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  • 1
    Publication Date: 2018-08-02
    Description: Titanium (Ti) is an ideal bone substitute due to its superior bio-compatibility and remarkable corrosion resistance. However, in order to improve the osteoconduction and osteoinduction capacities in clinical applications, different kinds of surface modifications are typically applied to Ti alloys. In this study, we fabricated a tightly attached polydopamine-assisted Fe 3 O 4 nanoparticle coating on Ti with magnetic properties, aiming to improve the osteogenesis of the Ti substrates. The PDA-assisted Fe 3 O 4 nanoparticle coatings were characterized by scanning electron microscopy, energy dispersive spectroscopy, atomic force microscopy and water contact angle measurements. The cell attachment and proliferation rate of the human bone mesenchymal stem cells (hBMSCs) on the Ti surface significantly improved with the Fe 3 O 4 /PDA coating when compared with the pure Ti without a coating. Furthermore, the results of in vitro alkaline phosphatase (ALP) activity at 7 and 14 days and alizarin red S staining at 14 days showed that the Fe 3 O 4 /PDA coating on Ti promoted the osteogenic differentiation of hBMSCs. Moreover, hBMSCs co-cultured with the Fe 3 O 4 /PDA-coated Ti for approximately 14 days also exhibited a significantly higher mRNA expression level of ALP, osteocalcin and runt-related transcription factor-2 (RUNX2). Our in vitro results revealed that the present PDA-assisted Fe 3 O 4 nanoparticle surface coating is an innovative method for Ti surface modification and shows great potential for clinical applications.
    Keywords: materials science, biomaterials, cellular biology
    Electronic ISSN: 2054-5703
    Topics: Natural Sciences in General
    Published by Royal Society
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  • 2
    Publication Date: 2018-09-04
    Description: Metabolic programs are crucial for regulatory T (T reg) cell stability and function, but the underlying mechanisms that regulate T reg cell metabolism are elusive. Here, we report that lysosomal TRAF3IP3 acts as a pivotal regulator in the maintenance of T reg cell metabolic fitness. T reg–specific deletion of Traf3ip3 impairs T reg cell function, causing the development of inflammatory disorders and stronger antitumor T cell responses in mice. Excessive mechanistic target of rapamycin complex 1 (mTORC1)–mediated hyper-glycolytic metabolism is responsible for the instability of TRAF3IP3-deficient T reg cells. Mechanistically, TRAF3IP3 restricts mTORC1 signaling by recruiting the serine-threonine phosphatase catalytic subunit (PP2Ac) to the lysosome, thereby facilitating the interaction of PP2Ac with the mTORC1 component Raptor. Our results define TRAF3IP3 as a metabolic regulator in T reg cell stability and function and suggest a lysosome-specific mTORC1 signaling mechanism that regulates T reg cell metabolism.
    Keywords: Tumor Immunology, Tolerance
    Print ISSN: 0022-1007
    Electronic ISSN: 1540-9538
    Topics: Medicine
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  • 3
    Publication Date: 2018-10-16
    Description: Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels were reported to express in the well-known vasomotor region, rostral ventrolateral medulla (RVLM), and can be inhibited by propofol. However, whether HCN channels in RVLM contribute to propofol-induced cardiovascular depression remains unclear. We recorded the hemodynamic changes when either continuous intravenous infusions or microinjections of propofol and ZD-7288 (4-ethylphenylamino-1,2-dimethyl-6-methylaminopyrimidinium chloride; HCN channel blocker) in RVLM. Expressions of HCN channels in RVLM neurons of mice of different ages were examined by quantitative real-time polymerase chain reaction and Western blotting. The effects of propofol and ZD-7288 on HCN channels and the excitability of RVLM neurons were examined by electrophysiological recording. Propofol (1.25, 2.5, 5, and 7.5 mg/kg per minute, i.v., 10 minutes) decreased mean arterial pressure (MAP) and heart rate (HR) in a concentration-dependent manner in wild-type mice that were markedly attenuated in HCN1 knockout mice. Bilateral microinjection of propofol (1%, 0.1 μ l) in RVLM caused a sharp and pronounced drop in MAP and HR values, which were abated by pretreatment with ZD-7288. In electrophysiological recording, propofol (5, 10, and 20 μ M) concentration-dependently inhibited HCN current, increased input resistance, decreased firing rate, and caused membrane hyperpolarization in RVLM neurons. These actions of propofol were attenuated by ZD-7288 pretreatment. The mRNA and protein level of HCN channels increased in an age-dependent manner, which may contribute to the age-dependent increase in the sensitivity to propofol. Our results indicated that the inhibition of HCN channels in RVLM neurons may contribute to propofol-induced cardiovascular inhibition.
    Print ISSN: 0026-895X
    Electronic ISSN: 1521-0111
    Topics: Chemistry and Pharmacology , Medicine
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  • 4
    Publication Date: 2018-11-06
    Description: Evidence for Weyl fermions in a canonical heavy-fermion semimetal YbPtBi Evidence for Weyl fermions in a canonical heavy-fermion semimetal YbPtBi, Published online: 05 November 2018; doi:10.1038/s41467-018-06782-1 Weyl fermions are evidenced in weakly correlated electron systems, but whether they survive strong electron correlations remains obscure. Here, Guo et al. report evidence of the chiral anomaly, topological Hall effect and a cubic temperature dependence of specific heat, suggesting existence of Weyl fermions in a heavy fermion semimetal YbPtBi.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2018-06-02
    Description: UDP-glucuronosyltransferases (UGTs) play an important role in the metabolism and detoxification of amine-containing chemicals; however, the disposition mechanisms for amines via UGT metabolism are not fully clear. We aimed to investigate a potential role of UGT2B10 in N-glucosidation and to determine the transporters for the excretion of N-glucosides. We first established a human embryonic kidney cell line 293 (HEK293) that stably overexpressed UGT2B10. Incubation of mianserin or cyclizine with the cells generated one N-glucuronide and one N-glucoside. Chemical inhibition (using specific chemical inhibitor Ko143) and biologic inhibition [using specific short hairpin RNA of breast cancer resistance protein (BCRP)] resulted in a significant reduction in efflux of N-glucuronide. Similar results were observed when multidrug resistance–associated protein (MRP4) was inhibited. Furthermore, inhibition of BCRP led to increased intracellular N-glucoside, whereas inhibition of MRP4 caused no changes in disposition of N-glucoside. Overall, the data indicated that BCRP, not MRP4, was responsible for the excretion of N-glucosides, whereas both BCRP and MRP4 contributed to excretion of N-glucuronides. Interestingly, downregulation of N-glucuronidation led to increased N-glucosidation in the cells, supporting the glucosidation as a potential complementary pathway for conventional glucuronidation. In conclusion, UGT2B10 was for the first time identified as an N-glucosidation enzyme. Generated N-glucosides were excreted primarily by the BCRP transporter.
    Print ISSN: 0090-9556
    Electronic ISSN: 1521-009X
    Topics: Chemistry and Pharmacology , Medicine
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  • 6
    Publication Date: 2012-05-25
    Description: Human apolipoprotein E has three isoforms: APOE2, APOE3 and APOE4. APOE4 is a major genetic risk factor for Alzheimer's disease and is associated with Down's syndrome dementia and poor neurological outcome after traumatic brain injury and haemorrhage. Neurovascular dysfunction is present in normal APOE4 carriers and individuals with APOE4-associated disorders. In mice, lack of Apoe leads to blood-brain barrier (BBB) breakdown, whereas APOE4 increases BBB susceptibility to injury. How APOE genotype affects brain microcirculation remains elusive. Using different APOE transgenic mice, including mice with ablation and/or inhibition of cyclophilin A (CypA), here we show that expression of APOE4 and lack of murine Apoe, but not APOE2 and APOE3, leads to BBB breakdown by activating a proinflammatory CypA-nuclear factor-kappaB-matrix-metalloproteinase-9 pathway in pericytes. This, in turn, leads to neuronal uptake of multiple blood-derived neurotoxic proteins, and microvascular and cerebral blood flow reductions. We show that the vascular defects in Apoe-deficient and APOE4-expressing mice precede neuronal dysfunction and can initiate neurodegenerative changes. Astrocyte-secreted APOE3, but not APOE4, suppressed the CypA-nuclear factor-kappaB-matrix-metalloproteinase-9 pathway in pericytes through a lipoprotein receptor. Our data suggest that CypA is a key target for treating APOE4-mediated neurovascular injury and the resulting neuronal dysfunction and degeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047116/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047116/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, Robert D -- Winkler, Ethan A -- Singh, Itender -- Sagare, Abhay P -- Deane, Rashid -- Wu, Zhenhua -- Holtzman, David M -- Betsholtz, Christer -- Armulik, Annika -- Sallstrom, Jan -- Berk, Bradford C -- Zlokovic, Berislav V -- R01 AG039452/AG/NIA NIH HHS/ -- R01 NS034467/NS/NINDS NIH HHS/ -- R01AG039452/AG/NIA NIH HHS/ -- R37 AG013956/AG/NIA NIH HHS/ -- R37 AG023084/AG/NIA NIH HHS/ -- R37 NS034467/NS/NINDS NIH HHS/ -- R37AG13956/AG/NIA NIH HHS/ -- R37AG23084/AG/NIA NIH HHS/ -- R37NS34467/NS/NINDS NIH HHS/ -- England -- Nature. 2012 May 16;485(7399):512-6. doi: 10.1038/nature11087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center, Rochester, New York 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22622580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein E2/deficiency/genetics/metabolism ; Apolipoprotein E3/deficiency/genetics/metabolism ; Apolipoprotein E4/deficiency/genetics/metabolism ; Apolipoproteins E/deficiency/genetics/*metabolism ; Blood-Brain Barrier/drug effects/*physiology/physiopathology ; Cerebrovascular Circulation/*physiology ; Cyclophilin A/antagonists & inhibitors/deficiency/*metabolism ; Hippocampus/metabolism/pathology ; Humans ; Matrix Metalloproteinase 9/metabolism ; Mice ; Mice, Transgenic ; Microcirculation ; NF-kappa B/metabolism ; Neurodegenerative Diseases/metabolism/pathology ; Neurons/metabolism/pathology ; Pericytes/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2013-10-25
    Description: Mutations in SHANK3 and large duplications of the region spanning SHANK3 both cause a spectrum of neuropsychiatric disorders, indicating that proper SHANK3 dosage is critical for normal brain function. However, SHANK3 overexpression per se has not been established as a cause of human disorders because 22q13 duplications involve several genes. Here we report that Shank3 transgenic mice modelling a human SHANK3 duplication exhibit manic-like behaviour and seizures consistent with synaptic excitatory/inhibitory imbalance. We also identified two patients with hyperkinetic disorders carrying the smallest SHANK3-spanning duplications reported so far. These findings indicate that SHANK3 overexpression causes a hyperkinetic neuropsychiatric disorder. To probe the mechanism underlying the phenotype, we generated a Shank3 in vivo interactome and found that Shank3 directly interacts with the Arp2/3 complex to increase F-actin levels in Shank3 transgenic mice. The mood-stabilizing drug valproate, but not lithium, rescues the manic-like behaviour of Shank3 transgenic mice raising the possibility that this hyperkinetic disorder has a unique pharmacogenetic profile.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923348/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923348/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Kihoon -- Holder, J Lloyd Jr -- Schaaf, Christian P -- Lu, Hui -- Chen, Hongmei -- Kang, Hyojin -- Tang, Jianrong -- Wu, Zhenyu -- Hao, Shuang -- Cheung, Sau Wai -- Yu, Peng -- Sun, Hao -- Breman, Amy M -- Patel, Ankita -- Lu, Hui-Chen -- Zoghbi, Huda Y -- 1R01NS070302/NS/NINDS NIH HHS/ -- 2T32NS043124/NS/NINDS NIH HHS/ -- P30HD024064/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Nov 7;503(7474):72-7. doi: 10.1038/nature12630. Epub 2013 Oct 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA [2] Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA [3] Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24153177" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/metabolism ; Actins/metabolism ; Adult ; Animals ; Behavior, Animal ; Bipolar Disorder/*drug therapy/genetics/*physiopathology ; Chromosomes, Human, Pair 22/genetics ; Disease Models, Animal ; Excitatory Postsynaptic Potentials ; Female ; Gene Dosage/genetics ; Gene Expression/genetics ; Genes, Duplicate/genetics ; Humans ; Hyperkinesis/genetics/physiopathology ; Inhibitory Postsynaptic Potentials ; Lithium/pharmacology ; Male ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/*genetics/*metabolism ; Seizures/genetics ; Valproic Acid/pharmacology/therapeutic use
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2014-03-29
    Description: Oesophageal cancer is one of the most aggressive cancers and is the sixth leading cause of cancer death worldwide. Approximately 70% of global oesophageal cancer cases occur in China, with oesophageal squamous cell carcinoma (ESCC) being the histopathological form in the vast majority of cases (〉90%). Currently, there are limited clinical approaches for the early diagnosis and treatment of ESCC, resulting in a 10% five-year survival rate for patients. However, the full repertoire of genomic events leading to the pathogenesis of ESCC remains unclear. Here we describe a comprehensive genomic analysis of 158 ESCC cases, as part of the International Cancer Genome Consortium research project. We conducted whole-genome sequencing in 17 ESCC cases and whole-exome sequencing in 71 cases, of which 53 cases, plus an additional 70 ESCC cases not used in the whole-genome and whole-exome sequencing, were subjected to array comparative genomic hybridization analysis. We identified eight significantly mutated genes, of which six are well known tumour-associated genes (TP53, RB1, CDKN2A, PIK3CA, NOTCH1, NFE2L2), and two have not previously been described in ESCC (ADAM29 and FAM135B). Notably, FAM135B is identified as a novel cancer-implicated gene as assayed for its ability to promote malignancy of ESCC cells. Additionally, MIR548K, a microRNA encoded in the amplified 11q13.3-13.4 region, is characterized as a novel oncogene, and functional assays demonstrate that MIR548K enhances malignant phenotypes of ESCC cells. Moreover, we have found that several important histone regulator genes (MLL2 (also called KMT2D), ASH1L, MLL3 (KMT2C), SETD1B, CREBBP and EP300) are frequently altered in ESCC. Pathway assessment reveals that somatic aberrations are mainly involved in the Wnt, cell cycle and Notch pathways. Genomic analyses suggest that ESCC and head and neck squamous cell carcinoma share some common pathogenic mechanisms, and ESCC development is associated with alcohol drinking. This study has explored novel biological markers and tumorigenic pathways that would greatly improve therapeutic strategies for ESCC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, Yongmei -- Li, Lin -- Ou, Yunwei -- Gao, Zhibo -- Li, Enmin -- Li, Xiangchun -- Zhang, Weimin -- Wang, Jiaqian -- Xu, Liyan -- Zhou, Yong -- Ma, Xiaojuan -- Liu, Lingyan -- Zhao, Zitong -- Huang, Xuanlin -- Fan, Jing -- Dong, Lijia -- Chen, Gang -- Ma, Liying -- Yang, Jie -- Chen, Longyun -- He, Minghui -- Li, Miao -- Zhuang, Xuehan -- Huang, Kai -- Qiu, Kunlong -- Yin, Guangliang -- Guo, Guangwu -- Feng, Qiang -- Chen, Peishan -- Wu, Zhiyong -- Wu, Jianyi -- Ma, Ling -- Zhao, Jinyang -- Luo, Longhai -- Fu, Ming -- Xu, Bainan -- Chen, Bo -- Li, Yingrui -- Tong, Tong -- Wang, Mingrong -- Liu, Zhihua -- Lin, Dongxin -- Zhang, Xiuqing -- Yang, Huanming -- Wang, Jun -- Zhan, Qimin -- England -- Nature. 2014 May 1;509(7498):91-5. doi: 10.1038/nature13176. Epub 2014 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China [2]. ; 1] BGI-Shenzhen, Shenzhen 518083, Guangdong 518083, China [2]. ; 1] State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China [2] Department of Neurosurgery, Chinese PLA General Hospital, Beijing 100853, China [3]. ; 1] Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong, China [2]. ; State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China. ; BGI-Shenzhen, Shenzhen 518083, Guangdong 518083, China. ; Institute of Oncologic Pathology, Shantou University Medical College, Shantou 515041, Guangdong, China. ; Department of Tumor Surgery, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-sen University, Shantou 515041, Guangdong, China. ; Department of Biochemistry and Molecular Biology, The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou 515041, Guangdong, China. ; Department of Neurosurgery, Chinese PLA General Hospital, Beijing 100853, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670651" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Drinking/adverse effects ; Biomarkers, Tumor/genetics ; Carcinoma, Squamous Cell/*genetics/pathology ; Cell Cycle/genetics ; Chromosomes, Human, Pair 11/genetics ; Comparative Genomic Hybridization ; DNA Copy Number Variations/genetics ; Esophageal Neoplasms/*genetics/pathology ; Exome/genetics ; Female ; Genome, Human/*genetics ; Genomics ; Histones/metabolism ; Humans ; Male ; MicroRNAs/genetics ; Mutation/*genetics ; Oncogenes/genetics ; Phenotype ; Receptors, Notch/genetics ; Risk Factors ; Wnt Signaling Pathway/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2014-05-16
    Description: Mice display robust, stereotyped behaviours towards pups: virgin males typically attack pups, whereas virgin females and sexually experienced males and females display parental care. Here we show that virgin males genetically impaired in vomeronasal sensing do not attack pups and are parental. Furthermore, we uncover a subset of galanin-expressing neurons in the medial preoptic area (MPOA) that are specifically activated during male and female parenting, and a different subpopulation that is activated during mating. Genetic ablation of MPOA galanin neurons results in marked impairment of parental responses in males and females and affects male mating. Optogenetic activation of these neurons in virgin males suppresses inter-male and pup-directed aggression and induces pup grooming. Thus, MPOA galanin neurons emerge as an essential regulatory node of male and female parenting behaviour and other social responses. These results provide an entry point to a circuit-level dissection of parental behaviour and its modulation by social experience.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105201/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4105201/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Zheng -- Autry, Anita E -- Bergan, Joseph F -- Watabe-Uchida, Mitsuko -- Dulac, Catherine G -- F32 DC010089/DC/NIDCD NIH HHS/ -- R01 DC003903/DC/NIDCD NIH HHS/ -- R01 DC009019/DC/NIDCD NIH HHS/ -- R01 DC013087/DC/NIDCD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 May 15;509(7500):325-30. doi: 10.1038/nature13307.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138, USA. ; Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24828191" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/physiology ; Animals ; Copulation ; Female ; Galanin/deficiency/genetics/*metabolism ; Grooming/physiology ; Male ; Maternal Behavior/*physiology ; Mice ; Neurons/*metabolism ; Optogenetics ; Paternal Behavior/*physiology ; Pheromones/analysis ; Preoptic Area/*cytology/metabolism ; TRPC Cation Channels/deficiency/genetics ; Vomeronasal Organ/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2014-11-07
    Description: High-efficiency acceleration of charged particle beams at high gradients of energy gain per unit length is necessary to achieve an affordable and compact high-energy collider. The plasma wakefield accelerator is one concept being developed for this purpose. In plasma wakefield acceleration, a charge-density wake with high accelerating fields is driven by the passage of an ultra-relativistic bunch of charged particles (the drive bunch) through a plasma. If a second bunch of relativistic electrons (the trailing bunch) with sufficient charge follows in the wake of the drive bunch at an appropriate distance, it can be efficiently accelerated to high energy. Previous experiments using just a single 42-gigaelectronvolt drive bunch have accelerated electrons with a continuous energy spectrum and a maximum energy of up to 85 gigaelectronvolts from the tail of the same bunch in less than a metre of plasma. However, the total charge of these accelerated electrons was insufficient to extract a substantial amount of energy from the wake. Here we report high-efficiency acceleration of a discrete trailing bunch of electrons that contains sufficient charge to extract a substantial amount of energy from the high-gradient, nonlinear plasma wakefield accelerator. Specifically, we show the acceleration of about 74 picocoulombs of charge contained in the core of the trailing bunch in an accelerating gradient of about 4.4 gigavolts per metre. These core particles gain about 1.6 gigaelectronvolts of energy per particle, with a final energy spread as low as 0.7 per cent (2.0 per cent on average), and an energy-transfer efficiency from the wake to the bunch that can exceed 30 per cent (17.7 per cent on average). This acceleration of a distinct bunch of electrons containing a substantial charge and having a small energy spread with both a high accelerating gradient and a high energy-transfer efficiency represents a milestone in the development of plasma wakefield acceleration into a compact and affordable accelerator technology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Litos, M -- Adli, E -- An, W -- Clarke, C I -- Clayton, C E -- Corde, S -- Delahaye, J P -- England, R J -- Fisher, A S -- Frederico, J -- Gessner, S -- Green, S Z -- Hogan, M J -- Joshi, C -- Lu, W -- Marsh, K A -- Mori, W B -- Muggli, P -- Vafaei-Najafabadi, N -- Walz, D -- White, G -- Wu, Z -- Yakimenko, V -- Yocky, G -- England -- Nature. 2014 Nov 6;515(7525):92-5. doi: 10.1038/nature13882.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉SLAC National Accelerator Laboratory, Menlo Park, California 94025, USA. ; 1] SLAC National Accelerator Laboratory, Menlo Park, California 94025, USA [2] Department of Physics, University of Oslo, 0316 Oslo, Norway. ; Department of Physics and Astronomy, University of California Los Angeles, Los Angeles, California 90095, USA. ; Department of Electrical Engineering, University of California Los Angeles, Los Angeles, California 90095, USA. ; Department of Engineering Physics, Tsinghua University, Beijing 100084, China. ; Max Planck Institute for Physics, Munich 80805, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25373678" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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