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  • Mice  (7)
  • Astrophysics  (5)
  • CC 4
  • Lasers and Masers
  • 2010-2014  (13)
  • 2000-2004
  • 2011  (13)
  • 1
    Publication Date: 2011-11-15
    Description: The structure of BPSL1549, a protein of unknown function from Burkholderia pseudomallei, reveals a similarity to Escherichia coli cytotoxic necrotizing factor 1. We found that BPSL1549 acted as a potent cytotoxin against eukaryotic cells and was lethal when administered to mice. Expression levels of bpsl1549 correlate with conditions expected to promote or suppress pathogenicity. BPSL1549 promotes deamidation of glutamine-339 of the translation initiation factor eIF4A, abolishing its helicase activity and inhibiting translation. We propose to name BPSL1549 Burkholderia lethal factor 1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3364511/" 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/PMC3364511/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruz-Migoni, Abimael -- Hautbergue, Guillaume M -- Artymiuk, Peter J -- Baker, Patrick J -- Bokori-Brown, Monika -- Chang, Chung-Te -- Dickman, Mark J -- Essex-Lopresti, Angela -- Harding, Sarah V -- Mahadi, Nor Muhammad -- Marshall, Laura E -- Mobbs, George W -- Mohamed, Rahmah -- Nathan, Sheila -- Ngugi, Sarah A -- Ong, Catherine -- Ooi, Wen Fong -- Partridge, Lynda J -- Phillips, Helen L -- Raih, M Firdaus -- Ruzheinikov, Sergei -- Sarkar-Tyson, Mitali -- Sedelnikova, Svetlana E -- Smither, Sophie J -- Tan, Patrick -- Titball, Richard W -- Wilson, Stuart A -- Rice, David W -- 085162/Wellcome Trust/United Kingdom -- BB/D011795/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/D524975/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E025293/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- WT085162AIA/Wellcome Trust/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2011 Nov 11;334(6057):821-4. doi: 10.1126/science.1211915.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Biotechnology, Krebs Institute, University of Sheffield, Sheffield S10 2TN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22076380" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Bacterial Proteins/*chemistry/genetics/metabolism/*toxicity ; Bacterial Toxins/*chemistry/genetics/metabolism/*toxicity ; Burkholderia pseudomallei/*chemistry/*pathogenicity ; Catalytic Domain ; Cell Line ; Crystallography, X-Ray ; Cytotoxins/chemistry/genetics/metabolism/toxicity ; Escherichia coli Proteins/chemistry ; Eukaryotic Initiation Factor-4A/*antagonists & inhibitors/metabolism ; Glutamine/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Mutant Proteins/toxicity ; Peptide Chain Initiation, Translational/drug effects ; Protein Binding ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2011-04-09
    Description: Cytotoxic T lymphocyte antigen 4 (CTLA-4) is an essential negative regulator of T cell immune responses whose mechanism of action is the subject of debate. CTLA-4 shares two ligands (CD80 and CD86) with a stimulatory receptor, CD28. Here, we show that CTLA-4 can capture its ligands from opposing cells by a process of trans-endocytosis. After removal, these costimulatory ligands are degraded inside CTLA-4-expressing cells, resulting in impaired costimulation via CD28. Acquisition of CD86 from antigen-presenting cells is stimulated by T cell receptor engagement and observed in vitro and in vivo. These data reveal a mechanism of immune regulation in which CTLA-4 acts as an effector molecule to inhibit CD28 costimulation by the cell-extrinsic depletion of ligands, accounting for many of the known features of the CD28-CTLA-4 system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3198051/" 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/PMC3198051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qureshi, Omar S -- Zheng, Yong -- Nakamura, Kyoko -- Attridge, Kesley -- Manzotti, Claire -- Schmidt, Emily M -- Baker, Jennifer -- Jeffery, Louisa E -- Kaur, Satdip -- Briggs, Zoe -- Hou, Tie Z -- Futter, Clare E -- Anderson, Graham -- Walker, Lucy S K -- Sansom, David M -- 17851/Arthritis Research UK/United Kingdom -- BB/D011000/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H013598/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0400931/Medical Research Council/United Kingdom -- G0401620/Medical Research Council/United Kingdom -- G0802382/Medical Research Council/United Kingdom -- G1000213/Medical Research Council/United Kingdom -- G9818340/Medical Research Council/United Kingdom -- Arthritis Research UK/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Apr 29;332(6029):600-3. doi: 10.1126/science.1202947. Epub 2011 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Immune Regulation, School of Immunity and Infection, Institute of Biomedical Research, University of Birmingham Medical School, Birmingham B15 2TT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21474713" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*immunology/metabolism ; Antigens, CD28/*immunology ; Antigens, CD80/*immunology/metabolism ; Antigens, CD86/*immunology/metabolism ; CHO Cells ; CTLA-4 Antigen ; Cricetinae ; Cricetulus ; Dendritic Cells/immunology ; *Endocytosis ; Humans ; Jurkat Cells ; Ligands ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Models, Biological ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; T-Lymphocyte Subsets/*immunology/metabolism ; T-Lymphocytes, Regulatory/immunology/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-11-04
    Description: Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells. Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16(Ink4a), to design a novel transgene, INK-ATTAC, for inducible elimination of p16(Ink4a)-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16(Ink4a)-positive senescent cells upon drug treatment. In tissues--such as adipose tissue, skeletal muscle and eye--in which p16(Ink4a) contributes to the acquisition of age-related pathologies, life-long removal of p16(Ink4a)-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468323/" 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/PMC3468323/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Darren J -- Wijshake, Tobias -- Tchkonia, Tamar -- LeBrasseur, Nathan K -- Childs, Bennett G -- van de Sluis, Bart -- Kirkland, James L -- van Deursen, Jan M -- AG13925/AG/NIA NIH HHS/ -- CA96985/CA/NCI NIH HHS/ -- P30 DK050456/DK/NIDDK NIH HHS/ -- R01 AG013925/AG/NIA NIH HHS/ -- R01 AG013925-14/AG/NIA NIH HHS/ -- R01 CA096985/CA/NCI NIH HHS/ -- R01 CA096985-10/CA/NCI NIH HHS/ -- England -- Nature. 2011 Nov 2;479(7372):232-6. doi: 10.1038/nature10600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22048312" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology/drug effects/pathology ; Aging/drug effects/*physiology ; Animals ; Bone Marrow Cells/cytology/drug effects ; Cell Aging/drug effects/*physiology ; Cell Count ; Cell Cycle Proteins ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/*metabolism ; Eye/cytology/drug effects/pathology ; Female ; Gene Expression ; Genotype ; Longevity/drug effects/physiology ; Male ; Mice ; Mice, Transgenic ; Muscle, Skeletal/cytology/drug effects/pathology ; Phenotype ; Progeria/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Tacrolimus/analogs & derivatives/pharmacology ; Time Factors ; Weaning
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2011-01-29
    Description: Imprinted genes, defined by their preferential expression of a single parental allele, represent a subset of the mammalian genome and often have key roles in embryonic development, but also postnatal functions including energy homeostasis and behaviour. When the two parental alleles are unequally represented within a social group (when there is sex bias in dispersal and/or variance in reproductive success), imprinted genes may evolve to modulate social behaviour, although so far no such instance is known. Predominantly expressed from the maternal allele during embryogenesis, Grb10 encodes an intracellular adaptor protein that can interact with several receptor tyrosine kinases and downstream signalling molecules. Here we demonstrate that within the brain Grb10 is expressed from the paternal allele from fetal life into adulthood and that ablation of this expression engenders increased social dominance specifically among other aspects of social behaviour, a finding supported by the observed increase in allogrooming by paternal Grb10-deficient animals. Grb10 is, therefore, the first example of an imprinted gene that regulates social behaviour. It is also currently alone in exhibiting imprinted expression from each of the parental alleles in a tissue-specific manner, as loss of the peripherally expressed maternal allele leads to significant fetal and placental overgrowth. Thus Grb10 is, so far, a unique imprinted gene, able to influence distinct physiological processes, fetal growth and adult behaviour, owing to actions of the two parental alleles in different tissues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031026/" 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/PMC3031026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garfield, Alastair S -- Cowley, Michael -- Smith, Florentia M -- Moorwood, Kim -- Stewart-Cox, Joanne E -- Gilroy, Kerry -- Baker, Sian -- Xia, Jing -- Dalley, Jeffrey W -- Hurst, Laurence D -- Wilkinson, Lawrence S -- Isles, Anthony R -- Ward, Andrew -- 093875/Wellcome Trust/United Kingdom -- G0300415/Medical Research Council/United Kingdom -- G0300415(66812)/Medical Research Council/United Kingdom -- G11786/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Jan 27;469(7331):534-8. doi: 10.1038/nature09651.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology & Biochemistry and Centre for Regenerative Medicine, University of Bath, Claverton Down, Bath BA2 7AY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21270893" target="_blank"〉PubMed〈/a〉
    Keywords: *Alleles ; Animals ; Behavior, Animal/*physiology ; Central Nervous System/embryology ; Female ; GRB10 Adaptor Protein/*genetics/*metabolism ; Gene Expression Regulation, Developmental ; Genomic Imprinting/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Social Dominance
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2011-07-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Monya -- England -- Nature. 2011 Jul 6;475(7354):123-8. doi: 10.1038/475123a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21734709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics/physiopathology ; Automation ; *Behavior, Animal/physiology ; Cues ; *Disease Models, Animal ; Environment ; Fragile X Syndrome/genetics/physiopathology ; Gene Knockout Techniques ; Grooming/physiology ; Housing, Animal ; Humans ; Informatics/methods ; Mental Disorders/diagnosis/*genetics/*physiopathology ; Mice ; Motor Activity/physiology ; Muscular Atrophy, Spinal/genetics/physiopathology ; Obesity/genetics/physiopathology ; Obsessive-Compulsive Disorder/genetics/physiopathology ; Rats ; Reproducibility of Results ; Rett Syndrome/genetics/physiopathology ; Schizophrenia/genetics/physiopathology ; Video Recording/instrumentation/methods
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Nature Publishing Group (NPG)
    Publication Date: 2011-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baker, Monya -- England -- Nature. 2011 Mar 31;471(7340):661-5. doi: 10.1038/471661a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21455183" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Testing Alternatives/instrumentation/*methods ; Animals ; Bioengineering/instrumentation/*methods ; Biomimetics/instrumentation/*methods ; Cell Culture Techniques/instrumentation/methods ; Drug Evaluation, Preclinical/instrumentation/methods ; Humans ; *Lab-On-A-Chip Devices ; Liver/drug effects/pathology/physiology/physiopathology ; Lung/blood supply/cytology/drug effects/immunology/physiology ; Mice ; Models, Animal ; *Models, Biological ; Nanotechnology/instrumentation/methods ; *Organ Specificity ; Reproducibility of Results ; Silicon/chemistry
    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: 2011-04-30
    Description: Stem cells cycle through active and quiescent states. Large populations of stem cells in an organ may cycle randomly or in a coordinated manner. Although stem cell cycling within single hair follicles has been studied, less is known about regenerative behavior in a hair follicle population. By combining predictive mathematical modeling with in vivo studies in mice and rabbits, we show that a follicle progresses through cycling stages by continuous integration of inputs from intrinsic follicular and extrinsic environmental signals based on universal patterning principles. Signaling from the WNT/bone morphogenetic protein activator/inhibitor pair is coopted to mediate interactions among follicles in the population. This regenerative strategy is robust and versatile because relative activator/inhibitor strengths can be modulated easily, adapting the organism to different physiological and evolutionary needs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321266/" 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/PMC3321266/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plikus, Maksim V -- Baker, Ruth E -- Chen, Chih-Chiang -- Fare, Clyde -- de la Cruz, Damon -- Andl, Thomas -- Maini, Philip K -- Millar, Sarah E -- Widelitz, Randall -- Chuong, Cheng-Ming -- AR47364/AR/NIAMS NIH HHS/ -- AR60306/AR/NIAMS NIH HHS/ -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR042177-17/AR/NIAMS NIH HHS/ -- R01 AR042177-18/AR/NIAMS NIH HHS/ -- R01 AR060306/AR/NIAMS NIH HHS/ -- R01 AR060306-02/AR/NIAMS NIH HHS/ -- R01 AR060306-03/AR/NIAMS NIH HHS/ -- R01-AR42177/AR/NIAMS NIH HHS/ -- R01-AR47709/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 29;332(6029):586-9. doi: 10.1126/science.1201647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Southern California (USC), Los Angeles, CA 90033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21527712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/*metabolism ; Computer Simulation ; Hair Follicle/*cytology/*growth & development/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Biological ; Rabbits ; *Regeneration ; *Signal Transduction ; Stem Cells/*physiology ; Stochastic Processes ; Wnt Proteins/*metabolism
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2019-07-12
    Description: Context. Transient neutrino sources such as Gamma-Ray Bursts (GRBs) and Supernovae (SNe) are hypothesized to emit bursts of high-energy neutrinos on a time-scale of 〈 or approx.100 s. While GRB neutrinos would be produced in high relativistic jets, core-collapse SNe might host soft-relativistic jets, which become stalled in the outer layers of the progenitor star leading to an efficient production of high-energy neutrinos. Aims. To increase the sensitivity to these neutrinos and identify their sources, a low-threshold optical follow-up program for neutrino multiplets detected with the IceCube observatory has been implemented. Methods. If a neutrino multiplet, i.e. two or more neutrinos from the same direction within 100 s, is found by IceCube a trigger is sent to the Robotic Optical Transient Search Experiment, ROTSE. The 4 ROTSE telescopes immediately start an observation program of the corresponding region of the sky in order to detect an optical counterpart to the neutrino events. Results. No statistically significant excess in the rate of neutrino multiplets has been observed and furthermore no coincidence with an optical counterpart was found. Conclusions. The search allows, for the first time, to set stringent limits on current models predicting a high-energy neutrino flux from soft relativistic hadronic jets in core-collapse SNe. We conclude that a sub-population of SNe with typical Lorentz boost factor and jet energy of 10 and 3 x 10(exp 51) erg, respectively, does not exceed 4:2% at 90% confidence.
    Keywords: Astrophysics
    Type: GSFC.JA.5925.2012
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  • 9
    Publication Date: 2019-07-19
    Description: Gravitational wave observations provide exceptional and unique opportunities for precision tests of gravitational physics, as predicted by general relativity (GR). Space-based gravitational wave measurements, with high signal-to-noise ratios and large numbers of observed events may provide the best-suited gravitational-wave observations for testing GR with unprecedented precision. These observations will be especially useful in testing the properties of gravitational waves and strong-field aspects of the theory which are less relevant in other observations. We review the proposed GR test based on observations of massive black hole mergers, extreme mass ratio inspirals, and galactic binary systems.
    Keywords: Astrophysics
    Type: GSFC.ABS.5948.2012 , Workshop for Gravitational-Wave Mission Architectural Concepts/Maritime Institute; Dec 20, 2011 - Dec 21, 2011; Linthicum, MD; United States
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  • 10
    Publication Date: 2019-07-12
    Description: Recent observations of GeV /TeV photon emission from several X-ray binaries have sparked a renewed interest in these objects as galactic particle accelerators. In spite of the available multi-wavelength data, their acceleration mechanisms are not determined, and the nature of the accelerated particles (hadrons or leptons) is unknown. While much evidence favors leptonic emission, it is very likely that a hadronic component is also accelerated in the jets of these binary systems. The observation of neutrino emission would be clear evidence for the presence of a hadronic component in the outflow of these sources. In this paper we look for periodic neutrino emission from binary systems. Such modulation, observed in the photon flux, would be caused by the geometry of these systems. The results of two searches are presented that differ in the treatment of the spectral shape and phase of the emission. The 'generic' search allows parameters to vary freely and best fit values, in a 'model-dependent' search, predictions are used to constrain these parameters. We use the IceCube data taken from May 31, 2007 to April 5, 2008 with its 22-string configuration, and from April 5, 2008 and May 20, 2009 with its 40-string configuration. For the generic search and the 40 string sample, we find that the most significant source in the catalog of 7 binary stars is Cygnus X-3 with a 1.8% probability after trials (2.10" sigma one-sided) of being produced by statistical fluctuations of the background. The model-dependent method tested a range of system geometries - the inclination and the massive star's disk size - for LS I+61 deg 303, no significant excess was found.
    Keywords: Astrophysics
    Type: GSFC.JA.5866.2012
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