bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of host plants on life history traits of Phenacoccus solenopsis (Homoptera: Pseudococcidae)
Authors: Dogar Abdul Manan , Ayyaz Mahmood , Abbas Naeem , Shad Sarfraz Ali , Naeem Afifa 
Published: September 2018

AbstractCotton mealybug,Phenacoccus solenopsisTinsley is an important polyphagous insect pest and causes severe losses to different crops worldwide. In the current study, we investigated the effect of different host plants, such asCaesalpinia pulcherrima,Plumeria rubra, Anthurium andraeanum, Jasminum sambac, andHibiscus rosasinensis, on the biological parameters ofP. solenopsis. The survival rate from crawler to adult, female nymphal duration, development time from crawler to female adult, and female adult weight were significantly different on the different hosts. Male nymphal duration, development time from crawler to male adult, pupal weight, emergence rate of male adults, and mean relative growth rate for male were similar on all the tested host plants. Pupal duration and generation time of male and female onH. rosasinensiswere significantly shorter than on the other hosts. Adult male and femaleP. solenopsislongevity was significantly shorter onH. rosasinensiscompared to other hosts. The fecundity was lower onC. pulcherrimaandA. andraeanumand hatchability was lower onC. pulcherrimathan on the other hosts. The net reproductive rate, the intrinsic rate of natural increase, and biotic potential and mean relative growth rate for female ofP. solenopsiswere significantly different on the tested hosts. Our results point to the role of host plants in increasing the populations ofP. solenopsisand could help to design cultural management strategies.
Fruits of Icacinaceae Miers from the Palaeocene of the Paris Basin (Oise, France)
Authors: Del Rio Cédric , Thomas Romain , De Franceschi Dario 
Published: September 2018

ABSTRACTIcacinaceae Miers are a family of trees, shrubs, and lianas with a current pantropical distribution. The family is well known in the fossil record, especially from the Palaeogene of Europe and North America, with the modern genus Iodes being particularly well represented. Here, we describe five new species of Iodes based on fossil endocarps with horn-like protrusions from the late Palaeocene Rivecourt deposits (Oise, France). Moreover, we propose a new combination for Iodes israelii Soudry & Gregor, as Icacinicarytes israelii (Soudry & Gregor) Del Rio, Thomas & De Franceschi, because it lacks the diagnostic morphological and anatomical characters of the genus Iodes. The significance of papillae, which has been emphasised in the literature, is discussed in light of new data, and a more standardised system of terminology is proposed. Given that, among modern members of Iodes, horn-like protrusions are only known from Asian species; the fossils described here suggest an affinity between the late Palaeocene flora of Europe and the modern flora of Asia. Finally, this study represents the first detailed investigation of Icacinaceae from the Paris Basin, where palaeocarpology remains understudied.
Evaporation From Layered Porous Medium in the Presence of Infrared Heating
Authors: Kumar Navneet , Arakeri Jaywant H. 
Published: September 2018

AbstractWe report an experimental study of evaporation of two configurations of layered porous media that are heated from above by infrared (IR) radiation having ~1,000 W/m2 intensity. We used nearly monodisperse glass beads in each of the layers. The two configurations are (1) coarse and fine beads, stacked side by side and (2) fine beads over coarse beads (FoC). The IR heater mimics the natural evaporation process in soils, and the aim is to study, using three diagnostic tools, how the layering affects the evaporation process, and compare it with the homogeneous porous medium case. For each experiment we use three diagnostics simultaneously, evaporation rate measurement using a precision balance, surface temperature imaging using an IR camera, and visualization of the evaporation process with fluorescein dye. The constant (evaporation) rate period (CRP) regime, found in homogeneous porous media, is drastically changed for the two layered configurations. We show new results for side‐by‐side configuration. In the FoC configuration we show that the near‐surface water content in the finer particles does not change in CRP and a true constant evaporation rate is possible. The average water depth at end of CRP in the porous medium, for a wide range of diameter ratios for the FoC configuration are compared with the predictions from theoretical relations proposed by Shokri et al. (2010, https://doi.org/10.1029/2009JB006743) and Assouline et al. (2014, https://doi.org/10.1002/2013WR014489). Using a simple surface energy budget, we show that knowing the surface temperature, the evaporation rate can be estimated with reasonable accuracy (±5%) during drying of a porous medium.
Climate Change and Women's Health: Impacts and Opportunities in India
Authors: Sorensen Cecilia , Saunik Sujata , Sehgal Meena , Tewary Anwesha , Govindan Mini , Lemery Jay , Balbus John 
Published: September 2018

AbstractClimate change impacts on health, including increased exposures to heat, poor air quality, extreme weather events, and altered vector‐borne disease transmission, reduced water quality, and decreased food security, affect men and women differently due to biologic, socioeconomic, and cultural factors. In India, where rapid environmental changes are taking place, climate change threatens to widen existing gender‐based health disparities. Integration of a gendered perspective into existing climate, development, and disaster‐risk reduction policy frameworks can decrease negative health outcomes. Modifying climate risks requires multisector coordination, improvement in data acquisition, monitoring of gender specific targets, and equitable stakeholder engagement. Empowering women as agents of social change can improve mitigation and adaptation policy interventions.
Changes in Marine Fog Over the North Pacific Under Different Climates in CMIP5 Multimodel Simulations
Authors: Kawai Hideaki , Koshiro Tsuyoshi , Endo Hirokazu , Arakawa Osamu 
Published: September 2018

AbstractIn this study, the changes in the occurrence of marine fog over the summer North Pacific in warmer sea surface temperature (SST) or increased CO2 climates were investigated based on atmospheric model simulations by using the fifth phase of the Climate Model Intercomparison Project (CMIP5) multimodel data. Initially, the marine fog representation in CMIP5 multimodels was briefly evaluated globally. We found that the simulated marine fog occurrence was represented relatively well in boreal summer but poorly in other seasons. The results indicated that the changes in the North Pacific high‐pressure system accompanied by changes in horizontal wind patterns control the changes in marine fog occurrence in the North Pacific. The magnitude of contrasting pair changes in marine fog occurrence in the western and eastern North Pacific are primarily determined by the magnitude of changes in the North Pacific high‐pressure system. Global‐scale changes in the vertical profiles of the atmosphere (stability changes) can also affect the marine fog changes. These changes in marine fog over the North Pacific were consistent among most CMIP5 models.
Wastewater treatment plant resistomes are shaped by bacterial composition, genetic exchange, and upregulated expression in the effluent microbiomes
Authors: Ju Feng , Beck Karin , Yin Xiaole , Maccagnan Andreas , McArdell Christa S , Singer Heinz P , Johnson David R , Zhang Tong , Bürgmann Helmut 
Published: September 2018

Abstract
Wastewater treatment plants (WWTPs) are implicated as hotspots for the dissemination of antibacterial resistance into the environment. However, the in situ processes governing removal, persistence, and evolution of resistance genes during wastewater treatment remain poorly understood. Here, we used quantitative metagenomic and metatranscriptomic approaches to achieve a broad-spectrum view of the flow and expression of genes related to antibacterial resistance to over 20 classes of antibiotics, 65 biocides, and 22 metals. All compartments of 12 WWTPs share persistent resistance genes with detectable transcriptional activities that were comparatively higher in the secondary effluent, where mobility genes also show higher relative abundance and expression ratios. The richness and abundance of resistance genes vary greatly across metagenomes from different treatment compartments, and their relative and absolute abundances correlate with bacterial community composition and biomass concentration. No strong drivers of resistome composition could be identified among the chemical stressors analyzed, although the sub-inhibitory concentration (hundreds of ng/L) of macrolide antibiotics in wastewater correlates with macrolide and vancomycin resistance genes. Contig-based analysis shows considerable co-localization between resistance and mobility genes and implies a history of substantial horizontal resistance transfer involving human bacterial pathogens. Based on these findings, we propose future inclusion of mobility incidence (M%) and host pathogenicity of antibiotic resistance genes in their quantitative health risk ranking models with an ultimate goal to assess the biological significance of wastewater resistomes with regard to disease control in humans or domestic livestock.
SP1-induced lncRNA-ZFAS1 contributes to colorectal cancer progression via the miR-150-5p/VEGFA axis
Authors: Chen Xiaoxiang , Zeng Kaixuan , Xu Mu , Hu Xiuxiu , Liu Xiangxiang , Xu Tao , He Bangshun , Pan Yuqin , Sun Huiling , Wang Shukui 
Published: September 2018

AbstractIncreasing long non-coding RNAs (lncRNAs) have been reported to play key roles in the development and progression of various malignancies. ZNFX1 antisense RNA1 (ZFAS1) has been reported to be aberrant expression and suggested as a tumor suppressor or oncogene in many cancers. However, the biological role and underlying molecular mechanism of ZFAS1, especially the miRNA sponge role of which in CRC remain largely unknown. We found that ZFAS1 expression was higher in CRC tissues, where it was associated with poor overall survival (OS), we also showed that ZFAS1 upregulation was induced by nuclear transcription factor SP1. Moreover, ZFAS1 and VEGFA are both targets of miR-150-5p, while ZFAS1 binds to miR-150-5p in an AGO2-dependent manner. Additionally, ZFAS1 upregulation markedly promoted as well as ZFAS1 knockdown significantly suppressed CRC cell proliferation, migration, invasion and angiogenesis, and the inhibitory effect caused by ZFAS1 knockdown could be reversed by antagomiR-150-5p. Lastly, we demonstrated that ZFAS1 knockdown inhibited EMT process and inactivated VEGFA/VEGFR2 and downstream Akt/mTOR signaling pathway in CRC. Our data demonstrated that SP1-induced ZFAS1 contributed to CRC progression by upregulating VEGFA via competitively binding to miR-150-5p, which acts as a tumor suppressor by targeting VEGFA in CRC.
Loperamide, pimozide, and STF-62247 trigger autophagy-dependent cell death in glioblastoma cells
Authors: Zielke Svenja , Meyer Nina , Mari Muriel , Abou-El-Ardat Khalil , Reggiori Fulvio , van Wijk Sjoerd J. L. , Kögel Donat , Fulda Simone 
Published: September 2018

AbstractAutophagy is a well-described degradation mechanism that promotes cell survival upon nutrient starvation and other forms of cellular stresses. In addition, there is growing evidence showing that autophagy can exert a lethal function via autophagic cell death (ACD). As ACD has been implicated in apoptosis-resistant glioblastoma (GBM), there is a high medical need for identifying novel ACD-inducing drugs. Therefore, we screened a library containing 70 autophagy-inducing compounds to induce ATG5-dependent cell death in human MZ-54 GBM cells. Here, we identified three compounds, i.e. loperamide, pimozide, and STF-62247 that significantly induce cell death in several GBM cell lines compared to CRISPR/Cas9-generated ATG5- or ATG7-deficient cells, pointing to a death-promoting role of autophagy. Further cell death analyses conducted using pharmacological inhibitors revealed that apoptosis, ferroptosis, and necroptosis only play minor roles in loperamide-, pimozide- or STF-62247-induced cell death. Intriguingly, these three compounds induce massive lipidation of the autophagy marker protein LC3B as well as the formation of LC3B puncta, which are characteristic of autophagy. Furthermore, loperamide, pimozide, and STF-62247 enhance the autophagic flux in parental MZ-54 cells, but not in ATG5 or ATG7 knockout (KO) MZ-54 cells. In addition, loperamide- and pimozide-treated cells display a massive formation of autophagosomes and autolysosomes at the ultrastructural level. Finally, stimulation of autophagy by all three compounds is accompanied by dephosphorylation of mammalian target of rapamycin complex 1 (mTORC1), a well-known negative regulator of autophagy. In summary, our results indicate that loperamide, pimozide, and STF-62247 induce ATG5- and ATG7-dependent cell death in GBM cells, which is preceded by a massive induction of autophagy. These findings emphasize the lethal function and potential clinical relevance of hyperactivated autophagy in GBM.
Proscillaridin A exerts anti-tumor effects through GSK3β activation and alteration of microtubule dynamics in glioblastoma
Authors: Berges Raphael , Denicolai Emilie , Tchoghandjian Aurélie , Baeza-Kallee Nathalie , Honore Stephane , Figarella-Branger Dominique , Braguer Diane 
Published: September 2018

AbstractGlioblastoma (GBM) is characterized by highly aggressive growth and invasive behavior. Due to the highly lethal nature of GBM, new therapies are urgently needed and repositioning of existing drugs is a promising approach. We have previously shown the activity of Proscillaridin A (ProA), a cardiac glycoside inhibitor of the Na(+)/K(+) ATPase (NKA) pump, against proliferation and migration of GBM cell lines. ProA inhibited tumor growth in vivo and increased mice survival after orthotopic grafting of GBM cells. This study aims to decipher the mechanism of action of ProA in GBM tumor and stem-like cells. ProA displayed cytotoxic activity on tumor and stem-like cells grown in 2D and 3D culture, but not on healthy cells as astrocytes or oligodendrocytes. Even at sub-cytotoxic concentration, ProA impaired cell migration and disturbed EB1 accumulation at microtubule (MT) plus-ends and MT dynamics instability. ProA activates GSK3β downstream of NKA inhibition, leading to EB1 phosphorylation on S155 and T166, EB1 comet length shortening and MT dynamics alteration, and finally inhibition of cell migration and cytotoxicity. Similar results were observed with digoxin. Therefore, we disclosed here a novel pathway by which ProA and digoxin modulate MT-governed functions in GBM tumor and stem-like cells. Altogether, our results support ProA and digoxin as potent candidates for drug repositioning in GBM.
POFUT1 promotes colorectal cancer development through the activation of Notch1 signaling
Authors: Du Yuheng , Li Daojiang , Li Nanpeng , Su Chen , Yang Chunxing , Lin Changwei , Chen Miao , Wu Runliu , Li Xiaorong , Hu Gui 
Published: September 2018

AbstractCopy number variations (CNVs) are key drivers of colorectal cancer (CRC). Our previous studies revealed that protein O-fucosyltransferase 1 (POFUT1) overexpression is driven by CNVs during CRC development. The potential role and underlying mechanisms of POFUT1 in CRC were not investigated. In this study, we analyzed the expression of POFUT1 in CRC from cosmic and TCGA databases and confirmed that POFUT1 is highly expressed in CRC. We used well characterized CRC cell lines, including SW620 and HCT116 to establish a model POFUT1 knockdown cell line. Using these cells, we investigated the role of POFUT1 in CRC. Our data revealed that silencing POFUT1 in CRC cells inhibits cell proliferation, decreases cell invasion and migration, arrests cell cycle progression, and stimulates CRC cell apoptosis in vitro. We further demonstrate that POFUT1 silencing dramatically suppresses CRC tumor growth and transplantation in vivo. We additionally reveal new mechanistic insights into the role of POFUT1 during CRC, through demonstrating that POFUT1 silencing inhibits Notch1 signaling. Taken together, our findings demonstrate that POFUT1 is a tumor activating gene during CRC development, which positively regulates CRC tumor progression through activating Notch1.
SIRT3 deficiency leads to induction of abnormal glycolysis in diabetic kidney with fibrosis
Authors: Srivastava Swayam Prakash , Li Jinpeng , Kitada Munehiro , Fujita Hiroki , Yamada Yuichiro , Goodwin Julie E. , Kanasaki Keizo , Koya Daisuke 
Published: September 2018

AbstractThe regulation of aberrant glucose metabolism in diabetes associated-kidney fibrosis is not well known. In this study we found the suppression of SIRT3 protein level in diabetic kidney, displays responsibility in fibrogenic programming associated with aberrant glycolysis and such abnormal glycolysis is the therapeutic target in diabetes associated-kidney fibrosis. When analyzing different strains of streptozotocin-induced diabetic mice model (fibrotic model: CD-1, less fibrotic model: C57Bl6), we found SIRT3 suppression was associated with kidney fibrosis in fibrotic CD-1; further SIRT3 suppression by systemic administration of SIRT3 siRNA in the diabetic mice, showed profound fibrogenic phenotype in the kidney. Such suppression in SIRT3 was associated with the induction of transforming growth factor-β (TGF-β)/smad signaling, higher level of HIF1α accumulation and PKM2 dimer formation; these alterations subsequently led to abnormal glycolysis and linked abnormal mesenchymal transformations in vivo and in vitro. Inhibition of such aberrant glycolysis suppressed fibrogenic programming and restored SIRT3 level as well. Such aberrant glycolysis was confirmed in the KK/Ta-Ins2Akita mouse, the mouse model of progressive diabetic kidney disease. These data demonstrate that SIRT3 deficiency promotes abnormal glycolysis which is responsible for the fibrogenic pathway in diabetic kidney. Restoration of SIRT3 could be an alternative strategy in combating diabetes associated-kidney fibrosis via inhibition of aberrant glycolysis.
Pharmacological activation of SIRT6 triggers lethal autophagy in human cancer cells
Authors: Iachettini Sara , Trisciuoglio Daniela , Rotili Dante , Lucidi Alessia , Salvati Erica , Zizza Pasquale , Di Leo Luca , Del Bufalo Donatella , Ciriolo Maria Rosa , Leonetti Carlo , Steegborn Clemens , Mai Antonello , Rizzo Angela , Biroccio Annamaria 
Published: September 2018

AbstractSirtuin 6 (SIRT6) is a member of the NAD+-dependent class III deacetylase sirtuin family, which plays a key role in cancer by controlling transcription, genome stability, telomere integrity, DNA repair, and autophagy. Here we analyzed the molecular and biological effects of UBCS039, the first synthetic SIRT6 activator. Our data demonstrated that UBCS039 induced a time-dependent activation of autophagy in several human tumor cell lines, as evaluated by increased content of the lipidated form of LC3B by western blot and of autophagosomal puncta by microscopy analysis of GFP-LC3. UBCS039-mediated activation of autophagy was strictly dependent on SIRT6 deacetylating activity since the catalytic mutant H133Y failed to activate autophagy. At the molecular level, SIRT6-mediated autophagy was triggered by an increase of ROS levels, which, in turn, resulted in the activation of the AMPK-ULK1-mTOR signaling pathway. Interestingly, antioxidants were able to completely counteract UBCS039-induced autophagy, suggesting that ROS burst had a key role in upstream events leading to autophagy commitment. Finally, sustained activation of SIRT6 resulted in autophagy-related cell death, a process that was markedly attenuated using either a pan caspases inhibitor (zVAD-fmk) or an autophagy inhibitor (CQ). Overall, our results identified UBCS039 as an efficient SIRT6 activator, thereby providing a proof of principle that modulation of the enzyme can influence therapeutic strategy by enhancing autophagy-dependent cell death.
Temporal genetic association and temporal genetic causality methods for dissecting complex networks
Authors: Lin Luan , Chen Quan , Hirsch Jeanne P. , Yoo Seungyeul , Yeung Kayee , Bumgarner Roger E. , Tu Zhidong , Schadt Eric E. , Zhu Jun 
Published: September 2018

AbstractA large amount of panomic data has been generated in populations for understanding causal relationships in complex biological systems. Both genetic and temporal models can be used to establish causal relationships among molecular, cellular, or phenotypical traits, but with limitations. To fully utilize high-dimension temporal and genetic data, we develop a multivariate polynomial temporal genetic association (MPTGA) approach for detecting temporal genetic loci (teQTLs) of quantitative traits monitored over time in a population and a temporal genetic causality test (TGCT) for inferring causal relationships between traits linked to the locus. We apply MPTGA and TGCT to simulated data sets and a yeast F2 population in response to rapamycin, and demonstrate increased power to detect teQTLs. We identify a teQTL hotspot locus interacting with rapamycin treatment, infer putative causal regulators of the teQTL hotspot, and experimentally validate RRD1 as the causal regulator for this teQTL hotspot.
Towards a comprehensive understanding of the structural dynamics of a bacterial diterpene synthase during catalysis
Authors: Driller Ronja , Janke Sophie , Fuchs Monika , Warner Evelyn , Mhashal Anil R. , Major Dan Thomas , Christmann Mathias , Brück Thomas , Loll Bernhard 
Published: September 2018

AbstractTerpenes constitute the largest and structurally most diverse natural product family. Most terpenoids exhibit a stereochemically complex macrocyclic core, which is generated by C–C bond forming of aliphatic oligo-prenyl precursors. This reaction is catalysed by terpene synthases (TPSs), which are capable of chaperoning highly reactive carbocation intermediates through an enzyme-specific reaction. Due to the instability of carbocation intermediates, the proteins’ structural dynamics and enzyme:substrate interactions during TPS catalysis remain elusive. Here, we present the structure of the diterpene synthase CotB2, in complex with an in crystallo cyclised abrupt reaction product and a substrate-derived diphosphate. We captured additional snapshots of the reaction to gain an overview of CotB2’s catalytic mechanism. To enhance insights into catalysis, structural information is augmented with multiscale molecular dynamic simulations. Our data represent fundamental TPS structure dynamics during catalysis, which ultimately enable rational engineering towards tailored terpene macrocycles that are inaccessible by conventional chemical synthesis.
Genus-wide sequencing supports a two-locus model for sex-determination in Phoenix
Authors: Torres Maria F. , Mathew Lisa S. , Ahmed Ikhlak , Al-Azwani Iman K. , Krueger Robert , Rivera-Nuñez Diego , Mohamoud Yasmin A. , Clark Andrew G. , Suhre Karsten , Malek Joel A. 
Published: September 2018

AbstractThe date palm tree is a commercially important member of the genus Phoenix whose 14 species are dioecious with separate male and female individuals. To identify sex determining genes we sequenced the genomes of 15 female and 13 male Phoenix trees representing all 14 species. We identified male-specific sequences and extended them using phased single-molecule sequencing or BAC clones. We observed that only four genes contained sequences conserved in all analyzed Phoenix males. Most of these sequences showed similarity to a single genomic locus in the closely related monoecious oil palm. CYP703 and GPAT3, two single copy genes present in males and critical for male flower development in other monocots, were absent in females. A LOG-like gene appears translocated into the Y-linked region and is suggested to play a role in suppressing female flowers. Our data are consistent with a two-mutation model for the evolution of dioecy in Phoenix.