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  • 1
    Electronic Resource
    Electronic Resource
    The ground state mass of147Gd from single-neutron-transfer reactions and its impact on derived mass values (1986)
    Springer
    The European physical journal 324 (1986), S. 27-34 
    Details
    ISSN: 1434-601X
    Keywords: 21.10.Dr ; 21.60.Cs ; 27.60.+j
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Using a148Gd radioactive target and the (p,d), (d,t), and (3He,α) single neutron pick-up reactions we have measured the147Gd mass excess as — 75,366(4) keV, which differs by 139(24) keV from the adopted value of the 1983 mass table. From this result, and from recently reported first transfer-reaction mass determinations for145Eu and146Eu, we have recalculated the masses of nuclei above146Gd from a previous shell model analysis of high-spin states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01290751
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  • 2
    Electronic Resource
    Electronic Resource
    Two-nucleon excitations in 66 148 Dy82 from Gamow-Teller decay of the 67 148 Ho81 6− isomer (1989)
    Springer
    The European physical journal 333 (1989), S. 29-38 
    Details
    ISSN: 1434-601X
    Keywords: 23.40.Hc ; 21.60.Cs ; 27.60.+j
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Two-particle excitations in the two-proton nucleus148Dy populated inβ-decay of 10-s 148Ho(6−) were investigated throughγ-ray measurements following on-line mass separation. Theπh 11/2s1/2 two-proton doublet and the (vh 9/2 s 1 2/−1 )5− neutron particle hole configuration are firmly identified, and theπh 11/2 d 5 2/−1 and πh11/2D3/2 multiplets are also observed. The results suggest dominantπh 11/2vs 1 2/−1 character for the148Ho 6−-isomer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01290107
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  • 3
    Electronic Resource
    Electronic Resource
    Collective excitations in148Gd populated in thep p′-reaction on a radioactive target (1990)
    Springer
    The European physical journal 336 (1990), S. 375-380 
    Details
    ISSN: 1434-601X
    Keywords: 21.60.-n ; 25.40.Ep ; 27.60.+j
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Collective excitations in the two-particle nucleus148Gd up to 2.9 MeV have been investigated by thepp′-reaction at 25 MeV beam energy, and angular distributions have been analyzed with standard DWBA calculations. It is found that148Gd has larger octupole- than quadrupole collectivity in the energy range investigated. The 3− strength distribution is in quantitative agreement with predicted results for the levels formed by the coupling of two valence particles to the146Gd core octupole phonon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01294110
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  • 4
    Electronic Resource
    Electronic Resource
    Beta-decay of 27/2− isomers inN=83 nuclei (1988)
    Springer
    The European physical journal 329 (1988), S. 11-20 
    Details
    ISSN: 1434-601X
    Keywords: 21.10.−k ; 27.60.+j ; 27.70.+q
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract In theN=83 nucleus151Er we observed the isomericE3 transition in conversion electron measurements following on-line mass separation and located its 0.6 s 27/2− isomer at 2.586 MeV. Gamma-ray data establish a 4.7(3)% Gamow-Tellerβ-decay branch proceeding to high-spin states above 2 MeV excitation in151Ho. A weakβ-decay branch of 0.7(3)% was also observed for the 0.5 s 27/2− isomer in the149Dy isotone, and it was established that a similar 27/2− E3-isomer does not occur in153Yb. First results on the151Tm and151Er ground-stateβ-decays are briefly discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01294811
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  • 5
    Electronic Resource
    Electronic Resource
    Three-nucleon yrast states in145Sm (1991)
    Springer
    The European physical journal 338 (1991), S. 417-421 
    Details
    ISSN: 1434-601X
    Keywords: 27.60.+j ; 21.60.Cs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract In-beamγ-ray and conversion electron measurements with (α, xn) reactions have established the145Sm highspin states up toI π=25/2+ at 3.5 MeV excitation. A shell model analysis using empirical two- and one-body energies from neighbouring nuclei classifies the low-lying odd-parity levels as 3-quasiparticle states formed by the144Sm two-proton-hole excitations and thef 7/2 valence neutron. The higher-lying positive-parity states involve particle-hole core excitations with one proton inh 11/2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01295769
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  • 6
    Electronic Resource
    Electronic Resource
    Beta-decay energy and atomic mass of148Tb (1995)
    Springer
    The European physical journal 352 (1995), S. 1-2 
    Details
    ISSN: 1434-601X
    Keywords: 21.10.Dr ; 27.60.+j
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract The Q EC values of the $${}^{148}Tb_{2^ - } $$ ground-state and the $${}^{148}Tb_{9^ + } $$ isomer were measured to the 5750(40) keV and 5846(50) keV, respectively, corresponding to a148Tb ground-state mass-excess of ⦓70527(30) keV. The impact on mass calculations near146Gd is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01292750
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  • 7
    Electronic Resource
    Electronic Resource
    Particle-hole multiplets in146Gd from in-beam studies of non-yrast levels (1986)
    Springer
    The European physical journal 324 (1986), S. 417-432 
    Details
    ISSN: 1434-601X
    Keywords: 21.30+y ; 21.60.Cs ; 27.60.+j
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract Non-yrast levels of146Gd have been investigated by in-beamγ-ray and conversion electron spectroscopy following the144Sm(α, 2n) reaction at 25.7 MeV, an energy which was determined to provide optimum population of levels above the yrast line. The detailed146Gd level scheme includes twenty-one newly identified levels, many of which can be characterized in terms of specific proton particle-hole configurations. Several twoparticle-twohole states involving the 3− phonon have also been identified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01290925
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  • 8
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    Notch and EGFR pathway interaction regulates neural stem cell number and self-renewal (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-09-17
    Description: Specialized cellular microenvironments, or 'niches', modulate stem cell properties, including cell number, self-renewal and fate decisions. In the adult brain, niches that maintain a source of neural stem cells (NSCs) and neural progenitor cells (NPCs) are the subventricular zone (SVZ) of the lateral ventricle and the dentate gyrus of the hippocampus. The size of the NSC population of the SVZ at any time is the result of several ongoing processes, including self-renewal, cell differentiation, and cell death. Maintaining the balance between NSCs and NPCs in the SVZ niche is critical to supply the brain with specific neural populations, both under normal conditions or after injury. A fundamental question relevant to both normal development and to cell-based repair strategies in the central nervous system is how the balance of different NSC and NPC populations is maintained in the niche. EGFR (epidermal growth factor receptor) and Notch signalling pathways have fundamental roles during development of multicellular organisms. In Drosophila and in Caenorhabditis elegans these pathways may have either cooperative or antagonistic functions. In the SVZ, Notch regulates NSC identity and self-renewal, whereas EGFR specifically affects NPC proliferation and migration. This suggests that interplay of these two pathways may maintain the balance between NSC and NPC numbers. Here we show that functional cell-cell interaction between NPCs and NSCs through EGFR and Notch signalling has a crucial role in maintaining the balance between these cell populations in the SVZ. Enhanced EGFR signalling in vivo results in the expansion of the NPC pool, and reduces NSC number and self-renewal. This occurs through a non-cell-autonomous mechanism involving EGFR-mediated regulation of Notch signalling. Our findings define a novel interaction between EGFR and Notch pathways in the adult SVZ, and thus provide a mechanism for NSC and NPC pool maintenance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941915/" 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/PMC2941915/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aguirre, Adan -- Rubio, Maria E -- Gallo, Vittorio -- K99NS057944/NS/NINDS NIH HHS/ -- P30HD40677/HD/NICHD NIH HHS/ -- R00 NS057944/NS/NINDS NIH HHS/ -- R01 DC006881/DC/NIDCD NIH HHS/ -- R01 DC006881-03/DC/NIDCD NIH HHS/ -- R01 DC006881-04/DC/NIDCD NIH HHS/ -- R01DC006881/DC/NIDCD NIH HHS/ -- R01NS045702/NS/NINDS NIH HHS/ -- R01NS056427/NS/NINDS NIH HHS/ -- R0O NS057944-03/NS/NINDS NIH HHS/ -- England -- Nature. 2010 Sep 16;467(7313):323-7. doi: 10.1038/nature09347.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuroscience Research, Children's National Medical Center, Washington, District of Columbia 20010, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20844536" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Division ; Humans ; Membrane Proteins/deficiency/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/deficiency/genetics/metabolism ; Neurons/*cytology ; Protein Binding ; Receptor, Epidermal Growth Factor/genetics/*metabolism ; Receptor, Notch1/metabolism ; Receptors, Notch/*metabolism ; *Signal Transduction ; Stem Cell Niche/cytology ; Stem Cells/*cytology ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    BRCA2 prevents R-loop accumulation and associates with TREX-2 mRNA export factor PCID2 (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-06-05
    Description: Genome instability is central to ageing, cancer and other diseases. It is not only proteins involved in DNA replication or the DNA damage response (DDR) that are important for maintaining genome integrity: from yeast to higher eukaryotes, mutations in genes involved in pre-mRNA splicing and in the biogenesis and export of messenger ribonucleoprotein (mRNP) also induce DNA damage and genome instability. This instability is frequently mediated by R-loops formed by DNA-RNA hybrids and a displaced single-stranded DNA. Here we show that the human TREX-2 complex, which is involved in mRNP biogenesis and export, prevents genome instability as determined by the accumulation of gamma-H2AX (Ser-139 phosphorylated histone H2AX) and 53BP1 foci and single-cell electrophoresis in cells depleted of the TREX-2 subunits PCID2, GANP and DSS1. We show that the BRCA2 repair factor, which binds to DSS1, also associates with PCID2 in the cell. The use of an enhanced green fluorescent protein-tagged hybrid-binding domain of RNase H1 and the S9.6 antibody did not detect R-loops in TREX-2-depleted cells, but did detect the accumulation of R-loops in BRCA2-depleted cells. The results indicate that R-loops are frequently formed in cells and that BRCA2 is required for their processing. This link between BRCA2 and RNA-mediated genome instability indicates that R-loops may be a chief source of replication stress and cancer-associated instability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhatia, Vaibhav -- Barroso, Sonia I -- Garcia-Rubio, Maria L -- Tumini, Emanuela -- Herrera-Moyano, Emilia -- Aguilera, Andres -- England -- Nature. 2014 Jul 17;511(7509):362-5. doi: 10.1038/nature13374. Epub 2014 Jun 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro Andaluz de Biologia Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Avenida Americo Vespucio s/n, 41092 Seville, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24896180" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/metabolism ; BRCA2 Protein/deficiency/genetics/*metabolism ; DNA Damage ; DNA Replication ; DNA, Single-Stranded/chemistry/*metabolism ; Exodeoxyribonucleases/chemistry/deficiency/*metabolism ; *Genomic Instability ; Histones/chemistry/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Nuclear Proteins/*metabolism ; Nucleic Acid Conformation ; Phosphoproteins/chemistry/deficiency/*metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; RNA/chemistry/*metabolism ; *RNA Transport ; Ribonuclease H/chemistry ; Ribonucleoproteins/biosynthesis/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-07-20
    Description: Genotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations, and large numbers of somatic genomic alterations, associated with a predisposition to cancer. However, it remains difficult to distinguish background, or 'passenger', cancer mutations from causal, or 'driver', mutations in these data sets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. Here we test the hypothesis that genomic variations and tumour viruses may cause cancer through related mechanisms, by systematically examining host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways, such as Notch signalling and apoptosis, that go awry in cancer. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on a par with their identification through functional genomics and large-scale cataloguing of tumour mutations. Together, these complementary approaches increase the specificity of cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate the prioritization of cancer-causing driver genes to advance the understanding of the genetic basis of human cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408847/" 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/PMC3408847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rozenblatt-Rosen, Orit -- Deo, Rahul C -- Padi, Megha -- Adelmant, Guillaume -- Calderwood, Michael A -- Rolland, Thomas -- Grace, Miranda -- Dricot, Amelie -- Askenazi, Manor -- Tavares, Maria -- Pevzner, Samuel J -- Abderazzaq, Fieda -- Byrdsong, Danielle -- Carvunis, Anne-Ruxandra -- Chen, Alyce A -- Cheng, Jingwei -- Correll, Mick -- Duarte, Melissa -- Fan, Changyu -- Feltkamp, Mariet C -- Ficarro, Scott B -- Franchi, Rachel -- Garg, Brijesh K -- Gulbahce, Natali -- Hao, Tong -- Holthaus, Amy M -- James, Robert -- Korkhin, Anna -- Litovchick, Larisa -- Mar, Jessica C -- Pak, Theodore R -- Rabello, Sabrina -- Rubio, Renee -- Shen, Yun -- Singh, Saurav -- Spangle, Jennifer M -- Tasan, Murat -- Wanamaker, Shelly -- Webber, James T -- Roecklein-Canfield, Jennifer -- Johannsen, Eric -- Barabasi, Albert-Laszlo -- Beroukhim, Rameen -- Kieff, Elliott -- Cusick, Michael E -- Hill, David E -- Munger, Karl -- Marto, Jarrod A -- Quackenbush, John -- Roth, Frederick P -- DeCaprio, James A -- Vidal, Marc -- F32 GM095284/GM/NIGMS NIH HHS/ -- F32GM095284/GM/NIGMS NIH HHS/ -- K08 CA122833/CA/NCI NIH HHS/ -- K08 HL098361/HL/NHLBI NIH HHS/ -- K08HL098361/HL/NHLBI NIH HHS/ -- K25 HG006031/HG/NHGRI NIH HHS/ -- K25HG006031/HG/NHGRI NIH HHS/ -- P01 CA050661/CA/NCI NIH HHS/ -- P01CA050661/CA/NCI NIH HHS/ -- P50 HG004233/HG/NHGRI NIH HHS/ -- P50HG004233/HG/NHGRI NIH HHS/ -- R01 CA047006/CA/NCI NIH HHS/ -- R01 CA063113/CA/NCI NIH HHS/ -- R01 CA066980/CA/NCI NIH HHS/ -- R01 CA081135/CA/NCI NIH HHS/ -- R01 CA085180/CA/NCI NIH HHS/ -- R01 CA093804/CA/NCI NIH HHS/ -- R01 CA131354/CA/NCI NIH HHS/ -- R01 HG001715/HG/NHGRI NIH HHS/ -- R01CA047006/CA/NCI NIH HHS/ -- R01CA063113/CA/NCI NIH HHS/ -- R01CA066980/CA/NCI NIH HHS/ -- R01CA081135/CA/NCI NIH HHS/ -- R01CA085180/CA/NCI NIH HHS/ -- R01CA093804/CA/NCI NIH HHS/ -- R01CA131354/CA/NCI NIH HHS/ -- R01HG001715/HG/NHGRI NIH HHS/ -- T32 HL007208/HL/NHLBI NIH HHS/ -- T32HL007208/HL/NHLBI NIH HHS/ -- U01 CA141583/CA/NCI NIH HHS/ -- U01CA141583/CA/NCI NIH HHS/ -- England -- Nature. 2012 Jul 26;487(7408):491-5. doi: 10.1038/nature11288.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis of Network Perturbations Center of Excellence in Genomic Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810586" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/metabolism/pathogenicity ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm/*genetics ; Genome, Human/*genetics ; Herpesvirus 4, Human/genetics/metabolism/pathogenicity ; *Host-Pathogen Interactions/genetics ; Humans ; Neoplasms/*genetics/*metabolism/pathology ; Oncogenic Viruses/genetics/metabolism/*pathogenicity ; Open Reading Frames/genetics ; Papillomaviridae/genetics/metabolism/pathogenicity ; Polyomavirus/genetics/metabolism/pathogenicity ; Receptors, Notch/metabolism ; Signal Transduction ; Two-Hybrid System Techniques ; Viral Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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