bluuebunny/crossref_metadata_2025_split huggingface dataset:
Do manufacturer ‘nutrient claims’ influence the efficacy of mandated front-of-package labels?
Authors: Acton Rachel B , Hammond David 
Published: October 2018

AbstractObjectiveTo examine consumers’ ability to correctly interpret front-of-package (FOP) ‘high in’ warnings in the presence of a voluntary claim for the same or a different nutrient.DesignA between-group experimental task assigned respondents to view food products labelled as ‘high in sodium’, with a ‘reduced sodium’ claim positioned next to the warning, away from the warning or absent. A second experiment assigned participants to view a food product labelled as ‘high in sugar’, with a ‘reduced fat’ claim positioned next to the warning, away from the warning or absent. For both tasks, respondents were asked to identify whether the products were high in the indicated nutrient.SettingOnline survey (2016).SubjectsCanadians aged 16–32 years (n 1000) were recruited in person from five major cities in Canada.ResultsRespondents were less likely to correctly identify a product as ‘high in sodium’ when packages also featured a voluntary ‘reduced sodium’ claim, with a stronger effect when the claim was positioned away from the FOP symbol (P<0·001). The number of correct responses was similar across conditions when the nutrient claim was for a different nutrient than the one featured in the FOP ‘high in’ warning.ConclusionsThe findings demonstrate that the presence of a voluntary nutrient claim can undermine the efficacy of mandated FOP labels for the same nutrient. Countries considering nutrient-specific FOP warnings, including Canada, should consider regulations that would prohibit claims for nutrients that exceed the threshold for nutrient-specific FOP warnings.
The effects of a nutrition education curriculum on improving young children’s fruit and vegetable preferences and nutrition and health knowledge
Authors: Schmitt Sara A , Bryant Lindsey M , Korucu Irem , Kirkham Lisa , Katare Bhagyashree , Benjamin Tamara 
Published: October 2018

AbstractObjectiveThe main objective of the present study was to develop and evaluate a nutrition education curriculum to enhance young children’s dietary behaviours and nutrition and health knowledge.DesignA randomized controlled design was utilized. The intervention was designed to improve children’s nutrition and health knowledge and preferences for fruits and vegetables through classroom lessons and activities, including direct instruction and tastings (implemented twice per week for 6 weeks).SettingThe study took place in elementary schools in a Midwestern US state.SubjectsOne hundred and thirty-one 2nd grade children from ten classrooms (n 82 intervention, n 49 control) participated.ResultsMultiple regression analyses that adjusted se for clustering by classroom were used to test hypotheses. Children in the intervention condition demonstrated significantly higher scores on the nutrition and health survey (β=0·47, P=0·001) and showed greater preferences for fruits and vegetables at post-test than the control group (β=0·19, P=0·003).ConclusionsFindings suggest that a short, 6-week intervention that aligns with educational standards has the ability to significantly enhance children’s outcomes and thus may be a more feasible option for teachers to incorporate into their classrooms than what is currently available.
RIT1 suppresses esophageal squamous cell carcinoma growth and metastasis and predicts good prognosis
Authors: Feng Yan-Fen , Lei Yi-Yan , Lu Jia-Bin , Xi Shao-Yan , Zhang Yu , Huang Qi-Tao , Wu Qiu-Liang , Wang Fang 
Published: October 2018

AbstractRas-like without CAAX1 (RIT1) protein is a member of Ras family, which plays critical roles in signaling pathways and cellular process regulation. However, the role of RIT1 in esophageal squamous cell carcinoma (ESCC) is unclear. In this study, we found that the expression of RIT1 is downregulated in ESCC compared to corresponding non-tumor tissues. The low-level expression of RIT1 was correlated with poorer prognosis. Then we showed that RIT1 inhibited proliferation, invasion, and migration of ESCC cells, and silencing RIT1 by shRNA promoted tumorigenicity and metastasis in nude mice. We further demonstrated that RIT1 inhibited the malignant behaviors of ESCC through inhibiting the PI3K/AKT and MAPK pathway and epithelial–mesenchymal transition in ESCC cells. Our study also revealed that RIT1 increased drug sensitivity to cisplatin (CDDP), and this function could be carried out through downregulating stemness of ESCC. In conclusion, our study indicates for the first time that RIT1 displays tumor-suppressing functions in ESCC, and these functions were carried out by inhibiting MAPK and PI3K/AKT signaling pathway, inhibiting EMT, and downregulating cancer stemness of ESCC cells.
Azithromycin promotes alternatively activated macrophage phenotype in systematic lupus erythematosus via PI3K/Akt signaling pathway
Authors: Wang Jie , Xie Lin , Wang Shangshang , Lin Jinran , Liang Jun , Xu Jinhua 
Published: October 2018

AbstractAlternatively activated macrophages have been reported to be helpful to alleviate systematic lupus erythematosus (SLE), and azithromycin could serve as an immunomodulator by promoting alternatively activated macrophage phenotype. However, the effect of azithromycin in SLE and the involved mechanism remain undetermined. The aim of this study is to characterize azithromycin and the underlying mechanism contributing to SLE therapy. First, we compared monocytes from SLE patients and matched healthy donors, and found monocytes from SLE patients exhibited more CD14+CD86+ cells, impaired phagocytic activity, and elevated interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α (the classical activated phenotype), which could be blocked by azithromycin. On the contrary, there were fewer CD14+CD163+ cells in SLE patients, accompanied by decreased arginase (Arg)-1 and found in inflammatory zone (Fizz)-1 (the alternatively activated phenotype). And IL-10, the crucial immune regulatory factor secreted by alternatively activated monocytes/macrophages, also showed a decreased trend in SLE patients. In addition, all these markers were up-regulated after azithromycin treatment. Next, we used activated lymphocyte-derived-DNA to imitate SLE macrophages in vitro to investigate the possible mechanism involved. Azithromycin showed the same effect in imitated SLE macrophages, with distinct Akt phosphorylation at 30 min and 12 h. After inhibiting Akt phosphorylation by LY294002, the down-regulation of CD80, IL-1β, IL-6, and TNF-α caused by azithromycin raised again, meanwhile, the up-regulation of CD206, Arg-1, Fizz-1, and IL-10 due to azithromycin was abolished. Additionally, insulin-like growth factor 1 (IGF-1), the specific agonist of Akt, played a similar role to azithromycin in imitated SLE macrophages. Taken together, our data indicated a novel role of azithromycin in alleviating SLE by promoting alternatively activated macrophage phenotype, and the PI3K/Akt signaling pathway was involved. Our findings provide a rationale for further investigation of novel therapeutic strategy for SLE patients.
APP promotes osteoblast survival and bone formation by regulating mitochondrial function and preventing oxidative stress
Authors: Pan Jin-Xiu , Tang Fulei , Xiong Fei , Xiong Lei , Zeng Peng , Wang Bo , Zhao Kai , Guo Haohan , Shun Cui , Xia Wen-Fang , Mei Lin , Xiong Wen-Cheng 
Published: October 2018

AbstractAmyloid precursor protein (APP) is ubiquitously expressed in various types of cells including bone cells. Mutations in App gene result in early-onset Alzheimer’s disease (AD). However, little is known about its physiological function in bone homeostasis. Here, we provide evidence for APP’s role in promoting bone formation. Mice that knocked out App gene (APP−/−) exhibit osteoporotic-like deficit, including reduced trabecular and cortical bone mass. Such a deficit is likely due in large to a decrease in osteoblast (OB)-mediated bone formation, as little change in bone resorption was detected in the mutant mice. Further mechanical studies of APP−/−OBs showed an impairment in mitochondrial function, accompanied with increased reactive oxygen species (ROS) and apoptosis. Intriguingly, these deficits, resemble to those in Tg2576 animal model of AD that expresses Swedish mutant APP (APPswe), were diminished by treatment with an anti-oxidant NAC (n-acetyl-l-cysteine), uncovering ROS as a critical underlying mechanism. Taken together, these results identify an unrecognized physiological function of APP in promoting OB survival and bone formation, implicate APPswe acting as a dominant negative factor, and reveal a potential clinical value of NAC in treatment of AD-associated osteoporotic deficits.
Cytoplasmic FLIP(S) and nuclear FLIP(L) mediate resistance of castrate-resistant prostate cancer to apoptosis induced by IAP antagonists
Authors: McCann Christopher , Crawford Nyree , Majkut Joanna , Holohan Caitriona , Armstrong Chris W. D. , Maxwell Pamela J. , Ong Chee Wee , LaBonte Melissa J. , McDade Simon S. , Waugh David J. , Longley Daniel B. 
Published: October 2018

AbstractExpression of tumor necrosis factor-α (TNFα) in the serum of prostate cancer patients is associated with poorer outcome and progression to castrate-resistant (CRPC) disease. TNFα promotes the activity of NFκB, which regulates a number of anti-apoptotic and proinflammatory genes, including those encoding the inhibitor of apoptosis proteins (IAPs); however, in the presence of IAP antagonists, TNFα can induce cell death. In the presence of recombinant or macrophage-derived TNFα, we found that IAP antagonists triggered degradation of cIAP1 and induced formation of Complex-IIb, consisting of caspase-8, FADD and RIPK1 in CRPC models; however, no, or modest levels of apoptosis were induced. This resistance was found to be mediated by both the long (L) and short (S) splice forms of the caspase-8 inhibitor, FLIP, another NFκB-regulated protein frequently overexpressed in CRPC. By decreasing FLIP expression at the post-transcriptional level in PC3 and DU145 cells (but not VCaP), the Class-I histone deacetylase (HDAC) inhibitor Entinostat promoted IAP antagonist-induced cell death in these models in a manner dependent on RIPK1, FADD and Caspase-8. Of note, Entinostat primarily targeted the nuclear rather than cytoplasmic pool of FLIP(L). While the cytoplasmic pool of FLIP(L) was highly stable, the nuclear pool was more labile and regulated by the Class-I HDAC target Ku70, which we have previously shown regulates FLIP stability. The efficacy of IAP antagonist (TL32711) and Entinostat combination and their effects on cIAP1 and FLIP respectively were confirmed in vivo, highlighting the therapeutic potential for targeting IAPs and FLIP in proinflammatory CRPC.
Chromatin-remodeling factor, RSF1, controls p53-mediated transcription in apoptosis upon DNA strand breaks
Authors: Min Sunwoo , Kim Keeeun , Kim Seong-Gwang , Cho Hyeseong , Lee Youngsoo 
Published: October 2018

AbstractRemodeling and spacing factor 1 (RSF1), which is one of chromatin-remodeling factors, has been linked to the DNA damage response (DDR) and DNA repair. However, the biological consequence of RSF1 deficiency in DDR in vivo and its molecular mechanisms remain unknown. Because defective DDR is related to neuropathological phenotypes, we developed neural-specific Rsf1 knockout mice. Rsf1 deficiency did not result in any neuropathological abnormalities, but prevented neural apoptosis triggered by excessive DNA strand breaks during neurogenesis. Likewise, cell death was significantly reduced in RSF1 deficient human cell lines after DNA damage, and the global transcriptome of these cells revealed that the expressions of p53 downstream genes were significantly reduced upon DNA strand breaks. Inactivation of these genes resulted from decreased binding of p53/p300 complex and subsequent reduction of H3 acetylation at their promoters. Our data show that RSF1 is necessary for p53-dependent gene expression in response to DNA strand breaks via controlling the accessibility of p53/p300 complex to its target genes and contributes to the maintenance of cellular integrity.
Common helical V1V2 conformations of HIV-1 Envelope expose the α4β7 binding site on intact virions
Authors: Wibmer Constantinos Kurt , Richardson Simone I. , Yolitz Jason , Cicala Claudia , Arthos James , Moore Penny L. , Morris Lynn 
Published: October 2018

AbstractThe α4β7 integrin is a non-essential HIV-1 adhesion receptor, bound by the gp120 V1V2 domain, facilitating rapid viral dissemination into gut-associated lymphoid tissues. Antibodies blocking this interaction early in infection can improve disease outcome, and V1V2-targeted antibodies were correlated with moderate efficacy reported from the RV144 HIV-1 vaccine trial. Monoclonal α4β7-blocking antibodies recognise two slightly different helical V2 conformations, and current structural data suggests their binding sites are occluded in prefusion envelope trimers. Here, we report cocrystal structures of two α4β7-blocking antibodies from an infected donor complexed with scaffolded V1V2 or V2 peptides. Both antibodies recognised the same helix-coil V2 conformation as RV144 antibody CH58, identifying a frequently sampled alternative conformation of full-length V1V2. In the context of Envelope, this α-helical form of V1V2 displays highly exposed α4β7-binding sites, potentially providing a functional role for non-native Envelope on virion or infected cell surfaces in HIV-1 dissemination, pathogenesis, and vaccine design.
Mutual inhibition between PTEN and PIP3 generates bistability for polarity in motile cells
Authors: Matsuoka Satomi , Ueda Masahiro 
Published: October 2018

AbstractPhosphatidylinositol 3,4,5-trisphosphate (PIP3) and PIP3 phosphatase (PTEN) are enriched mutually exclusively on the anterior and posterior membranes of eukaryotic motile cells. However, the mechanism that causes this spatial separation between the two molecules is unknown. Here we develop a method to manipulate PIP3 levels in living cells and used it to show PIP3 suppresses the membrane localization of PTEN. Single-molecule measurements of membrane-association and -dissociation kinetics and of lateral diffusion reveal that PIP3 suppresses the PTEN binding site required for stable PTEN membrane binding. Mutual inhibition between PIP3 and PTEN provides a mechanistic basis for bistability that creates a PIP3-enriched/PTEN-excluded state and a PTEN-enriched/PIP3-excluded state underlying the strict spatial separation between PIP3 and PTEN. The PTEN binding site also mediates the suppression of PTEN membrane localization in chemotactic signaling. These results illustrate that the PIP3-PTEN bistable system underlies a cell’s decision-making for directional movement irrespective of the environment.
Deconvolution of octahedral Pt3Ni nanoparticle growth pathway from in situ characterizations
Authors: Shen Xiaochen , Zhang Changlin , Zhang Shuyi , Dai Sheng , Zhang Guanghui , Ge Mingyuan , Pan Yanbo , Sharkey Stephen M. , Graham George W. , Hunt Adrian , Waluyo Iradwikanari , Miller Jeffrey T. , Pan Xiaoqing , Peng Zhenmeng 
Published: October 2018

AbstractUnderstanding the growth pathway of faceted alloy nanoparticles at the atomic level is crucial to morphology control and property tuning. Yet, it remains a challenge due to complexity of the growth process and technical limits of modern characterization tools. We report a combinational use of multiple cutting-edge in situ techniques to study the growth process of octahedral Pt3Ni nanoparticles, which reveal the particle growth and facet formation mechanisms. Our studies confirm the formation of octahedral Pt3Ni initiates from Pt nuclei generation, which is followed by continuous Pt reduction that simultaneously catalyzes Ni reduction, resulting in mixed alloy formation with moderate elemental segregation. Carbon monoxide molecules serve as a facet formation modulator and induce Ni segregation to the surface, which inhibits the (111) facet growth and causes the particle shape to evolve from a spherical cluster to an octahedron as the (001) facet continues to grow.
Non-catalytic signaling by pseudokinase ILK for regulating cell adhesion
Authors: Vaynberg Julia , Fukuda Koichi , Lu Fan , Bialkowska Katarzyna , Chen Yinghua , Plow Edward F. , Qin Jun 
Published: October 2018

AbstractDynamic communication between integrin-containing complexes (focal adhesions, FAs) and actin filaments is critical for regulating cell adhesion. Pseudokinase ILK plays a key role in this process but the underlying mechanism remains highly elusive. Here we show that by recruiting FA adaptors PINCH and Parvin into a heterotrimeric complex (IPP), ILK triggers F-actin filament bundling – a process known to generate force/mechanical signal to promote cytoskeleton reassembly and dynamic cell adhesion. Structural, biochemical, and functional analyses revealed that the F-actin bundling is orchestrated by two previously unrecognized WASP-Homology-2 actin binding motifs within IPP, one from PINCH and the other from Parvin. Strikingly, this process is also sensitized to Mg-ATP bound to the pseudoactive site of ILK and its dysregulation severely impairs stress fibers formation, cell spreading, and migration. These data identify a crucial mechanism for ILK, highlighting its uniqueness as a pseudokinase to transduce non-catalytic signal and regulate cell adhesion.
An optical reaction micro-turbine
Authors: Bianchi Silvio , Vizsnyiczai Gaszton , Ferretti Stefano , Maggi Claudio , Di Leonardo Roberto 
Published: October 2018

AbstractTo any energy flow there is an associated flow of momentum, so that recoil forces arise every time an object absorbs or deflects incoming energy. This same principle governs the operation of macroscopic turbines as well as that of microscopic turbines that use light as the working fluid. However, a controlled and precise redistribution of optical energy is not easy to achieve at the micron scale resulting in a low efficiency of power to torque conversion. Here we use direct laser writing to fabricate 3D light guiding structures, shaped as a garden sprinkler, that can precisely reroute input optical power into multiple output channels. The shape parameters are derived from a detailed theoretical analysis of losses in curved microfibers. These optical reaction micro-turbines can maximally exploit light’s momentum to generate a strong, uniform and controllable torque.
High-power hybrid biofuel cells using layer-by-layer assembled glucose oxidase-coated metallic cotton fibers
Authors: Kwon Cheong Hoon , Ko Yongmin , Shin Dongyeeb , Kwon Minseong , Park Jinho , Bae Wan Ki , Lee Seung Woo , Cho Jinhan 
Published: October 2018

AbstractElectrical communication between an enzyme and an electrode is one of the most important factors in determining the performance of biofuel cells. Here, we introduce a glucose oxidase-coated metallic cotton fiber-based hybrid biofuel cell with efficient electrical communication between the anodic enzyme and the conductive support. Gold nanoparticles are layer-by-layer assembled with small organic linkers onto cotton fibers to form metallic cotton fibers with extremely high conductivity (>2.1×104 S cm−1), and are used as an enzyme-free cathode as well as a conductive support for the enzymatic anode. For preparation of the anode, the glucose oxidase is sequentially layer-by-layer-assembled with the same linkers onto the metallic cotton fibers. The resulting biofuel cells exhibit a remarkable power density of 3.7 mW cm−2, significantly outperforming conventional biofuel cells. Our strategy to promote charge transfer through electrodes can provide an important tool to improve the performance of biofuel cells.
Integrative taxonomy resolves taxonomic uncertainty for freshwater mussels being considered for protection under the U.S. Endangered Species Act
Authors: Johnson Nathan A. , Smith Chase H. , Pfeiffer John M. , Randklev Charles R. , Williams James D. , Austin James D. 
Published: October 2018

AbstractObjectively delimiting species boundaries remains an important challenge in systematics and becomes urgent when unresolved taxonomy complicates conservation and recovery efforts. We examined species boundaries in the imperiled freshwater mussel genus Cyclonaias (Bivalvia: Unionidae) using morphometrics, molecular phylogenetics, and multispecies coalescent models to help guide pending conservation assessments and legislative decisions. Congruence across multiple lines of evidence indicated that current taxonomy overestimates diversity in the C. pustulosa species complex. The only genetically and morphologically diagnosable species in the C. pustulosa species complex were C. pustulosa and C. succissa and we consider C. aurea, C. houstonensis, C. mortoni, and C. refulgens to be synonyms of C. pustulosa. In contrast, all three species in the C. nodulata complex (C. necki, C. nodulata, and C. petrina) were genetically, geographically, and morphologically diagnosable. Our findings have important conservation and management implications, as three nominal species (C. aurea, C. houstonensis, and C. petrina) are being considered for protection under the Endangered Species Act.
Behavioral flexibility promotes collective consistency in a social insect
Authors: Garrison Linda Karen , Kleineidam Christoph Johannes , Weidenmüller Anja 
Published: October 2018

AbstractDeciphering the mechanisms that integrate individuals and their behavior into a functional unit is crucial for our understanding of collective behaviors. We here present empirical evidence for the impressive strength of social processes in this integration. We investigated collective temperature homeostasis in bumblebee (Bombus terrestris) colonies and found that bees are less likely to engage in thermoregulatory fanning and do so with less time investment when confronted with heat stress in a group setting than when facing the same challenge alone and that this down-regulation of individual stimulus-response behavior resulted in a consistent proportion of workers in a group engaged in the task of fanning. Furthermore, the bees that comprised the subset of fanning individuals changed from trial to trial and participation in the task was predominately unpredictable based on previous response behavior. Our results challenge basic assumptions in the most commonly used class of models for task allocation and contrast numerous collective behavior studies that emphasize the importance of fixed inter-individual variation for the functioning of animal groups. We demonstrate that bumblebee colonies maintain within-group behavioral heterogeneity and a consistent collective response pattern based on social responsiveness and behavioral flexibility at the individual level.
Solid-phase enzyme catalysis of DNA end repair and 3′ A-tailing reduces GC-bias in next-generation sequencing of human genomic DNA
Authors: Zhang Aihua , Li Shaohua , Apone Lynne , Sun Xiaoli , Chen Lixin , Ettwiller Laurence M. , Langhorst Bradley W. , Noren Christopher J. , Xu Ming-Qun 
Published: October 2018

AbstractThe use of next-generation sequencing (NGS) has been instrumental in advancing biological research and clinical diagnostics. To fully utilize the power of NGS, complete, uniform coverage of the entire genome is required. In this study, we identified the primary sources of bias observed in sequence coverage across AT-rich regions of the human genome with existing amplification-free DNA library preparation methods. We have found evidence that a major source of bias is the inefficient processing of AT-rich DNA in end repair and 3′ A-tailing, causing under-representation of extremely AT-rich regions. We have employed immobilized DNA modifying enzymes to catalyze end repair and 3′ A-tailing reactions, to notably reduce the GC bias observed with existing library construction methods.