bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tailoring spontaneous infrared emission of HgTe quantum dots with laser-printed plasmonic arrays
Authors: Sergeev A. A. , Pavlov D. V. , Kuchmizhak A. A. , Lapine M. V. , Yiu W. K. , Dong Y. , Ke N. , Juodkazis S. , Zhao N. , Kershaw S. V. , Rogach A. L. 
Published: February 2020

AbstractChemically synthesized near-infrared to mid-infrared (IR) colloidal quantum dots (QDs) offer a promising platform for the realization of devices including emitters, detectors, security, and sensor systems. However, at longer wavelengths, the quantum yield of such QDs decreases as the radiative emission rate drops following Fermi’s golden rule, while non-radiative recombination channels compete with light emission. Control over the radiative and non-radiative channels of the IR-emitting QDs is crucially important to improve the performance of IR-range devices. Here, we demonstrate strong enhancement of the spontaneous emission rate of near- to mid-IR HgTe QDs coupled to periodically arranged plasmonic nanoantennas, in the form of nanobumps, produced on the surface of glass-supported Au films via ablation-free direct femtosecond laser printing. The enhancement is achieved by simultaneous radiative coupling of the emission that spectrally matches the first-order lattice resonance of the arrays, as well as more efficient photoluminescence excitation provided by coupling of the pump radiation to the local surface plasmon resonances of the isolated nanoantennas. Moreover, coupling of the HgTe QDs to the lattice plasmons reduces the influence of non-radiative decay losses mediated by the formation of polarons formed between QD surface-trapped carriers and the IR absorption bands of dodecanethiol used as a ligand on the QDs, allowing us to improve the shape of the emission spectrum through a reduction in the spectral dip related to this ligand coupling. Considering the ease of the chemical synthesis and processing of the HgTe QDs combined with the scalability of the direct laser fabrication of nanoantennas with tailored plasmonic responses, our results provide an important step towards the design of IR-range devices for various applications.
Blood platelets stimulate cancer extravasation through TGFβ-mediated downregulation of PRH/HHEX
Authors: Marcolino Eudmar , Siddiqui Yusra Hasan , van den Bosch Marion , Poole Alastair W. , Jayaraman Padma-Sheela , Gaston Kevin 
Published: February 2020

AbstractCancer cells go through a process known as epithelial–mesenchymal transition (EMT) during which they acquire the ability to migrate and invade extracellular matrix. Some cells also acquire the ability to move across a layer of endothelial cells to enter and exit the bloodstream; intra- and extravasation, respectively. The transcription factor PRH/HHEX (proline-rich homeodomain/haematopoietically expressed homeobox) controls cell proliferation and cell migration/invasion in a range of cell types. Our previous work showed that PRH activity is downregulated in prostate cancer cells owing to increased inhibitory PRH phosphorylation and that this increases cell proliferation and invasion. PRH inhibits migration and invasion by prostate and breast epithelial cells in part by activating the transcription of Endoglin, a transforming growth factor β (TGFβ) co-receptor. Here we show that depletion of PRH in immortalised prostate epithelial cells results in increased extravasation in vitro. We show that blood platelets stimulate extravasation of cells with depleted PRH and that inhibition of TGFβ signalling blocks the effects of platelets on these cells. Moreover, TGFβ induces changes characteristic of EMT including decreased E-Cadherin expression and increased Snail expression. We show that in prostate cells PRH regulates multiple genes involved in EMT and TGFβ signalling. However, both platelets and TGFβ increase PRH phosphorylation. In addition, TGFβ increases binding of its effector pSMAD3 to the PRH/HHEX promoter and downregulates PRH protein and mRNA levels. Thus, TGFβ signalling downregulates PRH activity by multiple mechanisms and induces an EMT that facilitates extravasation and sensitises cells to TGFβ.
Chondroitin sulfate synthase 1 enhances proliferation of glioblastoma by modulating PDGFRA stability
Authors: Liao Wen-Chieh , Liao Chih-Kai , Tseng To-Jung , Ho Ying-Jui , Chen Ying-Ru , Lin Kuan-Hung , Lai Te-Jen , Lan Chyn-Tair , Wei Kuo-Chen , Liu Chiung-Hui 
Published: February 2020

AbstractChondroitin sulfate synthases, a family of enzyme involved in chondroitin sulfate (CS) polymerization, are dysregulated in various human malignancies, but their roles in glioma remain unclear. We performed database analysis and immunohistochemistry on human glioma tissue, to demonstrate that the expression of CHSY1 was frequently upregulated in glioma, and that it was associated with adverse clinicopathologic features, including high tumor grade and poor survival. Using a chondroitin sulfate-specific antibody, we showed that the expression of CHSY1 was significantly associated with CS formation in glioma tissue and cells. In addition, overexpression of CHSY1 in glioma cells enhanced cell viability and orthotopic tumor growth, whereas CHSY1 silencing suppressed malignant growth. Mechanistic investigations revealed that CHSY1 selectively regulates PDGFRA activation and PDGF-induced signaling in glioma cells by stabilizing PDGFRA protein levels. Inhibiting PDGFR activity with crenolanib decreased CHSY1-induced malignant characteristics of GL261 cells and prolonged survival in an orthotopic mouse model of glioma, which underlines the critical role of PDGFRA in mediating the effects of CHSY1. Taken together, these results provide information on CHSY1 expression and its role in glioma progression, and highlight novel insights into the significance of CHSY1 in PDGFRA signaling. Thus, our findings point to new molecular targets for glioma treatment.
Synergism between Corynebacterium and Streptococcus sanguinis reveals new interactions between oral commensals
Authors: Treerat Puthayalai , Redanz Ulrike , Redanz Sylvio , Giacaman Rodrigo A , Merritt Justin , Kreth Jens 
Published: February 2020

Abstract
The oral microbiome engages in a diverse array of highly sophisticated ecological interactions that are crucial for maintaining symbiosis with the host. Streptococci and corynebacteria are among the most abundant oral commensals and their interactions are critical for normal biofilm development. In this study, we discovered that Streptococcus sanguinis specifically responds to the presence of Corynebacterium durum by dramatically altering its chain morphology and improving its overall fitness. By employing gas chromatography-mass spectrometry (GC-MS) analysis, specific fatty acids were identified in C. durum supernatants that are responsible for the observed effect. Membrane vesicles (MVs) containing these fatty acids were isolated from C. durum supernatants and were able to replicate the chain morphology phenotype in S. sanguinis, suggesting MV as a mediator of interspecies interactions. Furthermore, S. sanguinis responds to C. durum lipids by decreasing the expression of key FASII genes involved in fatty acid synthesis. Several of these genes are also essential for the chain elongation phenotype, which implicates a regulatory connection between lipid metabolism and chain elongation. In addition, C. durum was found to affect the growth, cell aggregation, and phagocytosis of S. sanguinis, revealing a complex association of these species that likely supports oral commensal colonization and survival.
Predictive factors for early progression during induction chemotherapy and chemotherapy-free interval: analysis from PRODIGE 9 trial
Authors:   for PRODIGE investigators/collaborators, Aparicio Thomas , Bennouna Jaafar , Le Malicot Karine , Boige Valérie , Taieb Julien , Bouché Olivier , Phelip Jean-Marc , François Eric , Borel Christian , Faroux Roger , Dahan Laetitia , Bachet Jean-Baptiste , Egreteau Joelle , Kaminsky Marie-Christine , Gornet Jean-Marc , Cojocarasu Oana , Gasmi Mohamed , Guerin-Meyer Véronique , Lepage Côme , Ghiringhelli François 
Published: February 2020

Abstract
Background
Identifying patients with metastatic colorectal cancer who will have an early disease progression during induction chemotherapy (IC) and identifying patients who may have a chemotherapy-free interval (CFI) after IC are two major challenges.

Methods
A logistic model was used to identify factors associated with early progression during IC and with short duration of the first CFI in 488 patients enrolled in the PRODIGE 9 trial. Independent factors were defined with a threshold 0.10.

Results
In multivariate analysis, baseline leukocytes >10 × 109/L (OR = 1.98 [1.02–3.8], p = 0.04), and stable or increasing CEA at 2 months (OR = 3.61 [1.68–7.75], p = 0.01) were independent factors associated with progression during IC. Male gender (OR = 1.725 [0.92–3.325], p = 0.09) and no tumour response at first evaluation (OR = 1.90 [0.96–3.76], p = 0.07) were significantly associated with a short CFI. The presence of BRAF V600E mutation was also associated with short CFI (OR = 4.59 [0.95; 22.3], p = 0.058).

Conclusion
High baseline leukocyte count and the lack of CEA decrease level at first evaluation were associated with early progression, and could be in favour of early chemotherapy intensification. Male gender, no tumour response at first evaluation and BRAF mutation are associated with a short CFI, and may be considered for maintenance chemotherapy after IC.

Clinical trial number
NCT00952029.
Nintedanib inhibits intrahepatic cholangiocarcinoma aggressiveness via suppression of cytokines extracted from activated cancer-associated fibroblasts
Authors: Yamanaka Takahiro , Harimoto Norifumi , Yokobori Takehiko , Muranushi Ryo , Hoshino Kouki , Hagiwara Kei , Gantumur Dolgormaa , Handa Tadashi , Ishii Norihiro , Tsukagoshi Mariko , Igarashi Takamichi , Tanaka Hiroshi , Watanabe Akira , Kubo Norio , Araki Kenichiro , Shirabe Ken 
Published: February 2020

Abstract
Background
Intrahepatic cholangiocarcinoma (ICC) is a malignancy that is challenging to treat. Fibroblasts in ICC tissues have been identified as cancer-associated fibroblasts (CAFs) that promote the malignant behaviour of ICC cells. An antifibrotic drug nintedanib has been reported to suppress activated hepatic stellate cells in liver fibrosis.

Methods
We investigated whether nintedanib could suppress the cancer-promoting effect of CAFs derived from ICC tissues in vitro and in vivo.

Results
CAFs promoted the proliferation and invasion of ICC cells. Nintedanib suppressed activated CAFs expressing α-smooth muscle actin (α-SMA) and inhibited the ICC-promoting effects of CAFs. Nintedanib greatly reduced the levels of cancer-promoting cytokines, such as interleukin (IL)-6 (IL-6) and IL-8, secreted by CAFs. An in vivo study demonstrated that nintedanib reduced xenografted ICC growth and activated CAFs expressing α-SMA, and that combination therapy with nintedanib and gemcitabine against CAFs and ICC cells showed the strongest inhibition of tumour growth compared with the control and single-treatment groups.

Conclusions
Nintedanib inhibited the cancer-promoting effect of CAFs via the suppression of CAF activation and secretion of cancer-promoting cytokines. Our findings suggest that therapeutic strategies combining conventional cytotoxic agents with nintedanib targeting CAFs are promising for overcoming refractory ICC with activated CAFs.
Oncogene-dependent function of BRG1 in hepatocarcinogenesis
Authors: Wang Pan , Song Xinhua , Cao Dan , Cui Kairong , Wang Jingxiao , Utpatel Kirsten , Shang Runze , Wang Haichuan , Che Li , Evert Matthias , Zhao Keji , Calvisi Diego F. , Chen Xin 
Published: February 2020

AbstractHepatocellular carcinoma (HCC) is the major type of primary liver cancer. Genomic studies have revealed that HCC is a heterogeneous disease with multiple subtypes. BRG1, encoded by the SMARCA4 gene, is a key component of SWI/SNF chromatin-remodeling complexes. Based on TCGA studies, somatic mutations of SMARCA4 occur in ~3% of human HCC samples. Additional studies suggest that BRG1 is overexpressed in human HCC specimens and may promote HCC growth and invasion. However, the precise functional roles of BRG1 in HCC remain poorly delineated. Here, we analyzed BRG1 in human HCC samples as well as in mouse models. We found that BRG1 is overexpressed in most of human HCC samples, especially in those associated with poorer prognosis. BRG1 expression levels positively correlate with cell cycle and negatively with metabolic pathways in the Cancer Genome Atlas (TCGA) human HCC data set. In a murine HCC model induced by c-MYC overexpression, ablation of the Brg1 gene completely repressed HCC formation. In striking contrast, however, we discovered that concomitant deletion of Brg1 and overexpression of c-Met or mutant NRas (NRASV12) triggered HCC formation in mice. Altogether, the present data indicate that BRG1 possesses both oncogenic and tumor-suppressing roles depending on the oncogenic stimuli during hepatocarcinogenesis.
Loss of GFAT-1 feedback regulation activates the hexosamine pathway that modulates protein homeostasis
Authors: Ruegenberg Sabine , Horn Moritz , Pichlo Christian , Allmeroth Kira , Baumann Ulrich , Denzel Martin S. 
Published: February 2020

AbstractGlutamine fructose-6-phosphate amidotransferase (GFAT) is the key enzyme in the hexosamine pathway (HP) that produces uridine 5′-diphospho-N-acetyl-d-glucosamine (UDP-GlcNAc), linking energy metabolism with posttranslational protein glycosylation. In Caenorhabditis elegans, we previously identified gfat-1 gain-of-function mutations that elevate UDP-GlcNAc levels, improve protein homeostasis, and extend lifespan. GFAT is highly conserved, but the gain-of-function mechanism and its relevance in mammalian cells remained unclear. Here, we present the full-length crystal structure of human GFAT-1 in complex with various ligands and with important mutations. UDP-GlcNAc directly interacts with GFAT-1, inhibiting catalytic activity. The longevity-associated G451E variant shows drastically reduced sensitivity to UDP-GlcNAc inhibition in enzyme activity assays. Our structural and functional data point to a critical role of the interdomain linker in UDP-GlcNAc inhibition. In mammalian cells, the G451E variant potently activates the HP. Therefore, GFAT-1 gain-of-function through loss of feedback inhibition constitutes a potential target for the treatment of age-related proteinopathies.
Nexus of grazing management with plant and soil properties in northern China grasslands
Authors: Wang Li , Luan Limin , Hou Fujiang , Siddique Kadambot H. M. 
Published: February 2020

AbstractGrasslands provide habitats for living organisms and livelihoods for ~800 million people globally. Many grasslands in developing countries are severely degraded. Some measures have been taken to curb the trend of degradation for decades. It is important to determine how decade-long rejuvenation efforts affected grassland ecosystems. We identified 65 data-rich studies based on six criteria, from >2500 relevant publications, and generated a dataset with 997 rows and 12 variables. The dataset covers different grazing intensities (grazing exclusion, light, moderate, and heavy grazing) and their impacts on plant traits (vegetation coverage, aboveground and root biomass, and plant diversity) and soil physiochemical properties (bulk density, moisture content, organic C, total and available N, total and available P, C:N ratio, and pH). The dataset could be used to (i) quantify the effectiveness of rejuvenation processes by determining the impact on plant community and soil properties, (ii) perform comprehensive analyses to elucidate large-picture effects of grazing management and rejuvenation, and (iii) analyze the impact of grass–climate–soil–human interactions on grassland ecosystem sustainability.
Prosthetic model, but not stiffness or height, affects maximum running velocity in athletes with unilateral transtibial amputations
Authors: Taboga Paolo , Drees Emily K. , Beck Owen N. , Grabowski Alena M. 
Published: February 2020

AbstractThe running-specific prosthetic (RSP) configuration used by athletes with transtibial amputations (TTAs) likely affects performance. Athletes with unilateral TTAs are prescribed C- or J-shaped RSPs with a manufacturer-recommended stiffness category based on body mass and activity level, and height based on unaffected leg and residual limb length. We determined how 15 different RSP model, stiffness, and height configurations affect maximum running velocity (vmax) and the underlying biomechanics. Ten athletes with unilateral TTAs ran at 3 m/s to vmax on a force-measuring treadmill. vmax was 3.8–10.7% faster when athletes used J-shaped versus C-shaped RSP models (p < 0.05), but was not affected by stiffness category, actual stiffness (kN/m), or height (p = 0.72, p = 0.37, and p = 0.11, respectively). vmax differences were explained by vertical ground reaction forces (vGRFs), stride kinematics, leg stiffness, and symmetry. While controlling for velocity, use of J-shaped versus C-shaped RSPs resulted in greater stance average vGRFs, slower step frequencies, and longer step lengths (p < 0.05). Stance average vGRFs were less asymmetric using J-shaped versus C-shaped RSPs (p < 0.05). Contact time and leg stiffness were more asymmetric using the RSP model that elicited the fastest vmax (p < 0.05). Thus, RSP geometry (J-shape versus C-shape), but not stiffness or height, affects vmax in athletes with unilateral TTAs.
1RS arm of Secale cereanum ‘Kriszta’ confers resistance to stripe rust, improved yield components and high arabinoxylan content in wheat
Authors: Szakács Éva , Szőke-Pázsi Kitti , Kalapos Balázs , Schneider Annamária , Ivanizs László , Rakszegi Marianna , Vida Gyula , Molnár István , Molnár-Láng Márta 
Published: February 2020

AbstractWheat-rye T1BL.1RS translocation is widespread worldwide as the genes on 1RS arm have positive effect on stress resistance, grain yield and adaptation ability of wheat. Nowadays, the T1BL.1RS wheat cultivars have become susceptible to rust diseases because of the monophyletic (‘Petkus’) origin of 1RS. Here we report and discuss the production and detailed investigation of a new T1BL.1RS translocation line carrying 1RS with widened genetic base originating from Secale cereanum. Line ‘179’ exhibited improved spike morphology traits, resistance against stripe rust and leaf rust, as well as higher tillering capacity, fertility and dietary fiber (arabynoxylan) content than the parental wheat genotype. Comparative analyses based on molecular cytogenetic methods and molecular (SSR and DArTseq) makers indicate that the 1RS arm of line ‘179’ is a recombinant of S. cereale and S. strictum homologues, and approximately 16% of its loci were different from that of ‘Petkus’ origin. 162 (69.5%) 1RS-specific markers were associated with genes, including 10 markers with putative disease resistance functions and LRR domains found on the subtelomeric or pericentromeric regions of 1RS. Line ‘179’ will facilitate the map-based cloning of the resistance genes, and it can contribute to healthy eating and a more cost-efficient wheat production.
A kinetic method for measuring agonist efficacy and ligand bias using high resolution biosensors and a kinetic data analysis framework
Authors: Hoare Sam R. J. , Tewson Paul H. , Quinn Anne Marie , Hughes Thomas E. 
Published: February 2020

AbstractThe kinetics/dynamics of signaling are of increasing value for G-protein-coupled receptor therapeutic development, including spatiotemporal signaling and the kinetic context of biased agonism. Effective application of signaling kinetics to developing new therapeutics requires reliable kinetic assays and an analysis framework to extract kinetic pharmacological parameters. Here we describe a platform for measuring arrestin recruitment kinetics to GPCRs using a high quantum yield, genetically encoded fluorescent biosensor, and a data analysis framework to quantify the recruitment kinetics. The sensor enabled high temporal resolution measurement of arrestin recruitment to the angiotensin AT1 and vasopressin V2 receptors. The analysis quantified the initial rate of arrestin recruitment (kτ), a biologically-meaningful kinetic drug efficacy parameter, by fitting time course data using routine curve-fitting methods. Biased agonism was assessed by comparing kτ values for arrestin recruitment with those for Gq signaling via the AT1 receptor. The kτ ratio values were in good agreement with bias estimates from existing methods. This platform potentially improves and simplifies assessment of biased agonism because the same assay modality is used to compare pathways (potentially in the same cells), the analysis method is parsimonious and intuitive, and kinetic context is factored into the bias measurement.
A high visibility Talbot-Lau neutron grating interferometer to investigate stress-induced magnetic degradation in electrical steel
Authors: Neuwirth Tobias , Backs Alexander , Gustschin Alex , Vogt Simon , Pfeiffer Franz , Böni Peter , Schulz Michael 
Published: February 2020

AbstractNeutron grating interferometry (nGI) is a unique technique allowing to probe magnetic and nuclear properties of materials not accessible in standard neutron imaging. The signal-to-noise ratio of an nGI setup is strongly dependent on the achievable visibility. Hence, for analysis of weak signals or short measurement times a high visibility is desired. We developed a new Talbot-Lau interferometer using the third Talbot order with an unprecedented visibility (0.74) over a large field of view. Using the third Talbot order and the resulting decreased asymmetry allows to access a wide correlation length range. Moreover, we have used a novel technique for the production of the absorption gratings which provides nearly binary gratings even for thermal neutrons. The performance of the new interferometer is demonstrated by visualizing the local magnetic domain wall density in electrical steel sheets when influenced by residual stress induced by embossing. We demonstrate that it is possible to affect the density of the magnetic domain walls by embossing and therefore to engineer the guiding of magnetic fields in electrical steel sheets. The excellent performance of our new setup will also facilitate future studies of dynamic effects in electric steels and other systems.
Cold-water coral (Lophelia pertusa) response to multiple stressors: High temperature affects recovery from short-term pollution exposure
Authors: Weinnig Alexis M. , Gómez Carlos E. , Hallaj Adam , Cordes Erik E. 
Published: February 2020

AbstractThere are numerous studies highlighting the impacts of direct and indirect stressors on marine organisms, and multi-stressor studies of their combined effects are an increasing focus of experimental work.Lophelia pertusais a framework-forming cold-water coral that supports numerous ecosystem services in the deep ocean. These corals are threatened by increasing anthropogenic impacts to the deep-sea, such as global ocean change and hydrocarbon extraction. This study implemented two sets of experiments to assess the effects of future conditions (temperature: 8 °C and 12 °C, pH: 7.9 and 7.6) and hydrocarbon exposure (oil, dispersant, oil + dispersant combined) on coral health. Phenotypic response was assessed through three independent observations of diagnostic characteristics that were combined into an average health rating at four points during exposure and recovery. In both experiments, regardless of environmental condition, average health significantly declined during 24-hour exposure to dispersant alone but was not significantly altered in the other treatments. In the early recovery stage (24 hours), polyp health returned to the pre-exposure health state under ambient temperature in all treatments. However, increased temperature resulted in a delay in recovery (72 hours) from dispersant exposure. These experiments provide evidence that global ocean change can affect the resilience of corals to environmental stressors and that exposure to chemical dispersants may pose a greater threat than oil itself.