bluuebunny/crossref_metadata_2025_split huggingface dataset:
“Hearing faces and seeing voices”: Amodal coding of person identity in the human brain
Authors: Awwad Shiekh Hasan Bashar , Valdes-Sosa Mitchell , Gross Joachim , Belin Pascal 
Published: November 2016

AbstractRecognizing familiar individuals is achieved by the brain by combining cues from several sensory modalities, including the face of a person and her voice. Here we used functional magnetic resonance (fMRI) and a whole-brain, searchlight multi-voxel pattern analysis (MVPA) to search for areas in which local fMRI patterns could result in identity classification as a function of sensory modality. We found several areas supporting face or voice stimulus classification based on fMRI responses, consistent with previous reports; the classification maps overlapped across modalities in a single area of right posterior superior temporal sulcus (pSTS). Remarkably, we also found several cortical areas, mostly located along the middle temporal gyrus, in which local fMRI patterns resulted in identity “cross-classification”: vocal identity could be classified based on fMRI responses to the faces, or the reverse, or both. These findings are suggestive of a series of cortical identity representations increasingly abstracted from the input modality.
Wide-Field Detected Fourier Transform CARS Microscopy
Authors: Duarte Alex Soares , Schnedermann Christoph , Kukura Philipp 
Published: November 2016

AbstractWe present a wide-field imaging implementation of Fourier transform coherent anti-Stokes Raman scattering (wide-field detected FT-CARS) microscopy capable of acquiring high-contrast label-free but chemically specific images over the full vibrational ‘fingerprint’ region, suitable for a large field of view. Rapid resonant mechanical scanning of the illumination beam coupled with highly sensitive, camera-based detection of the CARS signal allows for fast and direct hyperspectral wide-field image acquisition, while minimizing sample damage. Intrinsic to FT-CARS microscopy, the ability to control the range of time-delays between pump and probe pulses allows for fine tuning of spectral resolution, bandwidth and imaging speed while maintaining full duty cycle. We outline the basic principles of wide-field detected FT-CARS microscopy and demonstrate how it can be used as a sensitive optical probe for chemically specific Raman imaging.
Netrin-1-Induced Stem Cell Bioactivity Contributes to the Regeneration of Injured Tissues via the Lipid Raft-Dependent Integrin α6β4 Signaling Pathway
Authors: Lee Soo Sang , Lee Sei-Jung , Lee Sang Hun , Ryu Jung Min , Lim Hyeon Su , Kim Jun Sung , Song Eun Ju , Jung Young Hyun , Lee Hyun Jik , Kim Chung Hun , Han Ho Jae 
Published: November 2016

AbstractNetrin-1 (Ntn-1) is a multifunctional neuronal signaling molecule; however, its physiological significance, which improves the tissue-regeneration capacity of stem cells, has not been characterized. In the present study, we investigate the mechanism by which Ntn-1 promotes the proliferation of hUCB-MSCs with regard to the regeneration of injured tissues. We found that Ntn-1 induces the proliferation of hUCB-MSCs mainly via Inα6β4 coupled with c-Src. Ntn-1 induced the recruitment of NADPH oxidases and Rac1 into membrane lipid rafts to facilitate ROS production. The Inα6β4 signaling of Ntn-1 through ROS production is uniquely mediated by the activation of SP1 for cell cycle progression and the transcriptional occupancy of SP1 on the VEGF promoter. Moreover, Ntn-1 has the ability to induce the F-actin reorganization of hUCB-MSCs via the Inα6β4 signaling pathway. In anin vivomodel, transplantation of hUCB-MSCs pre-treated with Ntn-1 enhanced the skin wound healing process, where relatively more angiogenesis was detected. The potential effect of Ntn-1 on angiogenesis is further verified by the mouse hindlimb ischemia model, where the pre-activation of hUCB-MSCs with Ntn-1 significantly improved vascular regeneration. These results demonstrate that Ntn-1 plays an important role in the tissue regeneration process of hUCB-MSC via the lipid raft-mediated Inα6β4 signaling pathway.
Disturbed phospholipid homeostasis in endoplasmic reticulum initiates tri-o-cresyl phosphate-induced delayed neurotoxicity
Authors: Zhu Li , Wang Pan , Sun Ying-Jian , Xu Ming-Yuan , Wu Yi-Jun 
Published: November 2016

AbstractTri-o-cresyl phosphate (TOCP) is a widely used organophosphorus compound, which can cause a neurodegenerative disorder, i.e., organophosphate-induced delayed neurotoxicity (OPIDN). The biochemical events in the initiation of OPIDN were not fully understood except for the essential inhibition of neuropathy target esterase (NTE). NTE, located in endoplasmic reticulum (ER), catalyzes the deacylation of phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) to glycerophosphocholine (GPC). The present study aims to study the changes of ER phospholipids profile as well as levels of important intermediates of phospholipid synthesis such as diacylglycerol (DAG) and phosphatidic acid (PA) at the initiation stage of OPIDN. Hens are the most commonly used animal models of OPIDN. The spinal cord phospholipidomic profiles of hens treated by TOCP were studied by using HPLC-MS-MS. The results revealed that TOCP induced an increase of PC, LPC, and sphingomyelin (SM) levels and a decrease of GPC, phosphatidylethanolamine (PE), lysophosphatidylethanolamine (LPE), lysophosphatidylserine (LPS), phosphatidylglycerol (PG), and phosphatidylinositol (PI) levels., Levels of DAG and PA were also decreased. Pretreatment with phenylmethylsulfonyl fluoride (PMSF) 24 h before TOCP administration prevented OPIDN and restored the TOCP-induced changes of phospholipids except GPC. Thus, the disruption of ER phospholipid homeostasis may contribute to the initiation of organophosphate-induced delayed neurotoxicity.
Inhibition of lysophosphatidic acid receptors 1 and 3 attenuates atherosclerosis development in LDL-receptor deficient mice
Authors: Kritikou Eva , van Puijvelde Gijs H. M. , van der Heijden Thomas , van Santbrink Peter J. , Swart Maarten , Schaftenaar Frank H. , Kröner Mara J. , Kuiper Johan , Bot Ilze 
Published: November 2016

AbstractLysophosphatidic acid (LPA) is a natural lysophospholipid present at high concentrations within lipid-rich atherosclerotic plaques. Upon local accumulation in the damaged vessels, LPA can act as a potent activator for various types of immune cells through its specific membrane receptors LPA1/3. LPA elicits chemotactic, pro-inflammatory and apoptotic effects that lead to atherosclerotic plaque progression. In this study we aimed to inhibit LPA signaling by means of LPA1/3 antagonism using the small molecule Ki16425. We show that LPA1/3 inhibition significantly impaired atherosclerosis progression. Treatment with Ki16425 also resulted in reduced CCL2 production and secretion, which led to less monocyte and neutrophil infiltration. Furthermore, we provide evidence that LPA1/3 blockade enhanced the percentage of non-inflammatory, Ly6Clow monocytes and CD4+ CD25+ FoxP3+ T-regulatory cells. Finally, we demonstrate that LPA1/3 antagonism mildly reduced plasma LDL cholesterol levels. Therefore, pharmacological inhibition of LPA1/3 receptors may prove a promising approach to diminish atherosclerosis development.
Detecting and utilizing minority phases in heterogeneous catalysis
Authors: Hartfelder Urs , Singh Jagdeep , Haase Johannes , Nachtegaal Maarten , Grolimund Daniel , van Bokhoven Jeroen A. 
Published: November 2016

AbstractHighly active phases in carbon monoxide oxidation are known, however they are transient in nature. Here, we determined for the first time the structure of such a highly active phase on platinum nanoparticles in an actual reactor. Unlike generally assumed, the surface of this phase is virtually free of adsorbates and co-exists with carbon-monoxide covered and surface oxidized platinum. Understanding the relation between gas composition and catalyst structure at all times and locations within a reactor enabled the rational design of a reactor concept, which maximizes the amount of the highly active phase and minimizes the amount of platinum needed.
17-oxo-DHA displays additive anti-inflammatory effects with fluticasone propionate and inhibits the NLRP3 inflammasome
Authors: Cipollina Chiara , Di Vincenzo Serena , Siena Liboria , Di Sano Caterina , Gjomarkaj Mark , Pace Elisabetta 
Published: November 2016

AbstractChronic obstructive pulmonary disease (COPD) is characterized by reduced lung function associated with increased local and systemic inflammatory markers, such as TNFα and IL-1β. Glucocorticoids are used to treat this chronic disease, however their efficacy is low and new drugs are very much required. 17-oxo-DHA is a cyclooxygenase-2-dependent, electrophilic, α,β-unsaturated keto-derivative of docosahexaenoic acid with anti-inflammatory properties. We evaluated the action of 17-oxo-DHA alone or in combination with the steroid fluticasone propionate (FP) in peripheral blood mononuclear cells (PBMCs) from COPD patients and healthy individuals exposed to lipopolysaccharide. We show that PBMCs from COPD patients released higher levels of TNFα and IL-1β compared to controls. 17-oxo-DHA displayed strong anti-inflammatory effects. The addition of 17-oxo-DHA in combination with FP showed enhanced anti-inflammatory effects through the modulation of transcriptional and post-transcriptional mechanisms. 17-oxo-DHA, but not FP, was able to suppress the release of mature IL-1β through inhibition of the NLRP3 inflammasome. Furthermore, 17-oxo-DHA inhibited inflammasome-dependent degradation of the glucocorticoid receptor (GR). Our findings suggest that 17-oxo-DHA in combination with FP or other steroids might achieve higher therapeutic efficacy than steroids alone. Combined treatment might be particularly relevant in those conditions where increased inflammasome activation may lead to GR degradation and steroid-unresponsive inflammation.
A comparison of the performance of molecularly imprinted polymer nanoparticles for small molecule targets and antibodies in the ELISA format
Authors: Smolinska-Kempisty Katarzyna , Guerreiro Antonio , Canfarotta Francesco , Cáceres César , Whitcombe Michael J. , Piletsky Sergey 
Published: November 2016

AbstractHere we show that molecularly imprinted polymer nanoparticles, prepared in aqueous media by solid phase synthesis with immobilised L-thyroxine, glucosamine, fumonisin B2 or biotin as template, can demonstrate comparable or better performance to commercially produced antibodies in enzyme-linked competitive assays. Imprinted nanoparticles-based assays showed detection limits in the pM range and polymer-coated microplates are stable to storage at room temperature for at least 1 month. No response to analyte was detected in control experiments with nanoparticles imprinted with an unrelated template (trypsin) but prepared with the same polymer composition. The ease of preparation, high affinity of solid-phase synthesised imprinted nanoparticles and the lack of requirement for cold chain logistics make them an attractive alternative to traditional antibodies for use in immunoassays.
Nucleoside-Diphosphate-Kinase of P. gingivalis is Secreted from Epithelial Cells In the Absence of a Leader Sequence Through a Pannexin-1 Interactome
Authors: Atanasova Kalina , Lee Jungnam , Roberts JoAnn , Lee Kyulim , Ojcius David M , Yilmaz Özlem 
Published: November 2016

AbstractNucleoside-diphosphate-kinases (NDKs) are leaderless, multifunctional enzymes. The mode(s) of NDK secretion is currently undefined, while extracellular translocation of bacterial NDKs is critical for avoidance of host pathogen clearance by opportunistic pathogens such as Porphyromonas gingivalis. P. gingivalis-NDK during infection inhibits extracellular-ATP (eATP)/P2X7-receptor mediated cell death in gingival epithelial cells (GECs) via eATP hydrolysis. Furthermore, depletion of pannexin-1-hemichannel (PNX1) coupled with P2X7-receptor blocks the infection-induced eATP release in GECs, and P. gingivalis-NDK impacts this pathway. Ultrastructural and confocal microscopy of P. gingivalis-co-cultured GECs or green-fluorescent-protein (GFP)-P. gingivalis-NDK transfected GECs revealed a perinuclear/cytoplasmic localization of NDK. eATP stimulation induced NDK recruitment to the cell periphery. Depletion of PNX1 by siRNA or inhibition by probenecid resulted in significant blocking of extracellular NDK activity and secretion using ATPase and ELISA assays. Co-immunoprecipitation-coupled Mass-spectrometry method revealed association of P. gingivalis-NDK to the myosin-9 motor molecule. Interestingly, inhibition of myosin-9, actin, and lipid-rafts, shown to be involved in PNX1-hemichannel function, resulted in marked intracellular accumulation of NDK and decreased NDK secretion from infected GECs. These results elucidate for the first time PNX1-hemichannels as potentially main extracellular translocation pathway for NDKs from an intracellular pathogen, suggesting that PNX1-hemichannels may represent a therapeutic target for chronic opportunistic infections.
Thermodynamic origin of instability in hybrid halide perovskites
Authors: Tenuta E. , Zheng C. , Rubel O. 
Published: November 2016

AbstractDegradation of hybrid halide perovskites under the influence of environmental factors impairs future prospects of using these materials as absorbers in solar cells. First principle calculations can be used as a guideline in search of new materials, provided we can rely on their predictive capabilities. We show that the instability of perovskites can be captured using ab initio total energy calculations for reactants and products augmented with additional thermodynamic data to account for finite temperature effects. Calculations suggest that the instability of CH3NH3PbI3 in moist environment is linked to the aqueous solubility of the CH3NH3I salt, thus making other perovskite materials with soluble decomposition products prone to degradation. Properties of NH3OHPbI3, NH3NH2PbI3, PH4PbI3, SbH4PbI3, CsPbBr3, and a new hypothetical SF3PbI3 perovskite are studied in the search for alternative solar cell absorber materials with enhanced chemical stability.
Questioning the Mpemba effect: hot water does not cool more quickly than cold
Authors: Burridge Henry C. , Linden Paul F. 
Published: November 2016

AbstractThe Mpemba effect is the name given to the assertion that it is quicker to cool water to a given temperature when the initial temperature is higher. This assertion seems counter-intuitive and yet references to the effect go back at least to the writings of Aristotle. Indeed, at first thought one might consider the effect to breach fundamental thermodynamic laws, but we show that this is not the case. We go on to examine the available evidence for the Mpemba effect and carry out our own experiments by cooling water in carefully controlled conditions. We conclude, somewhat sadly, that there is no evidence to support meaningful observations of the Mpemba effect.
Role of ectonucleotide pyrophosphatase/phosphodiesterase 2 in the midline axis formation of zebrafish
Authors: Frisca Frisca , Colquhoun Daniel , Goldshmit Yona , Änkö Minna-Liisa , Pébay Alice , Kaslin Jan 
Published: November 2016

AbstractLysophosphatidic acid (LPA) is a unique bioactive lysophospholipid that induces pleiotropic effects in various cell types and organisms by acting on its specific receptors. LPA is mainly synthetised extracellularly by the ectonucleotide pyrophosphatase/phosphodiesterase 2/autotaxin (enpp2). Altered LPA signalling is associated with embryonic abnormalities, suggesting critical roles for LPA during development. However, the role of LPA signalling during early embryogenesis is not well established. We demonstrate that enpp2/LPA signalling in the early zebrafish embryo results in altered axis and midline formation, defects in left right (L-R) patterning, ciliogenesis of the Kupffer’s vesicle (KV), through the modulation of cell migration during gastrulation in a lpar1–3 Rho/ROCK-dependant manner. Overall, this study demonstrates an essential role of enpp2/LPA signalling during early embryogenesis.
Ground states of a Bose-Einstein Condensate in a one-dimensional laser-assisted optical lattice
Authors: Sun Qing , Hu Jie , Wen Lin , Liu W.-M. , Juzeliūnas G. , Ji An-Chun 
Published: November 2016

AbstractWe study the ground-state behavior of a Bose-Einstein Condensate (BEC) in a Raman-laser-assisted one-dimensional (1D) optical lattice potential forming a multilayer system. We find that, such system can be described by an effective model with spin-orbit coupling (SOC) of pseudospin (N-1)/2, where N is the number of layers. Due to the intricate interplay between atomic interactions, SOC and laser-assisted tunnelings, the ground-state phase diagrams generally consist of three phases–a stripe, a plane wave and a normal phase with zero-momentum, touching at a quantum tricritical point. More important, even though the single-particle states only minimize at zero-momentum for odd N, the many-body ground states may still develop finite momenta. The underlying mechanisms are elucidated. Our results provide an alternative way to realize an effective spin-orbit coupling of Bose gas with the Raman-laser-assisted optical lattice, and would also be beneficial to the studies on SOC effects in spinor Bose systems with large spin.
Alpha band disruption in the AD-continuum starts in the Subjective Cognitive Decline stage: a MEG study
Authors: López-Sanz D. , Bruña R. , Garcés P. , Camara C. , Serrano N. , Rodríguez-Rojo I. C. , Delgado M. L. , Montenegro M. , López-Higes R. , Yus M. , Maestú F. 
Published: November 2016

AbstractThe consideration of Subjective Cognitive Decline (SCD) as a preclinical stage of AD remains still a matter of debate. Alpha band alterations represent one of the most significant changes in the electrophysiological profile of AD. In particular, AD patients exhibit reduced alpha relative power and frequency. We used alpha band activity measured with MEG to study whether SCD and MCI elders present these electrophysiological changes characteristic of AD, and to determine the evolution of the observed alterations across AD spectrum. The total sample consisted of 131 participants: 39 elders without SCD, 41 elders with SCD and 51 MCI patients. All of them underwent MEG and MRI scans and neuropsychological assessment. SCD and MCI patients exhibited a similar reduction in alpha band activity compared with the no SCD group. However, only MCI patients showed a slowing in their alpha peak frequency compared with both SCD and no SCD. These changes in alpha band were related to worse cognition. Our results suggest that AD-related alterations may start in the SCD stage, with a reduction in alpha relative power. It is later, in the MCI stage, where the slowing of the spectral profile takes place, giving rise to objective deficits in cognitive functioning.
Highly expressed ribosomal protein L34 indicates poor prognosis in osteosarcoma and its knockdown suppresses osteosarcoma proliferation probably through translational control
Authors: Luo Shuju , Zhao Jinmin , Fowdur Mitra , Wang Kun , Jiang Tenglong , He Maolin 
Published: November 2016

AbstractOsteosarcoma has devastating health implications on children and adolescents. However, due to its low incidence and high tumor heterogeneity, it is hard to achieve any further improvements in therapy and overall survival. Ribosomal protein L34 (RPL34) has been increasingly recognized to promote the proliferation of malignant cells, but its role in osteosarcoma has not been investigated. In this study, real-time quantitative PCR (RT-qPCR) and immunohistochemistry revealed that RPL34 was highly expressed in osteosarcoma tissues when compared to adjacent tissues and normal bone tissues. Survival analysis showed that high expression of RPL34 predicted a poor prognosis for osteosarcoma patients. Knockdown of RPL34 in Saos-2 cells via lentivirus-mediated small interfering RNA (siRNA) significantly inhibited cell proliferation, induced cell apoptosis and G2/M phase arrest. Moreover, screening of transcription factors using University of California Santa Cruz (UCSC) Genome Browser, protein-protein interaction (PPI) network analysis, Gene Ontology (GO) and pathway enrichment analysis revealed that MYC participates in the transcriptional regulation of RPL34, which interacts with the subunits of eukaryotic translation initiation factor 3 (eIF3) and probably involves the translational control of growth-promoting proteins. Our findings suggest that RPL34 plays an important role in the proliferation of osteosarcoma cells.
Mycobacterium tuberculosis-triggered Hippo pathway orchestrates CXCL1/2 expression to modulate host immune responses
Authors: Boro Monoranjan , Singh Vikas , Balaji Kithiganahalli Narayanaswamy 
Published: November 2016

AbstractMycobacterium tuberculosis (Mtb) pathogenesis encompasses a plethora of finely regulated alterations within the host which eventually coin the outcome of infection. Chemokines are important components in directing immune cell recruitment to the site of infection, and shaping the disease progression. Here, we demonstrate that Hippo (mammalian sterile 20–like 1 and 2 kinases, MST1/2, in mammals), is activated during mycobacterial infection in a toll-like receptor (TLR) 2-interleukin receptor-1 associated kinases (IRAK1/4)-dependent manner. Mtb-triggered Hippo signaling modulates the expression and secretion of chemokines (CXCL1 and CXCL2); as silencing MST1/2 compromised the ability of Mtb to furnish the same. Further insight into the mechanism of Hippo-mediated regulation of chemokines revealed the role for a non-canonical Hippo effector interferon (IFN) regulatory factor (IRF) 3 in the process and marked the effect to be independent of LATS1. Alongside their ability to guide directed recruitment of immune cells, we have uncovered a paracrine role for Hippo-mediated secretion of CXCL1 and CXCL2 in the production of anti-microbial peptides (beta-defensins), iNOS, NOX2 and pro-inflammatory molecules during mycobacterial infection of the host. This study highlights the involvement of TLR2-IRAK1/4-MST1/2-IRF3 axis in Mtb-triggered modulation of chemokines and identifies Hippo signaling as a novel regulator of host-mycobacterial interactions.
The mevalonate pathway regulates primitive streak formation via protein farnesylation
Authors: Okamoto-Uchida Yoshimi , Yu Ruoxing , Miyamura Norio , Arima Norie , Ishigami-Yuasa Mari , Kagechika Hiroyuki , Yoshida Suguru , Hosoya Takamitsu , Nawa Makiko , Kasama Takeshi , Asaoka Yoichi , Alois Reiner Wimmer , Elling Ulrich , Penninger Josef M. , Nishina Sachiko , Azuma Noriyuki , Nishina Hiroshi 
Published: November 2016

AbstractThe primitive streak in peri-implantation embryos forms the mesoderm and endoderm and controls cell differentiation. The metabolic cues regulating primitive streak formation remain largely unknown. Here we utilised a mouse embryonic stem (ES) cell differentiation system and a library of well-characterised drugs to identify these metabolic factors. We found that statins, which inhibit the mevalonate metabolic pathway, suppressed primitive streak formation in vitro and in vivo. Using metabolomics and pharmacologic approaches we identified the downstream signalling pathway of mevalonate and revealed that primitive streak formation requires protein farnesylation but not cholesterol synthesis. A tagging-via-substrate approach revealed that nuclear lamin B1 and small G proteins were farnesylated in embryoid bodies and important for primitive streak gene expression. In conclusion, protein farnesylation driven by the mevalonate pathway is a metabolic cue essential for primitive streak formation.