bluuebunny/crossref_metadata_2025_split huggingface dataset:
Broadband perovskite quantum dot spectrometer beyond human visual resolution
Authors: Zhu Xiaoxiu , Bian Liheng , Fu Hao , Wang Lingxue , Zou Bingsuo , Dai Qionghai , Zhang Jun , Zhong Haizheng 
Published: April 2020

AbstractThe quantum dot spectrometer, fabricated by integrating different quantum dots with an image sensor to reconstruct the target spectrum from spectral-coupled measurements, is an emerging and promising hyperspectrometry technology with high resolution and a compact size. The spectral resolution and spectral range of quantum dot spectrometers have been limited by the spectral variety of the available quantum dots and the robustness of algorithmic reconstruction. Moreover, the spectrometer integration of quantum dots also suffers from inherent photoluminescence emission and poor batch-to-batch repeatability. In this work, we developed nonemissive in situ fabricated MA3Bi2X9 and Cs2SnX6 (MA = CH3NH3; X = Cl, Br, I) perovskite-quantum-dot-embedded films (PQDFs) with precisely tunable transmittance spectra for quantum dot spectrometer applications. The resulting PQDFs contain in situ fabricated perovskite nanocrystals with homogenous dispersion in a polymeric matrix, giving them advantageous features such as high transmittance efficiency and good batch-to-batch repeatability. By integrating a filter array of 361 kinds of PQDFs with a silicon-based photodetector array, we successfully demonstrated the construction of a perovskite quantum dot spectrometer combined with a compressive-sensing-based total-variation optimization algorithm. A spectral resolution of ~1.6 nm was achieved in the broadband of 250–1000 nm. The performance of the perovskite quantum dot spectrometer is well beyond that of human eyes in terms of both the spectral range and spectral resolution. This advancement will not only pave the way for using quantum dot spectrometers for practical applications but also significantly impact the development of artificial intelligence products, clinical treatment equipment, scientific instruments, etc.
TGFβ and EGF signaling orchestrates the AP-1- and p63 transcriptional regulation of breast cancer invasiveness
Authors: Sundqvist Anders , Vasilaki Eleftheria , Voytyuk Oleksandr , Bai Yu , Morikawa Masato , Moustakas Aristidis , Miyazono Kohei , Heldin Carl-Henrik , ten Dijke Peter , van Dam Hans 
Published: April 2020

AbstractActivator protein (AP)-1 transcription factors are essential elements of the pro-oncogenic functions of transforming growth factor-β (TGFβ)-SMAD signaling. Here we show that in multiple HER2+ and/or EGFR+ breast cancer cell lines these AP-1-dependent tumorigenic properties of TGFβ critically rely on epidermal growth factor receptor (EGFR) activation and expression of the ΔN isoform of transcriptional regulator p63. EGFR and ΔNp63 enabled and/or potentiated the activation of a subset of TGFβ-inducible invasion/migration-associated genes, e.g., ITGA2, LAMB3, and WNT7A/B, and enhanced the recruitment of SMAD2/3 to these genes. The TGFβ- and EGF-induced binding of SMAD2/3 and JUNB to these gene loci was accompanied by p63-SMAD2/3 and p63-JUNB complex formation. p63 and EGFR were also found to strongly potentiate TGFβ induction of AP-1 proteins and, in particular, FOS family members. Ectopic overexpression of FOS could counteract the decrease in TGFβ-induced gene activation after p63 depletion. p63 is also involved in the transcriptional regulation of heparin binding (HB)-EGF and EGFR genes, thereby establishing a self-amplification loop that facilitates and empowers the pro-invasive functions of TGFβ. These cooperative pro-oncogenic functions of EGFR, AP-1, p63, and TGFβ were efficiently inhibited by clinically relevant chemical inhibitors. Our findings may, therefore, be of importance for therapy of patients with breast cancers with an activated EGFR-RAS-RAF pathway.
ACSL4 promotes hepatocellular carcinoma progression via c-Myc stability mediated by ERK/FBW7/c-Myc axis
Authors: Chen Junru , Ding Chaofeng , Chen Yunhao , Hu Wendi , Lu Yuejie , Wu Wenxuan , Zhang Yanpeng , Yang Beng , Wu Hao , Peng Chuanhui , Xie Haiyang , Zhou Lin , Wu Jian , Zheng Shusen 
Published: April 2020

AbstractHepatocellular carcinoma (HCC) is a highly heterogeneous, multigene-driven malignant tumor. Long chain acyl-CoA synthetase 4 (ACSL4), an enzyme has pivotal roles in arachidonic acid (AA) metabolism. However, its function and the underlying molecular mechanisms in HCC are still not fully elucidated. Here, we identified ACSL4 as a novel marker for AFP high subtype HCC through transcriptome profiling. ACSL4 was frequently upregulated in HCC samples and associated with poor prognosis. Functionally, ACSL4 knockdown resulted in decreased cell growth, whereas ectopic ACSL4 expression facilitated tumor formation in vitro and in vivo. Mechanistically, ACSL4 stabilized the oncoprotein c-Myc through ubiquitin–proteasome system in an ERK/FBW7-dependent manner. Cell growth ability mediated by ACSL4 elevation was partly attenuated by c-Myc depletion using siRNA or its inhibitor 10058-F4. In contrast, the effects of ACSL4 silencing were partially reversed by c-Myc overexpression via FBW7 knockdown. Clinically, ACSL4 expression was positively correlated with c-Myc in HCC. In conclusion, ACSL4 is a novel marker for AFP high subtype HCC. Our data uncovered a new mechanism by which ACSL4 promotes HCC progression via c-Myc stability mediated by ERK/FBW7/c-Myc axis and could be a valuable prognostic biomarker and a potential therapeutic target in HCC.
KLF4-mediated upregulation of CD9 and CD81 suppresses hepatocellular carcinoma development via JNK signaling
Authors: Li Yandong , Yu Shijun , Li Li , Chen Jingde , Quan Ming , Li Qinchuan , Gao Yong 
Published: April 2020

AbstractTetraspanins CD9 and CD81 frequently serve as the surface markers of exosomes, which are involved in intercellular communication during tumor progression. KLF4 is a well-known tumor suppressor in various cancers. This study aims to investigate the relationship between KLF4 and CD9/CD81 in hepatocellular carcinoma (HCC). The results showed that CD9 and CD81 were transcriptionally activated by KLF4 in HCC cell lines. Decreased expressions of CD9 and CD81 were found in most HCC tumor tissues and predicted advanced stages. Furthermore, KLF4 expression was positively associated with CD9 and CD81 expression in HCC specimens. Functionally, overexpression of CD9 and CD81 inhibited HCC cell proliferation in vitro and in vivo and silencing CD9 and CD81 displayed opposite phenotypes. Mechanistically, we found that JNK signaling pathway may be involved in the growth suppression mediated by CD9 and CD81. In addition, increased expression of KLF4, CD9 or CD81 had no obvious impact on exosome secretion from HCC cells. Collectively, we identified CD9 and CD81 as new transcriptional targets of KLF4 and the dysregulated KLF4-CD9/CD81-JNK signaling contributes to HCC development. Our findings will provide new promising targets against this disease.
Synthetic hybrids of six yeast species
Authors: Peris David , Alexander William G. , Fisher Kaitlin J. , Moriarty Ryan V. , Basuino Mira G. , Ubbelohde Emily J. , Wrobel Russell L. , Hittinger Chris Todd 
Published: April 2020

AbstractAllopolyploidy generates diversity by increasing the number of copies and sources of chromosomes. Many of the best-known evolutionary radiations, crops, and industrial organisms are ancient or recent allopolyploids. Allopolyploidy promotes differentiation and facilitates adaptation to new environments, but the tools to test its limits are lacking. Here we develop an iterative method of Hybrid Production (iHyPr) to combine the genomes of multiple budding yeast species, generating Saccharomyces allopolyploids of at least six species. When making synthetic hybrids, chromosomal instability and cell size increase dramatically as additional copies of the genome are added. The six-species hybrids initially grow slowly, but they rapidly regain fitness and adapt, even as they retain traits from multiple species. These new synthetic yeast hybrids and the iHyPr method have potential applications for the study of polyploidy, genome stability, chromosome segregation, and bioenergy.
Data-driven analysis and forecasting of highway traffic dynamics
Authors: Avila A. M. , Mezić I. 
Published: April 2020

AbstractThe unpredictable elements involved in a vehicular traffic system, like human interaction and weather, lead to a very complicated, high-dimensional, nonlinear dynamical system. Therefore, it is difficult to develop a mathematical or artificial intelligence model that describes the time evolution of traffic systems. All the while, the ever-increasing demands on transportation systems has left traffic agencies in dire need of a robust method for analyzing and forecasting traffic. Here we demonstrate how the Koopman mode decomposition can offer a model-free, data-driven approach for analyzing and forecasting traffic dynamics. By obtaining a decomposition of data sets collected by the Federal Highway Administration and the California Department of Transportation, we are able to reconstruct observed data, distinguish any growing or decaying patterns, and obtain a hierarchy of previously identified and never before identified spatiotemporal patterns. Furthermore, it is demonstrated how this methodology can be utilized to forecast highway network conditions.
Targeting codon 158 p53-mutant cancers via the induction of p53 acetylation
Authors: Kong Li Ren , Ong Richard Weijie , Tan Tuan Zea , Mohamed Salleh Nur Afiqah Binte , Thangavelu Matan , Chan Jane Vin , Koh Lie Yong Judice , Periyasamy Giridharan , Lau Jieying Amelia , Le Thi Bich Uyen , Wang Lingzhi , Lee Miyoung , Kannan Srinivasaraghavan , Verma Chandra S. , Lim Chwee Ming , Chng Wee Joo , Lane David P. , Venkitaraman Ashok , Hung Huynh The , Cheok Chit Fang , Goh Boon Cher 
Published: April 2020

AbstractGain of function (GOF) DNA binding domain (DBD) mutations of TP53 upregulate chromatin regulatory genes that promote genome-wide histone methylation and acetylation. Here, we therapeutically exploit the oncogenic GOF mechanisms of p53 codon 158 (Arg158) mutation, a DBD mutant found to be prevalent in lung carcinomas. Using high throughput compound screening and combination analyses, we uncover that acetylating mutp53R158G could render cancers susceptible to cisplatin-induced DNA stress. Acetylation of mutp53R158G alters DNA binding motifs and upregulates TRAIP, a RING domain-containing E3 ubiquitin ligase which dephosphorylates IĸB and impedes nuclear translocation of RelA (p65), thus repressing oncogenic nuclear factor kappa-B (NF-ĸB) signaling and inducing apoptosis. Given that this mechanism of cytotoxic vulnerability appears inapt in p53 wild-type (WT) or other hotspot GOF mutp53 cells, our work provides a therapeutic opportunity specific to Arg158-mutp53 tumors utilizing a regimen consisting of DNA-damaging agents and mutp53 acetylators, which is currently being pursued clinically.
Partial impairment of insulin receptor expression mimics fasting to prevent diet-induced fatty liver disease
Authors: Merry Troy L. , Hedges Chris P. , Masson Stewart W. , Laube Beate , Pöhlmann Doris , Wueest Stephan , Walsh Michael E. , Arnold Myrtha , Langhans Wolfgang , Konrad Daniel , Zarse Kim , Ristow Michael 
Published: April 2020

AbstractExcessive insulin signaling through the insulin receptor (IR) may play a role in the pathogenesis of diet-induced metabolic disease, including obesity and type 2 diabetes. Here we investigate whether heterozygous impairment of insulin receptor (IR) expression limited to peripheral, i.e. non-CNS, tissues of adult mice impacts the development of high-fat diet-induced metabolic deterioration. While exhibiting some features of insulin resistance, PerIRKO+/−mice display a hepatic energy deficit accompanied by induction of energy-sensing AMPK, mitochondrial biogenesis, PPARα, unexpectedly leading to protection from, and reversal of hepatic lipid accumulation (steatosis hepatis, NAFLD). Consistently, and unlike in control mice, the PPARα activator fenofibrate fails to further affect hepatic lipid accumulation in PerIRKO+/−mice. Taken together, and opposing previously established diabetogenic features of insulin resistance, incomplete impairment of insulin signaling may mimic central aspects of calorie restriction to limit hepatic lipid accumulation during conditions of metabolic stress.
Local conditions and policy design determine whether ecological compensation can achieve No Net Loss goals
Authors: Sonter Laura J. , Simmonds Jeremy S. , Watson James E. M. , Jones Julia P. G. , Kiesecker Joseph M. , Costa Hugo M. , Bennun Leon , Edwards Stephen , Grantham Hedley S. , Griffiths Victoria F. , Jones Kendall , Sochi Kei , Puydarrieux Philippe , Quétier Fabien , Rainer Helga , Rainey Hugo , Roe Dilys , Satar Musnanda , Soares-Filho Britaldo S. , Starkey Malcolm , ten Kate Kerry , Victurine Ray , von Hase Amrei , Wells Jessie A. , Maron Martine 
Published: April 2020

AbstractMany nations use ecological compensation policies to address negative impacts of development projects and achieve No Net Loss (NNL) of biodiversity and ecosystem services. Yet, failures are widely reported. We use spatial simulation models to quantify potential net impacts of alternative compensation policies on biodiversity (indicated by native vegetation) and two ecosystem services (carbon storage, sediment retention) across four case studies (in Australia, Brazil, Indonesia, Mozambique). No policy achieves NNL of biodiversity in any case study. Two factors limit their potential success: the land available for compensation (existing vegetation to protect or cleared land to restore), and expected counterfactual biodiversity losses (unregulated vegetation clearing). Compensation also fails to slow regional biodiversity declines because policies regulate only a subset of sectors, and expanding policy scope requires more land than is available for compensation activities. Avoidance of impacts remains essential in achieving NNL goals, particularly once opportunities for compensation are exhausted.
The intensification of Arctic warming as a result of CO2 physiological forcing
Authors: Park So-Won , Kim Jin-Soo , Kug Jong-Seong 
Published: April 2020

AbstractStomatal closure is one of the main physiological responses to increasing CO2 concentration, which leads to a reduction in plant water loss. This response has the potential to trigger changes in the climate system by regulating surface energy budgets—a phenomenon known as CO2 physiological forcing. However, its remote impacts on the Arctic climate system are unclear. Here we show that vegetation at high latitudes enhances the Arctic amplification via remote and time-delayed physiological forcing processes. Surface warming occurs at mid-to-high latitudes due to the physiological acclimation-induced reduction in evaporative cooling and resultant increase in sensible heat flux. This excessive surface heat energy is transported to the Arctic ocean and contributes to the sea ice loss, thereby enhancing Arctic warming. The surface warming in the Arctic is further amplified by local feedbacks, and consequently the contribution of physiological effects to Arctic warming represents about 10% of radiative forcing effects.
In-situ resonant band engineering of solution-processed semiconductors generates high performance n-type thermoelectric nano-inks
Authors: Sahu Ayaskanta , Russ Boris , Liu Miao , Yang Fan , Zaia Edmond W. , Gordon Madeleine P. , Forster Jason D. , Zhang Ya-Qian , Scott Mary C. , Persson Kristin A. , Coates Nelson E. , Segalman Rachel A. , Urban Jeffrey J. 
Published: April 2020

AbstractThermoelectric devices possess enormous potential to reshape the global energy landscape by converting waste heat into electricity, yet their commercial implementation has been limited by their high cost to output power ratio. No single “champion” thermoelectric material exists due to a broad range of material-dependent thermal and electrical property optimization challenges. While the advent of nanostructuring provided a general design paradigm for reducing material thermal conductivities, there exists no analogous strategy for homogeneous, precise doping of materials. Here, we demonstrate a nanoscale interface-engineering approach that harnesses the large chemically accessible surface areas of nanomaterials to yield massive, finely-controlled, and stable changes in the Seebeck coefficient, switching a poor nonconventional p-type thermoelectric material, tellurium, into a robust n-type material exhibiting stable properties over months of testing. These remodeled, n-type nanowires display extremely high power factors (~500 µW m−1K−2) that are orders of magnitude higher than their bulk p-type counterparts.
Network-directed efficient isolation of previously uncultivated Chloroflexi and related bacteria in hot spring microbial mats
Authors: Xian Wen-Dong , Salam Nimaichand , Li Meng-Meng , Zhou En-Min , Yin Yi-Rui , Liu Ze-Tao , Ming Yu-Zhen , Zhang Xiao-Tong , Wu Geng , Liu Lan , Xiao Min , Jiang Hong-Chen , Li Wen-Jun 
Published: April 2020

AbstractThe perplexity of the complex multispecies community interactions is one of the many reasons why majority of the microorganisms are still uncultivated. We analyzed the entire co-occurrence networks between the OTUs of Tibet and Yunnan hot spring samples, and found that less abundant OTUs such as genus Tepidimonas (relative abundant <1%) had high-degree centricity (key nodes), while dominant OTUs particularly genus Chloroflexus (relative abundant, 13.9%) formed the peripheral vertexes. A preliminary growth-promotion assay determined that Tepidimonas sp. strain SYSU G00190W enhanced the growth of Chloroflexus sp. SYSU G00190R. Exploiting this result, an ameliorated isolation medium containing 10% spent-culture supernatant of Tepidimonas sp. strain SYSU G00190W was prepared for targeted isolation of Chloroflexi in the Tibet and Yunnan hot spring samples. 16S rRNA gene fingerprinting characterized majority of the colonies isolated from these media as previously uncultivated Chloroflexi, of which 36 are potential novel species (16S rRNA sequence identity <98.5%). Metabolomes studies indicated that the spent-culture supernatant comprises several low-molecular-weight organic substrates that can be utilized as potential nutrients for the growth of these bacteria. These findings suggested that limited knowledge on the interaction of microbes provide threshold to traditional isolation method.
Fuzziness of muscle synergies in patients with multiple sclerosis indicates increased robustness of motor control during walking
Authors: Janshen Lars , Santuz Alessandro , Ekizos Antonis , Arampatzis Adamantios 
Published: April 2020

AbstractDeficits during gait poses a significant threat to the quality of life in patients with Multiple Sclerosis (MS). Using the muscle synergy concept, we investigated the modular organization of the neuromuscular control during walking in MS patients compared to healthy participants (HP). We hypothesized a widening and increased fuzziness of motor primitives (e.g. increased overlap intervals) in MS patients compared to HP allowing the motor system to increase robustness during walking. We analysed temporal gait parameters, local dynamic stability and muscle synergies from myoelectric signals of 13 ipsilateral leg muscles using non-negative matrix factorization. Compared to HP, MS patients showed a significant decrease in the local dynamic stability of walking during both, preferred and fixed (0.7 m/s) speed. MS patients demonstrated changes in time-dependent activation patterns (motor primitives) and alterations of the relative muscle contribution to the specific synergies (motor modules). We specifically found a widening in three out of four motor primitives during preferred speed and in two out of four during fixed speed in MS patients compared to HP. The widening increased the fuzziness of motor control in MS patients, which allows the motor system to increase its robustness when coping with pathology-related motor deficits during walking.
Taphonomic criteria for identifying Iberian lynx dens in quaternary deposits
Authors: Rodríguez-Hidalgo Antonio , Sanz Montserrat , Daura Joan , Sánchez-Marco Antonio 
Published: April 2020

AbstractFor decades, taphonomists have dedicated their efforts to assessing the nature of the massive leporid accumulations recovered at archaeological sites in the northwestern Mediterranean region. Their interest lying in the fact that the European rabbit constituted a critical part of human subsistence during the late Pleistocene and early Holocene. However, rabbits are also a key prey in the food webs of Mediterranean ecosystems and the base of the diet for several specialist predators, including the Iberian lynx (Lynx pardinus). For this reason, the origin of rabbit accumulations in northwestern Mediterranean sites has proved a veritable conundrum. Here, we present the zooarchaeological and taphonomic study of more than 3000 faunal and 140 coprolite remains recovered in layer IIIa of Cova del Gegant (Catalonia, Spain). Our analysis indicates that this layer served primarily as a den for the Iberian lynx. The lynxes modified and accumulated rabbit remains and also died at the site creating an accumulation dominated by the two taxa. However, other agents and processes, including human, intervened in the final configuration of the assemblage. Our study contributes to characterizing the Iberian lynx fossil accumulation differentiating between the faunal assemblages accumulated by lynxes and hominins.
The orphan solute carrier SLC10A7 is a novel negative regulator of intracellular calcium signaling
Authors: Karakus Emre , Wannowius Marie , Müller Simon Franz , Leiting Silke , Leidolf Regina , Noppes Saskia , Oswald Stefan , Diener Martin , Geyer Joachim 
Published: April 2020

AbstractSLC10A7 represents an orphan member of the Solute Carrier Family SLC10. Recently, mutations in the human SLC10A7 gene were associated with skeletal dysplasia, amelogenesis imperfecta, and decreased bone mineral density. However, the exact molecular function of SLC10A7 and the mechanisms underlying these pathologies are still unknown. For this reason, the role of SLC10A7 on intracellular calcium signaling was investigated. SLC10A7 protein expression was negatively correlated with store-operated calcium entry (SOCE) via the plasma membrane. Whereas SLC10A7 knockout HAP1 cells showed significantly increased calcium influx after thapsigargin, ionomycin and ATP/carbachol treatment, SLC10A7 overexpression reduced this calcium influx. Intracellular Ca2+ levels were higher in the SLC10A7 knockout cells and lower in the SLC10A7-overexpressing cells. The SLC10A7 protein co-localized with STIM1, Orai1, and SERCA2. Most of the previously described human SLC10A7 mutations had no effect on the calcium influx and thus were confirmed to be functionally inactive. In the present study, SLC10A7 was established as a novel negative regulator of intracellular calcium signaling that most likely acts via STIM1, Orai1 and/or SERCA2 inhibition. Based on this, SLC10A7 is suggested to be named as negative regulator of intracellular calcium signaling (in short: RCAS).