bluuebunny/crossref_metadata_2025_split huggingface dataset:
Molecular serogrouping ofEscherichia coli
Authors: DebRoy Chitrita , Fratamico Pina M. , Roberts Elisabeth 
Published: February 2018

AbstractO-antigens present on the surface ofEscherichia coliprovide antigenic specificity for the strain and are the main components for O-serogroup designation. Serotyping using O-group-specific antisera for the identification ofE. coliO-serogroups has been traditionally the gold-standard for distinguishingE. colistrains. Knowledge of the O-group is important for determining pathogenic lineage, classifyingE. colifor epidemiological studies, for determining virulence, and for tracing outbreaks of diseases and sources of infection. However, serotyping has limitations, as the antisera generated against each specific O-group may cross-react, many strains are non-typeable, and others can autoagglutinate or be rough (lacking an O-antigen). Currently, the nucleotide sequences are available for most of the 187 designatedE. coliO-groups. Public health and other laboratories are considering whole genome sequencing to develop genotypic methods to determine O-groups. These procedures require instrumentation and analysis that may not be accessible and may be cost-prohibitive at this time. In this review, we have identified unique gene sequences within the O-antigen gene clusters and have targeted these genes for identification of O-groups using the polymerase chain reaction. This information can be used to distinguish O-groups by developing other platforms forE. colidiagnostics in the future.
Why policy needs history (and historians)
Authors: Berridge Virginia 
Published: February 2018

AbstractPolicy makers like the idea of new initiatives and fresh starts, unencumbered by, even actively overthrowing, what has been done in the past. At the same time, history can be pigeonholed as fusty and antiquarian, dealing with long past events of no relevance to the present. Academic historians are sometimes bound up in their own worlds. The debates central to academe may have little direct relevance to the immediate concerns of policy making. The paper argues that history, as the evidence-based discipline par excellence, is as relevant as other approaches to evidence-based policy making. Case studies can show us the nature of that relevance. How to achieve influence for history also needs discussion. The relationship is not straightforward and will vary according to time and place. History is an interpretative discipline, not just a collection of ‘facts’. The paper discusses how historians work and why it is important for policy makers to engage, not just with history, but with historians as well. Historians too need to think about the value of bringing their analysis into policy.
Weed Management in 2050: Perspectives on the Future of Weed Science
Authors: Westwood James H. , Charudattan Raghavan , Duke Stephen O. , Fennimore Steven A. , Marrone Pam , Slaughter David C. , Swanton Clarence , Zollinger Richard 
Published: February 2018

AbstractThe discipline of weed science is at a critical juncture. Decades of efficient chemical weed control have led to a rise in the number of herbicide-resistant weed populations, with few new herbicides with unique modes of action to counter this trend and often no economical alternatives to herbicides in large-acreage crops. At the same time, the world population is swelling, necessitating increased food production to feed an anticipated 9 billion people by the year 2050. Here, we consider these challenges along with emerging trends in technology and innovation that offer hope of providing sustainable weed management into the future. The emergence of natural product leads in discovery of new herbicides and biopesticides suggests that new modes of action can be discovered, while genetic engineering provides additional options for manipulating herbicide selectivity and creating entirely novel approaches to weed management. Advances in understanding plant pathogen interactions will contribute to developing new biological control agents, and insights into plant–plant interactions suggest that crops can be improved by manipulating their response to competition. Revolutions in computing power and automation have led to a nascent industry built on using machine vision and global positioning system information to distinguish weeds from crops and deliver precision weed control. These technologies open multiple possibilities for efficient weed management, whether through chemical or mechanical mechanisms. Information is also needed by growers to make good decisions, and will be delivered with unprecedented efficiency and specificity, potentially revolutionizing aspects of extension work. We consider that meeting the weed management needs of agriculture by 2050 and beyond is a challenge that requires commitment by funding agencies, researchers, and students to translate new technologies into durable weed management solutions. Integrating old and new weed management technologies into more diverse weed management systems based on a better understanding of weed biology and ecology can provide integrated weed management and resistance management strategies that will be more sustainable than the technologies that are now failing.
Histone deacetylase inhibitor ITF2357 leads to apoptosis and enhances doxorubicin cytotoxicity in preclinical models of human sarcoma
Authors: Di Martile Marta , Desideri Marianna , Tupone Maria Grazia , Buglioni Simonetta , Antoniani Barbara , Mastroiorio Carlotta , Falcioni Rita , Ferraresi Virginia , Baldini Nicola , Biagini Roberto , Milella Michele , Trisciuoglio Daniela , Del Bufalo Donatella 
Published: February 2018

AbstractSarcomas are rare tumors with generally poor prognosis, for which current therapies have shown limited efficacy. Histone deacetylase inhibitors (HDACi) are emerging anti-tumor agents; however, little is known about their effect in sarcomas. By using established and patient-derived sarcoma cells with different subtypes, we showed that the pan-HDACi, ITF2357, potently inhibited in vitro survival in a p53-independent manner. ITF2357-mediated cell death implied the activation of mitochondrial apoptosis, as attested by induction of pro-apoptotic BH3-only proteins and a caspases-dependent mechanism. ITF2357 also induced autophagy, which protected sarcoma cells from apoptotic cell death. ITF2357 activated forkhead box (FOXO) 1 and 3a transcription factors and their downstream target genes, however, silencing of both FOXO1 and 3a did not protect sarcoma cells against ITF2357-induced apoptosis and upregulated FOXO4 and 6. Notably, ITF2357 synergized with Doxorubicin to induce cell death of established and patient-derived sarcoma cells. Furthermore, combination treatment strongly impaired xenograft tumor growth in vivo, when compared to single treatments, suggesting that combination of ITF2357 with Doxorubicin has the potential to enhance sensitization in different preclinical models of sarcoma. Overall, our study highlights the therapeutic potential of ITF2357, alone or in rational combination therapies, for bone and soft tissue sarcomas management.
Embryonic lethality in mice lacking Trim59 due to impaired gastrulation development
Authors: Su Xiaomin , Wu Chenglei , Ye Xiaoying , Zeng Ming , Zhang Zhujun , Che Yongzhe , Zhang Yuan , Liu Lin , Lin Yushuang , Yang Rongcun 
Published: February 2018

AbstractTRIM family members have been implicated in a variety of biological processes such as differentiation and development. We here found that Trim59 plays a critical role in early embryo development from blastocyst stage to gastrula. There existed delayed development and empty yolk sacs from embryonic day (E) 8.5 in Trim59−/− embryos. No viable Trim59−/− embryos were observed beyond E9.5. Trim59 deficiency affected primary germ layer formation at the beginning of gastrulation. At E6.5 and E7.5, the expression of primary germ layer formation-associated genes including Brachyury, lefty2, Cer1, Otx2, Wnt3, and BMP4 was reduced in Trim59−/− embryos. Homozygous mutant embryonic epiblasts were contracted and the mesoderm was absent. Trim59 could interact with actin- and myosin-associated proteins. Its deficiency disturbed F-actin polymerization during inner cell mass differentiation. Trim59-mediated polymerization of F-actin was via WASH K63-linked ubiquitination. Thus, Trim59 may be a critical regulator for early embryo development from blastocyst stage to gastrula through modulating F-actin assembly.
Estradiol signaling mediates gender difference in visceral adiposity via autophagy
Authors: Tao Zhipeng , Zheng Louise D. , Smith Cayleen , Luo Jing , Robinson Alex , Almeida Fabio A. , Wang Zongwei , Olumi Aria F. , Liu Dongmin , Cheng Zhiyong 
Published: February 2018

AbstractExcessive adiposity (particularly visceral fat mass) increases the risks of developing metabolic syndrome. Women have lower deposit of visceral fat than men, and this pattern becomes diminished postmenopausally, but the underlying mechanism remains largely unknown. Here, we show that the gender difference in visceral fat distribution is controlled by an estradiol–autophagy axis. In C57BL/6J and wild-type control mice, a higher visceral fat mass was detected in the males than in the females, which was associated with lower expression of estrogen receptor α (ERα) and more active autophagy in males vs. females. However, deletion of ERα normalized autophagy activity and abolished the gender difference in visceral adiposity. In line with the adiposity-reducing effect of the ERα–autophagy axis, we found that downregulation of ERα and increased autophagy activity were required for adipogenesis, while induction of estradiol signaling dampened autophagy and drastically prevented adipogenesis. Mechanistically, the estradiol-ERα signaling activated mTOR, which phosphorylated and inhibited ULK1, thereby suppressing autophagy and adipogenesis. Together, our study suggests that the lower visceral adiposity in the females (vs. the males) arises from a more active estradiol-ERα signaling, which tunes down autophagy and adipogenesis.
Dual properties of a hydrogen oxidation Ni-catalyst entrapped within a polymer promote self-defense against oxygen
Authors: Oughli Alaa A. , Ruff Adrian , Boralugodage Nilusha Priyadarshani , Rodríguez-Maciá Patricia , Plumeré Nicolas , Lubitz Wolfgang , Shaw Wendy J. , Schuhmann Wolfgang , Rüdiger Olaf 
Published: February 2018

AbstractThe Ni(P2N2)2 catalysts are among the most efficient non-noble-metal based molecular catalysts for H2 cycling. However, these catalysts are O2 sensitive and lack long term stability under operating conditions. Here, we show that in a redox silent polymer matrix the catalyst is dispersed into two functionally different reaction layers. Close to the electrode surface is the “active” layer where the catalyst oxidizes H2 and exchanges electrons with the electrode generating a current. At the outer film boundary, insulation of the catalyst from the electrode forms a “protection” layer in which H2 is used by the catalyst to convert O2 to H2O, thereby providing the “active” layer with a barrier against O2. This simple but efficient polymer-based electrode design solves one of the biggest limitations of these otherwise very efficient catalysts enhancing its stability for catalytic H2 oxidation as well as O2 tolerance.
Heritable DNA methylation marks associated with susceptibility to breast cancer
Authors: Joo Jihoon E. , Dowty James G. , Milne Roger L. , Wong Ee Ming , Dugué Pierre-Antoine , English Dallas , Hopper John L. , Goldgar David E. , Giles Graham G. , Southey Melissa C. ,   kConFab, Sexton Adrienne , Christian Alice , Trainer Alison , Spigelman Allan , Fellows Andrew , Shelling Andrew , De Fazio Anna , Blackburn Anneke , Crook Ashley , Meiser Bettina , Patterson Briony , Clarke Christine , Saunders Christobel , Hunt Clare , Scott Clare , Amor David , Marsh Deborah , Edkins Edward , Salisbury Elizabeth , Haan Eric , Neidermayr Eveline , Macrae Finlay , Farshid Gelareh , Lindeman Geoff , Chenevix-Trench Georgia , Mann Graham , Gill Grantley , Thorne Heather , Campbell Ian , Hickie Ian , Winship Ingrid , Goldblatt Jack , Flanagan James , Kollias James , Visvader Jane , Stone Jennifer , Taylor Jessica , Burke Jo , Saunus Jodi , Forbes John , Beesley Jonathan , Kirk Judy , French Juliet , Tucker Kathy , Wu Kathy , Phillips Kelly , Lipton Lara , Andrews Leslie , Lobb Elizabeth , Walker Logan , Kentwell Maira , Spurdle Amanda , Cummings Margaret , Gleeson Margaret , Harris Marion , Jenkins Mark , Young Mary Anne , Delatycki Martin , Wallis Mathew , Burgess Matthew , Price Melanie , Brown Melissa , Bogwitz Michael , Field Michael , Friedlander Michael , Gattas Michael , Saleh Mona , Hayward Nick , Pachter Nick , Cohen Paul , Duijf Pascal , James Paul , Simpson Peter , Fong Peter , Butow Phyllis , Williams Rachael , Kefford Richard , Scott Rodney , Balleine Rosemary , Dawson Sarah-Jane , Lok Sheau , O’Connell Shona , Greening Sian , Nightingale Sophie , Edwards Stacey , Fox Stephen , McLachlan Sue-Anne , Lakhani Sunil , Thomas Susan , Antill Yoland 
Published: February 2018

AbstractMendelian-like inheritance of germline DNA methylation in cancer susceptibility genes has been previously reported. We aimed to scan the genome for heritable methylation marks associated with breast cancer susceptibility by studying 25 Australian multiple-case breast cancer families. Here we report genome-wide DNA methylation measured in 210 peripheral blood DNA samples provided by family members using the Infinium HumanMethylation450. We develop and apply a new statistical method to identify heritable methylation marks based on complex segregation analysis. We estimate carrier probabilities for the 1000 most heritable methylation marks based on family structure, and we use Cox proportional hazards survival analysis to identify 24 methylation marks with corresponding carrier probabilities significantly associated with breast cancer. We replicate an association with breast cancer risk for four of the 24 marks using an independent nested case–control study. Here, we report a novel approach for identifying heritable DNA methylation marks associated with breast cancer risk.
3D printing of robotic soft actuators with programmable bioinspired architectures
Authors: Schaffner Manuel , Faber Jakob A. , Pianegonda Lucas , Rühs Patrick A. , Coulter Fergal , Studart André R. 
Published: February 2018

AbstractSoft actuation allows robots to interact safely with humans, other machines, and their surroundings. Full exploitation of the potential of soft actuators has, however, been hindered by the lack of simple manufacturing routes to generate multimaterial parts with intricate shapes and architectures. Here, we report a 3D printing platform for the seamless digital fabrication of pneumatic silicone actuators exhibiting programmable bioinspired architectures and motions. The actuators comprise an elastomeric body whose surface is decorated with reinforcing stripes at a well-defined lead angle. Similar to the fibrous architectures found in muscular hydrostats, the lead angle can be altered to achieve elongation, contraction, or twisting motions. Using a quantitative model based on lamination theory, we establish design principles for the digital fabrication of silicone-based soft actuators whose functional response is programmed within the material's properties and architecture. Exploring such programmability enables 3D printing of a broad range of soft morphing structures.
Monovalent manganese based anodes and co-solvent electrolyte for stable low-cost high-rate sodium-ion batteries
Authors: Firouzi Ali , Qiao Ruimin , Motallebi Shahrokh , Valencia Christian W. , Israel Hannah S. , Fujimoto Mai , Wray L. Andrew , Chuang Yi-De , Yang Wanli , Wessells Colin D. 
Published: February 2018

AbstractThe demand of sustainable power supply requires high-performance cost-effective energy storage technologies. Here we report a high-rate long-life low-cost sodium-ion battery full-cell system by innovating both the anode and the electrolyte. The redox couple of manganese(I/II) in Prussian blue analogs enables a high-rate and stable anode. Soft X-ray absorption spectroscopy and resonant inelastic X-ray scattering provide direct evidence suggesting the existence of monovalent manganese in the charged anode. There is a strong hybridization between cyano ligands and manganese-3d states, which benefits the electronic property for improving rate performance. Additionally, we employ an organic–aqueous cosolvent electrolyte to solve the long-standing solubility issue of Prussian blue analogs. A full-cell sodium-ion battery with low-cost Prussian blue analogs in both electrodes and co-solvent electrolyte retains 95% of its initial discharge capacity after 1000 cycles at 1C and 95% depth of discharge. The revealed manganese(I/II) redox couple inspires conceptual innovations of batteries based on atypical oxidation states.
PAN-cancer analysis of S-phase enriched lncRNAs identifies oncogenic drivers and biomarkers
Authors: Ali Mohamad Moustafa , Akhade Vijay Suresh , Kosalai Subazini Thankaswamy , Subhash Santhilal , Statello Luisa , Meryet-Figuiere Matthieu , Abrahamsson Jonas , Mondal Tanmoy , Kanduri Chandrasekhar 
Published: February 2018

AbstractDespite improvement in our understanding of long noncoding RNAs (lncRNAs) role in cancer, efforts to find clinically relevant cancer-associated lncRNAs are still lacking. Here, using nascent RNA capture sequencing, we identify 1145 temporally expressed S-phase-enriched lncRNAs. Among these, 570 lncRNAs show significant differential expression in at least one tumor type across TCGA data sets. Systematic clinical investigation of 14 Pan-Cancer data sets identified 633 independent prognostic markers. Silencing of the top differentially expressed and clinically relevant S-phase-enriched lncRNAs in several cancer models affects crucial cancer cell hallmarks. Mechanistic investigations on SCAT7 in multiple cancer types reveal that it interacts with hnRNPK/YBX1 complex and affects cancer cell hallmarks through the regulation of FGF/FGFR and its downstream PI3K/AKT and MAPK pathways. We also implement a LNA-antisense oligo-based strategy to treat cancer cell line and patient-derived tumor (PDX) xenografts. Thus, this study provides a comprehensive list of lncRNA-based oncogenic drivers with potential prognostic value.
Assembly of 913 microbial genomes from metagenomic sequencing of the cow rumen
Authors: Stewart Robert D. , Auffret Marc D. , Warr Amanda , Wiser Andrew H. , Press Maximilian O. , Langford Kyle W. , Liachko Ivan , Snelling Timothy J. , Dewhurst Richard J. , Walker Alan W. , Roehe Rainer , Watson Mick 
Published: February 2018

AbstractThe cow rumen is adapted for the breakdown of plant material into energy and nutrients, a task largely performed by enzymes encoded by the rumen microbiome. Here we present 913 draft bacterial and archaeal genomes assembled from over 800 Gb of rumen metagenomic sequence data derived from 43 Scottish cattle, using both metagenomic binning and Hi-C-based proximity-guided assembly. Most of these genomes represent previously unsequenced strains and species. The draft genomes contain over 69,000 proteins predicted to be involved in carbohydrate metabolism, over 90% of which do not have a good match in public databases. Inclusion of the 913 genomes presented here improves metagenomic read classification by sevenfold against our own data, and by fivefold against other publicly available rumen datasets. Thus, our dataset substantially improves the coverage of rumen microbial genomes in the public databases and represents a valuable resource for biomass-degrading enzyme discovery and studies of the rumen microbiome.
Prediction of Postnatal Growth Failure among Very Low Birth Weight Infants
Authors: Lee Soon Min , Kim Namhyo , Namgung Ran , Park Minsoo , Park Kookin , Jeon Jihyun 
Published: February 2018

AbstractPostnatal growth failure (PGF) in preterm infants remains an important clinical issue. In this study, we analysed the incidence of PGF among very low birth weight (VLBW) infants and evaluated the risk factors for PGF based on the data of 2799 VLBW infants obtained from the Korean Neonatal Network database from 2013 to 2014. PGF was defined as a decrease in weight Z score between birth and discharge of more than −1.28 using the Fenton growth charts. Risk factors were evaluated in relation to birth weight for gestational age, namely small (SGA) or appropriate (AGA) for gestational age, using propensity score matching used for between-group differences. The overall incidence of PGF was 45.5%, with a rate of 68.9% in the SGA group and 36.2% in the AGA group. PGF was negatively correlated with gestation and birth weight; additionally, PGF was associated with a higher incidence of co-morbidities. Predictors of PGF in the SGA group were respiratory distress syndrome and days to attain 100 mL/kg of enteral feeding. The only predictor of PGF in the AGA group was days to attain 100 mL/kg of enteral feeding. Early initiation and aggressive progression of enteral nutrition may decrease the incidence of PGF.
Nox4 is a Target for Tuberin Deficiency Syndrome
Authors: Shi Qian , Viswanadhapalli Suryavathi , Friedrichs William E. , Velagapudi Chakradhar , Szyndralewiez Cédric , Bansal Shweta , Bhat Manzoor A. , Choudhury Goutam Ghosh , Abboud Hanna E. 
Published: February 2018

AbstractThe mechanism by which TSC2 inactivation or deficiency contributes to the pathology of tuberous sclerosis complex (TSC) is not fully clear. We show that renal angiomyolipomas from TSC patients and kidney cortex from Tsc2+/− mice exhibit elevated levels of reactive oxygen species (ROS). Downregulation of tuberin (protein encoded by TSC2 gene) in renal proximal tubular epithelial cells significantly increased ROS concomitant with enhanced Nox4. Similarly, we found elevated levels of Nox4 in the renal cortex of Tsc2+/− mice and in the renal angiomyolipomas from TSC patients. Tuberin deficiency is associated with activation of mTORC1. Rapamycin, shRNAs targeting raptor, or inhibition of S6 kinase significantly inhibited the expression of Nox4, resulting in attenuation of production of ROS in tuberin-downregulated proximal tubular epithelial cells. In contrast, activation of mTORC1 increased Nox4 and ROS. These results indicate that Nox4 may be a potential target for tuberin-deficiency-derived diseases. Using a xenograft model from tuberin-null tubular cells in nude mice, both anti-sense Nox4 and GKT137831, a specific inhibitor of Nox1/4, significantly inhibited the tumor growth. Thus, our results demonstrate the presence of an antagonistic relationship between tuberin and Nox4 to drive oncogenesis in the tuberin deficiency syndrome and identify Nox4 as a target to develop a therapy for TSC.
Ablation of Bax and Bak protects skeletal muscle against pressure-induced injury
Authors: Tam Bjorn T. , Yu Angus P. , Tam Eric W. , Monks Douglas A. , Wang Xu P. , Pei Xiao M. , Koh Su P. , Sin Thomas K. , Law Helen K. W. , Ugwu Felix N. , Supriya Rashmi , Yung Benjamin Y. , Yip Shea P. , Wong S. C. , Chan Lawrence W. , Lai Christopher W. , Ouyang Pin , Siu Parco M. 
Published: February 2018

AbstractPressure-induced injury (PI), such as a pressure ulcer, in patients with limited mobility is a healthcare issue worldwide. PI is an injury to skin and its underlying tissue such as skeletal muscle. Muscle compression, composed of mechanical deformation of muscle and external load, leads to localized ischemia and subsequent unloading reperfusion and, hence, a pressure ulcer in bed-bound patients. Although the gross factors involved in PI have been identified, little is known about the exact disease mechanism or its links to apoptosis, autophagy and inflammation. Here, we report that PI is mediated by intrinsic apoptosis and exacerbated by autophagy. Conditional ablation of Bax and Bak activates the Akt-mTOR pathway and Bnip3-mediated mitophagy and preserves mitochondrial contents in compressed muscle. Moreover, we find that the presence/absence of Bax and Bak alters the roles and functions of autophagy in PI. Our results suggest that manipulating apoptosis and autophagy are potential therapeutic targets for treatment and prevention of PI.