bluuebunny/crossref_metadata_2025_split huggingface dataset:
Are organic compounds good candidates to substitute rare earth materials in fluorescent applications?
Authors: Carbonaro Carlo Maria , Chiriu Daniele , Ricci Pier Carlo 
Published: September 2016

AbstractThe optical properties of some organic compounds in solution or embedded within suitable host matrices are reported and discussed in terms of their performances for possible applications in lighting, photonic or biomedicine. The aim of the paper is to briefly review the presence of rare earth elements in these fields and to enlighten the possibility of their substitution because of global market cost/effectiveness considerations. The easiness of green chemical synthesis and functionalization, the fluorescence tunability over the visible spectrum range of dye molecules and their fluorescence quantum efficiency promote organic compounds as promising good candidate to substitute rare earth materials. (© 2016 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Luminescent point defect formation in 3C‐SiC by ion implantation
Authors: Al Atem Abdul Salam , Ferrier Lydie , Canut Bruno , Chauvin Nicolas , Guillot Gérard , Bluet Jean‐Marie 
Published: September 2016

AbstractOptically active point defects in SiC are attracting a growing interest thanks to their prospect of emission in the near‐infrared (NIR) spectral region (application in optical fiber communications and for in vivo imaging) and also thanks to the possibility to control optically their spin. Most of the results have been obtained for the hexagonal SiC polytypes. In this work, we focus on the optical properties of point defects in the 3C‐SiC polytype after ion implantation. Different ions, fluences and post‐implantation annealing were performed to optimize the defect formation. Photoluminescence results show that the optimal conditions for intense D1 defect related PL emission in the 600‐850 nm range are high temperature annealing (up to 1200 °C) and a displacement density not exceeding 1020 cm‐3 at the projected range. The creation of Ky5 defect at 1.12 eV has also been demonstrated for lower temperature annealing (800 °C). (© 2016 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Elliptic curve coding technique application for digital signature
Authors: Yildiz Kazim , Buldu Ali , Saritas Hasan 
Published: September 2016

AbstractAn elliptic curve coding technique application is proposed in this study. It is one of the asymmetric coding techniques and so crucial in today's world. The application codes messages between two different console screens by using elliptical curve coding technique. It is created by using C# with the class of Crypto Next Generation (CNG) which brings into consideration the messaging system as four different security levels. The aim is to use the necessary additional security precautions when using asymmetric techniques. Cryptography techniques are not used for connection, and messaging occurs in security level 1. Security level 2 describes the public channel for the connection between two console screens which is used for sending and receiving key pair; then messaging occurs. Public channel for the connection between two console screens is used for sending and receiving signed key pair and encrypted data; then messaging occurs in security level 3. Security level 4 is the safest one. A private channel for the connection between two console screens is used for sending and receiving a signed key pair and encrypted data, and then messaging occurs. In addition, Advanced Encryption Standard (AES) technique is used in applications which is one of the symmetric cryptographic techniques for encrypting data. Copyright © 2016 John Wiley & Sons, Ltd.
Algebraic techniques on searching linear diffusion layers in block cipher
Authors: Zhang Wenying , Zhang Wenyu 
Published: September 2016

AbstractMaximum branch number permutation plays an efficacious role in providing resistance against the most well‐known attacks on block ciphers, such as differential cryptanalysis and linear cryptanalysis. In this paper, we propose algebraic techniques in searching permutations with maximal branch number, which can be employed as the linear diffusion layers in block ciphers. We focus on permutations composed of simple operations such as word‐level XORs and rotations. Some necessary conditions are proposed to filter out linear permutations that cannot achieve the maximal branch number. With these conditions, the searching process of maximum permutation on 32‐bit word can be finished in 1 s, contrast to the previous searching method which spent several days on two computers. What is the most important is that it can be generalized to 64‐bit word and show that there is no 8‐byte word permutation, which is XOR of 9 right‐rotations or 11 right‐rotations with maximum branch number. Copyright © 2016 John Wiley & Sons, Ltd.
Conversion of Nonproliferating Astrocytes into Neurogenic Neural Stem Cells: Control by FGF2 and Interferon-γ
Authors: Kleiderman Susanne , Gutbier Simon , Ugur Tufekci Kemal , Ortega Felipe , Sá João V. , Teixeira Ana P. , Brito Catarina , Glaab Enrico , Berninger Benedikt , Alves Paula M. , Leist Marcel 
Published: September 2016

Abstract
Conversion of astrocytes to neurons, via de-differentiation to neural stem cells (NSC), may be a new approach to treat neurodegenerative diseases and brain injuries. The signaling factors affecting such a cell conversion are poorly understood, and they are hard to identify in complex disease models or conventional cell cultures. To address this question, we developed a serum-free, strictly controlled culture system of pure and homogeneous “astrocytes generated from murine embryonic stem cells (ESC).” These stem cell derived astrocytes (mAGES), as well as standard primary astrocytes resumed proliferation upon addition of FGF. The signaling of FGF receptor tyrosine kinase converted GFAP-positive mAGES to nestin-positive NSC. ERK phosphorylation was necessary, but not sufficient, for cell cycle re-entry, as EGF triggered no de-differentiation. The NSC obtained by de-differentiation of mAGES were similar to those obtained directly by differentiation of ESC, as evidenced by standard phenotyping, and also by transcriptome mapping, metabolic profiling, and by differentiation to neurons or astrocytes. The de-differentiation was negatively affected by inflammatory mediators, and in particular, interferon-γ strongly impaired the formation of NSC from mAGES by a pathway involving phosphorylation of STAT1, but not the generation of nitric oxide. Thus, two antagonistic signaling pathways were identified here that affect fate conversion of astrocytes independent of genetic manipulation. The complex interplay of the respective signaling molecules that promote/inhibit astrocyte de-differentiation may explain why astrocytes do not readily form neural stem cells in most diseases. Increased knowledge of such factors may provide therapeutic opportunities to favor such conversions.
Prediction of stillbirth from maternal factors, fetal biometry and uterine artery Doppler at 19–24 weeks
Authors: Akolekar R. , Tokunaka M. , Ortega N. , Syngelaki A. , Nicolaides K. H. 
Published: September 2016

ABSTRACTObjectivesTo evaluate the performance of screening for all stillbirths and those due to impaired placentation and unexplained or other causes using a combination of maternal factors, fetal biometry and uterine artery pulsatility index (UtA‐PI) at 19–24 weeks' gestation and to compare this performance with that of screening by UtA‐PI alone.MethodsThis was a prospective screening study of 70 003 singleton pregnancies including 69 735 live births and 268 (0.38%) antepartum stillbirths; 159 (59%) were secondary to impaired placentation and 109 (41%) were due to other or unexplained causes. Multivariable logistic regression analysis was used to develop a model for prediction of stillbirth based on a combination of maternal factors, fetal biometry and UtA‐PI.ResultsCombined screening predicted 55% of all stillbirths, including 75% of those due to impaired placentation and 23% of those that were unexplained or due to other causes, at a false‐positive rate of 10%. Within the impaired placentation group, the detection rate of stillbirth < 32 weeks' gestation was higher than that of stillbirth ≥ 37 weeks (88% vs 46%; P < 0.001). The performance of screening by the combined test was superior to that of selecting the high‐risk group on the basis of UtA‐PI > 90th percentile for gestational age, which predicted 48% of all stillbirths, 70% of those due to impaired placentation and 15% of those that were unexplained or due to other causes.ConclusionsSecond‐trimester screening by a combination of UtA‐PI with maternal factors and fetal biometry can predict a high proportion of stillbirths and, in particular, those that are due to impaired placentation. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.
Network dynamics: quantitative analysis of complex behavior in metabolism, organelles, and cells, from experiments to models and back
Authors: Kurz Felix T. , Kembro Jackelyn M. , Flesia Ana G. , Armoundas Antonis A. , Cortassa Sonia , Aon Miguel A. , Lloyd David 
Published: September 2016

Advancing from two core traits of biological systems: multilevel network organization and nonlinearity, we review a host of novel and readily available techniques to explore and analyze their complex dynamic behavior within the framework of experimental–computational synergy. In the context of concrete biological examples, analytical methods such as wavelet, power spectra, and metabolomics–fluxomics analyses, are presented, discussed, and their strengths and limitations highlighted. Further shown is how time series from stationary and nonstationary biological variables and signals, such as membrane potential, high‐throughput metabolomics,O2andCO2levels, bird locomotion, at the molecular, (sub)cellular, tissue, and whole organ and animal levels, can reveal important information on the properties of the underlying biological networks. Systems biology‐inspired computational methods start to pave the way for addressing the integrated functional dynamics of metabolic, organelle and organ networks. As our capacity to unravel the control and regulatory properties of these networks and their dynamics under normal or pathological conditions broadens, so is our ability to address endogenous rhythms and clocks to improve health‐span in human aging, and to manage complex metabolic disorders, neurodegeneration, and cancer.WIREs Syst Biol Med2017, 9:e1352. doi: 10.1002/wsbm.1352This article is categorized under:Analytical and Computational Methods > Computational MethodsLaboratory Methods and Technologies > MetabolomicsPhysiology > Physiology of Model Organisms
Data sources for in vivo molecular profiling of human phenotypes
Authors: Cardozo Timothy , Gupta Priyanka , Ni Eric , Young Lauren M. , Tivon Doreen , Felsovalyi Klara 
Published: September 2016

Molecular profiling of human diseases has been approached at the genetic (DNA), expression (RNA), and proteomic (protein) levels. An important goal of these efforts is to map observed molecular patterns to specific, mechanistic organic entities, such as loci in the genome, individual RNA molecules or defined proteins or protein assemblies. Importantly, such maps have been historically approached in the more intuitive context of a theoretical individual cell, but diseases are better described in reality using an in vivo framework, namely a library of several tissue‐specific maps. In this article, we review the existing data atlases that can be used for this purpose and identify critical gaps that could move the field forward from cellular to in vivo dimensions. WIREs Syst Biol Med 2016, 8:472–484. doi: 10.1002/wsbm.1354This article is categorized under:

Biological Mechanisms > Chemical Biology
Laboratory Methods and Technologies > Genetic/Genomic Methods
Laboratory Methods and Technologies > Proteomics Methods
In silico bone mechanobiology: modeling a multifaceted biological system
Authors: Giorgi Mario , Verbruggen Stefaan W. , Lacroix Damien 
Published: September 2016

Mechanobiology, the study of the influence of mechanical loads on biological processes through signaling to cells, is fundamental to the inherent ability of bone tissue to adapt its structure in response to mechanical stimulation. The immense contribution of computational modeling to the nascent field of bone mechanobiology is indisputable, having aided in the interpretation of experimental findings and identified new avenues of inquiry. Indeed, advances in computational modeling have spurred the development of this field, shedding new light on problems ranging from the mechanical response to loading by individual cells to tissue differentiation during events such as fracture healing. To date, in silico bone mechanobiology has generally taken a reductive approach in attempting to answer discrete biological research questions, with research in the field broadly separated into two streams: (1) mechanoregulation algorithms for predicting mechanobiological changes to bone tissue and (2) models investigating cell mechanobiology. Future models will likely take advantage of advances in computational power and techniques, allowing multiscale and multiphysics modeling to tie the many separate but related biological responses to loading together as part of a larger systems biology approach to shed further light on bone mechanobiology. Finally, although the ever‐increasing complexity of computational mechanobiology models will inevitably move the field toward patient‐specific models in the clinic, the determination of the context in which they can be used safely for clinical purpose will still require an extensive combination of computational and experimental techniques applied to in vitro and in vivo applications. WIREs Syst Biol Med 2016, 8:485–505. doi: 10.1002/wsbm.1356This article is categorized under:

Analytical and Computational Methods > Computational Methods
Models of Systems Properties and Processes > Organ, Tissue, and Physiological Models
Physiology > Physiology of Model Organisms
Transition metal catalysis in the mitochondria of living cells
Authors: Tomás-Gamasa María , Martínez-Calvo Miguel , Couceiro José R. , Mascareñas José L. 
Published: September 2016

AbstractThe development of transition metal catalysts capable of promoting non-natural transformations within living cells can open significant new avenues in chemical and cell biology. Unfortunately, the complexity of the cell makes it extremely difficult to translate standard organometallic chemistry to living environments. Therefore, progress in this field has been very slow, and many challenges, including the possibility of localizing active metal catalysts into specific subcellular sites or organelles, remain to be addressed. Herein, we report a designed ruthenium complex that accumulates preferentially inside the mitochondria of mammalian cells, while keeping its ability to react with exogenous substrates in a bioorthogonal way. Importantly, we show that the subcellular catalytic activity can be used for the confined release of fluorophores, and even allows selective functional alterations in the mitochondria by the localized transformation of inert precursors into uncouplers of the membrane potential.
Type II enteropathy-associated T-cell lymphoma features a unique genomic profile with highly recurrent SETD2 alterations
Authors: Roberti Annalisa , Dobay Maria Pamela , Bisig Bettina , Vallois David , Boéchat Cloé , Lanitis Evripidis , Bouchindhomme Brigitte , Parrens Marie- Cécile , Bossard Céline , Quintanilla-Martinez Leticia , Missiaglia Edoardo , Gaulard Philippe , de Leval Laurence 
Published: September 2016

AbstractEnteropathy-associated T-cell lymphoma (EATL), a rare and aggressive intestinal malignancy of intraepithelial T lymphocytes, comprises two disease variants (EATL-I and EATL-II) differing in clinical characteristics and pathological features. Here we report findings derived from whole-exome sequencing of 15 EATL-II tumour-normal tissue pairs. The tumour suppressor gene SETD2 encoding a non-redundant H3K36-specific trimethyltransferase is altered in 14/15 cases (93%), mainly by loss-of-function mutations and/or loss of the corresponding locus (3p21.31). These alterations consistently correlate with defective H3K36 trimethylation. The JAK/STAT pathway comprises recurrent STAT5B (60%), JAK3 (46%) and SH2B3 (20%) mutations, including a STAT5B V712E activating variant. In addition, frequent mutations in TP53, BRAF and KRAS are observed. Conversely, in EATL-I, no SETD2, STAT5B or JAK3 mutations are found, and H3K36 trimethylation is preserved. This study describes SETD2 inactivation as EATL-II molecular hallmark, supports EATL-I and -II being two distinct entities, and defines potential new targets for therapeutic intervention.
NK cell development requires Tsc1-dependent negative regulation of IL-15-triggered mTORC1 activation
Authors: Yang Meixiang , Chen Shasha , Du Juan , He Junming , Wang Yuande , Li Zehua , Liu Guangao , Peng Wanwen , Zeng Xiaokang , Li Dan , Xu Panglian , Guo Wei , Chang Zai , Wang Song , Tian Zhigang , Dong Zhongjun 
Published: September 2016

AbstractActivation of metabolic signalling by IL-15 is required for natural killer (NK) cell development. Here we show that Tsc1, a repressor of mTOR, is dispensable for the terminal maturation, survival and function of NK cells but is critical to restrict exhaustive proliferation of immature NK cells and activation downstream of IL-15 during NK cell development. Tsc1 is expressed in immature NK cells and is upregulated by IL-15. Haematopoietic-specific deletion of Tsc1 causes a marked decrease in the number of NK cells and compromises rejection of ‘missing-self’ haematopoietic tumours and allogeneic bone marrow. The residual Tsc1-null NK cells display activated, pro-apoptotic phenotype and elevated mTORC1 activity. Deletion of Raptor, a component of mTORC1, largely reverses these defects. Tsc1-deficient NK cells express increased levels of T-bet and downregulate Eomes and CD122, a subunit of IL-15 receptor. These results reveal a role for Tsc1-dependent inhibition of mTORC1 activation during immature NK cell development.
Vancomycin susceptibility in methicillin-resistant Staphylococcus aureus is mediated by YycHI activation of the WalRK essential two-component regulatory system
Authors: Cameron David R. , Jiang Jhih-Hang , Kostoulias Xenia , Foxwell Daniel J. , Peleg Anton Y. 
Published: September 2016

AbstractThe treatment of infections caused by methicillin-resistant Staphylococcus aureus is complicated by the emergence of strains with intermediate-level resistance to vancomycin (termed VISA). We have characterised a molecular pathway involved in the in vivo evolution of VISA mediated by the regulatory proteins YycH and YycI. In contrast to their function in other bacterial species, we report a positive role for these auxiliary proteins in regulation of the two-component regulator WalRK. Transcriptional profiling of yycH and yycI deletion mutants revealed downregulation of the ‘WalRK regulon’ including cell wall hydrolase genes atlA and sle1, with functional autolysis assays supporting these data by showing an impaired autolytic phenotype for each deletion strain. Using bacterial-two hybrid assays, we showed that YycH and YycI interact and that YycHI also interacts with the sensor kinase WalK, forming a ternary protein complex. Mutation to YycH or YycI associated with clinical VISA strains had a deleterious impact on the YycHI/WalK complex, suggesting that the interaction is important for the regulation of WalRK. Taken together, we have described a novel antibiotic resistance strategy for the human pathogen S. aureus, whereby YycHI mutations are selected for in vivo leading to reduced WalRK activation, impaired cell wall turnover and ultimately reduced vancomycin efficacy.
Coherence-Gated Sensorless Adaptive Optics Multiphoton Retinal Imaging
Authors: Cua Michelle , Wahl Daniel J. , Zhao Yuan , Lee Sujin , Bonora Stefano , Zawadzki Robert J. , Jian Yifan , Sarunic Marinko V. 
Published: September 2016

AbstractMultiphoton microscopy enables imaging deep into scattering tissues. The efficient generation of non-linear optical effects is related to both the pulse duration (typically on the order of femtoseconds) and the size of the focused spot. Aberrations introduced by refractive index inhomogeneity in the sample distort the wavefront and enlarge the focal spot, which reduces the multiphoton signal. Traditional approaches to adaptive optics wavefront correction are not effective in thick or multi-layered scattering media. In this report, we present sensorless adaptive optics (SAO) using low-coherence interferometric detection of the excitation light for depth-resolved aberration correction of two-photon excited fluorescence (TPEF) in biological tissue. We demonstrate coherence-gated SAO TPEF using a transmissive multi-actuator adaptive lens for in vivo imaging in a mouse retina. This configuration has significant potential for reducing the laser power required for adaptive optics multiphoton imaging and for facilitating integration with existing systems.
miR-564 acts as a dual inhibitor of PI3K and MAPK signaling networks and inhibits proliferation and invasion in breast cancer
Authors: Mutlu Merve , Saatci Özge , Ansari Suhail A. , Yurdusev Emre , Shehwana Huma , Konu Özlen , Raza Umar , Şahin Özgür 
Published: September 2016

AbstractDysregulation of PI3K and MAPK pathways promotes uncontrolled cell proliferation, apoptotic inhibition and metastasis. Individual targeting of these pathways using kinase inhibitors has largely been insufficient due to the existence of cross-talks between these parallel cascades. MicroRNAs are small non-coding RNAs targeting several genes simultaneously and controlling cancer-related processes. To identify miRNAs repressing both PI3K and MAPK pathways in breast cancer, we re-analyzed our previous miRNA mimic screen data with reverse phase protein array (RPPA) output and identified miR-564 inhibiting both PI3K and MAPK pathways causing markedly decreased cell proliferation through G1 arrest. Moreover, ectopic expression of miR-564 blocks epithelial-mesenchymal transition (EMT) and reduces migration and invasion of aggressive breast cancer cells. Mechanistically, miR-564 directly targets a network of genes comprising AKT2, GNA12, GYS1 and SRF, thereby facilitating simultaneous repression of PI3K and MAPK pathways. Notably, combinatorial knockdown of these target genes using a cocktail of siRNAs mimics the phenotypes exerted upon miR-564 expression. Importantly, high miR-564 expression or low expression of target genes in combination is significantly correlated with better distant relapse-free survival of patients. Overall, miR-564 is a potential dual inhibitor of PI3K and MAPK pathways and may be an attractive target and prognostic marker for breast cancer.