bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of modeling strategies for assessing self‐thinning behavior and carrying capacity
Authors: Salas‐Eljatib Christian , Weiskittel Aaron R. 
Published: November 2018

AbstractSelf‐thinning and site maximum carrying capacity are key concepts for understanding and predicting ecosystem dynamics as they represent the outcome of several fundamental ecological processes (e.g., mortality and growth). Relationships are often derived using alternative modeling strategies, depending on the statistical approach, model formulation, and underlying data with unclear implications of these various assumptions. In this analysis, the influence of contrasting modeling strategies for estimating the self‐thinning relationship and maximum carrying capacity in long‐term, permanent plot data (n = 130) from the mixedNothofagusforests in southern Chile was assessed and compared. Seven contrasting modeling strategies were used including ordinary least squares, quantile, and nonlinear regression that were formulated based on static (no remeasurements) or dynamic data (with remeasurements). Statistically distinct differences among these seven approaches were identified with mean maximum carrying capacity ranging from 1,050 to 1,912 stems/ha depending on the approach. The population‐level static approach based on quantile regression produced an estimate closest to the overall mean with site‐level carrying capacity depending on tree species diversity and climate.Synthesis and applications. Overall, the findings highlight strong variability within and between contrasting methods of determining self‐thinning and site maximum carry capacity, which may influence ecological inferences.
Habitat segregation between brown bears and gray wolves in a human‐dominated landscape
Authors: Milleret Cyril , Ordiz Andrés , Chapron Guillaume , Andreassen Harry Peter , Kindberg Jonas , Månsson Johan , Tallian Aimee , Wabakken Petter , Wikenros Camilla , Zimmermann Barbara , Swenson Jon E. , Sand Håkan 
Published: November 2018

AbstractIdentifying how sympatric species belonging to the same guild coexist is a major question of community ecology and conservation. Habitat segregation between two species might help reduce the effects of interspecific competition and apex predators are of special interest in this context, because their interactions can have consequences for lower trophic levels. However, habitat segregation between sympatric large carnivores has seldom been studied. Based on monitoring of 53 brown bears (Ursus arctos) and seven sympatric adult gray wolves (Canis lupus) equipped with GPS collars in Sweden, we analyzed the degree of interspecific segregation in habitat selection within their home ranges in both late winter and spring, when their diets overlap the most. We used the K‐select method, a multivariate approach that relies on the concept of ecological niche, and randomization methods to quantify habitat segregation between bears and wolves. Habitat segregation between bears and wolves was greater than expected by chance. Wolves tended to select for moose occurrence, young forests, and rugged terrain more than bears, which likely reflects the different requirements of an omnivore (bear) and an obligate carnivore (wolf). However, both species generally avoided human‐related habitats during daytime. Disentangling the mechanisms that can drive interspecific interactions at different spatial scales is essential for understanding how sympatric large carnivores occur and coexist in human‐dominated landscapes, and how coexistence may affect lower trophic levels. The individual variation in habitat selection detected in our study may be a relevant mechanism to overcome intraguild competition and facilitate coexistence.
Social structure contains epidemics and regulates individual roles in disease transmission in a group‐living mammal
Authors: Rozins Carly , Silk Matthew J. , Croft Darren P. , Delahay Richard J. , Hodgson Dave J. , McDonald Robbie A. , Weber Nicola , Boots Mike 
Published: November 2018

AbstractPopulation structure is critical to infectious disease transmission. As a result, theoretical and empirical contact network models of infectious disease spread are increasingly providing valuable insights into wildlife epidemiology. Analyzing an exceptionally detailed dataset on contact structure within a high‐density population of European badgersMeles meles,we show that a modular contact network produced by spatially structured stable social groups, lead to smaller epidemics, particularly for infections with intermediate transmissibility. The key advance is that we identify considerable variation among individuals in their role in disease spread, with these new insights made possible by the detail in the badger dataset. Furthermore, the important impacts on epidemiology are found even though the modularity of the Badger network is much lower than the threshold that previous work suggested was necessary. These findings reveal the importance of stable social group structure for disease dynamics with important management implications for socially structured populations.
Do slower movers have lower reproductive success and higher mutation load?
Authors: Walsh Carly B. , McGuigan Katrina 
Published: November 2018

AbstractDeleterious mutations occur frequently in eukaryotes, resulting in individuals carrying multiple alleles that decrease their fitness. At a population level, if unchecked, accumulation of this mutation load can ultimately lead to extinction. How selection counters the accumulation of mutation load, limiting declines in population fitness, is not well understood. Here, we use manipulative experiments in zebrafish (Danio rerio) to investigate the opportunities for selection on mutation load. Inducing high mutation load through mutagenesis, we applied one generation of within-family selection on locomotor performance and characterized both the direct response to this selection and the indirect response of reproductive success. Offspring of slow swimming parents exhibited age-dependent declines in swimming speed, whereas their cousins, with faster swimming parents, did not. This pattern mimics previously documented differences between high and low mutation load populations of zebrafish, suggesting that slow swimming siblings inherited (and transmitted) more mutations than their faster swimming siblings. Crosses among offspring of slow swimming fish had, on average, &lt;75% of the reproductive success of crosses among offspring of fast swimming parents, or crosses of offspring of slow swimmers with offspring of fast swimmers. This evidence of mutationally correlated swimming speed and reproductive success reveals the potential for concordant selection on mutation load through different fitness components. There was no evidence that crosses within families (where parents potentially shared the same mutations inherited from their common ancestor) had lower reproductive success than crosses among families, suggesting that viability selection was not acting predominantly through lethal recessive homozygotes. Rather, patterns of reproductive success are suggestive of effects of mutation number per se on embryo viability. Overall, our results highlight the potential for early life mortality to remove deleterious mutations, and the need to account for this mortality when investigating the evolutionary dynamics of mutation load.
Evolution of longevity improves immunity inDrosophila
Authors: Fabian Daniel K. , Garschall Kathrin , Klepsatel Peter , Santos-Matos Gonçalo , Sucena Élio , Kapun Martin , Lemaitre Bruno , Schlötterer Christian , Arking Robert , Flatt Thomas 
Published: November 2018

AbstractMuch has been learned about the genetics of aging from studies in model organisms, but still little is known about naturally occurring alleles that contribute to variation in longevity. For example, analysis of mutants and transgenes has identified insulin signaling as a major regulator of longevity, yet whether standing variation in this pathway underlies microevolutionary changes in lifespan and correlated fitness traits remains largely unclear. Here, we have analyzed the genomes of a set of Drosophila melanogaster lines that have been maintained under direct selection for postponed reproduction and indirect selection for longevity, relative to unselected control lines, for over 35 years. We identified many candidate loci shaped by selection for longevity and late-life fertility, but – contrary to expectation – we did not find overrepresentation of canonical longevity genes. Instead, we found an enrichment of immunity genes, particularly in the Toll pathway, suggesting that evolutionary changes in immune function might underpin – in part – the evolution of late-life fertility and longevity. To test whether this genomic signature is causative, we performed functional experiments. In contrast to control flies, long-lived flies tended to downregulate the expression of antimicrobial peptides upon infection with age yet survived fungal, bacterial, and viral infections significantly better, consistent with alleviated immunosenescence. To examine whether genes of the Toll pathway directly affect longevity, we employed conditional knockdown using in vivo RNAi. In adults, RNAi against the Toll receptor extended lifespan, whereas silencing the pathway antagonist cactus-–causing immune hyperactivation – dramatically shortened lifespan. Together, our results suggest that genetic changes in the age-dependent regulation of immune homeostasis might contribute to the evolution of longer life.
Crosstalk of mTOR/PKM2 and STAT3/c‐Myc signaling pathways regulate the energy metabolism and acidic microenvironment of gastric cancer
Authors: Gao Sumeng , Chen Min , Wei Wei , Zhang Xiaoqi , Zhang Mingming , Yao Yuling , Lv Ying , Ling Tingsheng , Wang Lei , Zou Xiaoping 
Published: November 2018

AbstractCancer cells consume large amounts of glucose to produce lactate, even in the presence of ample oxygen. This phenomenon is called the Warburg effect. c‐Myc is an important member of the Myc gene family and is involved in the development of various tumors. It plays an important role in the regulation of tumor energy metabolism, which can regulate glycolysis to promote the Warburg effect in a tumor. Our study aimed to improve the malignant biological behavior by controlling the energy metabolism of gastric cancer through the mTOR/PKM2 and signal transduction and activator 3 (STAT3)/c‐Myc signaling pathways through a series of in vitro experiments. Human gastric cancer AGS and HGC‐27 cells were treated with PKM2 and c‐Myc lentivirus, and the effects of the knockdown of PKM2 and/or c‐Myc were analyzed on cell proliferation, cell apoptosis, the ability of cell migration, and the growth signaling pathway in vitro. The expressions of PKM2, c‐Myc, LDHA, STAT3, P‐STAT3, GLUT‐1 gene were identified by the quantitative real‐time polymerase chain reaction and Western blot analysis. Lactate and glucose levels were tested by the corresponding kit. Our findings showed that PKM2 and c‐Myc were upregulated in human gastric cancer. Knockdown of c‐Myc in gastric cancer cells suppressed cell proliferation capacity and glycolysis level, and the inhibitory effects on gastric cancer cells upon co‐knockdown of PKM2 and c‐Myc were more obvious compared with knockout of PKM2 or c‐Myc alone. And there was a correlation between the mTOR/PKM2 and the STAT3/c‐Myc signaling pathways. Our results suggested that c‐Myc might be considered a potential therapeutic target for gastric cancer and PKM2 combined with c‐Myc could better inhibit the malignant biological behaviors of gastric cancer.
CircABCB10 promotes nonsmall cell lung cancer cell proliferation and migration by regulating the miR‐1252/FOXR2 axis
Authors: Tian Xufeng , Zhang Lin , Jiao Yan , Chen Junsheng , Shan Ying , Yang Wenfeng 
Published: November 2018

AbstractCircular RNA (circRNA) is a key regulator in the development and progression of human cancers. Previous studies confirmed circRNA‐0008717 (circABCB10) as an oncogene in osteosarcoma, but the regulatory effect of circABCB10 in nonsmall cell lung cancer (NSCLC) is still unclear. In the current study, we examined the expression of circABCB10 in different NSCLC cell lines. Bioinformatics analysis, Cell Counting Kit‐8 assays, Transwell migration, fluorescein reporting experiments, and xenografts in mice were used to detect the effect of circABCB10 on NSCLC cell proliferation and migration in vitro and tumor growth in vivo. The results showed that the expression of circABCB10 in NSCLC cell lines was increased. Downregulation of circABCB10 suppressed NSCLC cell proliferation and migration by promoting microRNA miR‐1252 expression and suppressing Forkhead box 2 (FOXR2). Fluorescein reporting experiments confirmed that circABCB10 expression increased FOXR2 levels by sponging miR‐1252, and in vivo experiments found that knockdown of circABCB10 decreased tumor growth. These data suggested that circABCB10 acted as a tumor promoter through a novel miR‐1252/FOXR2 axis, providing potential biomarkers and therapeutic targets for the management of NSCLC.
The diagnostic accuracy of procalcitonin and C‐reactive protein for sepsis: A systematic review and meta‐analysis
Authors: Tan Meichun , Lu Yunxia , Jiang Hao , Zhang Liandong 
Published: November 2018

AbstractBackgroundThe objective of this study was to systematically evaluate the clinical value of procalcitonin and C‐reactive protein in the diagnosis of adult patients with sepsis.MethodPubMed, Cochrane, Embase, Wanfang, China National Knowledge Infrastructure, and VIP database were searched by the index words to identify the qualified prospective studies, and relevant literature sources were also searched. The most recent research was done in the April 2017. The only languages included were English or Chinese. In the experiment group, patients were diagnosed with sepsis, severe sepsis, or septic shock; in the control group, the patients were of noninfectious origin or a systemic inflammatory response syndrome. The diagnostic accuracy was analyzed by heterogeneity, diagnostic odds ratio (DOR), sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and the summary receiver‐operating characteristic curve.ResultsAt least nine studies were involved in the meta‐analysis with 495 patients in the sepsis group and 873 patients in the nonsepsis group. In terms of the diagnostic accuracy of C‐reactive protein (CRP) for sepsis, the overall area under the summary receiver operator characteristic (SROC) curve was 0.73 (95% confidence interval [CI], 0.69‐0.77), with a sensitivity and specificity of 0.80 (95% CI, 0.63‐0.90) and 0.61 (95% CI, 0.50‐0.72) respectively, and the DOR was 6.89 (95% CI, 3.86‐12.31). In terms of the diagnostic accuracy of procalcitonin (PCT) for sepsis, the overall area under the SROC curve was 0.85 (95% CI, 0.82‐0.88), with a sensitivity and specificity of 0.80 (95% CI, 0.69‐0.87) and 0.77 (95% CI, 0.60‐0.88) respectively, and the DOR was 12.50 (95% CI, 3.65‐42.80).ConclusionIn this meta‐analysis, our results together indicate a moderate degree of value of PCT and CRP for the diagnosis of sepsis in adult patients. The diagnosis accuracy and specificity of PCT are higher than those of CRP.
Hypermethylated in cancer 1 (HIC1) suppresses bladder cancer progression by targeting yes‐associated protein (YAP) pathway
Authors: Zhou Xiaoguang , Zhang Peng , Han Hu , Lei Hongen , Zhang Xiaodong 
Published: November 2018

AbstractObjectivesBladder cancer (BCa) is the most common malignant tumor in the urinary system. Growing evidence suggests that as a tumor suppressor gene, hypermethylated in cancer 1 (HIC1) is correlated with various malignancies in the modulation of tumor progression. This study aims to investigate the effect of HIC1 on regulating the proliferation, migration, and invasion of BCa.MethodsQuantitative reverse transcription polymerase chain reaction (qRT‐PCR) and Western blot (WB) were used to evaluate the expression of HIC1 messenger RNA and protein in human BCa tissues and cells. Proliferation, migration and invasion assays, and flow cytometry assay were performed to assess the biological functional role of HIC1 in BCa. Co‐immunoprecipitation (Co‐IP) examined the protein‐protein interaction. The signaling pathways involved in the mode of action of HIC1 in BCa were also investigated.ResultsHIC1 was found downregulated in tested samples. Cloning formation assay and cell‐proliferation activity analysis showed that overexpression of HIC1 significantly inhibited the proliferation of BCa cells, while knockdown led to the opposite, namely the promotion of the proliferation. Flow cytometry assay confirmed the arrest of the cell cycle at the G1 phase with overexpression of HIC1 observed. Moreover, HIC1 inhibited migration and invasion of BCa. Co‐IP showed the binding between YAP (yes‐associated protein) and TEAD (TEA domain/transcription enhancer factor family members) as well as the cancerostatic activity of HIC1, partially manifested via its negative regulation of YAP signaling pathway.ConclusionsOur data unprecedently showed that HIC1 was responsible for the inhibition of proliferation, migration, and invasion of BCa via the YAP signaling pathway. These findings suggested that therapeutic strategies regulating HIC1 expression might provide effective treatments for BCa.
Wnt/β‐catenin signaling enhances transcription of the CX43 gene in murine Sertoli cells
Authors: López Camila , Aguilar Rodrigo , Nardocci Gino , Cereceda Karina , Vander Stelt Karen , Slebe Juan Carlos , Montecino Martin , Concha Ilona I. 
Published: November 2018

AbstractSertoli cells provide the nutritional and metabolic support for germ cells. Wnt/β‐catenin signaling is important for the development of the seminiferous epithelium during embryonic age, although after birth this pathway is downregulated. Cx43 gene codes for a protein that is critical during testicular development. The Cx43 promoter contains TCF/β‐catenin binding elements (TBEs) that contribute CX43 expression in different cell types and which may also be regulating the expression of this gene in Sertoli cells. In this study, we demonstrate that 42GPA9 Sertoli cells respond to treatments that result in accumulation of β‐catenin within the nucleus and in upregulation of CX43 gene transcription. β‐Catenin binds to TBEs located both upstream and downstream of the transcriptional start site (TSS). Luciferase reporter experiments revealed that TBEs located upstream of the TSS are necessary for β‐catenin‐mediated upregulation. Our results also indicate that the Wnt/β‐catenin‐dependent upregulation of the Cx43 gene in Sertoli cells is accompanied by changes in epigenetic parameters that may be directly contributing to generating a chromatin environment that facilitates the establishment of the transcriptional machinery at this promoter.
Epitope‐based immunoinformatics approach on RNA‐dependent RNA polymerase (RdRp) protein complex of Nipah virus (NiV)
Authors: Ravichandran Lavanya , Venkatesan Arthi , Febin Prabhu Dass J. 
Published: November 2018

AbstractPersistent outbreaks of Nipah virus (NiV) with severe case fatality throw a major challenge on researchers to develop a drug or vaccine to combat the disease. With little knowledge of its molecular mechanisms, we utilized the proteome data of NiV to evaluate the potency of three major proteins (phosphoprotein, polymerase, and nucleocapsid protein) in the RNA‐dependent RNA polymerase complex to count as a possible candidate for epitope‐based vaccine design. Profound computational analysis was used on the above proteins individually to explore the T‐cell immune properties like antigenicity, immunogenicity, binding to major histocompatibility complex class I and class II alleles, conservancy, toxicity, and population coverage. Based on these predictions the peptide ‘ELRSELIGY’ of phosphoprotein and ‘YPLLWSFAM’ of nulceocapsid protein were identified as the best‐predicted T‐cell epitopes and molecular docking with human leukocyte antigen‐C (HLA‐C*12:03) molecule was effectuated followed by validation with molecular dynamics simulation. The B‐cell epitope predictions suggest that the sequence positions 421 to 471 in phosphoprotein, 606 to 640 in polymerase and 496 to 517 in nucleocapsid protein are the best‐predicted regions for B‐cell immune response. However, the further experimental circumstance is required to test and validate the efficacy of the subunit peptide for potential candidacy against NiV.
Evaluation of Osteopontin and Pokémon genes expression in hepatitis C virus–associated hepatocellular carcinoma
Authors: El‐Khazragy Nashwa , Khalifa Mona M. , Salem Ahmed M. , Swellam Menha , Hegazy Marwa 
Published: November 2018

AbstractOsteopontin and Pokémon genes may have an important role in the pathogenesis of different malignancies. Osteopontin is a glycoprotein of the extracellular matrix, and Pokémon is a regulator of transcription. Both have been hypothesized to be useful as therapeutic targets or diagnostic markers. We aim to assess the role of both in hepatocellular carcinoma and liver fibrosis due to hepatitis C virus (HCV) infection. We conducted our study on 50 patients and classified them into three groups—Group I: Patients with HCV‐related hepatocellular carcinoma (HCC) (n = 30); Group II: Patients with hepatitis C cirrhosis (n = 10); and Group III: Patients with hepatitis C fibrosis (n = 10). We found high levels of Osteopontin and Pokémon gene expression in group I. Osteopontin levels were higher also in patients with liver fibrosis was correlated to high levels of parameters such as alpha fetoprotein and caspase. We conclude that HCC is associated with overexpression of both Osteopontin and Pokémon and that Osteopontin plays a significant role in liver fibrosis due to hepatitis C infection.
Retracted: Long noncoding RNA MEG3 inhibits proliferation and migration but induces autophagy by regulation of Sirt7 and PI3K/AKT/mTOR pathway in glioma cells
Authors: Xu Dong‐Hui , Chi Guo‐Nan , Zhao Cong‐Hai , Li Dong‐Yuan 
Published: November 2018

AbstractGlioma is a common primary brain tumor with high mortality rate and poor prognosis. Long noncoding RNA maternally expressed gene 3 (MEG3) is a tumor suppressor in diverse cancer types. However, the role of MEG3 in glioma remains unclear. We aimed to explore the effects of MEG3 on U251 cells as well as the underlying mechanisms. U251 cells were stably transfected with different recombined plasmids to overexpress or silence MEG3. Effects of aberrantly expressed MEG3 on cell viability, migration, apoptosis, expressions of apoptosis‐associated and autophagy‐associated proteins, and phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all evaluated. Then, messenger RNA (mRNA) and protein expression of Sirt7 in cells abnormally expressing MEG3 were estimated. In addition, effects of abnormally expressed MEG3 and Sirt7 on U251 cells were determined to reveal the underlying mechanism of MEG3‐associated modulation. Cell viability and migration were significantly reduced by MEG3 overexpression whereas cell apoptosis as well as Bax and cleaved caspase‐3/‐9 proteins were obviously induced. Beclin‐1 and LC3‐II/LC3‐I were upregulated and p62 was downregulated in MEG3 overexpressed cells. In addition, the autophagy pharmacological inhibitor (3‐methyladenine, 3‐MA) affected the effect of MEG3 overexpression on cell proliferation. Furthermore, the phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathway were all reduced by MEG3 overexpression. Sirt7 was positively regulated by MEG3 expression, and effects of MEG3 overexpression on U251 cells were ameliorated by Sirt7 silence. MEG3 suppressed cell proliferation and migration but promoted autophagy in U251 cells through positively regulating Sirt7, involving in the inhibition of the PI3K/AKT/mTOR pathway.