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  1. Article ; Online: Hyperfunction of post-synaptic density protein 95 promotes seizure response in early-stage aβ pathology.

    Yook, Yeeun / Lee, Kwan Young / Kim, Eunyoung / Lizarazo, Simon / Yu, Xinzhu / Tsai, Nien-Pei

    EMBO reports

    2024  Volume 25, Issue 3, Page(s) 1233–1255

    Abstract: Accumulation of amyloid-beta (Aβ) can lead to the formation of aggregates that contribute to neurodegeneration in Alzheimer's disease (AD). Despite globally reduced neural activity during AD onset, recent studies have suggested that Aβ induces ... ...

    Abstract Accumulation of amyloid-beta (Aβ) can lead to the formation of aggregates that contribute to neurodegeneration in Alzheimer's disease (AD). Despite globally reduced neural activity during AD onset, recent studies have suggested that Aβ induces hyperexcitability and seizure-like activity during the early stages of the disease that ultimately exacerbate cognitive decline. However, the underlying mechanism is unknown. Here, we reveal an Aβ-induced elevation of postsynaptic density protein 95 (PSD-95) in cultured neurons in vitro and in an in vivo AD model using APP/PS1 mice at 8 weeks of age. Elevation of PSD-95 occurs as a result of reduced ubiquitination caused by Akt-dependent phosphorylation of E3 ubiquitin ligase murine-double-minute 2 (Mdm2). The elevation of PSD-95 is consistent with the facilitation of excitatory synapses and the surface expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors induced by Aβ. Inhibition of PSD-95 corrects these Aβ-induced synaptic defects and reduces seizure activity in APP/PS1 mice. Our results demonstrate a mechanism underlying elevated seizure activity during early-stage Aβ pathology and suggest that PSD-95 could be an early biomarker and novel therapeutic target for AD.
    MeSH term(s) Animals ; Mice ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Disease Models, Animal ; Mice, Transgenic ; Post-Synaptic Density/metabolism ; Post-Synaptic Density/pathology ; Receptors, AMPA/metabolism ; Seizures
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Receptors, AMPA ; Dlg4 protein, mouse
    Language English
    Publishing date 2024-02-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.1038/s44319-024-00090-0
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    Zs.A 5433: Show issues Location:
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  2. Article ; Online: Amyloid beta induces Fmr1-dependent translational suppression and hyposynchrony of neural activity via phosphorylation of eIF2α and eEF2.

    Lizarazo, Simon / Yook, Yeeun / Tsai, Nien-Pei

    Journal of cellular physiology

    2022  Volume 237, Issue 7, Page(s) 2929–2942

    Abstract: Alzheimer's disease (AD) is the most common cause of dementia, with the accumulation of amyloid beta peptide (Aβ) being one of the main causes of the disease. Fragile X mental retardation protein (FMRP), encoded by fragile X mental retardation 1 (Fmr1), ... ...

    Abstract Alzheimer's disease (AD) is the most common cause of dementia, with the accumulation of amyloid beta peptide (Aβ) being one of the main causes of the disease. Fragile X mental retardation protein (FMRP), encoded by fragile X mental retardation 1 (Fmr1), is an RNA-binding protein that represses translation of its bound mRNAs or exerts other indirect mechanisms that result in translational suppression. Because the accumulation of Aβ has been shown to cause translational suppression resulting from the elevated cellular stress response, in this study we asked whether and how Fmr1 is involved in Aβ-induced translational regulation. Our data first showed that the application of synthetic Aβ peptide induces the expression of Fmr1 in cultured primary neurons. We followed by showing that Fmr1 is required for Aβ-induced translational suppression, hyposynchrony of neuronal firing activity, and loss of excitatory synapses. Mechanistically, we revealed that Fmr1 functions to repress the expression of phosphatases including protein phosphatase 2A (PP2A) and protein phosphatase 1 (PP1), leading to elevated phosphorylation of eukaryotic initiation factor 2-α (eIF2α) and eukaryotic elongation factor 2 (eEF2), and subsequent translational suppression. Finally, our data suggest that such translational suppression is critical to Aβ-induced hyposynchrony of firing activity, but not the loss of synapses. Altogether, our study uncovers a novel mechanism by which Aβ triggers translational suppression and we reveal the participation of Fmr1 in altered neural plasticity associated with Aβ pathology. Our study may also provide information for a better understanding of Aβ-induced cellular stress responses in AD.
    MeSH term(s) Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; Eukaryotic Initiation Factor-2/genetics ; Eukaryotic Initiation Factor-2/metabolism ; Fragile X Mental Retardation Protein/genetics ; Fragile X Mental Retardation Protein/metabolism ; Humans ; Mice ; Peptide Elongation Factor 2/metabolism ; Phosphorylation
    Chemical Substances Amyloid beta-Peptides ; Eukaryotic Initiation Factor-2 ; Fmr1 protein, mouse ; Peptide Elongation Factor 2 ; Fragile X Mental Retardation Protein (139135-51-6)
    Language English
    Publishing date 2022-04-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.30754
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  3. Article ; Online: Tumor suppressor p53 modulates activity-dependent synapse strengthening, autism-like behavior and hippocampus-dependent learning.

    Lee, Kwan Young / Wang, Haohan / Yook, Yeeun / Rhodes, Justin S / Christian-Hinman, Catherine A / Tsai, Nien-Pei

    Molecular psychiatry

    2023  Volume 28, Issue 9, Page(s) 3782–3794

    Abstract: Synaptic potentiation underlies various forms of behavior and depends on modulation by multiple activity-dependent transcription factors to coordinate the expression of genes necessary for sustaining synaptic transmission. Our current study identified ... ...

    Abstract Synaptic potentiation underlies various forms of behavior and depends on modulation by multiple activity-dependent transcription factors to coordinate the expression of genes necessary for sustaining synaptic transmission. Our current study identified the tumor suppressor p53 as a novel transcription factor involved in this process. We first revealed that p53 could be elevated upon chemically induced long-term potentiation (cLTP) in cultured primary neurons. By knocking down p53 in neurons, we further showed that p53 is required for cLTP-induced elevation of surface GluA1 and GluA2 subunits of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR). Because LTP is one of the principal plasticity mechanisms underlying behaviors, we employed forebrain-specific knockdown of p53 to evaluate the role of p53 in behavior. Our results showed that, while knocking down p53 in mice does not alter locomotion or anxiety-like behavior, it significantly promotes repetitive behavior and reduces sociability in mice of both sexes. In addition, knocking down p53 also impairs hippocampal LTP and hippocampus-dependent learning and memory. Most importantly, these learning-associated defects are more pronounced in male mice than in female mice, suggesting a sex-specific role of p53 in these behaviors. Using RNA sequencing (RNAseq) to identify p53-associated genes in the hippocampus, we showed that knocking down p53 up- or down-regulates multiple genes with known functions in synaptic plasticity and neurodevelopment. Altogether, our study suggests p53 as an activity-dependent transcription factor that mediates the surface expression of AMPAR, permits hippocampal synaptic plasticity, represses autism-like behavior, and promotes hippocampus-dependent learning and memory.
    MeSH term(s) Animals ; Female ; Male ; Mice ; Autistic Disorder/metabolism ; Hippocampus/metabolism ; Long-Term Potentiation/physiology ; Neuronal Plasticity/genetics ; Receptors, AMPA/genetics ; Receptors, AMPA/metabolism ; Synapses/metabolism ; Transcription Factors/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Receptors, AMPA ; Transcription Factors ; Tumor Suppressor Protein p53 ; Trp53 protein, mouse
    Language English
    Publishing date 2023-09-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-023-02268-9
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    Zs.A 4812: Show issues Location:
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  4. Article ; Online: Chronic Activation of Gp1 mGluRs Leads to Distinct Refinement of Neural Network Activity through Non-Canonical p53 and Akt Signaling.

    Liu, Dai-Chi / Soriano, Stephanie / Yook, Yeeun / Lizarazo, Simon / Eagleman, Daphne E / Tsai, Nien-Pei

    eNeuro

    2020  Volume 7, Issue 2

    Abstract: Group 1 metabotropic glutamate receptors (Gp1 mGluRs), including mGluR1 and mGluR5, are critical regulators for neuronal and synaptic plasticity. Dysregulated Gp1 mGluR signaling is observed with various neurologic disorders, including Alzheimer's ... ...

    Abstract Group 1 metabotropic glutamate receptors (Gp1 mGluRs), including mGluR1 and mGluR5, are critical regulators for neuronal and synaptic plasticity. Dysregulated Gp1 mGluR signaling is observed with various neurologic disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and autism spectrum disorders (ASDs). It is well established that acute activation of Gp1 mGluRs leads to elevation of neuronal intrinsic excitability and long-term synaptic depression. However, it remains unknown how chronic activation of Gp1 mGluRs can affect neural activity and what molecular mechanisms might be involved. In the current study, we employed a multielectrode array (MEA) recording system to evaluate neural network activity of primary mouse cortical neuron cultures. We demonstrated that chronic activation of Gp1 mGluRs leads to elevation of spontaneous spike frequency while burst activity and cross-electrode synchronization are maintained at the baseline. We further showed that these neural network properties are achieved through proteasomal degradation of Akt that is dependent on the tumor suppressor p53. Genetically knocking down p53 disrupts the elevation of spontaneous spike frequency and alters the burst activity and cross-electrode synchronization following chronic activation of Gp1 mGluRs. Importantly, these deficits can be restored by pharmacologically inhibiting Akt to mimic inactivation of Akt mediated by p53. Together, our findings reveal the effects of chronic activation of Gp1 mGluRs on neural network activity and identify a unique signaling pathway involving p53 and Akt for these effects. Our data can provide insights into constitutively active Gp1 mGluR signaling observed in many neurologic and psychiatric disorders.
    MeSH term(s) Animals ; Mice ; Neural Networks, Computer ; Neurons ; Proto-Oncogene Proteins c-akt ; Signal Transduction ; Tumor Suppressor Protein p53/genetics
    Chemical Substances Tumor Suppressor Protein p53 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2020-03-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2800598-3
    ISSN 2373-2822 ; 2373-2822
    ISSN (online) 2373-2822
    ISSN 2373-2822
    DOI 10.1523/ENEURO.0438-19.2020
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  5. Article: IL-18 gene expression pattern in exogenously treated AML cells.

    Seo, Minji / Park, Minha / Yook, Yeonjoo / Kwon, Young Sook / Suh, Young Ju / Kim, Min Jung / Cho, Daeho / Park, Jong Hoon

    BMB reports

    2008  Volume 41, Issue 6, Page(s) 461–465

    Abstract: IL-18 production may enhance immune system defense against KG-1 cells ... NB4 cells, which are associated with good prognosis, do not produce IL-18. In this study, we treated KG-1 cells with IL-18 and used microarray technology to assess subsequent effects ...

    Abstract IL-18 production may enhance immune system defense against KG-1 cells

    NB4 cells, which are associated with good prognosis, do not produce IL-18. In this study, we treated KG-1 cells with IL-18 and used microarray technology to assess subsequent effects on gene expression. In UniGene-array of 7488 human genes, expression of 57 genes, including stress related genes, increased at least 2-fold, whereas expression of 48 genes decreased at least 2-fold. Following exogenous exposure of KG-1 cells to IL-18, expression of CRYGC, NF(kappa)BIA and NACA gene were monitored. The latter is a transcriptional coactivator potentiating c-Jun-mediated transcription. NF(kappa)BIA is an inhibitor of NF(kappa)B, and affects growth regulation, apoptosis and hypoxic stress. Studies, such as this one, are beginning to clarify the differences between cells associated with good and bad cancer prognoses, which may ultimately assist in medical treatment for acute myeloid leukemia.
    MeSH term(s) Blotting, Western ; Cell Line, Tumor ; Down-Regulation ; Gene Expression/drug effects ; Gene Expression Profiling ; Humans ; Interleukin-18/biosynthesis ; Interleukin-18/genetics ; Interleukin-18/pharmacology ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; NF-kappa B/metabolism ; Oligonucleotide Array Sequence Analysis ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances Interleukin-18 ; NF-kappa B
    Language English
    Publishing date 2008-07-01
    Publishing country Korea (South)
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2410389-5
    ISSN 1976-670X ; 1976-6696
    ISSN (online) 1976-670X
    ISSN 1976-6696
    DOI 10.5483/bmbrep.2008.41.6.461
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    Zs.A 4202: Show issues Location:
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  6. Article ; Online: First Simultaneous Determination of Inclusive and Exclusive |V_{ub}|.

    Cao, L / Bernlochner, F / Tackmann, K / Adachi, I / Aihara, H / Al Said, S / Asner, D M / Atmacan, H / Aushev, T / Ayad, R / Babu, V / Bahinipati, S / Banerjee, Sw / Behera, P / Belous, K / Bennett, J / Bessner, M / Bhuyan, B / Bilka, T /
    Biswas, D / Bobrov, A / Bodrov, D / Borah, J / Bozek, A / Bračko, M / Branchini, P / Browder, T E / Budano, A / Campajola, M / Červenkov, D / Chang, M-C / Cheon, B G / Chilikin, K / Cho, H E / Cho, K / Cho, S-J / Choi, S-K / Choi, Y / Choudhury, S / Cinabro, D / Cunliffe, S / Das, S / de Marino, G / De Nardo, G / De Pietro, G / Dhamija, R / Di Capua, F / Dingfelder, J / Doležal, Z / Dong, T V / Ferber, T / Ferlewicz, D / Frey, A / Fulsom, B G / Gaur, V / Garmash, A / Giri, A / Goldenzweig, P / Graziani, E / Gu, T / Guan, Y / Gudkova, K / Hadjivasiliou, C / Halder, S / Hara, T / Hartbrich, O / Hayasaka, K / Hayashii, H / Hedges, M T / Herrmann, D / Hou, W-S / Hsu, C-L / Iijima, T / Inami, K / Ipsita, N / Ishikawa, A / Itoh, R / Iwasaki, M / Jacobs, W W / Jang, E-J / Jia, S / Jin, Y / Joo, K K / Kalita, D / Kang, K H / Kiesling, C / Kim, C H / Kim, D Y / Kim, K-H / Kim, Y-K / Kinoshita, K / Kodyš, P / Konno, T / Korobov, A / Korpar, S / Kovalenko, E / Križan, P / Krokovny, P / Kuhr, T / Kumar, R / Kumara, K / Kuzmin, A / Kwon, Y-J / Lange, J S / Laurenza, M / Lee, S C / Lewis, P / Li, J / Li, L K / Li, Y / Libby, J / Lin, Y-R / Liventsev, D / Luo, T / Ma, Y / Martini, A / Masuda, M / Matsuda, T / Matvienko, D / Maurya, S K / Meier, F / Merola, M / Metzner, F / Miyabayashi, K / Mizuk, R / Mohanty, G B / Mrvar, M / Mussa, R / Nakamura, I / Nakao, M / Natkaniec, Z / Natochii, A / Nayak, L / Nayak, M / Nisar, N K / Nishida, S / Ogawa, K / Ogawa, S / Ono, H / Oskin, P / Pakhlov, P / Pakhlova, G / Pang, T / Pardi, S / Park, H / Park, J / Park, S-H / Passeri, A / Patra, S / Paul, S / Pedlar, T K / Pestotnik, R / Piilonen, L E / Podobnik, T / Prencipe, E / Prim, M T / Rout, N / Rozanska, M / Russo, G / Sandilya, S / Sangal, A / Santelj, L / Savinov, V / Schnell, G / Schwanda, C / Seino, Y / Senyo, K / Sevior, M E / Shan, W / Shapkin, M / Sharma, C / Shen, C P / Shiu, J-G / Shwartz, B / Sokolov, A / Solovieva, E / Starič, M / Stottler, Z S / Sumihama, M / Sutcliffe, W / Takizawa, M / Tamponi, U / Tanida, K / Tenchini, F / Tiwary, R / Trabelsi, K / Uchida, M / Uglov, T / Unno, Y / Uno, K / Uno, S / Ushiroda, Y / Usov, Y / Vahsen, S E / Varner, G / Varvell, K E / Vossen, A / Wang, D / Wang, E / Wang, M-Z / Watanuki, S / Werbycka, O / Won, E / Xu, X / Yabsley, B D / Yan, W / Yang, S B / Yin, J H / Yook, Y / Yusa, Y / Zhang, Z P / Zhilich, V / Zhukova, V

    Physical review letters

    2023  Volume 131, Issue 21, Page(s) 211801

    Abstract: The first simultaneous determination of the absolute value of the Cabibbo-Kobayashi-Maskawa matrix element V_{ub} using inclusive and exclusive decays is performed with the full Belle data set at the ϒ(4S) resonance, corresponding to an integrated ... ...

    Abstract The first simultaneous determination of the absolute value of the Cabibbo-Kobayashi-Maskawa matrix element V_{ub} using inclusive and exclusive decays is performed with the full Belle data set at the ϒ(4S) resonance, corresponding to an integrated luminosity of 711  fb^{-1}. We analyze collision events in which one B meson is fully reconstructed in hadronic modes. This allows for the reconstruction of the hadronic X_{u} system of the semileptonic b→uℓν[over ¯]_{ℓ} decay. We separate exclusive B→πℓν[over ¯]_{ℓ} decays from other inclusive B→X_{u}ℓν[over ¯]_{ℓ} and backgrounds with a two-dimensional fit that utilizes the number of charged pions in the X_{u} system and the four-momentum transfer q^{2} between the B and X_{u} systems. Combining our measurement with information from lattice QCD and QCD calculations of the inclusive partial rate as well as external experimental information on the shape of the B→πℓν[over ¯]_{ℓ} form factor, we determine |V_{ub}^{excl}|=(3.78±0.23±0.16±0.14)×10^{-3} and |V_{ub}^{incl}|=(3.88±0.20±0.31±0.09)×10^{-3}, respectively, with the uncertainties being the statistical error, systematic errors, and theory errors. The ratio of |V_{ub}^{excl}|/|V_{ub}^{incl}|=0.97±0.12 is compatible with unity.
    Language English
    Publishing date 2023-09-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 208853-8
    ISSN 1079-7114 ; 0031-9007
    ISSN (online) 1079-7114
    ISSN 0031-9007
    DOI 10.1103/PhysRevLett.131.211801
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  7. Article ; Online: Identification of 11 novel mutations in 49 Korean patients with mucopolysaccharidosis type II.

    Sohn, Y B / Ki, C-S / Kim, C-H / Ko, A-R / Yook, Y-J / Lee, S-J / Kim, S J / Park, S W / Yeau, S / Kwon, E-K / Han, S J / Choi, E W / Lee, S-Y / Kim, J-W / Jin, D-K

    Clinical genetics

    2012  Volume 81, Issue 2, Page(s) 185–190

    Abstract: Mucopolysaccharidosis type II (MPS II) or Hunter syndrome is a rare lysosomal storage disorder caused by a deficiency of iduronate-2-sulfatase (IDS). As MPS II is X-linked, patients are usually males with heterogeneous mutations ranging from point ... ...

    Abstract Mucopolysaccharidosis type II (MPS II) or Hunter syndrome is a rare lysosomal storage disorder caused by a deficiency of iduronate-2-sulfatase (IDS). As MPS II is X-linked, patients are usually males with heterogeneous mutations ranging from point mutations to gross deletions and recombination. In 2003, we reported a mutation analysis of 25 patients with MPS II. In this study, 31 mutations in another 49 Korean patients (45 families) with MPS II are reported: 12 missense, nine deletions, four splicing, two nonsense, two insertions, one deletion/insertion, and IDS-IDS2 recombination mutations. Among these mutations, 11 were novel ones (4 missense mutations: Ser61Pro, Pro97Arg, Pro228Ala, and Pro261Ala; 5 deletions: c.344delA, c.420delG, c.768delT, c.1112delC and c.1402delC; 1 deletion/insertion: c.1222delinsTA; and 1 insertion mutation: c.359_360insATCC). The IDS-IDS2 recombination mutations were most frequently observed; all patients with this mutation had the severe MPS II phenotype. However, most of the patients (5/7) with the G374G splicing mutation had an attenuated phenotype, except for two sibling cases with the severe phenotype. Except for a few recurrent mutations such as the G374G, R443X, L522P, and recombination mutations, each patient had a unique individual mutation. Therefore, careful interpretation of genotype-phenotype correlations is warranted.
    MeSH term(s) Asian Continental Ancestry Group/genetics ; Humans ; Iduronate Sulfatase/genetics ; Mucopolysaccharidosis II/diagnosis ; Mucopolysaccharidosis II/genetics ; Mutation ; Mutation Rate ; Phenotype ; Republic of Korea
    Chemical Substances Iduronate Sulfatase (EC 3.1.6.13)
    Language English
    Publishing date 2012-02
    Publishing country Denmark
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 221209-2
    ISSN 1399-0004 ; 0009-9163
    ISSN (online) 1399-0004
    ISSN 0009-9163
    DOI 10.1111/j.1399-0004.2011.01641.x
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    Zs.A 413: Show issues Location:
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  8. Article: Isolation and Characterization of Plant Growth Promoting Rhizobacterium Bacillus subtilis YK-5 from soil

    Yeo, S.H., Korean Food Research for Globalization, NAAS, RDA, Suwon, Republic of Korea / Yook, Y.M., Keimyung Biotech Co., Seongju, Republic of Korea / Kim, H.S., Keimyung University, Daegu, Republic of Korea

    Korean Society for Biotechnology and Bioengineering Journal

    (Aug 2009)  Volume v. 24, Issue (4), Page(s) p. 334–340

    Abstract: For the isolation of a plant growth-promoting rhizobacteria, strain YK-5 was selected from approximately 400 thermostable strains isolated from special soil samples. Strain YK-5 produced an antifungal compound, and optimum carbon and nitrogen sources for ...

    Abstract For the isolation of a plant growth-promoting rhizobacteria, strain YK-5 was selected from approximately 400 thermostable strains isolated from special soil samples. Strain YK-5 produced an antifungal compound, and optimum carbon and nitrogen sources for the production of the antifungal compound were investigated against Aspergillus flavus as a test strain. Modified LB medium containing 1% peptone, 1% yeast extract and 5% black sugar was determined to be the optimal medium for growth and antifungal compound production. Culture broth of strain YK-5 potently inhibited growth of the phytopathogenic fungus Fusarium oxysporum KACC 40052 for 7 days. The plant growth-promotion function of strain YK-5 was tested against radish and rice in pot trials. Leaf number, plant height and root length in YK-5-treated radish markedly exceeded (greater than 60%) those of untreated radish. Leaf length and white rootlet development were markedly more prominent than in commercially-treated rice plants. Strain YK-5 was determined to be Bacillus subtilis YK-5 by physiological, chemotaxonomical, and phylogenetical analyses.
    Keywords SOIL ; SOL ; SUELO
    Language Korean
    Document type Article
    ISSN 1225-7117
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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  9. Article ; Online: Search for the dark photon and the dark Higgs boson at belle.

    Jaegle, I / Adachi, I / Aihara, H / Al Said, S / Asner, D M / Aushev, T / Ayad, R / Bakich, A M / Bansal, V / Barrett, M / Bhuyan, B / Bozek, A / Bračko, M / Browder, T E / Červenkov, D / Chang, M-C / Cheon, B G / Chilikin, K / Cho, K /
    Chobanova, V / Choi, S-K / Choi, Y / Cinabro, D / Dalseno, J / Doležal, Z / Drásal, Z / Drutskoy, A / Dutta, D / Eidelman, S / Epifanov, D / Farhat, H / Fast, J E / Ferber, T / Frost, O / Gaur, V / Gabyshev, N / Ganguly, S / Garmash, A / Getzkow, D / Gillard, R / Goh, Y M / Golob, B / Grzymkowska, O / Hayasaka, K / Hayashii, H / He, X H / Hedges, M / Hou, W-S / Iijima, T / Inami, K / Ishikawa, A / Iwasaki, Y / Julius, T / Kang, K H / Kato, E / Kawasaki, T / Kim, D Y / Kim, J B / Kim, J H / Kim, S H / Kinoshita, K / Ko, B R / Kodyš, P / Korpar, S / Križan, P / Krokovny, P / Kuzmin, A / Kwon, Y-J / Lange, J S / Lee, I S / Lewis, P / Li Gioi, L / Libby, J / Liventsev, D / Matvienko, D / Miyata, H / Mizuk, R / Mohanty, G B / Moll, A / Mussa, R / Nakano, E / Nakao, M / Nisar, N K / Nishida, S / Ogawa, S / Pakhlov, P / Pakhlova, G / Park, H / Pedlar, T K / Pesántez, L / Petrič, M / Piilonen, L E / Ritter, M / Rostomyan, A / Sakai, Y / Sandilya, S / Santelj, L / Sanuki, T / Sato, Y / Savinov, V / Schneider, O / Schnell, G / Schwanda, C / Semmler, D / Senyo, K / Seon, O / Seong, I / Sevior, M E / Shebalin, V / Shibata, T-A / Shiu, J-G / Shwartz, B / Simon, F / Sinha, R / Sohn, Y-S / Starič, M / Sumihama, M / Sumisawa, K / Tamponi, U / Tatishvili, G / Teramoto, Y / Thorne, F / Uchida, M / Uehara, S / Unno, Y / Uno, S / Vahsen, S E / Van Hulse, C / Vanhoefer, P / Varner, G / Vinokurova, A / Wagner, M N / Wang, C H / Wang, M-Z / Wang, P / Wang, X L / Watanabe, M / Watanabe, Y / Williams, K M / Won, E / Yamaoka, J / Yashchenko, S / Yook, Y / Yusa, Y / Zhilich, V / Zhulanov, V / Zupanc, A

    Physical review letters

    2015  Volume 114, Issue 21, Page(s) 211801

    Abstract: The dark photon A^{'} and the dark Higgs boson h^{'} are hypothetical constituents featured in a number of recently proposed dark sector models. Assuming prompt decays of both dark particles, we search for their production in the so-called Higgstrahlung ... ...

    Abstract The dark photon A^{'} and the dark Higgs boson h^{'} are hypothetical constituents featured in a number of recently proposed dark sector models. Assuming prompt decays of both dark particles, we search for their production in the so-called Higgstrahlung channel e^{+}e^{-}→A^{'}h^{'}, with h^{'}→A^{'}A^{'}. We investigate ten exclusive final states with A^{'}→e^{+}e^{-}, μ^{+}μ^{-}, or π^{+}π^{-} in the mass ranges 0.1  GeV/c^{2} <m_{A^{'}}<3.5  GeV/c^{2} and 0.2  GeV/c^{2} <m_{h^{'}}<10.5  GeV/c^{2}. We also investigate three inclusive final states 2(e^{+}e^{-})X, 2(μ^{+}μ^{-})X, and (e^{+}e^{-})(μ^{+}μ^{-})X, where X denotes a dark photon candidate detected via missing mass, in the mass ranges 1.1  GeV/c^{2} <m_{A^{'}}<3.5  GeV/c^{2} and 2.2  GeV/c^{2} <m_{h^{'}}<10.5  GeV/c^{2}. Using the entire 977  fb^{-1} data set collected by Belle, we observe no significant signal. We obtain individual and combined 90% credibility level upper limits on the branching fraction times the Born cross section, B×σ_{Born}, on the Born cross section σ_{Born}, and on the dark photon coupling to the dark Higgs boson times the kinetic mixing between the standard model photon and the dark photon, α_{D}×ε^{2}. These limits improve upon and cover wider mass ranges than previous experiments. The limits from the final states 3(π^{+}π^{-}) and 2(e^{+}e^{-})X are the first placed by any experiment. For α_{D} equal to 1/137, m_{h^{'}}< 8  GeV/c^{2}, and m_{A^{'}}<1  GeV/c^{2}, we exclude values of the mixing parameter ε above ∼8×10^{-4}.<br />
    Language English
    Publishing date 2015-05-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 208853-8
    ISSN 1079-7114 ; 0031-9007
    ISSN (online) 1079-7114
    ISSN 0031-9007
    DOI 10.1103/PhysRevLett.114.211801
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Search for Lepton-Flavor-Violating τ Decays to a Lepton and an Invisible Boson at Belle II.

    Adachi, I / Adamczyk, K / Aggarwal, L / Ahmed, H / Aihara, H / Akopov, N / Aloisio, A / Anh Ky, N / Asner, D M / Aushev, T / Aushev, V / Bae, H / Bahinipati, S / Bambade, P / Banerjee, Sw / Baudot, J / Bauer, M / Baur, A / Beaubien, A /
    Becker, J / Behera, P K / Bennett, J V / Bernieri, E / Bernlochner, F U / Bertacchi, V / Bertemes, M / Bertholet, E / Bessner, M / Bettarini, S / Bhuyan, B / Bianchi, F / Bilka, T / Bilokin, S / Biswas, D / Bodrov, D / Bolz, A / Borah, J / Bozek, A / Bračko, M / Branchini, P / Browder, T E / Budano, A / Bussino, S / Campajola, M / Cao, L / Casarosa, G / Cecchi, C / Chang, M-C / Chang, P / Cheaib, R / Cheema, P / Chekelian, V / Chen, Y Q / Cheon, B G / Chilikin, K / Chirapatpimol, K / Cho, H-E / Cho, K / Cho, S-J / Choi, S-K / Choudhury, S / Cinabro, D / Corona, L / Cunliffe, S / Das, S / Dattola, F / De La Cruz-Burelo, E / De La Motte, S A / De Nardo, G / De Nuccio, M / De Pietro, G / de Sangro, R / Destefanis, M / Dey, S / De Yta-Hernandez, A / Dhamija, R / Di Canto, A / Di Capua, F / Dingfelder, J / Doležal, Z / Domínguez Jiménez, I / Dong, T V / Dorigo, M / Dort, K / Dossett, D / Dreyer, S / Dubey, S / Dujany, G / Ecker, P / Eliachevitch, M / Epifanov, D / Feichtinger, P / Ferber, T / Ferlewicz, D / Fillinger, T / Finck, C / Finocchiaro, G / Flood, K / Fodor, A / Forti, F / Fulsom, B G / Gabrielli, A / Ganiev, E / Garcia-Hernandez, M / Gaur, V / Gaz, A / Gellrich, A / Ghevondyan, G / Giordano, R / Giri, A / Glazov, A / Gobbo, B / Godang, R / Goldenzweig, P / Gradl, W / Granderath, S / Graziani, E / Greenwald, D / Gruberová, Z / Gu, T / Gudkova, K / Guilliams, J / Hara, T / Hayasaka, K / Hayashii, H / Hazra, S / Hearty, C / Heredia de la Cruz, I / Hernández Villanueva, M / Hershenhorn, A / Higuchi, T / Hill, E C / Hohmann, M / Hsu, C-L / Humair, T / Iijima, T / Inami, K / Inguglia, G / Ipsita, N / Ishikawa, A / Ito, S / Itoh, R / Iwasaki, M / Jackson, P / Jacobs, W W / Jaffe, D E / Jang, E-J / Ji, Q P / Jia, S / Jin, Y / Joo, K K / Junkerkalefeld, H / Kakuno, H / Kaliyar, A B / Kandra, J / Kang, K H / Kang, S / Karl, R / Karyan, G / Kiesling, C / Kim, C-H / Kim, D Y / Kim, K-H / Kim, Y-K / Kindo, H / Kinoshita, K / Kodyš, P / Koga, T / Kohani, S / Kojima, K / Konno, T / Korobov, A / Korpar, S / Kovalenko, E / Kowalewski, R / Kraetzschmar, T M G / Križan, P / Krokovny, P / Kuhr, T / Kumar, J / Kumar, R / Kumara, K / Kunigo, T / Kuzmin, A / Kwon, Y-J / Lacaprara, S / Lam, T / Lanceri, L / Lange, J S / Laurenza, M / Lautenbach, K / Leboucher, R / Le Diberder, F R / Leitl, P / Lewis, P M / Li, C / Li, L K / Li, Y B / Libby, J / Lieret, K / Liptak, Z / Liu, Q Y / Liventsev, D / Longo, S / Lozar, A / Lueck, T / Luo, T / Lyu, C / Maggiora, M / Maiti, R / Maity, S / Manfredi, R / Manoni, E / Manthei, A / Marcello, S / Marinas, C / Martel, L / Martini, A / Martinov, T / Massaccesi, L / Masuda, M / Matsuda, T / Matsuoka, K / Matvienko, D / Maurya, S K / McKenna, J A / Meier, F / Merola, M / Metzner, F / Milesi, M / Miller, C / Miyabayashi, K / Mizuk, R / Mohanty, G B / Molina-Gonzalez, N / Moneta, S / Moser, H-G / Mrvar, M / Mussa, R / Nakamura, I / Nakamura, K R / Nakao, M / Nakayama, H / Nakazawa, Y / Narimani Charan, A / Naruki, M / Natochii, A / Nayak, L / Nayak, M / Nazaryan, G / Niebuhr, C / Nisar, N K / Nishida, S / Ogawa, S / Ono, H / Onuki, Y / Oskin, P / Pakhlov, P / Pakhlova, G / Paladino, A / Panta, A / Paoloni, E / Pardi, S / Parham, K / Park, H / Park, S-H / Paschen, B / Passeri, A / Patra, S / Paul, S / Pedlar, T K / Peruzzi, I / Peschke, R / Pestotnik, R / Pham, F / Piccolo, M / Piilonen, L E / Pinna Angioni, G / Podesta-Lerma, P L M / Podobnik, T / Pokharel, S / Polat, L / Praz, C / Prell, S / Prencipe, E / Prim, M T / Purwar, H / Rad, N / Rados, P / Raeuber, G / Raiz, S / Ramirez Morales, A / Reif, M / Reiter, S / Remnev, M / Ripp-Baudot, I / Rizzo, G / Robertson, S H / Rodríguez Pérez, D / Roney, J M / Rostomyan, A / Rout, N / Russo, G / Sanders, D A / Sandilya, S / Sangal, A / Santelj, L / Sato, Y / Savinov, V / Scavino, B / Schueler, J / Schwanda, C / Seino, Y / Selce, A / Senyo, K / Serrano, J / Sevior, M E / Sfienti, C / Shen, C P / Shi, X D / Shillington, T / Shiu, J-G / Shwartz, B / Sibidanov, A / Simon, F / Singh, J B / Skorupa, J / Sobie, R J / Soffer, A / Sokolov, A / Solovieva, E / Spataro, S / Spruck, B / Starič, M / Stefkova, S / Stottler, Z S / Stroili, R / Strube, J / Sue, Y / Sumihama, M / Sumisawa, K / Sutcliffe, W / Suzuki, S Y / Svidras, H / Takizawa, M / Tamponi, U / Tanida, K / Tanigawa, H / Tenchini, F / Thaller, A / Tiwary, R / Tonelli, D / Torassa, E / Toutounji, N / Trabelsi, K / Uchida, M / Ueda, I / Uematsu, Y / Uglov, T / Unger, K / Unno, Y / Uno, K / Uno, S / Ushiroda, Y / Vahsen, S E / van Tonder, R / Varner, G S / Varvell, K E / Vinokurova, A / Vitale, L / Vobbilisetti, V / Wakeling, H M / Wang, E / Wang, M-Z / Wang, X L / Warburton, A / Watanabe, M / Watanuki, S / Welsch, M / Wessel, C / Wiechczynski, J / Xu, X P / Yabsley, B D / Yamada, S / Yan, W / Yang, S B / Ye, H / Yelton, J / Yin, J H / Yook, Y M / Yoshihara, K / Yuan, C Z / Yusa, Y / Zani, L / Zhang, Y / Zhilich, V / Zhou, Q D / Zhou, X Y / Zhukova, V I / Žlebčík, R

    Physical review letters

    2023  Volume 130, Issue 18, Page(s) 181803

    Abstract: We search for lepton-flavor-violating τ^{-}→e^{-}α and τ^{-}→μ^{-}α decays, where α is an invisible spin-0 boson. The search uses electron-positron collisions at 10.58 GeV center-of-mass energy with an integrated luminosity of 62.8  fb^{-1}, produced by ... ...

    Abstract We search for lepton-flavor-violating τ^{-}→e^{-}α and τ^{-}→μ^{-}α decays, where α is an invisible spin-0 boson. The search uses electron-positron collisions at 10.58 GeV center-of-mass energy with an integrated luminosity of 62.8  fb^{-1}, produced by the SuperKEKB collider and collected with the Belle II detector. We search for an excess in the lepton-energy spectrum of the known τ^{-}→e^{-}ν[over ¯]_{e}ν_{τ} and τ^{-}→μ^{-}ν[over ¯]_{μ}ν_{τ} decays. We report 95% confidence-level upper limits on the branching-fraction ratio B(τ^{-}→e^{-}α)/B(τ^{-}→e^{-}ν[over ¯]_{e}ν_{τ}) in the range (1.1-9.7)×10^{-3} and on B(τ^{-}→μ^{-}α)/B(τ^{-}→μ^{-}ν[over ¯]_{μ}ν_{τ}) in the range (0.7-12.2)×10^{-3} for α masses between 0 and 1.6  GeV/c^{2}. These results provide the most stringent bounds on invisible boson production from τ decays.
    Language English
    Publishing date 2023-03-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 208853-8
    ISSN 1079-7114 ; 0031-9007
    ISSN (online) 1079-7114
    ISSN 0031-9007
    DOI 10.1103/PhysRevLett.130.181803
    Database MEDical Literature Analysis and Retrieval System OnLINE

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