bluuebunny/crossref_metadata_2025_split huggingface dataset:
Superconductivity in the antiperovskite Dirac-metal oxide Sr3−xSnO
Authors: Oudah Mohamed , Ikeda Atsutoshi , Hausmann Jan Niklas , Yonezawa Shingo , Fukumoto Toshiyuki , Kobayashi Shingo , Sato Masatoshi , Maeno Yoshiteru 
Published: December 2016

AbstractInvestigations of perovskite oxides triggered by the discovery of high-temperature and unconventional superconductors have had crucial roles in stimulating and guiding the development of modern condensed-matter physics. Antiperovskite oxides are charge-inverted counterpart materials to perovskite oxides, with unusual negative ionic states of a constituent metal. No superconductivity was reported among the antiperovskite oxides so far. Here we present the first superconducting antiperovskite oxide Sr3−xSnO with the transition temperature of around 5 K. Sr3SnO possesses Dirac points in its electronic structure, and we propose from theoretical analysis a possibility of a topological odd-parity superconductivity analogous to the superfluid 3He-B in moderately hole-doped Sr3−xSnO. We envision that this discovery of a new class of oxide superconductors will lead to a rapid progress in physics and chemistry of antiperovskite oxides consisting of unusual metallic anions.
Conditional repair by locally switching the thermal healing capability of dynamic covalent polymers with light
Authors: Fuhrmann Anne , Göstl Robert , Wendt Robert , Kötteritzsch Julia , Hager Martin D. , Schubert Ulrich S. , Brademann-Jock Kerstin , Thünemann Andreas F. , Nöchel Ulrich , Behl Marc , Hecht Stefan 
Published: December 2016

AbstractHealable materials could play an important role in reducing the environmental footprint of our modern technological society through extending the life cycles of consumer products and constructions. However, as most healing processes are carried out by heat alone, the ability to heal damage generally kills the parent material’s thermal and mechanical properties. Here we present a dynamic covalent polymer network whose thermal healing ability can be switched ‘on’ and ‘off’ on demand by light, thereby providing local control over repair while retaining the advantageous macroscopic properties of static polymer networks. We employ a photoswitchable furan-based crosslinker, which reacts with short and mobile maleimide-substituted poly(lauryl methacrylate) chains forming strong covalent bonds while simultaneously allowing the reversible, spatiotemporally resolved control over thermally induced de- and re-crosslinking. We reason that our system can be adapted to more complex materials and has the potential to impact applications in responsive coatings, photolithography and microfabrication.
Inhibition of Notch pathway arrests PTEN-deficient advanced prostate cancer by triggering p27-driven cellular senescence
Authors: Revandkar Ajinkya , Perciato Maria Luna , Toso Alberto , Alajati Abdullah , Chen Jingjing , Gerber Hermeto , Dimitrov Mitko , Rinaldi Andrea , Delaleu Nicolas , Pasquini Emiliano , D’Antuono Rocco , Pinton Sandra , Losa Marco , Gnetti Letizia , Arribas Alberto , Fraering Patrick , Bertoni Francesco , Nepveu Alain , Alimonti Andrea 
Published: December 2016

AbstractActivation of NOTCH signalling is associated with advanced prostate cancer and treatment resistance in prostate cancer patients. However, the mechanism that drives NOTCH activation in prostate cancer remains still elusive. Moreover, preclinical evidence of the therapeutic efficacy of NOTCH inhibitors in prostate cancer is lacking. Here, we provide evidence that PTEN loss in prostate tumours upregulates the expression ofADAM17, thereby activating NOTCH signalling. Using prostate conditional inactivation of bothPtenandNotch1along with preclinical trials carried out inPten-null prostate conditional mouse models, we demonstrate thatPten-deficient prostate tumours are addicted to the NOTCH signalling. Importantly, we find that pharmacological inhibition of γ-secretase promotes growth arrest in bothPten-null andPten/Trp53-null prostate tumours by triggering cellular senescence. Altogether, our findings describe a novel pro-tumorigenic network that links PTEN loss to ADAM17 and NOTCH signalling, thus providing the rational for the use of γ-secretase inhibitors in advanced prostate cancer patients.
Universal structural parameter to quantitatively predict metallic glass properties
Authors: Ding Jun , Cheng Yong-Qiang , Sheng Howard , Asta Mark , Ritchie Robert O. , Ma Evan 
Published: December 2016

AbstractQuantitatively correlating the amorphous structure in metallic glasses (MGs) with their physical properties has been a long-sought goal. Here we introduce ‘flexibility volume’ as a universal indicator, to bridge the structural state the MG is in with its properties, on both atomic and macroscopic levels. The flexibility volume combines static atomic volume with dynamics information via atomic vibrations that probe local configurational space and interaction between neighbouring atoms. We demonstrate that flexibility volume is a physically appropriate parameter that can quantitatively predict the shear modulus, which is at the heart of many key properties of MGs. Moreover, the new parameter correlates strongly with atomic packing topology, and also with the activation energy for thermally activated relaxation and the propensity for stress-driven shear transformations. These correlations are expected to be robust across a very wide range of MG compositions, processing conditions and length scales.
Additional energy scale in SmB6 at low-temperature
Authors: Jiao L. , Rößler S. , Kim D. J. , Tjeng L. H. , Fisk Z. , Steglich F. , Wirth S. 
Published: December 2016

AbstractTopological insulators give rise to exquisite electronic properties because of their spin-momentum locked Dirac-cone-like band structure. Recently, it has been suggested that the required opposite parities between valence and conduction band along with strong spin-orbit coupling can be realized in correlated materials. Particularly, SmB6 has been proposed as candidate material for a topological Kondo insulator. Here we observe, by utilizing scanning tunnelling microscopy and spectroscopy down to 0.35 K, several states within the hybridization gap of about ±20 meV on well characterized (001) surfaces of SmB6. The spectroscopic response to impurities and magnetic fields allows to distinguish between dominating bulk and surface contributions to these states. The surface contributions develop particularly strongly below about 7 K, which can be understood in terms of a suppressed Kondo effect at the surface. Our high-resolution data provide insight into the electronic structure of SmB6, which reconciles many current discrepancies on this compound.
Hall effect in charged conducting ferroelectric domain walls
Authors: Campbell M. P. , McConville J.P.V. , McQuaid R.G.P. , Prabhakaran D. , Kumar A. , Gregg J. M. 
Published: December 2016

AbstractEnhanced conductivity at specific domain walls in ferroelectrics is now an established phenomenon. Surprisingly, however, little is known about the most fundamental aspects of conduction. Carrier types, densities and mobilities have not been determined and transport mechanisms are still a matter of guesswork. Here we demonstrate that intermittent-contact atomic force microscopy (AFM) can detect the Hall effect in conducting domain walls. Studying YbMnO3 single crystals, we have confirmed that p-type conduction occurs in tail-to-tail charged domain walls. By calibration of the AFM signal, an upper estimate of ∼1 × 1016 cm−3 is calculated for the mobile carrier density in the wall, around four orders of magnitude below that required for complete screening of the polar discontinuity. A carrier mobility of∼50 cm2V−1s−1 is calculated, about an order of magnitude below equivalent carrier mobilities in p-type silicon, but sufficiently high to preclude carrier-lattice coupling associated with small polarons.
Kefir peptides prevent high-fructose corn syrup-induced non-alcoholic fatty liver disease in a murine model by modulation of inflammation and the JAK2 signaling pathway
Authors: Chen H L , Tsai T C , Tsai Y C , Liao J W , Yen C C , Chen C M 
Published: December 2016

Abstract
Objective:
In recent years, people have changed their eating habits, and high-fructose-containing bubble tea has become very popular. High-fructose intake has been suggested to be a key factor that induces non-alcoholic fatty liver disease (NAFLD). Kefir, a fermented milk product composed of microbial symbionts, has demonstrated numerous biological activities, including antibacterial, antioxidant and immunostimulating effects. The present study aims to evaluate the effects of kefir peptides on high-fructose-induced hepatic steatosis and the possible molecular mechanism.

Results:
An animal model of 30% high-fructose-induced NAFLD in C57BL/6J mice was established. The experiment is divided into the following six groups: (1) normal: H2O drinking water; (2) mock: H2O+30% fructose; (3) KL: low-dose kefir peptides (50 mg kg−1)+30% fructose; (4) KM: medium-dose kefir peptides (100 mg kg−1)+30% fructose; (5) KH: high-dose kefir peptides (150 mg kg−1)+30% fructose; and (6) CFM: commercial fermented milk (100 mg kg−1)+30% fructose. The results show that kefir peptides improve fatty liver syndrome by decreasing body weight, serum alanine aminotransferase, triglycerides, insulin and hepatic triglycerides, cholesterol, and free fatty acids as well as the inflammatory cytokines (TNF-α, IL-6 and IL-1β) that had been elevated in fructose-induced NAFLD mice. In addition, kefir peptides markedly increased phosphorylation of AMPK to downregulate its targeted enzymes, ACC (acetyl-CoA carboxylase) and SREBP-1c (sterol regulatory element-binding protein 1), and inhibited de novo lipogenesis. Furthermore, kefir peptides activated JAK2 to stimulate STAT3 phosphorylation, which can translocate to the nucleus, and upregulated several genes, including the CPT1 (carnitine palmitoyltransferase-1) involved in fatty acid oxidation.

Conclusion:
Our data have demonstrated that kefir peptides can improve the symptoms of NAFLD, including body weight, energy intake, inflammatory reaction and the formation of fatty liver by activating JAK2 signal transduction through the JAK2/STAT3 and JAK2/AMPK pathways in the high-fructose-induced fatty liver animal model. Therefore, kefir peptides may have the potential for clinical application for the prevention or treatment of clinical metabolic syndrome.
ERK-mediated NF-κB activation through ASIC1 in response to acidosis
Authors: Chen B , Liu J , Ho T-T , Ding X , Mo Y-Y 
Published: December 2016

AbstractAcidic microenvironment is a common feature of solid tumors. We have previously shown that neuron specific acid-sensing ion channel 1 (ASIC1) is expressed in breast cancer, and it is responsible for acidosis-induced cellular signaling through AKT, leading to nuclear factor-κB (NF-κB) activation, and cell invasion and metastasis. However, AKT is frequently activated in cancer. Thus, a key question is whether ASIC1-mediated cell signaling still takes place in the cancer cells carrying constitutively active AKT. In the present study, we show that among four prostate cancer cell lines tested, 22Rv1 cells express the highest level of phosphorylated AKT that is not impacted by acidosis. However, acidosis can still induce NF-κB activation during which extracellular signal-regulated kinase (ERK) serves as an alternative pathway for ASIC-mediated cell signaling. Inhibition of ERK by chemical inhibitors or small interfering RNAs suppresses the acidosis-induced NF-κB activity through regulation of the inhibitory subunit IκBα phosphorylation. Furthermore, suppression of ASIC1-mediated generation of reactive oxygen species (ROS) by ROS scavengers, such as glutathione or N-acetyl-cysteine causes a decrease in ERK phosphorylation and degradation of IκBα. Finally, ASIC1 is upregulated in a subset of prostate cancer cases and ASIC1 knockout by CRISPR/Cas9 significantly suppresses cell invasion, and castration resistance both in vitro and in vivo. Together, these results support the significance of ASIC1-ROS-ERK-IκBα-NF-κB axis in prostate tumorigenesis, especially in the constitutively active AKT background.
G-rich DNA-induced stress response blocks type-I-IFN but not CXCL10 secretion in monocytes
Authors: Herzner Anna-Maria , Wolter Steven , Zillinger Thomas , Schmitz Saskia , Barchet Winfried , Hartmann Gunther , Bartok Eva , Schlee Martin 
Published: December 2016

AbstractExcessive inflammation can cause damage to host cells and tissues. Thus, the secretion of inflammatory cytokines is tightly regulated at transcriptional, post-transcriptional and post-translational levels and influenced by cellular stress responses, such as endoplasmic reticulum (ER) stress or apoptosis. Here, we describe a novel type of post-transcriptional regulation of the type-I-IFN response that was induced in monocytes by cytosolic transfection of a short immunomodulatory DNA (imDNA), a G-tetrad forming CpG-free derivative of the TLR9 agonist ODN2216. When co-transfected with cytosolic nucleic acid stimuli (DNA or 3P-dsRNA), imDNA induced caspase-3 activation, translational shutdown and upregulation of stress-induced genes. This stress response inhibited the type-I-IFN induction at the translational level. By contrast, the induction of most type-I-IFN-associated chemokines, including Chemokine (C-X-C Motif) Ligand (CXCL)10 was not affected, suggesting a differential translational regulation of chemokines and type-I-IFN. Pan-caspase inhibitors could restore IFN-β secretion, yet, strikingly, caspase inhibition did not restore global translation but instead induced a compensatory increase in the transcription of IFN-β but not CXCL10. Altogether, our data provide evidence for a differential regulation of cytokine release at both transcriptional and post-transcriptional levels which suppresses type-I-IFN induction yet allows for CXCL10 secretion during imDNA-induced cellular stress.
VRK3-mediated nuclear localization of HSP70 prevents glutamate excitotoxicity-induced apoptosis and Aβ accumulation via enhancement of ERK phosphatase VHR activity
Authors: Song Haengjin , Kim Wanil , Kim Sung-Hoon , Kim Kyong-Tai 
Published: December 2016

AbstractMost of neurodegenerative disorders are associated with protein aggregation. Glutamate-induced excitotoxicity and persistent extracellular signal-regulated kinase (ERK) activation are also implicated in neurodegenerative diseases. Here, we found that vaccinia-related kinase 3 (VRK3) facilitates nuclear localization of glutamate-induced heat shock protein 70 (HSP70). Nuclear HSP70 leads to enhancement of vaccinia H1-related phosphatase (VHR) activity via protein-protein interaction rather than its molecular chaperone activity, thereby suppressing excessive ERK activation. Moreover, glutamate-induced ERK activation stimulates the expression of HSP70 and VRK3 at the transcriptional level. Downregulation of either VRK3 or HSP70 rendered cells vulnerable to glutamate-induced apoptosis. Overexpression of HSP70 fused to a nuclear localization signal attenuated apoptosis more than HSP70 alone. The importance of nuclear localization of HSP70 in the negative regulation of glutamate-induced ERK activation was further confirmed in VRK3-deficient neurons. Importantly, we showed a positive correlation between levels of VRK3 and HSP70 in the progression of Alzheimer’s and Parkinson’s diseases in humans, and neurons with HSP70 nuclear localization exhibited less Aβ accumulation in brains from patients with Alzheimer’s disease. Therefore, HSP70 and VRK3 could potentially serve as diagnostic and therapeutic targets in neurodegenerative diseases.
Meandering instability of air flow in a granular bed: self-similarity and fluid-solid duality
Authors: Yoshimura Yuki , Yagisawa Yui , Okumura Ko 
Published: December 2016

AbstractMeandering instability is familiar to everyone through river meandering or small rivulets of rain flowing down a windshield. However, its physical understanding is still premature, although it could inspire researchers in various fields, such as nonlinear science, fluid mechanics and geophysics, to resolve their long-standing problems. Here, we perform a small-scale experiment in which air flow is created in a thin granular bed to successfully find a meandering regime, together with other remarkable fluidized regimes, such as a turbulent regime. We discover that phase diagrams of the flow regimes for different types of grains can be universally presented as functions of the flow rate and the granular-bed thickness when the two quantities are properly renormalized. We further reveal that the meandering shapes are self-similar as was shown for meandering rivers. The experimental findings are explained by theory, with elucidating the physics. The theory is based on force balance, a minimum-dissipation principle, and a linear-instability analysis of a continuum equation that takes into account the fluid-solid duality, i.e., the existence of fluidized and solidified regions of grains along the meandering path. The present results provide fruitful links to related issues in various fields, including fluidized bed reactors in industry.
Nanosomes carrying doxorubicin exhibit potent anticancer activity against human lung cancer cells
Authors: Srivastava Akhil , Amreddy Narsireddy , Babu Anish , Panneerselvam Janani , Mehta Meghna , Muralidharan Ranganayaki , Chen Allshine , Zhao Yan Daniel , Razaq Mohammad , Riedinger Natascha , Kim Hogyoung , Liu Shaorong , Wu Si , Abdel-Mageed Asim B. , Munshi Anupama , Ramesh Rajagopal 
Published: December 2016

AbstractSuccessful chemotherapeutic intervention for management of lung cancer requires an efficient drug delivery system. Gold nanoparticles (GNPs) can incorporate various therapeutics; however, GNPs have limitations as drug carriers. Nano-sized cellular vesicles like exosomes (Exo) can ferry GNP-therapeutic complexes without causing any particle aggregation or immune response. In the present study, we describe the development and testing of a novel Exo-GNP-based therapeutic delivery system -‘nanosomes’- for lung cancer therapy. This system consists of GNPs conjugated to anticancer drug doxorubicin (Dox) by a pH-cleavable bond that is physically loaded onto the exosomes (Exo-GNP-Dox). The therapeutic efficacy of Dox in nanosomes was assessed in H1299 and A549 non-small cell lung cancer cells, normal MRC9 lung fibroblasts, and Dox-sensitive human coronary artery smooth muscle cells (HCASM). The enhanced rate of drug release under acidic conditions, successful uptake of the nanosomes by the recipient cells and the cell viability assays demonstrated that nanosomes exhibit preferential cytotoxicity towards cancer cells and have minimal activity on non-cancerous cells. Finally, the underlying mechanism of cytotoxicity involved ROS-mediated DNA damage. Results from this study mark the establishment of an amenable drug delivery vehicle and highlight the advantages of a natural drug carrier that demonstrates reduced cellular toxicity and efficient delivery of therapeutics to cancer cells.
Nuclear Factor Erythroid 2-related Factor 2 Deficiency Exacerbates Lupus Nephritis in B6/lpr mice by Regulating Th17 Cell Function
Authors: Zhao Mei , Chen Huanpeng , Ding Qingfeng , Xu Xiaoxie , Yu Bolan , Huang Zhaofeng 
Published: December 2016

AbstractLupus nephritis (LN) is the major clinical manifestation of systemic lupus erythematosus. LN is promoted by T helper 17 (Th17) cells, which are the major pro-inflammatory T cell subset contributing to autoimmunity regulation. Nuclear factor erythroid 2-related factor 2 (NRF2) is critical for suppressing reactive oxygen species (ROS) and relieving oxidant stress by regulating antioxidant gene expression. Previous studies have demonstrated that Nrf2 deficiency promotes drug-induced or spontaneous LN. However, whether NRF2 regulates Th17 function during LN development is still unclear. In this study, we introduced Nrf2 deficiency into a well-known LN model, the B6/lpr mouse strain, and found that it promoted early-stage LN with altered Th17 activation. Th17 cells and their relevant cytokines were dramatically increased in these double-mutant mice. We also demonstrated that naïve T cells from the double-mutant mice showed significantly increased differentiation into Th17 cells in vitro, with decreased expression of the Th17 differentiation suppressor Socs3 and increased phosphorylation of STAT3. Our results demonstrated that Nrf2 deficiency promoted Th17 differentiation and function during LN development. Moreover, our results suggested that the regulation of Th17 differentiation via NRF2 could be a therapeutic target for the treatment of subclinical LN patients.
Development of an oxide-dispersion-strengthened steel by introducing oxygen carrier compound into the melt aided by a general thermodynamic model
Authors: Moghadasi Mohammad Amin , Nili-Ahmadabadi Mahmoud , Forghani Farsad , Kim Hyoung Seop 
Published: December 2016

AbstractIn general, melting process is not a common method for the production of oxide dispersion strengthened (ODS) alloys due to agglomeration and coarsening of oxide particles. However, vacuum casting process has recently been employed as a promising process to produce micro-scale oxide dispersed alloys. In this paper, we report the process and characterization of in situ formation and uniform dispersion of nano-scale Y-Ti oxide particles in Fe-10Ni-7Mn (wt.%) alloy. The processing route involves a solid-liquid reaction between the added TiO2 as an oxygen carrier and dissolved yttrium in liquid metal leading to an optimal microstructure with nano-sized dispersed oxide particles. The developed thermodynamic model shows the independence of the final phase constituents from experimental conditions such as melting temperature or vacuum system pressure which offers a general pathway for the manufacture of oxide dispersion strengthened materials.
Effects of dextromethorphan on MDMA-induced serotonergic aberration in the brains of non-human primates using [123I]-ADAM/SPECT
Authors: Ma Kuo-Hsing , Liu Tsung-Ta , Weng Shao-Ju , Chen Chien-Fu F. , Huang Yuahn-Sieh , Chueh Sheau-Huei , Liao Mei-Hsiu , Chang Kang-Wei , Sung Chi-Chang , Hsu Te-Hung , Huang Wen-Sheng , Cheng Cheng-Yi 
Published: December 2016

Abstract3,4-Methylenedioxymethamphetamine (MDMA), a common recreational drug, is known to cause serotonergic neurotoxicity in the brain. Dextromethorphan (DM) is a widely used antitussive reported to exert anti-inflammatory effectin vivo. In this study, we examined the long-term effect of MDMA on the primate serotonergic system and the protective property of DM against MDMA-induced serotonergic abnormality using single photon emission computed tomography (SPECT). Nine monkeys (Macaca cyclopis) were divided into three groups, namely control, MDMA and co-treatment (MDMA/DM). [123I]-ADAM was used as the radioligand for serotonin transporters (SERT) in SPECT scans. SERT levels of the brain were evaluated and presented as the uptake ratios (URs) of [123I]-ADAM in several regions of interest of the brain including midbrain, thalamus and striatum. We found that the URs of [123I]-ADAM were significantly lower in the brains of MDMA than control group, indicating lower brain SERT levels in the MDMA-treated monkeys. This MDMA-induced decrease in brain SERT levels could persist for over four years. However, the loss of brain SERT levels was not observed in co-treatment group. These results suggest that DM may exert a protective effect against MDMA-induced serotonergic toxicity in the brains of the non-human primate.