bluuebunny/crossref_metadata_2025_split huggingface dataset:
Deleterious alleles in the context of domestication, inbreeding, and selection
Authors: Bosse Mirte , Megens Hendrik‐Jan , Derks Martijn F. L. , de Cara Ángeles M. R. , Groenen Martien A. M. 
Published: August 2018

AbstractEach individual has a certain number of harmful mutations in its genome. These mutations can lower the fitness of the individual carrying them, dependent on their dominance and selection coefficient. Effective population size, selection, and admixture are known to affect the occurrence of such mutations in a population. The relative roles of demography and selection are a key in understanding the process of adaptation. These are factors that are potentially influenced and confounded in domestic animals. Here, we hypothesize that the series of events of bottlenecks, introgression, and strong artificial selection associated with domestication increased mutational load in domestic species. Yet, mutational load is hard to quantify, so there are very few studies available revealing the relevance of evolutionary processes. The precise role of artificial selection, bottlenecks, and introgression in further increasing the load of deleterious variants in animals in breeding and conservation programmes remains unclear. In this paper, we review the effects of domestication and selection on mutational load in domestic species. Moreover, we test some hypotheses on higher mutational load due to domestication and selective sweeps using sequence data from commercial pig and chicken lines. Overall, we argue that domestication by itself is not a prerequisite for genetic erosion, indicating that fitness potential does not need to decline. Rather, mutational load in domestic species can be influenced by many factors, but consistent or strong trends are not yet clear. However, methods emerging from molecular genetics allow discrimination of hypotheses about the determinants of mutational load, such as effective population size, inbreeding, and selection, in domestic systems. These findings make us rethink the effect of our current breeding schemes on fitness of populations.
Ethylenediaminetetraacetic acid (EDTA) anticoagulant affects the refractometric measurement of total protein concentration in equine synovial fluid
Authors: Hann M. J. , Parker R. A. , South V. E. N. , Underwood C. E. 
Published: August 2018

SummaryThe objectives of this study were to (i) determine the effect of ethylenediaminetetraacetic acid (EDTA) concentration on the refractometric measurement of the total protein (TP) concentration of equine synovial fluid and (ii) assess the effect of time and temperature on the refractometric measurement of TP concentration. Synovial fluid was retrieved aseptically from horses presenting to Liphook Equine Hospital either (a) immediately after euthanasia or (b) from those requiring arthrocentesis as part of their clinical investigation. Samples were aliquoted into commercially available (i) plain tubes (0.5 mL; control) and (ii) EDTA tubes (at different volumes to obtain serial dilutions of EDTA:synovial fluid). TP concentration was measured by two independent observers using a calibrated hand‐held refractometer. Samples from a separate group of horses were stored for 24 h at 4°C and 20°C before analysis to assess the effects of time and temperature. Results were compared using repeated measures ANOVA. TP concentration was significantly higher at all EDTA concentrations compared to control samples, with the greatest effect seen with higher concentrations (P<0.0001 for samples with ≥3.17 mg EDTA/mL). Storage time or temperature did not significantly affect TP concentration. Refractometric measurement of small volumes of synovial fluid in commercially available EDTA tubes leads to artificially elevated TP concentrations. Delays in sample analysis and alterations in storage conditions did not significantly affect TP concentration within the parameters studied. The magnitude of overestimation of synovial total protein concentration could result in misclassification of suspect synovial sepsis cases where EDTA tubes are used.
Risk of diabetes with fibrates and statins: a pharmacoepidemiological study in VigiBase®
Authors: Montastruc François , Benevent Justine , Rousseau Vanessa , Durrieu Geneviève , Sommet Agnès , Montastruc Jean‐Louis 
Published: August 2018

AbstractIn contrast to statins, the risk of diabetes with fibrates was not clearly studied. This study investigates a putative signal of diabetes associated with the use of fibrates using the World Health Organization (WHO) global individual case safety reports database, VigiBase®. We included all reports registered until the 31st December 2017 in VigiBase® to measure the risk of reporting ‘hyperglycemia or new onset of diabetes’ (SMQ term) compared with all other reports [as a reporting odds ratio (ROR 95% CI)] for fibrates, statins, and the combination fibrates + statins. The likelihood that diabetes resulted from statin–fibrate interaction was also estimated. According to the interaction additive model, a ROR value for coexposure exceeding the sum of the RORs estimated for each individual class of drug supports a potential drug–drug interaction (DDI). To assess the stability of our results, we performed several sensitivity analyses, according to outcome definition and after exclusion of putative competitive (hyperglycemic) drugs. We included 19 149 patients exposed to fibrates (without statins), 177 323 to statins (without fibrates) and 3 247 to statins plus fibrates. In contrast to statins (ROR = 1.75, 95% CI 1.72–1.78), no association was found for fibrates (ROR = 0.76, 95% CI 0.71–0.82). The ROR value was lower for the combination statins plus fibrates (ROR = 1.46, 95% CI 1.28–1.67). Similar trends were found in sensitivity analyses. This study, performed in the real conditions of use, failed to find a signal of diabetes with fibrates. It strengths the association previously described with statin without any evidence for a statin–fibrate DDI.
Histone H3K36M mutation and trimethylation patterns in chondroblastoma
Authors: Lu Chuanyong , Ramirez Daniel , Hwang Sinchun , Jungbluth Achim , Frosina Denise , Ntiamoah Peter , Healey John , Zhu Guo , Chen Wen , Klein Michael , Hameed Meera 
Published: August 2018

AimsHistones are essential components of chromatin, and mutations in histones lead to alterations in methylation and acetylation, which play an important role in tumorigenesis. Most of the chondroblastomas harbour the H3K36M mutation. With the availability of a mutation‐specific antibody, we sought to assess the sensitivity of this antibody and the alterations of histone methylation in a series of chondroblastoma cases.Methods and resultsImmunohistochemical staining with antibodies against H3K36M, trimethylated histones (H3K27me3 and H3K36me3) and an osteoblastic marker (SATB2) was performed on 27 chondroblastomas from 27 patients. The clinical and radiological characteristics of each patient were reviewed. All 27 tumours showed typical radiological and histological features of chondroblastoma, with a subset of cases showing secondary aneurysmal bone cyst changes (11/27), giant‐cell‐rich foci (4/27), and matrix‐rich areas mimicking chondromyxoid fibroma (1/27). All except one case (26/27, 96%) showed positive H3K36M immunostaining (nuclear). In the majority of cases, there was a diffuse staining pattern. Immunohistochemical staining for H3K27me3 and H3K36me3 showed a heterogeneous staining pattern in all cases, regardless of mutation status. None of the cases showed loss of positivity or diffuse positivity. Focal or diffuse SATB2 expression was seen in 21 of 26 tumours (81%).ConclusionOur results demonstrate that the vast majority of chondroblastomas are positive for H3K36M by immunohistochemical analysis, confirming its diagnostic value. H3K27me3 expression and H3K36me3 expression are heterogeneous in these tumours.
Electrical properties of Y/Mg modified NiO simple oxides for negative temperature coefficient thermistors
Authors: He Zhenli , Li Zhicheng , Xiang Qinghua , Yan Weiqin , Zhang Hong 
Published: August 2018

AbstractThe semiconductors based on simple oxide have unique features with controllable electrical property by element doping. Y3+ doped NiO (Ni1−xYxO, x ≤ 0.01) and Mg2+ substituted Ni0.995Y0.005O (Ni0.995−yY0.005MgyO, y ≤ 0.5) powders were synthesized by a wet chemical method. The related ceramics were obtained by conventional ceramic processing. Phase component, microstructure, electrical property and temperature sensitivity of the prepared ceramics were investigated. All ceramics have a rock‐salt type crystalline structure. The room‐temperature resistivity of the ceramics can be widely adjusted from 254 to 12 322 Ω·cm by changing the concentrations of Y3+ and Mg2+ ions. The samples show typical characteristics of negative temperature coefficient of resistivity and have high temperature sensitivity with material constants higher than 4745 K. The analysis of impedance spectra indicates that the electrical properties resulted from both grain effect and grain boundary effect. Both band conduction and small polaron hopping were proposed as possible conduction mechanisms in the studied ceramics.
Investigating photocatalytic property of TiO2 nanorods fabricated hydrothermally at equal molar ratio of KOH and NaOH
Authors: Naseri Katayoon , Allahverdi Ali 
Published: August 2018

AbstractTiO2 photocatalysts were prepared by hydrothermal method at temperatures of 110, 155, and 200°C for 24 hours, using KOH (5 mol/L):NaOH (5 mol/L) solution and anatase TiO2 powder with an average particle size of 0.13 μm as precursor and by calcining at two different temperatures of 450 and 700°C. An overall photocatalytic removal efficiency of 93% was achieved for Rhodamine B dye under UV light irradiation by the photocatalyst obtained at synthesis and calcination temperatures of 155 and 700°C, respectively, which indicated a nanorod morphology with a mean diameter of about 34 nm.
Interleukin‐33 contributes to disease severity in Dengue virus infection in mice
Authors: Marques Rafael E. , Besnard Anne‐Gaëlle , Maillet Isabelle , Fagundes Caio T. , Souza Danielle G. , Ryffel Bernhard , Teixeira Mauro M. , Liew Foo Y. , Guabiraba Rodrigo 
Published: August 2018

SummaryThe excessive inflammation often present in patients with severe dengue infection is considered both a hallmark of disease and a target for potential treatments. Interleukin‐33 (IL‐33) is a pleiotropic cytokine with pro‐inflammatory effects whose role in dengue has not been fully elucidated. We demonstrate that IL‐33 plays a disease‐exacerbating role during experimental dengue infection in immunocompetent mice. Mice infected with dengue virus serotype 2 (DENV2) produced high levels of IL‐33. DENV2‐infected mice treated with recombinant IL‐33 developed markedly more severe disease compared with untreated mice as assessed by mortality, granulocytosis, liver damage and pro‐inflammatory cytokine production. Conversely, ST2−/− mice (deficient in IL‐33 receptor) infected with DENV2 developed significantly less severe disease compared with wild‐type mice. Furthermore, the increased disease severity and the accompanying pathology induced by IL‐33 during dengue infection were reversed by the simultaneous treatment with a CXCR2 receptor antagonist (DF2156A). Together, these results indicate that IL‐33 plays a disease‐exacerbating role in experimental dengue infection, probably driven by CXCR2‐expressing cells, leading to elevated pro‐inflammatory response‐mediated pathology. Our results also indicate that IL‐33 is a potential therapeutic target for dengue infection.
The inflammasomes, immune guardians at defence barriers
Authors: Palazon‐Riquelme Pablo , Lopez‐Castejon Gloria 
Published: August 2018

SummaryAs a result of its strategic location, the epithelium is constantly exposed to a wide variety of pathogen and danger signals. Traditionally, the epithelium has been perceived as a defensive but passive barrier; however, it has now become evident that the epithelium senses and actively responds to these signals in order to maintain barrier homeostasis and contributes to the inflammatory response. One way it does this is by producing pro‐inflammatory cytokines including interleukin‐1β (IL‐1β) and IL‐18. These two cytokines are synthesized as inactive precursors, the maturation of which is mediated by pro‐inflammatory caspases after the activation and assembly of macromolecular complexes called inflammasomes. Epithelial cells express a large panel of inflammasome components, and although the molecular mechanisms underlying the activation of these complexes in haematopoietic cells are well understood, how epithelial cells react to danger signals to activate the inflammasome remains unclear. We review and discuss how different inflammasomes contribute to barrier homeostasis and inflammation at several barrier sites, their mechanisms and how their aberrant regulation contributes to disease at the different epithelia.
YY1 binds to the E3ʹ enhancer and inhibits the expression of the immunoglobulin κ gene via epigenetic modifications
Authors: Zhou Xiaorong , Xian Weiwei , Zhang Jie , Zhu Yiqing , Shao Xiaoyi , Han Yu , Qi Yue , Ding Xiaoling , Wang Xiaoying 
Published: August 2018

SummaryThe rearrangement and expression of immunoglobulin genes are regulated by enhancers and their binding transcriptional factors that activate or suppress the activities of the enhancers. The immunoglobulin κ (Igκ) gene locus has three important enhancers: the intrinsic enhancer (Ei), 3′ enhancer (E3′), and distal enhancer (Ed). Ei and E3′ are both required for Igκ gene rearrangement during early stages of B‐cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3′ and Ed. The transcription factor YY1 affects the expression of many genes involved in B‐cell development, probably by mediating interactions between their enhancers and promoters. Herein, we found that YY1 binds to the E3ʹ enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer. Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3ʹ enhancer. Moreover, in germinal centre B cells and plasma cells, YY1 expression was reversely associated with Igκ levels, implying that YY1 might facilitate antibody affinity maturation in germinal centre B cells through the transient attenuation of Igκ expression.
The impact of inflationary cytomegalovirus‐specific memory T cells on anti‐tumour immune responses in patients with cancer
Authors: Luo Xiao‐Hua , Meng Qingda , Rao Martin , Liu Zhenjiang , Paraschoudi Georgia , Dodoo Ernest , Maeurer Markus 
Published: August 2018

SummaryHuman cytomegalovirus (CMV) is a ubiquitous, persistent beta herpesvirus. CMV infection contributes to the accumulation of functional antigen‐specific CD8+ T‐cell pools with an effector‐memory phenotype and enrichment of these immune cells in peripheral organs. We review here this ‘memory T‐cell inflation’ phenomenon and associated factors including age and sex. ‘Collateral damage’ due to CMV‐directed immune reactivity may occur in later stages of life – arising from CMV‐specific immune responses that were beneficial in earlier life. CMV may be considered an age‐dependent immunomodulator and a double‐edged sword in editing anti‐tumour immune responses. Emerging evidence suggests that CMV is highly prevalent in patients with a variety of cancers, particularly glioblastoma. A better understanding of CMV‐associated immune responses and its implications for immune senescence, especially in patients with cancer, may aid in the design of more clinically relevant and tailored, personalized treatment regimens. ‘Memory T‐cell inflation’ could be applied in vaccine development strategies to enrich for immune reactivity where long‐term immunological memory is needed, e.g. in long‐term immune memory formation directed against transformed cells.
Climate risk on two vegetation axes—Tropical wet‐to‐dry and temperate arid‐to‐moist forests
Authors: Williams John N. , Rivera Raul , Choe Hyeyeong , Schwartz Mark W. , Thorne James H. 
Published: August 2018

AbstractAimAssess climatic risk to vegetation types associated with tropical and temperate ecosystems based on exposure analysis, which models future risk as a function of deviation from current climate variable distributions.LocationOaxaca State, Mexico.TaxonBroadly defined vegetation types used in state‐ and national‐level vegetation classification systems. These types can be grouped into series representing dry‐to‐wet conditions for tropical and temperate vegetation.MethodsWe used climate exposure analysis to compare current and future climate parameters for the major vegetation types of Oaxaca. This technique integrates a recent vegetation map with historical climate data (1981–2010) to produce a baseline climate layer that is compared to climate projections made with five different global circulation models for near‐future (2015–2039) and end‐century (2075–2099) periods using two emissions scenarios (RCP4.5 and 8.5). We classified the frequency distribution of the baseline climate into five exposure classes where the closer values are to mean climate conditions, the lower the exposure. Future exposure was estimated by classifying the vegetation pixels into the same exposure classes, now based on future climate values. Increased exposure risk was assessed based on the fraction of pixels that moved into higher exposure classes from one period to another.Results and main conclusionsOur analysis showed four general trends: (a) the higher, current track emissions scenario produced much larger end‐century climate exposure; (b) for the tropical vegetation series, tropical evergreen forests are projected as most exposed by end‐century; (c) for the temperate vegetation series the matorral‐shrubland and conifer forests are the most impacted; and (d) the fiveGCMs considered showed some convergence in their end‐century climate exposure predictions, with coastal and low‐elevation areas of the State projected to experience the greatest exposure, and the interior mountain slopes and central region projected to experience the least exposure and be the most climatically stable.
An ancient and a recent colonization of islands by an Australian sap‐feeding insect
Authors: Fromont Caroline , Rymer Paul D. , Riegler Markus , Cook James M. 
Published: August 2018

AbstractAimTo assess the genetic structure, biogeography, and the potential for speciation, of a highly host‐specific insect pest with mainland and island populations.LocationEast coast of Australia, Lord Howe Island (LHI), and New Zealand.MethodsWe focussed on Mycopsylla fici, a plant sap‐feeding insect host‐specific to the fig tree Ficus macrophylla. We genotyped 152 insects from across the natural and extended host plant range at 14 microsatellite loci and analysed the data using standard population genetics statistics, Discriminant Analysis of Principal Components, genetic autocorrelation, and two Bayesian clustering approaches.ResultsGenetic analyses revealed that the northeastern Australian mainland population (Brisbane) is the centre of genetic diversity. Northeastern and southeastern (Sydney) mainland populations are genetically differentiated and interconnected in a stepping‐stone pattern. The LHI population is the most distinct genetically and Bayesian estimates indicated that the most recent colonization occurred c. 2,000‐17,500 years ago from a northeastern mainland origin. In contrast, the New Zealand population is little differentiated from the Sydney population and probably diverged by colonization within the past 200 years.Main conclusionsThe strong differentiation in nuclear microsatellites mirrors previous evidence for divergence of the LHI population from both mtDNA and endosymbiont DNA. The LHI population may be undergoing speciation from the mainland populations, with an oceanic barrier to gene flow. In contrast, the geographically isolated population in Auckland represents a far more recent colonization reflecting the contemporary naturalization of the plant host in New Zealand.
MelaNostrum: a consensus questionnaire of standardized epidemiologic and clinical variables for melanoma risk assessment by the melanostrum consortium
Authors: Stratigos Alexander J. , Fargnoli Maria Concetta , De Nicolo Arcangela , Peris Ketty , Puig Susana , Soura Efthymia , Menin Chiara , Calista Donato , Ghiorzo Paola , Mandala Mario , Massi Daniela , Rodolfo Monica , Del Regno Laura , Stefanaki Irene , Gogas Helen , Bataille Veronique , Tucker Margaret A. , Whiteman David , Nagore Eduardo , Landi Maria Teresa 
Published: August 2018

AbstractBackgroundMany melanoma observational studies have been carried out across different countries and geographic areas using heterogeneous assessments of epidemiologic risk factors and clinical variables.AimTo develop a consensus questionnaire to standardize epidemiologic and clinical data collection for melanoma risk assessment.MethodsWe used a stepwise strategy that included: compilation of variables from case–control datasets collected at various centres of the MelaNostrum Consortium; integration of variables from published case–control studies; consensus discussion of the collected items by MelaNostrum members; revision by independent experts; addition of online tools and image‐based charts; questionnaire testing across centres and generation of a final draft.ResultsWe developed a core consensus questionnaire (MelanoQ) that includes four separate sections: A. general and demographic data; B. phenotypic and ultraviolet radiation exposure risk factors and lifestyle habits; C. clinical examination, medical and family history; and D. diagnostic data on melanoma (cases only). Accompanying online tools, informative tables, and image‐based charts aid standardization. Different subsections of the questionnaire are designed for self‐administration, patient interviews performed by a physician or study nurse, and data collection from medical records.ConclusionsThe MelanoQ questionnaire is a useful tool for the collection and standardization of epidemiologic and clinical data across different studies, centres, cultures and languages. This will expedite ongoing efforts to compile high‐quality data for pooled analyses or meta‐analyses and offer a solid base for the design of clinical, epidemiologic and translational studies on melanoma.