bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fermionic Light Dark Matter Particles and the New Physics of Neutron Stars
Authors: Cermeño M. , Pérez-García M. Ángeles , Silk Joseph 
Published: October 2017

AbstractDark Matter constitutes most of the matter in the presently accepted cosmological model for our Universe. The extreme conditions of ordinary baryonic matter, namely high density and compactness, in Neutron Stars make these objects suitable to gravitationally accrete such a massive component provided interaction strength between both, luminous and dark sectors, at current experimental level of sensitivity. We consider several different DM phenomenological models from the myriad of those presently allowed. In this contribution, we review astrophysical aspects of interest in the interplay of ordinary matter and a fermionic light Dark Matter component. We focus in the interior nuclear medium in the core and external layers, i.e. the crust, discussing the impact of a novel dark sector in relevant stellar quantities for (heat) energy transport such as thermal conductivity or emissivities.
BEHAVIOURAL ECONOMICS AND PATERNALISM
Authors: Hausman Daniel M. 
Published: October 2017

Abstract:Contemporary behavioural economics has documented common failures of reasoning that apparently make possible policies that benefit individuals by contravening or correcting their judgements. These policies appear to be paternalistic, even though a traditional view would deny that they are paternalistic on the grounds that policies such as nudges do not restrict individual liberty. It appears to many that a new definition of paternalism that takes its cue from behavioural economics is needed. Furthermore, if one revises the definition of paternalism, one must revisit traditional views concerning whether paternalist policies are wise. In Government Paternalism, Julian Le Grand and Bill New make a valuable start, although some corrections are needed. This essay provides a general setting for revising the definition of paternalism and suggests a revised definition of paternalism.
Notions of computation as monoids
Authors: RIVAS EXEQUIEL , JASKELIOFF MAURO 
Published: October 2017

AbstractThere are different notions of computation, the most popular being monads, applicative functors, and arrows. In this article, we show that these three notions can be seen as instances of a unifying abstract concept: monoids in monoidal categories. We demonstrate that even when working at this high level of generality, one can obtain useful results. In particular, we give conditions under which one can obtain free monoids and Cayley representations at the level of monoidal categories, and we show that their concretisation results in useful constructions for monads, applicative functors, and arrows. Moreover, by taking advantage of the uniform presentation of the three notions of computation, we introduce a principled approach to the analysis of the relation between them.
DEXTER: A workbench for automatic term extraction with specialized corpora
Authors: PERIÑAN-PASCUAL CARLOS 
Published: October 2017

AbstractAutomatic term extraction has become a priority area of research within corpus processing. Despite the extensive literature in this field, there are still some outstanding issues that should be dealt with during the construction of term extractors, particularly those oriented to support research in terminology and terminography. In this regard, this article describes the design and development of DEXTER, an online workbench for the extraction of simple and complex terms from domain-specific corpora in English, French, Italian and Spanish. In this framework, three issues contribute to placing the most important terms in the foreground. First, unlike the elaborate morphosyntactic patterns proposed by most previous research, shallow lexical filters have been constructed to discard term candidates. Second, a large number of common stopwords are automatically detected by means of a method that relies on the IATE database together with the frequency distribution of the domain-specific corpus and a general corpus. Third, the term-ranking metric, which is grounded on the notions of salience, relevance and cohesion, is guided by the IATE database to display an adequate distribution of terms.
Association between green tea intake and risk of gastric cancer: a systematic review and dose–response meta-analysis of observational studies
Authors: Huang Yanhong , Chen Hongru , Zhou Liang , Li Gaoming , Yi Dali , Zhang Yanqi , Wu Yazhou , Liu Xiaoyu , Wu Xiaojiao , Song Qiuyue , Liu Ling , Yi Dong 
Published: October 2017

AbstractObjectiveTo examine and quantify the potential dose–response relationship between green tea intake and the risk of gastric cancer.DesignWe searched PubMed, EMBASE, Web of Science, CBM, CNKI and VIP up to December 2015 without language restrictions.SettingA systematic review and dose–response meta-analysis of observational studies.SubjectsFive cohort studies and eight case–control studies.ResultsCompared with the lowest level of green tea intake, the pooled relative risk (95 % CI) of gastric cancer was 1·05 (0·90, 1·21, I2=20·3 %) for the cohort studies and the pooled OR (95 % CI) was 0·84 (0·74, 0·95, I2=48·3 %) for the case–control studies. The pooled relative risk of gastric cancer was 0·79 (0·63, 0·97, I2=63·8 %) for intake of 6 cups green tea/d, 0·59 (0·42, 0·82, I2=1·0 %) for 25 years of green tea intake and 7·60 (1·67, 34·60, I2=86·5 %) for drinking very hot green tea.ConclusionsDrinking green tea has a certain preventive effect on reducing the risk of gastric cancer, particularly for long-term and high-dose consumption. Drinking too high-temperature green tea may increase the risk of gastric cancer, but it is still unclear whether high-temperature green tea is a risk factor for gastric cancer. Further studies should be performed to obtain more detailed results, including other gastric cancer risk factors such as smoking and alcohol consumption and the dose of the effective components in green tea, to provide more reliable evidence-based medical references for the relationship between green tea and gastric cancer.
Direct and indirect effects of parent stress on child obesity risk and added sugar intake in a sample of Southern California adolescents
Authors: Shonkoff Eleanor T , Dunton Genevieve F , Chou Chih-Ping , Leventhal Adam M , Bluthenthal Ricky , Pentz Mary Ann 
Published: October 2017

AbstractObjectiveResearch indicates that children are at higher risk for obesity if their parents have been exposed to a larger number of stressors, yet little is known about effects of parents’ subjective, perceived experience of stress on children’s eating behaviours and adiposity and whether weight-related parenting practices (i.e. parent rules and positive family meal practices) mediate this relationship. The present study evaluated the direct and mediated relationship between parent perceived stress and child waist circumference and parent stress and child consumption of added sugars one year later.DesignLongitudinal panel data.SettingEleven communities in Southern California, USA.SubjectsData were collected over two waves from parent–child dyads (n599). Most parents were female (81 %) and Hispanic (51 %); children were 11 years old on average (sd1·53; range 7–15 years) and 31 % received free school lunch.ResultsPerceived parent stress was not significantly associated with child waist circumference or consumption of added sugars one year later, and mediating pathways through parenting practices were not significant. However, parent rules were significantly associated with lower child consumption of added sugars (β=−0·14,P<0·001).ConclusionsResults suggest that parent rules about the types of foods children can eat, clearly explained to children, may decrease child consumption of added sugars but not necessarily lead to changes in obesity risk. Parent- and family-based interventions that support development of healthy rules about child eating have the potential to improve child dietary nutrient intake.
Targeting redox homeostasis in rhabdomyosarcoma cells: GSH-depleting agents enhance auranofin-induced cell death
Authors: Habermann Karoline Johanna , Grünewald Leon , van Wijk Sjoerd , Fulda Simone 
Published: October 2017

AbstractRhabdomyosarcoma (RMS) cells have recently been reported to be sensitive to oxidative stress. Therefore, we investigated whether concomitant inhibition of the two main antioxidant defense pathways, that is, the thioredoxin (TRX) and the glutathione (GSH) systems, presents a new strategy to trigger cell death in RMS. In this study, we discover that GSH-depleting agents, i.e. γ-glutamylcysteine synthetase inhibitor, buthionine sulfoximine (BSO) or the cystine/glutamate antiporter inhibitor erastin (ERA), synergize with thioredoxin reductase (TrxR) inhibitor auranofin (AUR) to induce cell death in RMS cells. Interestingly, AUR causes accumulation of ubiquitinated proteins when combined with BSO or ERA, in line with recent reports showing that AUR inhibits the proteasome besides TrxR. Consistently, AUR/BSO or AUR/ERA cotreatment increases ubiquitination and expression of the short-lived proteins NOXA and MCL-1, accompanied by increased binding of NOXA to MCL-1. Notably, NOXA knockdown significantly rescues RMS cells from AUR/BSO- or AUR/ERA-induced cell death. In addition, AUR acts together with BSO or ERA to stimulate BAX/BAK and caspase activation. Of note, BSO or ERA abolish the AUR-stimulated increase in GSH levels, leading to reduced GSH levels upon cotreatment. Although AUR/BSO or AUR/ERA cotreatment enhances reactive oxygen species (ROS) production, only thiol-containing antioxidants (i.e., N-acetylcysteine (NAC), GSH), but not the non-thiol-containing ROS scavenger α-Tocopherol consistently suppress AUR/BSO- and AUR/ERA-stimulated cell death in both cell lines. Importantly, re-supply of GSH or its precursor NAC completely prevents AUR/ERA- and AUR/BSO-induced accumulation of ubiquitinated proteins, NOXA upregulation and cell death, indicating that GSH depletion rather than ROS production is critical for AUR/BSO- or AUR/ERA-mediated cell death. Thus, by demonstrating that GSH-depleting agents enhance the antitumor activity of AUR, we highlight new treatment options for RMS by targeting the redox homeostasis.
NLRP3 inflammasome activation contributes to VSMC phenotypic transformation and proliferation in hypertension
Authors: Sun Hai-Jian , Ren Xing-Sheng , Xiong Xiao-Qing , Chen Yun-Zhi , Zhao Ming-Xia , Wang Jue-Jin , Zhou Ye-Bo , Han Ying , Chen Qi , Li Yue-Hua , Kang Yu-Ming , Zhu Guo-Qing 
Published: October 2017

AbstractInflammation is involved in pathogenesis of hypertension. NLRP3 inflammasome activation is a powerful mediator of inflammatory response via caspase-1 activation. The present study was designed to determine the roles and mechanisms of NLRP3 inflammasome in phenotypic modulation and proliferation of vascular smooth muscle cells (VSMCs) in hypertension. Experiments were conducted in spontaneously hypertensive rats (SHR) and primary aortic VSMCs. NLRP3 inflammasome activation was observed in the media of aorta in SHR and in the VSMCs from SHR. Knockdown of NLRP3 inhibited inflammasome activation, VSMC phenotypic transformation and proliferation in SHR-derived VSMCs. Increased NFκB activation, histone acetylation and histone acetyltransferase expression were observed in SHR-derived VSMCs and in media of aorta in SHR. Chromatin immunoprecipitation analysis revealed the increased histone acetylation, p65-NFκB and Pol II occupancy at the NLRP3 promoterin vivoandin vitro. Inhibition of NFκB with BAY11-7082 or inhibition of histone acetyltransferase with curcumin prevented the NLRP3 inflammasome activation, VSMC phenotype switching and proliferation in VSMCs from SHR. Moreover, curcumin repressed NFκB activation. Silencing of NLRP3 gene ameliorated hypertension, vascular remodeling, NLRP3 inflammasome activation and phenotype switching in the aorta of SHR. These results indicate that NLRP3 inflammasome activation response to histone acetylation and NFκB activation contributes to VSMC phenotype switching and proliferation and vascular remodeling in hypertension.
miRNA-223 upregulated by MYOD inhibits myoblast proliferation by repressing IGF2 and facilitates myoblast differentiation by inhibiting ZEB1
Authors: Li Guihuan , Luo Wen , Abdalla Bahareldin A , Ouyang Hongjia , Yu Jiao , Hu Fan , Nie Qinghua , Zhang Xiquan 
Published: October 2017

AbstractSkeletal muscle differentiation can be regulated by various transcription factors and non-coding RNAs. In our previous work, miR-223 is differentially expressed in the skeletal muscle of chicken with different growth rates, but its role, expression and action mechanism in muscle development still remains unknown. Here, we found that MYOD transcription factor can upregulate miR-223 expression by binding to an E-box region of the gga-miR-223 gene promoter during avian myoblast differentiation. IGF2 and ZEB1 are two target genes of miR-223. The target inhibition of miR-223 on IGF2 and ZEB1 are dynamic from proliferation to differentiation of myoblast. miR-223 inhibits IGF2 expression only in the proliferating myoblast, whereas it inhibits ZEB1 mainly in the differentiating myoblast. The inhibition of IGF2 by miR-223 resulted in the repression of myoblast proliferation. During myoblast differentiation, miR-223 would be upregulated owing to the promoting effect of MYOD, and the upregulation of miR-223 would inhibit ZEB1 to promote myoblast differentiation. These results not only demonstrated that the well-known muscle determination factor MYOD can promote myoblast differentiation by upregulate miR-223 transcription, but also identified that miR-223 can influence myoblast proliferation and differentiation by a dynamic manner regulates the expression of its target genes.
Overactive type 2 cannabinoid receptor induces meiosis in fetal gonads and impairs ovarian reserve
Authors: De Domenico Emanuela , Todaro Federica , Rossi Gabriele , Dolci Susanna , Geremia Raffaele , Rossi Pellegrino , Grimaldi Paola 
Published: October 2017

AbstractType 2 cannabinoid receptor (CB2R) has been proposed to promote in vitro meiotic entry of postnatal male germ cells and to maintain the temporal progression of spermatogenesis in vivo. However, no information is presently available on the role played by CB2R in male and female fetal gonads. Here we show that in vitro pharmacological stimulation with JWH133, a CB2R agonist, induced activation of the meiotic program in both male and female fetal gonads. Upon stimulation, gonocytes initiated the meiotic program but became arrested at early stages of prophase I, while oocytes showed an increased rate of meiotic entry and progression toward more advanced stage of meiosis. Acceleration of meiosis in oocytes was accompanied by a strong increase in the percentage of γ-H2AX-positive pachytene and diplotene cells, paralleled by an increase of TUNEL-positive cells, suggesting that DNA double-strand breaks were not correctly repaired during meiosis, leading to oocyte apoptosis. Interestingly, in vivo pharmacological stimulation of CB2R in fetal germ cells through JWH133 administration to pregnant females caused a significant reduction of primordial and primary follicles in the ovaries of newborns with a consequent depletion of ovarian reserve and reduced fertility in adult life, while no alterations of spermatogenesis in the testis of the offspring were detected. Altogether our findings highlight a pro-meiotic role of CB2R in male and female germ cells and suggest that the use of cannabis in pregnant female might represent a risk for fertility and reproductive lifespan in female offspring.
A novel acridine derivative, LS-1-10 inhibits autophagic degradation and triggers apoptosis in colon cancer cells
Authors: Fu Wan , Li Xue , Lu Xiaopeng , Zhang Luyao , Li Ran , Zhang Nan , Liu Shan , Yang Xin , Wang Yue , Zhao Ying , Meng Xiangbao , Zhu Wei-Guo 
Published: October 2017

AbstractAutophagy promotes cancer cell survival and drug resistance by degrading harmful cellular components and maintaining cellular energy levels. Disruption of autophagy may be a promising approach to sensitize cancer cells to anticancer drugs. The combination of autophagic inhibitors, such as chloroquine (CQ) and lucanthone with conventional cancer therapeutics has been investigated in clinical trials, but adverse drug–drug interactions are a high possibility. Here we designed and synthesized a novel, small-molecule library based on an acridine skeleton and the CQ structure with various modifications and substitutions and screened the compounds for effective autophagy inhibition. We found that 9-chloro-2-(3-(dimethylamino)propyl)pyrrolo[2,3,4-kl]acridin-1(2H)-one (LS-1-10) was the most effective from our library at inhibiting autophagic-mediated degradation and could decrease the viability of multiple colon cancer cells. In addition, LS-1-10 induced DNA damage and caspase 8-mediated apoptosis. Overall, this small molecule was more efficient at reducing the viability of cancer cells than other conventional chemotherapeutic agents, such as CQ and amsacrine. The anticancer and autophagy-inhibiting activities of LS-1-10 were confirmed in vivo in a xenograft mouse model. Collectively, this study has identified a new and efficient single compound with both autophagy-inhibiting and anticancer activity, which may provide a novel approach for cancer therapy.
Is trehalose an autophagic inducer? Unraveling the roles of non-reducing disaccharides on autophagic flux and alpha-synuclein aggregation
Authors: Yoon Ye-Seul , Cho Eun-Duk , Jung Ahn Woo , Won Lee Kyung , Lee Seung-Jae , Lee He-Jin 
Published: October 2017

AbstractAutophagy is a pivotal intracellular process by which cellular macromolecules are degraded upon various stimuli. A failure in the degradation of autophagic substrates such as impaired organelles and protein aggregates leads to their accumulations, which are characteristics of many neurodegenerative diseases. Pharmacological activation of autophagy has thus been considered a prospective therapeutic approach for treating neurodegenerative diseases. Among a number of autophagy-inducing agents, trehalose has received attention for its beneficial effects in different disease models of neurodegeneration. However, how trehalose promotes autophagy has not been fully revealed. We investigated the influence of trehalose and other disaccharides upon autophagic flux and aggregation ofα-synuclein, a protein linked to Parkinson's disease. In differentiated human neuroblastoma and primary rat cortical neuron culture models, treatment with trehalose and other disaccharides resulted in accumulation of lipidated LC3 (LC3-II), p62, and autophagosomes, whereas it decreased autolysosomes. On the other hand, addition of Bafilomycin A1 to trehalose treatments had relatively marginal effect, an indicative of autophagic flux blockage. In concordance with these results, the cells treated with trehalose exhibited an incremental tendency inα-synuclein aggregation. Secretion ofα-synuclein was also elevated in the culture medium upon trehalose treatment, thereby significantly increasing intercellular transmission of this protein. Despite the substantial increase inα-synuclein aggregation, which normally leads to cell death, cell viability was not affected upon treatment with trehalose, suggesting an autophagy-independent protective function of trehalose against protein aggregates. This study demonstrates that, although trehalose has been widely considered an autophagic inducer, it may be actually a potent blocker of the autophagic flux.
HDAC6 inhibition reverses axonal transport defects in motor neurons derived from FUS-ALS patients
Authors: Guo Wenting , Naujock Maximilian , Fumagalli Laura , Vandoorne Tijs , Baatsen Pieter , Boon Ruben , Ordovás Laura , Patel Abdulsamie , Welters Marc , Vanwelden Thomas , Geens Natasja , Tricot Tine , Benoy Veronick , Steyaert Jolien , Lefebvre-Omar Cynthia , Boesmans Werend , Jarpe Matthew , Sterneckert Jared , Wegner Florian , Petri Susanne , Bohl Delphine , Vanden Berghe Pieter , Robberecht Wim , Van Damme Philip , Verfaillie Catherine , Van Den Bosch Ludo 
Published: October 2017

AbstractAmyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disorder due to selective loss of motor neurons (MNs). Mutations in the fused in sarcoma (FUS) gene can cause both juvenile and late onset ALS. We generated and characterized induced pluripotent stem cells (iPSCs) from ALS patients with different FUS mutations, as well as from healthy controls. Patient-derived MNs show typical cytoplasmic FUS pathology, hypoexcitability, as well as progressive axonal transport defects. Axonal transport defects are rescued by CRISPR/Cas9-mediated genetic correction of the FUS mutation in patient-derived iPSCs. Moreover, these defects are reproduced by expressing mutant FUS in human embryonic stem cells (hESCs), whereas knockdown of endogenous FUS has no effect, confirming that these pathological changes are mutant FUS dependent. Pharmacological inhibition as well as genetic silencing of histone deacetylase 6 (HDAC6) increase α-tubulin acetylation, endoplasmic reticulum (ER)–mitochondrial overlay, and restore the axonal transport defects in patient-derived MNs.
High-throughput screens using photo-highlighting discover BMP signaling in mitochondrial lipid oxidation
Authors: Yu Yong , Mutlu Ayse Sena , Liu Harrison , Wang Meng C. 
Published: October 2017

AbstractHigh-throughput screens at microscopic resolution can uncover molecular mechanisms of cellular dynamics, but remain technically challenging in live multicellular organisms. Here we present a genetic screening method using photo-highlighting for candidate selection on microscopes. We apply this method to stimulated Raman scattering (SRS) microscopy and systematically identify 57 Caenorhabditis elegans mutants with altered lipid distribution. Four of these mutants target the components of the Bone Morphogenetic Protein (BMP) signaling pathway, revealing that BMP signaling inactivation causes exhaustion of lipid reserves in somatic tissues. Using SRS-based isotope tracing assay to quantitatively track lipid synthesis and mobilization, we discover that the BMP signaling mutants have increased rates of lipid mobilization. Furthermore, this increase is associated with the induction of mitochondrial β-oxidation and mitochondrial fusion. Together these studies demonstrate a photo-highlighting microscopic strategy for genome-scale screens, leading to the discovery of new roles for BMP signaling in linking mitochondrial homeostasis and lipid metabolism.
Quasi-two-dimensional superconductivity from dimerization of atomically ordered AuTe2Se4/3 cubes
Authors: Guo J. G. , Chen X. , Jia X. Y. , Zhang Q. H. , Liu N. , Lei H. C. , Li S. Y. , Gu L. , Jin S. F. , Chen X. L. 
Published: October 2017

AbstractThe emergent phenomena such as superconductivity and topological phase transitions can be observed in strict two-dimensional (2D) crystalline matters. Artificial interfaces and one atomic thickness layers are typical 2D materials of this kind. Although having 2D characters, most bulky layered compounds, however, do not possess these striking properties. Here, we report quasi-2D superconductivity in bulky AuTe2Se4/3, where the reduction in dimensionality is achieved through inducing the elongated covalent Te–Te bonds. The atomic-resolution images reveal that the Au, Te, and Se are atomically ordered in a cube, among which are Te–Te bonds of 3.18 and 3.28 Å. The superconductivity at 2.85 K is discovered, which is unraveled to be the quasi-2D nature owing to the Berezinsky–Kosterlitz–Thouless topological transition. The nesting of nearly parallel Fermi sheets could give rise to strong electron–phonon coupling. It is proposed that further depleting the thickness could result in more topologically-related phenomena.