of rearrangement evolution by studying how a rearrangement covaries with sexual and ecological trait divergence within a species. Previously, a chromosomal rearrangement that suppresses recombination on the Z (sex) chromosome was identified in European corn borer moths (Ostrinia nubilalis). We further characterize this recombination suppressor and explore its association with variation in sex pheromone communication and seasonal ecological adaptation in pairs of populations that are divergent in one or both of these characteristics. Direct estimates of recombination suppression in pedigree mapping families indicated that more than 39% of the Z chromosome (encompassing up to ~10 megabases and ~300 genes) resides within a nonrecombining unit, including pheromone olfactory receptor genes and a major quantitative trait locus that contributes to ecotype differences (Pdd). Combining direct and indirect estimates of recombination suppression, we found that the rearrangement was occasionally present between sexually isolated strains (E vs. Z) and between divergent ecotypes (univoltine vs. bivoltine). However, it was only consistently present when populations differed in both sexual and ecological traits. Our results suggest that independent of the forces that drove the initial establishment of the rearrangement, a combination of sexual and ecological divergence is required for rearrangement spread during speciation.
Transcriptomic responses to seawater acidification among sea urchin populations inhabiting a natural pH mosaic
Authors: Evans Tyler G. , Pespeni Melissa H. , Hofmann Gretchen E. , Palumbi Stephen R. , Sanford Eric 
Published: January 2017

AbstractIncreasing awareness of spatial and temporal variation in ocean pH suggests some marine populations may be adapted to local pH regimes and will therefore respond differently to present‐day pH variation and to long‐term ocean acidification. In the Northeast Pacific Ocean, differences in the strength of coastal upwelling cause latitudinal variation in prevailing pH regimes that are hypothesized to promote local adaptation and unequal pH tolerance among resident populations. In this study, responses to experimental seawater acidification were compared among embryos and larvae from six populations of purple sea urchins (Strongylocentrotus purpuratus) inhabiting areas that differ in their frequency of low pH exposure and that prior research suggests are locally adapted to seawater pH. Transcriptomic analyses demonstrate urchin populations most frequently exposed to low pH seawater responded to experimental acidification by expressing genes within major ATP‐producing pathways at greater levels than populations encountering low pH less often. Multiple genes within the tricarboxylic acid cycle, electron transport chain and fatty acid beta oxidation pathways were upregulated in urchin populations experiencing low pH conditions most frequently. These same metabolic pathways were significantly over‐represented among genes both expressed in a population‐specific manner and putatively under selection to enhance low pH tolerance. Collectively, these data suggest natural selection is acting on metabolic gene networks to redirect ATP toward maintaining acid–base homeostasis and enhance tolerance of seawater acidification. As a trade‐off, marine populations more tolerant of low pH may have less energy to put towards other aspects of fitness and to respond to additional ocean change.
Cryphonectria parasitica, the causal agent of chestnut blight: invasion history, population biology and disease control
Authors: Rigling Daniel , Prospero Simone 
Published: January 2017

SummaryChestnut blight, caused by Cryphonectria parasitica, is a devastating disease infecting American and European chestnut trees. The pathogen is native to East Asia and was spread to other continents via infected chestnut plants. This review summarizes the current state of research on this pathogen with a special emphasis on its interaction with a hyperparasitic mycovirus that acts as a biological control agent of chestnut blight.TaxonomyCryphonectria parasitica (Murr.) Barr. is a Sordariomycete (ascomycete) fungus in the family Cryphonectriaceae (Order Diaporthales). Closely related species that can also be found on chestnut include Cryphonectria radicalis, Cryphonectria naterciae and Cryphonectria japonica.Host rangeMajor hosts are species in the genus Castanea (Family Fagaceae), particularly the American chestnut (C. dentata), the European chestnut (C. sativa), the Chinese chestnut (C. mollissima) and the Japanese chestnut (C. crenata). Minor incidental hosts include oaks (Quercus spp.), maples (Acer spp.), European hornbeam (Carpinus betulus) and American chinkapin (Castanea pumila).Disease symptomsCryphonectria parasitica causes perennial necrotic lesions (so‐called cankers) on the bark of stems and branches of susceptible host trees, eventually leading to wilting of the plant part distal to the infection. Chestnut blight cankers are characterized by the presence of mycelial fans and fruiting bodies of the pathogen. Below the canker the tree may react by producing epicormic shoots. Non‐lethal, superficial or callusing cankers on susceptible host trees are usually associated with mycovirus‐induced hypovirulence.Disease controlAfter the introduction of C. parasitica into a new area, eradication efforts by cutting and burning the infected plants/trees have mostly failed. In Europe, the mycovirus Cryphonectria hypovirus 1 (CHV‐1) acts as a successful biological control agent of chestnut blight by causing so‐called hypovirulence. CHV‐1 infects C. parasitica and reduces its parasitic growth and sporulation capacity. Individual cankers can be therapeutically treated with hypovirus‐infected C. parasitica strains. The hypovirus may subsequently spread to untreated cankers and become established in the C. parasitica population. Hypovirulence is present in many chestnut‐growing regions of Europe, either resulting naturally or after biological control treatments. In North America, disease management of chestnut blight is mainly focused on breeding with the goal to backcross the Chinese chestnut's blight resistance into the American chestnut genome.
Silencing of OTUB1 inhibits migration of human glioma cells in vitro
Authors: Xu Li , Li Jinquan , Bao Zhen , Xu Peng , Chang Hao , Wu Jingjing , Bei Yuanqi , Xia Liuwan , Wu Peizhang , Yan Ke , Lu Bing , Cui Gang 
Published: January 2017

OTU domain‐containing ubiquitin aldehyde‐binding protein 1 (OTUB1) protein, a deubiquitinating enzyme (DUB) which belongs to the ovarian tumor (OTU) family, was reported to be associated with the development of various malignancies. However, the potential function of OTUB1 in human gliomas was still unclear. In this study, we sought to investigate the function of OTUB1 in the pathological process of gliomas and analyze its related clinical significance. Western blot and immunohistochemistry analyses demonstrated that OTUB1 was overexpressed in glioma tissues, and statistical analysis suggested the expression level of OTUB1 was significantly correlated with the WHO grades of human gliomas (P < 0.05). Moreover, Kaplan–Meier curve also indicated that high expression of OTUB1 was correlated with a poor prognosis. In vitro, silencing OTUB1 retarded the migration ability of glioma cells. Knockdown of OTUB1 increases epithelial‐mesenchymal transition‐related protein E‐cadherin expression, but decreases simultaneously the expression of vimentin and snail. Furthermore, down‐regulated expression of OTUB1 also resulted in decreased expression of some extracellular matrix degradation‐related proteins, such as matrix metallopeptidase (MMP)2 and MMP9. All results suggested that OTUB1 was a valuable marker in the pathogenesis of human gliomas and could be used as a novel biomarker for glioma therapy in the future.
MicroRNA‐125a promotes resistance to BRAF inhibitors through suppression of the intrinsic apoptotic pathway
Authors: Koetz‐Ploch Lisa , Hanniford Douglas , Dolgalev Igor , Sokolova Elena , Zhong Judy , Díaz‐Martínez Marta , Bernstein Emily , Darvishian Farbod , Flaherty Keith T. , Chapman Paul B. , Tawbi Hussein , Hernando Eva 
Published: January 2017

SummaryMelanoma patients with BRAFV600E‐mutant tumors display striking responses to BRAF inhibitors (BRAFi); however, almost all invariably relapse with drug‐resistant disease. Here, we report that microRNA‐125a (miR‐125a) expression is upregulated in human melanoma cells and patient tissues upon acquisition of BRAFi resistance. We show that miR‐125a induction confers resistance to BRAFV600E melanoma cells to BRAFi by directly suppressing pro‐apoptotic components of the intrinsic apoptosis pathway, including BAK1 and MLK3. Apoptotic suppression and prolonged survival favor reactivation of the MAPK and AKT pathways by drug‐resistant melanoma cells. We demonstrate that miR‐125a inhibition suppresses the emergence of resistance to BRAFi and, in a subset of resistant melanoma cell lines, leads to partial drug resensitization. Finally, we show that miR‐125a upregulation is mediated by TGFβ signaling. In conclusion, the identification of this novel role for miR‐125a in BRAFi resistance exposes clinically relevant mechanisms of melanoma cell survival that can be exploited therapeutically.
Impact of exacerbations on adherence and outcomes of pulmonary rehabilitation in patients with COPD
Authors: Braeken Dionne C.W. , Spruit Martijn A. , Houben‐Wilke Sarah , Smid Dionne E. , Rohde Gernot G.U. , Wouters Emiel F.M. , Franssen Frits M.E. 
Published: January 2017

ABSTRACT
Background and objectiveDropout or lack of response is an important issue in pulmonary rehabilitation (PR), which underlines the need to identify predictors of dropout and response. Acute exacerbations (AEs) of COPD may influence dropout rates and PR response. We aimed to assess differences in dropout and outcomes of PR between COPD with and without AEs.MethodsClinically stable patients with moderate‐to‐very severe COPD (age: 64.1 ± 9.1 years, 55.6% males, forced expiratory volume in 1 s (FEV1
): 48.6 ± 20.0% predicted) were assessed during PR (inpatient and outpatient). Mild‐to‐moderate AEs were defined as ‘the prescription of systemic glucocorticosteroids and/or antibiotics, following an acute increase in respiratory symptoms’. Severe AEs were defined as ‘a hospital admission due to an AE’. Health status was measured by COPD Assessment Test (CAT), COPD‐specific version of the St George's Respiratory Questionnaire (SGRQ‐C) and Clinical COPD Questionnaire (CCQ). Symptoms of anxiety and depression were measured by Hospital Anxiety and Depression Scale (HADS). Exercise capacity was measured with the 6‐min walking test (6MWT) and constant work rate test (CWRT).ResultsA total of 518 patients were assessed during a pre‐rehabilitation assessment. Four hundred and seventy‐six patients started PR, of whom 419 (88.0%) completed it. A larger proportion of patients who dropped out had a severe AE during PR (20.0% vs 3.5%, P < 0.001). Completers with severe AE showed a deterioration in 6MWT, while completers without AE and with mild‐to‐moderate AE improved (−24.8 (95% CI: −94.0 to 44.5) vs 24.2 (95% CI: 16.0 to 32.5) vs 25.1 (95% CI: 14.0 to 36.3) metres, P = 0.042). No other significant differences were observed in outcomes comparing completers with and without AE during PR.ConclusionMild‐to‐moderate AEs do not affect dropout or response of PR, although severe AEs are associated with dropout. AEs should not lead to discontinuation of PR, as response is in general not affected.
Coexistence of fusion and concrescence of primary teeth: in a child with Down syndrome
Authors: Singh Akshara , Bhatia Hind Pal , Sharma Naresh 
Published: January 2017

ABSTRACTDown syndrome is one of the most common congenital anomaly. It is most frequently caused by trisomy of chromosome 21. Other causes can be mosaicism and translocation. Such patients are commonly encountered in routine dental practice. This syndrome has wide range of medical and dental abnormalities. This paper presents a unique case of fusion and concrescence of retained primary teeth in a child with Down syndrome. The incidence of such anomalies is quite low in these cases. Thus, a better awareness of such conditions on part of a dental practitioner will aid in the provision of enhanced dental care to these patients.
Plasma volume reduction and hematological fluctuations in high‐level athletes after an increased training load
Authors: Bejder J. , Andersen A. B. , Goetze J. P. , Aachmann‐Andersen N. J. , Nordsborg N. B. 
Published: January 2017

The time course of plasma volume (PV) reduction following an increased training load period is unknown and was investigated. The accompanying fluctuations in [Hb] and OFF‐hr score were analyzed in the Athlete Biological Passport. Further, whether fluctuations in plasma albumin, soluble transferrin receptors (sTfR), and pro‐atrial natriuretic peptide (proANP) concentrations correlate with PV fluctuations was investigated. Eleven high‐level competitive cyclists were investigated for 3 weeks. After initial measurements in week 1, training load was increased ~250% in week 2 followed by a reversion to baseline training load in week 3. PV and hematological variables were determined frequently during all weeks. The higher training load in week 2 increased (P<.001) PV 10%, while [Hb] and OFF‐hr score decreased ~6% (P<.01) and ~16% (P<.001), respectively. PV and [Hb] returned to baseline within 2 and 4 days after week 2, respectively, while OFF‐hr score remained reduced for 6 days. Further, one and three atypical blood profiles of the ABP occurred during weeks 2 and 3, respectively. Individual changes in albumin, sTfR, and proANP only correlated weakly (R2<.20) with PV fluctuations. In conclusion, PV and [Hb] fluctuations caused by an elevated training load period were reverted within 2 and 4 days after returning to baseline training load, respectively, while OFF‐hr remained altered for 6 days. Furthermore, some atypical blood profiles were induced during and subsequent to the increased training load, demonstrating the importance of knowledge on naturally occurring hematological fluctuations. Finally, concentrations of albumin, sTfR, and proANP could not explain PV fluctuations.
The twisted structure of the Achilles tendon unraveled: A detailed quantitative and qualitative anatomical investigation
Authors: Pękala P. A. , Henry B. M. , Ochała A. , Kopacz P. , Tatoń G. , Młyniec A. , Walocha J. A. , Tomaszewski K. A. 
Published: January 2017

The Achilles tendon (AT) consists of fibers originating from the soleus muscle (SOL), which lies deep, and the medial (GM) and lateral (GL) heads of the gastrocnemius muscle, which lie superficial. As the fibers descend toward the insertion of the AT, the individual subtendons twist around each other. The aim of this study was to investigate the twisted structure of the AT and its individual subtendons. Specimens of the AT, with preserved calcaneal bone and a fragment of the triceps surae muscle, were obtained from 53 fresh‐frozen, male cadavers (n=106 lower limbs). The angle of torsion of each of the AT's subtendons was measured using a specially designed and 3D‐printed tool. The mean distance between the most distal fibers of the triceps surae muscle and the superior border of the calcaneal bone was 60.77±14.15 mm. The largest component of the AT at the level of its insertion into the calcaneal bone is the subtendon from the GL (44.43%), followed by the subtendon from SOL (27.89%), and the subtendon from GM (27.68%). The fibers originating from the GM rotate on average 28.17±15.15°, while the fibers originating from the GL and SOL twist 135.98±33.58° and 128.58±29.63°, respectively. The torsion of superficial fibers (GM) comprising the AT is significantly lower than that of deeper fibers (GL and SOL). The cross‐sectional area of the AT is smaller at the level of the musculo‐tendinous junction than at the level of its insertion. This study illustrates the three types of the AT with differently twisting subtendons, as well as a generalized model of the AT. Types of AT torsion may potentially alter the biomechanical properties of the tendon, thus possibly influencing the pathophysiologic mechanisms leading to the development of various tendinopathies.
CATALYTIC SURFACE MODIFICATION OF ALUMINA MEMBRANE FOR OXYGEN SEPARATION
Authors: Sihar ‘Ainun Sailah , Shahrudin Munawar Zaman , Alias Nur Hashimah , Che Abdul Rahim 'Azzah Nazihah , Othman Nur Hidayati , A. Rahman Mukhlis 
Published: January 2017

Two types of alumina ceramic membrane in hollow fibre shape was used in this study. Both alumina hollow fibres (AHF) were sintered at different temperatures; (a) 1350oC and (b) 1450oC. In order to improve the catalytic activity of the alumina membrane for oxygen separation purposes, surface modification of the membranes was carried out using La0.6Sr0.4Co0.2Fe0.8O3-δ (LSCF) perovskite catalyst. LSCF was synthesised using simple Pechini sol-gel method. The evaporation time and temperature of the LSCF-sol were varied to obtain various viscosity of catalytic sol. From XRD analysis, pure LSCF perovskite structure formed at temperature at 850oC. The morphological of unmodified and surface-modified alumina hollow fibre membranes (AHF) were studied using FESEM. The effect of LSCF catalytic sol viscosity was studied and it was found that as the viscosity of the sol increases, the amount of catalyst deposited on the alumina hollow fibre were increased. Besides, the amount of catalyst deposited on 1350 AHF was found to be higher than 1450 AHF. This result is supported by the result of pore distribution data whereby 1350 AHF was observed to be more porous than 1450 AHF, with porosity percentage of 40.38% and 28.80%, respectively. Although higher viscosity of catalytic sol could lead to a high amount of catalyst deposited on the AHF substrate, there is a tendency for micro-cracks to develop. Thus, the viscosity of the catalytic sol is important to control in order to have higher oxygen permeation flux.
URSODEOXYCHOLIC ACID REGULATES CASPASE-9 AND ROS PRODUCTION IN PROTECTING CARDIOMYOCYTES AGAINST HYPOXIA
Authors: Hanafi Noorul Izzati , Sheikh Abdul Kadir Siti Hamimah , Mohamed Anis Syamimi , Md Noor Julina , Osman Nora Julianna , Siran Rosfaiizah , Ab Rahim Sharaniza , Abdul Hamid Hasani Narimah 
Published: January 2017

Ursodeoxycholic acid (UDCA) is known as a therapeutic agent in treating cholestasis and liver diseases. Recently, UDCA has been suggested as a therapeutic drug for heart related diseases. Cardioprotective effect of UDCA against the development of ischemia has been studied. Yet, the mechanism of UDCA-cardioprotection is not clearly understood. Therefore, this study aimed to elucidate the mechanisms of UDCA cardioprotection against hypoxia by investigating the expression of caspase -3/-9 and ROS generation using an in vitro hypoxic heart model. A newborn (0-2 days old) rat heart was isolated for primary cell culture of cardiomyocytes. Hypoxia was chemically induced by using CoCl2. Cardiomyocytes were then incubated with UDCA. The treated cardiomyocytes were subjected for ROS generation detection assay, QuantiGene Plex assay for caspase-3/-9 gene expression and ELISA for caspase-3/-9 protein expression. The data were analyzed by using sample paired t-test and One-way ANOVA. Our results showed that UDCA abolishes the effects on CoCl2 in ROS production and UDCA downregulates caspase-9 protein expression in CoCl2 treated cardiomyocytes. This study provides an insight of UDCA in protecting cardiomyocytes against hypoxia mediated by anti-apoptosis mechanism.
A Short Double-Stapled Peptide Inhibits Respiratory Syncytial Virus Entry and Spreading
Authors: Gaillard Vanessa , Galloux Marie , Garcin Dominique , Eléouët Jean-François , Le Goffic Ronan , Larcher Thibaut , Rameix-Welti Marie-Anne , Boukadiri Abdelhak , Héritier Julien , Segura Jean-Manuel , Baechler Elodie , Arrell Miriam , Mottet-Osman Geneviève , Nyanguile Origène 
Published: January 2017

ABSTRACT
Synthetic peptides derived from the heptad repeat (HR) of fusion (F) proteins can be used as dominant negative inhibitors to inhibit the fusion mechanism of class I viral F proteins. Here, we have performed a stapled-peptide scan across the HR2 domain of the respiratory syncytial virus (RSV) F protein with the aim to identify a minimal domain capable of disrupting the formation of the postfusion six-helix bundle required for viral cell entry. Constraining the peptides with a single staple was not sufficient to inhibit RSV infection. However, the insertion of double staples led to the identification of novel short stapled peptides that display nanomolar potency in HEp-2 cells and are exceptionally robust to proteolytic degradation. By replacing each amino acid of the peptides by an alanine, we found that the substitution of residues 506 to 509, located in a patch of polar contacts between HR2 and HR1, severely affected inhibition. Finally, we show that intranasal delivery of the most potent peptide to BALB/c mice significantly decreased RSV infection in upper and lower respiratory tracts. The discovery of this minimal HR2 sequence as a means for inhibition of RSV infection provides the basis for further medicinal chemistry efforts toward developing RSV fusion antivirals.
Antimicrobial Effects of Antipyretics
Authors: Zimmermann Petra , Curtis Nigel 
Published: January 2017

ABSTRACT
Antipyretics are some of the most commonly used drugs. Since they are often coadministered with antimicrobial therapy, it is important to understand the interactions between these two classes of drugs. Our review is the first to summarize the antimicrobial effects of antipyretic drugs and the underlying mechanisms involved. Antipyretics can inhibit virus replication, inhibit or promote bacterial or fungal growth, alter the expression of virulence factors, change the surface hydrophobicity of microbes, influence biofilm production, affect the motility, adherence, and metabolism of pathogens, interact with the transport and release of antibiotics by leukocytes, modify the susceptibility of bacteria to antibiotics, and induce or reduce the frequency of mutations leading to antimicrobial resistance. While antipyretics may compromise the efficacy of antimicrobial therapy, they can also be beneficial, for example, in the management of biofilm-associated infections, in reducing virulence factors, in therapy of resistant pathogens, and in inducing synergistic effects. In an era where it is becoming increasingly difficult to find new antimicrobial drugs, targeting virulence factors, enhancing the efficacy of antimicrobial therapy, and reducing resistance may be important strategies.
Characterization of β-
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-Hydroxycytidine as a Novel Inhibitor of Chikungunya Virus
Authors: Ehteshami Maryam , Tao Sijia , Zandi Keivan , Hsiao Hui-Mien , Jiang Yong , Hammond Emily , Amblard Franck , Russell Olivia O. , Merits Andres , Schinazi Raymond F. 
Published: January 2017

ABSTRACT

Chikungunya virus (CHIKV) represents a reemerging global threat to human health. Recent outbreaks across Asia, Europe, Africa, and the Caribbean have prompted renewed scientific interest in this mosquito-borne alphavirus. There are currently no vaccines against CHIKV, and treatment has been limited to nonspecific antiviral agents, with suboptimal outcomes. Herein, we have identified β-
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-hydroxycytidine (NHC) as a novel inhibitor of CHIKV. NHC behaves as a pyrimidine ribonucleoside and selectively inhibits CHIKV replication in cell culture.