bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monolithically integrated stretchable photonics
Authors: Li Lan , Lin Hongtao , Qiao Shutao , Huang Yi-Zhong , Li Jun-Ying , Michon Jérôme , Gu Tian , Alosno-Ramos Carlos , Vivien Laurent , Yadav Anupama , Richardson Kathleen , Lu Nanshu , Hu Juejun 
Published: February 2018

AbstractMechanically stretchable photonics provides a new geometric degree of freedom for photonic system design and foresees applications ranging from artificial skins to soft wearable electronics. Here we describe the design and experimental realization of the first single-mode stretchable photonic devices. These devices, made of chalcogenide glass and epoxy polymer materials, are monolithically integrated on elastomer substrates. To impart mechanical stretching capability to devices built using these intrinsically brittle materials, our design strategy involves local substrate stiffening to minimize shape deformation of critical photonic components, and interconnecting optical waveguides assuming a meandering Euler spiral geometry to mitigate radiative optical loss. Devices fabricated following such design can sustain 41% nominal tensile strain and 3000 stretching cycles without measurable degradation in optical performance. In addition, we present a rigorous analytical model to quantitatively predict stress-optical coupling behavior in waveguide devices of arbitrary geometry without using a single fitting parameter.
Modulation of nuclear factor-kappa B activation by the endoplasmic reticulum stress sensor PERK to mediate estrogen-induced apoptosis in breast cancer cells
Authors: Fan Ping , Tyagi Amit K. , Agboke Fadeke A. , Mathur Rohit , Pokharel Niranjana , Jordan V. Craig 
Published: February 2018

AbstractStress responses are critical for estrogen (E2)-induced apoptosis in E2-deprived breast cancer cells. Nuclear factor-kappa B (NF-κB) is an important therapeutic target to prevent stress responses in chronic inflammatory diseases including cancer. However, whether E2 activates NF-κB to participate in stress-associated apoptosis in E2-deprived breast cancer cells is unknown. Here, we demonstrated that E2 differentially modulates NF-κB activity according to treatment time. E2 initially has significant potential to suppress NF-κB activation; it completely blocks tumor necrosis factor alpha (TNFα)-induced activation of NF-κB. We found that E2 preferentially and constantly enhances the expression of the adipogenic transcription factor CCAAT/enhancer binding protein beta (C/EBPβ), which is responsible for the suppression of NF-κB activation by E2 in MCF-7:5C cells. Interestingly, NF-κB p65 DNA-binding activity is increased when E2 is administered for 48 h, leading to the induction of TNFα and associated apoptosis. Blocking the nuclear translocation of NF-κB can completely prevent the induction of TNFα and apoptosis induced by E2. Further examination revealed that protein kinase RNA-like endoplasmic reticulum kinase (PERK), a stress sensor of unfolded protein response (UPR), plays an essential role in the late activation of NF-κB by E2. This modulation between PERK and NF-κB is mainly mediated by a stress responsive transcription factor, transducer and activator of transcription 3 (STAT3), independently of the classic canonical IκBα signaling pathway. Thus, inhibition of PERK kinase activity completely blocks the DNA binding of both STAT3 and NF-κB, thereby preventing induction of NF-κB-dependent genes and E2-induced apoptosis. All of these findings suggest that PERK is a key regulator to convey stress signals from the endoplasmic reticulum to the nucleus and illustrate a crucial role for the novel PERK/STAT3/NF-κB/TNFα axis in E2-induced apoptosis in E2-deprived breast cancer cells.
Aggregation-fragmentation and individual dynamics of active clusters
Authors: Ginot F. , Theurkauff I. , Detcheverry F. , Ybert C. , Cottin-Bizonne C. 
Published: February 2018

AbstractA remarkable feature of active matter is the propensity to self-organize. One striking instance of this ability to generate spatial structures is the cluster phase, where clusters broadly distributed in size constantly move and evolve through particle exchange, breaking or merging. Here we propose an exhaustive description of the cluster dynamics in apolar active matter. Exploiting large statistics gathered on thousands of Janus colloids, we measure the aggregation and fragmentation rates and rationalize the resulting cluster size distribution and fluctuations. We also show that the motion of individual clusters is entirely consistent with a model positing random orientation of colloids. Our findings establish a simple, generic model of cluster phase, and pave the way for a thorough understanding of clustering in active matter.
Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL
Authors: Schrader A. , Crispatzu G. , Oberbeck S. , Mayer P. , Pützer S. , von Jan J. , Vasyutina E. , Warner K. , Weit N. , Pflug N. , Braun T. , Andersson E. I. , Yadav B. , Riabinska A. , Maurer B. , Ventura Ferreira M. S. , Beier F. , Altmüller J. , Lanasa M. , Herling C. D. , Haferlach T. , Stilgenbauer S. , Hopfinger G. , Peifer M. , Brümmendorf T. H. , Nürnberg P. , Elenitoba-Johnson K. S. J. , Zha S. , Hallek M. , Moriggl R. , Reinhardt H. C. , Stern M.-H. , Mustjoki S. , Newrzela S. , Frommolt P. , Herling M. 
Published: February 2018

AbstractT-cell prolymphocytic leukemia (T-PLL) is a rare and poor-prognostic mature T-cell malignancy. Here we integrated large-scale profiling data of alterations in gene expression, allelic copy number (CN), and nucleotide sequences in 111 well-characterized patients. Besides prominent signatures of T-cell activation and prevalent clonal variants, we also identify novel hot-spots for CN variability, fusion molecules, alternative transcripts, and progression-associated dynamics. The overall lesional spectrum of T-PLL is mainly annotated to axes of DNA damage responses, T-cell receptor/cytokine signaling, and histone modulation. We formulate a multi-dimensional model of T-PLL pathogenesis centered around a unique combination of TCL1 overexpression with damaging ATM aberrations as initiating core lesions. The effects imposed by TCL1 cooperate with compromised ATM toward a leukemogenic phenotype of impaired DNA damage processing. Dysfunctional ATM appears inefficient in alleviating elevated redox burdens and telomere attrition and in evoking a p53-dependent apoptotic response to genotoxic insults. As non-genotoxic strategies, synergistic combinations of p53 reactivators and deacetylase inhibitors reinstate such cell death execution.
Mutations in CFAP43 and CFAP44 cause male infertility and flagellum defects in Trypanosoma and human
Authors: Coutton Charles , Vargas Alexandra S. , Amiri-Yekta Amir , Kherraf Zine-Eddine , Ben Mustapha Selima Fourati , Le Tanno Pauline , Wambergue-Legrand Clémentine , Karaouzène Thomas , Martinez Guillaume , Crouzy Serge , Daneshipour Abbas , Hosseini Seyedeh Hanieh , Mitchell Valérie , Halouani Lazhar , Marrakchi Ouafi , Makni Mounir , Latrous Habib , Kharouf Mahmoud , Deleuze Jean-François , Boland Anne , Hennebicq Sylviane , Satre Véronique , Jouk Pierre-Simon , Thierry-Mieg Nicolas , Conne Beatrice , Dacheux Denis , Landrein Nicolas , Schmitt Alain , Stouvenel Laurence , Lorès Patrick , El Khouri Elma , Bottari Serge P. , Fauré Julien , Wolf Jean-Philippe , Pernet-Gallay Karin , Escoffier Jessica , Gourabi Hamid , Robinson Derrick R. , Nef Serge , Dulioust Emmanuel , Zouari Raoudha , Bonhivers Mélanie , Touré Aminata , Arnoult Christophe , Ray Pierre F. 
Published: February 2018

AbstractSpermatogenesis defects concern millions of men worldwide, yet the vast majority remains undiagnosed. Here we report men with primary infertility due to multiple morphological abnormalities of the sperm flagella with severe disorganization of the sperm axoneme, a microtubule-based structure highly conserved throughout evolution. Whole-exome sequencing was performed on 78 patients allowing the identification of 22 men with bi-allelic mutations in DNAH1 (n = 6), CFAP43 (n = 10), and CFAP44 (n = 6). CRISPR/Cas9 created homozygous CFAP43/44 male mice that were infertile and presented severe flagellar defects confirming the human genetic results. Immunoelectron and stimulated-emission-depletion microscopy performed on CFAP43 and CFAP44 orthologs in Trypanosoma brucei evidenced that both proteins are located between the doublet microtubules 5 and 6 and the paraflagellar rod. Overall, we demonstrate that CFAP43 and CFAP44 have a similar structure with a unique axonemal localization and are necessary to produce functional flagella in species ranging from Trypanosoma to human.
Discovery of a magnetic conductive interface in PbZr0.2Ti0.8O3 /SrTiO3 heterostructures
Authors: Zhang Yi , Xie Lin , Kim Jeongwoo , Stern Alex , Wang Hui , Zhang Kui , Yan Xingxu , Li Linze , Liu Henry , Zhao Gejian , Chi Hang , Gadre Chaitanya , Lin Qiyin , Zhou Yichun , Uher Ctirad , Chen Tingyong , Chu Ying-Hao , Xia Jing , Wu Ruqian , Pan Xiaoqing 
Published: February 2018

AbstractEmergent physical properties often arise at interfaces of complex oxide heterostructures due to the interplay between various degrees of freedom, especially those with polar discontinuities. It is desirable to explore if these structures may generate pure and controllable spin currents, which are needed to attain unmatched performance and energy efficiency in the next-generation spintronic devices. Here we report the emergence of a spin-polarized two-dimensional electron gas (SP-2DEG) at the interface of two insulators, SrTiO3 and PbZr0.2Ti0.8O3. This SP-2DEG is strongly localized at the interfacial Ti atoms, due to the interplay between Coulomb interaction and band bending, and can be tuned by the ferroelectric polarization. Our findings open a door for engineering ferroelectric/insulator interfaces to create tunable ferroic orders for magnetoelectric device applications and provide opportunities for designing multiferroic materials in heterostructures.
USP35 regulates mitotic progression by modulating the stability of Aurora B
Authors: Park Jinyoung , Kwon Mi-Sun , Kim Eunice EunKyeong , Lee Hyunsook , Song Eun Joo 
Published: February 2018

AbstractAlthough approximately 100 deubiquitinating enzymes (DUBs) are encoded in the human genome, very little is known about the DUBs that function in mitosis. Here, we demonstrate that DUB USP35 functions as a mitotic regulator by controlling the protein levels and downstream signaling of Aurora B and the depletion of USP35 eventually leads to several mitotic defects including cytokinesis failures. USP35 binds to and deubiquitinates Aurora B, and inhibits the APCCDH1-mediated proteasomal degradation of Aurora B, thus maintaining its steady-state levels during mitosis. In addition, the loss of USP35 decreases the phosphorylation of histone H3-Ser10, an Aurora B substrate. Finally, the transcription factor FoxM1 promotes the expression of USP35, as well as that of Aurora B, during the cell cycle. Our findings suggest that USP35 regulates the stability and function of Aurora B by blocking APCCDH1-induced proteasomal degradation, thereby controlling mitotic progression.
Inference of field reversed configuration topology and dynamics during Alfvenic transients
Authors: Romero J. A. , Dettrick S. A. , Granstedt E. , Roche T. , Mok Y. 
Published: February 2018

AbstractActive control of field reversed configuration (FRC) devices requires a method to determine the flux surface geometry and dynamic properties of the plasma during both transient and steady-state conditions. The current tomography (CT) method uses Bayesian inference to determine the plasma current density distribution using both the information from magnetic measurements and a physics model in the prior. Here we show that, from the inferred current sources, the FRC topology and its axial stability properties are readily obtained. When Gaussian process priors are used and the forward model is linear, the CT solution involves non-iterative matrix operations and is then ideally suited for deterministic real-time applications. Because no equilibrium assumptions are used in this case, inference of plasma topology and dynamics up to Alfvenic frequencies then becomes possible. Inference results for the C-2U device exhibit self-consistency of motions and forces during Alfvenic transients, as well as good agreement with plasma imaging diagnostics.
Clonal polymorphism and high heterozygosity in the celibate genome of the Amazon molly
Authors: Warren Wesley C. , García-Pérez Raquel , Xu Sen , Lampert Kathrin P. , Chalopin Domitille , Stöck Matthias , Loewe Laurence , Lu Yuan , Kuderna Lukas , Minx Patrick , Montague Michael J. , Tomlinson Chad , Hillier LaDeana W. , Murphy Daniel N. , Wang John , Wang Zhongwei , Garcia Constantino Macias , Thomas Gregg C. W. , Volff Jean-Nicolas , Farias Fabiana , Aken Bronwen , Walter Ronald B. , Pruitt Kim D. , Marques-Bonet Tomas , Hahn Matthew W. , Kneitz Susanne , Lynch Michael , Schartl Manfred 
Published: February 2018

AbstractThe extreme rarity of asexual vertebrates in nature is generally explained by genomic decay due to absence of meiotic recombination, thus leading to extinction of such lineages. We explore features of a vertebrate asexual genome, the Amazon molly, Poecilia formosa, and find few signs of genetic degeneration but unique genetic variability and ongoing evolution. We uncovered a substantial clonal polymorphism and, as a conserved feature from its interspecific hybrid origin, a 10-fold higher heterozygosity than in the sexual parental species. These characteristics seem to be a principal reason for the unpredicted fitness of this asexual vertebrate. Our data suggest that asexual vertebrate lineages are scarce not because they are at a disadvantage, but because the genomic combinations required to bypass meiosis and to make up a functioning hybrid genome are rarely met in nature.
Assessing cetacean surveys throughout the Mediterranean Sea: a gap analysis in environmental space
Authors: Mannocci Laura , Roberts Jason J. , Halpin Patrick N. , Authier Matthieu , Boisseau Oliver , Bradai Mohamed Nejmeddine , Cañadas Ana , Chicote Carla , David Léa , Di-Méglio Nathalie , Fortuna Caterina M. , Frantzis Alexandros , Gazo Manel , Genov Tilen , Hammond Philip S. , Holcer Draško , Kaschner Kristin , Kerem Dani , Lauriano Giancarlo , Lewis Tim , Notarbartolo di Sciara Giuseppe , Panigada Simone , Raga Juan Antonio , Scheinin Aviad , Ridoux Vincent , Vella Adriana , Vella Joseph 
Published: February 2018

AbstractHeterogeneous data collection in the marine environment has led to large gaps in our knowledge of marine species distributions. To fill these gaps, models calibrated on existing data may be used to predict species distributions in unsampled areas, given that available data are sufficiently representative. Our objective was to evaluate the feasibility of mapping cetacean densities across the entire Mediterranean Sea using models calibrated on available survey data and various environmental covariates. We aggregated 302,481 km of line transect survey effort conducted in the Mediterranean Sea within the past 20 years by many organisations. Survey coverage was highly heterogeneous geographically and seasonally: large data gaps were present in the eastern and southern Mediterranean and in non-summer months. We mapped the extent of interpolationversusextrapolation and the proportion of data nearby in environmental space when models calibrated on existing survey data were used for prediction across the entire Mediterranean Sea. Using model predictions to map cetacean densities in the eastern and southern Mediterranean, characterised by warmer, less productive waters, and more intense eddy activity, would lead to potentially unreliable extrapolations. We stress the need for systematic surveys of cetaceans in these environmentally unique Mediterranean waters, particularly in non-summer months.
Common surgical procedures in pilonidal sinus disease: A meta-analysis, merged data analysis, and comprehensive study on recurrence
Authors: Stauffer V. K. , Luedi M. M. , Kauf P. , Schmid M. , Diekmann M. , Wieferich K. , Schnüriger B. , Doll D. 
Published: February 2018

AbstractWe systematically searched available databases. We reviewed 6,143 studies published from 1833 to 2017. Reports in English, French, German, Italian, and Spanish were considered, as were publications in other languages if definitive treatment and recurrence at specific follow-up times were described in an English abstract. We assessed data in the manner of a meta-analysis of RCTs; further we assessed non-RCTs in the manner of a merged data analysis. In the RCT analysis including 11,730 patients, Limberg & Dufourmentel operations were associated with low recurrence of 0.6% (95%CI 0.3–0.9%) 12 months and 1.8% (95%CI 1.1–2.4%) respectively 24 months postoperatively. Analysing 89,583 patients from RCTs and non-RCTs, the Karydakis & Bascom approaches were associated with recurrence of only 0.2% (95%CI 0.1–0.3%) 12 months and 0.6% (95%CI 0.5–0.8%) 24 months postoperatively. Primary midline closure exhibited long-term recurrence up to 67.9% (95%CI 53.3–82.4%) 240 months post-surgery. For most procedures, only a few RCTs without long term follow up data exist, but substitute data from numerous non-RCTs are available. Recurrence in PSD is highly dependent on surgical procedure and by follow-up time; both must be considered when drawing conclusions regarding the efficacy of a procedure.
Analysis combining correlated glaucoma traits identifies five new risk loci for open-angle glaucoma
Authors: Gharahkhani Puya , Burdon Kathryn P. , Cooke Bailey Jessica N. , Hewitt Alex W. , Law Matthew H. , Pasquale Louis R. , Kang Jae H. , Haines Jonathan L. , Souzeau Emmanuelle , Zhou Tiger , Siggs Owen M. , Landers John , Awadalla Mona , Sharma Shiwani , Mills Richard A. , Ridge Bronwyn , Lynn David , Casson Robert , Graham Stuart L. , Goldberg Ivan , White Andrew , Healey Paul R. , Grigg John , Lawlor Mitchell , Mitchell Paul , Ruddle Jonathan , Coote Michael , Walland Mark , Best Stephen , Vincent Andrea , Gale Jesse , RadfordSmith Graham , Whiteman David C. , Montgomery Grant W. , Martin Nicholas G. , Mackey David A , Wiggs Janey L. , MacGregor Stuart , Craig Jamie E. ,   The NEIGHBORHOOD consortium, Allingham R. Rand , Brilliant Murray , Budenz Donald L. , Fingert John H. , Gaasterland Douglas , Gaasterland Teresa , Hark Lisa , Hauser Michael , Igo Robert P. , Kraft Peter , Lee Richard K. , Lichter Paul R. , Liu Yutao , Moroi Syoko , Pericak-Vance Margaret , Realini Anthony , Rhee Doug , Richards Julia E. , Ritch Robert , Schuman Joel S. , Scott William K. , Singh Kuldev , Sit Arthur J. , Vollrath Douglas , Wollstein Gadi , Zack Donald J. 
Published: February 2018

AbstractOpen-angle glaucoma (OAG) is a major cause of blindness worldwide. To identify new risk loci for OAG, we performed a genome-wide association study in 3,071 OAG cases and 6,750 unscreened controls, and meta-analysed the results with GWAS data for intraocular pressure (IOP) and optic disc parameters (the overall meta-analysis sample size varying between 32,000 to 48,000 participants), which are glaucoma-related traits. We identified and independently validated four novel genome-wide significant associations within or near MYOF and CYP26A1, LINC02052 and CRYGS, LMX1B, and LMO7 using single variant tests, one additional locus (C9) using gene-based tests, and two genetic pathways - “response to fluid shear stress” and “abnormal retina morphology” - in pathway-based tests. Interestingly, some of the new risk loci contribute to risk of other genetically-correlated eye diseases including myopia and age-related macular degeneration. To our knowledge, this study is the first integrative study to combine genetic data from OAG and its correlated traits to identify new risk variants and genetic pathways, highlighting the future potential of combining genetic data from genetically-correlated eye traits for the purpose of gene discovery and mapping.
Chronic ETA antagonist reverses hypertension and impairment of structure and function of peripheral small arteries in aortic stiffening
Authors: Guo Xiaomei , Chen Huan , Han Ling , Haulon Stephan , Kassab Ghassan S. 
Published: February 2018

AbstractArterial stiffness may contribute to the pathogenesis of hypertension. The goal of this study is to elucidate the role of Endothelin-1 (ET-1) in aortic stiffening-induced hypertension through ETA receptor activation. An increase in aortic stiffness was created by use of a non-constrictive restraint, NCR on the abdominal aortic surface. A group of rats underwent aortic NCR or sham operation for 12 weeks and were then treated with ETA receptor antagonist BQ-123 for 3 weeks. We found that 12 weeks of aortic NCR significantly increased pulse and mean pressure and altered peripheral flow pattern, accompanied by an increased serum ET-1 level (p < 0.05). The increase in aortic stiffness (evidenced by an elevated pulse wave velocity) caused hypertrophic structural remodeling and decreased arterial compliance, along with an impaired endothelial function in peripheral small arteries. BQ-123 treatment only partially attenuated peripheral arterial hypertrophy and restored arterial compliance, but completely recovered endothelium function, and consequently restored local flow and lowered blood pressure. Our findings underscore the hemodynamic coupling between aortic stiffening and peripheral arterial vessels and flow dynamics through an ETA-dependent mechanism. ETA receptor blockade may have therapeutic potential for improving peripheral vessel structure and function in the treatment of aortic stiffness-induced hypertension.
Optimising the decellularization of human elastic cartilage with trypsin for future use in ear reconstruction
Authors: Rahman Shafiq , Griffin Michelle , Naik Anish , Szarko Matthew , Butler Peter E. M. 
Published: February 2018

AbstractDecellularized scaffolds can induce chondrogenic differentiation of stem cells. This study compares different methods to optimise the decellularization of auricular cartilage. The process consisted of an initial 12 hour dry freeze thaw which froze the cartilage specimens in an empty tube at −20 °C. Samples were allowed to thaw at room temperature followed by submersion in phosphate buffer solution in which they were frozen at −20 °C for a 12 hour period. They were then allowed to thaw at room temperature as before. Protocol A subsequently involved subjecting specimens to both deoxyribonuclease and sodium deoxycholate. Protocol B and C were adaptations of this using 0.25% trypsin (7 cycles) and a 0.5 molar solution of ethylenediaminetetraacetic acid (3 hours for each cycle) respectively as additional steps. Trypsin accelerated the decellularization process with a reduction in DNA content from 55.4 ng/μL (native) to 17.3 ng/μL (P-value < 0.05) after 14 days. Protocol B showed a faster reduction in DNA content when compared with protocol A. In comparison to protocol C after 14 days, trypsin also showed greater decellularization with a mean difference of 11.7 ng/μL (P-value < 0.05). Histological analysis with H&E and DAPI confirmed depletion of cells at 14 days with trypsin.