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  1. Article ; Online: Measurement of the ^{13}C(α, n_{0})^{16}O Differential Cross Section from 0.8 to 6.5 MeV.

    deBoer, R J / Febbraro, M / Bardayan, D W / Boomershine, C / Brandenburg, K / Brune, C / Coil, S / Couder, M / Derkin, J / Dede, S / Fang, R / Fritsch, A / Gula, A / Gyürky, Gy / Hackett, B / Hamad, G / Jones-Alberty, Y / Kelmar, R / Manukyan, K /
    Matney, M / McDonaugh, J / Meisel, Z / Moylan, S / Nattress, J / Odell, D / O'Malley, P / Paris, M W / Robertson, D / Shahina / Singh, N / Smith, K / Smith, M S / Stech, E / Tan, W / Wiescher, M

    Physical review letters

    2024  Volume 132, Issue 6, Page(s) 62702

    Abstract: The cross section of the ^{13}C(α,n)^{16}O reaction is needed for nuclear astrophysics and applications to a precision of 10% or better, yet inconsistencies among 50 years of experimental studies currently lead to an uncertainty of ≈15%. Using a state-of- ...

    Abstract The cross section of the ^{13}C(α,n)^{16}O reaction is needed for nuclear astrophysics and applications to a precision of 10% or better, yet inconsistencies among 50 years of experimental studies currently lead to an uncertainty of ≈15%. Using a state-of-the-art neutron detection array, we have performed a high resolution differential cross section study covering a broad energy range. These measurements result in a dramatic improvement in the extrapolation of the cross section to stellar energies potentially reducing the uncertainty to ≈5% and resolving long standing discrepancies in higher energy data.
    Language English
    Publishing date 2024-02-23
    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.132.062702
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Fibromyalgia as a disorder related to distress and its therapeutic implications.

    Schweinhardt, Petra / Fitzcharles, Mary-Ann / Boomershine, Chad / Vierck, Charles / Yunus, Muhammad B

    Pain research and treatment

    2012  Volume 2012, Page(s) 950602

    Language English
    Publishing date 2012-03-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2603578-9
    ISSN 2090-1550 ; 2090-1542
    ISSN (online) 2090-1550
    ISSN 2090-1542
    DOI 10.1155/2012/950602
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Synergistic interaction of catecholamine hormones and Mycobacterium avium results in the induction of interleukin-10 mRNA expression by murine peritoneal macrophages.

    Chen, L / Boomershine, C / Wang, T / Lafuse, W P / Zwilling, B S

    Journal of neuroimmunology

    1999  Volume 93, Issue 1-2, Page(s) 149–155

    Abstract: The results of this investigation provides evidence that catecholamine hormones interact with macrophages that are infected with Mycobacterium avium resulting in the induction of IL-10 mRNA and protein. The effect of catecholamine hormones was prevented ... ...

    Abstract The results of this investigation provides evidence that catecholamine hormones interact with macrophages that are infected with Mycobacterium avium resulting in the induction of IL-10 mRNA and protein. The effect of catecholamine hormones was prevented by treating the cells with the beta-adrenergic receptor antagonist propranolol but not by alpha-adrenergic antagonist phentolamine. The effect of catecholamine stimulation was mimicked by the addition of beta-2 adrenergic agonists and by the addition of cAMP to the infected macrophage cultures. These observations suggest that sympathetic nervous system activation together with microbial infection results in a synergistic interaction that could result in the control of inflammatory processes.
    MeSH term(s) Adrenergic alpha-Agonists/pharmacology ; Adrenergic alpha-Antagonists/pharmacology ; Adrenergic beta-Agonists/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Animals ; Antigens, Bacterial/immunology ; Antigens, Bacterial/pharmacology ; Bucladesine/pharmacology ; Cyclic AMP/pharmacology ; Dobutamine/pharmacology ; Drug Synergism ; Epinephrine/pharmacology ; Gene Expression/drug effects ; Gene Expression/immunology ; Interleukin-10/genetics ; Interleukin-10/immunology ; Macrophages, Peritoneal/drug effects ; Macrophages, Peritoneal/immunology ; Macrophages, Peritoneal/microbiology ; Male ; Metoprolol/pharmacology ; Mice ; Mice, Inbred BALB C ; Mycobacterium avium/immunology ; Phentolamine/pharmacology ; Propanolamines/pharmacology ; Propranolol/pharmacology ; RNA, Messenger/analysis ; Terbutaline/pharmacology
    Chemical Substances Adrenergic alpha-Agonists ; Adrenergic alpha-Antagonists ; Adrenergic beta-Agonists ; Adrenergic beta-Antagonists ; Antigens, Bacterial ; Propanolamines ; RNA, Messenger ; Interleukin-10 (130068-27-8) ; Dobutamine (3S12J47372) ; ICI 118551 (46OL1UC10R) ; Bucladesine (63X7MBT2LQ) ; Propranolol (9Y8NXQ24VQ) ; Cyclic AMP (E0399OZS9N) ; Metoprolol (GEB06NHM23) ; Terbutaline (N8ONU3L3PG) ; Epinephrine (YKH834O4BH) ; Phentolamine (Z468598HBV)
    Language English
    Publishing date 1999-01-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 8335-5
    ISSN 1872-8421 ; 0165-5728
    ISSN (online) 1872-8421
    ISSN 0165-5728
    DOI 10.1016/s0165-5728(98)00220-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Beta2-adrenergic receptor stimulation inhibits nitric oxide generation by Mycobacterium avium infected macrophages.

    Boomershine, C S / Lafuse, W P / Zwilling, B S

    Journal of neuroimmunology

    1999  Volume 101, Issue 1, Page(s) 68–75

    Abstract: Catecholamine regulation of nitric oxide (NO) production by IFNgamma-primed macrophages infected with Mycobacterium avium was investigated. Epinephrine treatment of IFNgamma-primed macrophages at the time of M. avium infection inhibited the anti- ... ...

    Abstract Catecholamine regulation of nitric oxide (NO) production by IFNgamma-primed macrophages infected with Mycobacterium avium was investigated. Epinephrine treatment of IFNgamma-primed macrophages at the time of M. avium infection inhibited the anti-mycobacterial activity of the cells. The anti-mycobacterial activity of macrophages correlated with NO production. Using specific adrenergic receptor agonists, the abrogation of mycobacterial killing and decreased NO production by catecholamines was shown to be mediated via the beta2-adrenergic receptor. Elevation of intracellular cAMP levels mimicked the catecholamine-mediated inhibition of NO in both M. avium infected and LPS stimulated macrophages. Specific inhibitors of both adenylate cyclase and protein kinase A prevented the beta2-adrenoceptor-mediated inhibition of nitric oxide production. Beta2-adrenoreceptor stimulation at the time of M. avium infection of IFNgamma-primed macrophages also inhibited expression of iNOS mRNA. These observations show that catecholamine hormones can affect the outcome of macrophage-pathogen interactions and suggest that one result of sympathetic nervous system activation is the suppression of the capacity of macrophages to produce anti-microbial effector molecules.
    MeSH term(s) Animals ; Cells, Cultured ; Cyclic AMP/physiology ; Epinephrine/pharmacology ; Interferon-gamma/pharmacology ; Macrophages/metabolism ; Macrophages/microbiology ; Male ; Mice ; Mice, Inbred BALB C ; Mycobacterium avium/physiology ; Nitric Oxide/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; RNA, Messenger/analysis ; Receptors, Adrenergic, beta-2/physiology ; Terbutaline/pharmacology
    Chemical Substances RNA, Messenger ; Receptors, Adrenergic, beta-2 ; Nitric Oxide (31C4KY9ESH) ; Interferon-gamma (82115-62-6) ; Cyclic AMP (E0399OZS9N) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; Terbutaline (N8ONU3L3PG) ; Epinephrine (YKH834O4BH)
    Language English
    Publishing date 1999-11-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 8335-5
    ISSN 1872-8421 ; 0165-5728
    ISSN (online) 1872-8421
    ISSN 0165-5728
    DOI 10.1016/s0165-5728(99)00134-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Autoimmune pancreatitis results from loss of TGFbeta signalling in S100A4-positive dendritic cells.

    Boomershine, C S / Chamberlain, A / Kendall, P / Afshar-Sharif, A-R / Huang, H / Washington, M K / Lawson, W E / Thomas, J W / Blackwell, T S / Bhowmick, N A

    Gut

    2009  Volume 58, Issue 9, Page(s) 1267–1274

    Abstract: Background and aims: Autoimmune pancreatitis (AIP) is a poorly understood human disease affecting the exocrine pancreas. The goal of the present study was to elucidate the pathogenic mechanisms underlying pancreatic autoimmunity in a murine disease ... ...

    Abstract Background and aims: Autoimmune pancreatitis (AIP) is a poorly understood human disease affecting the exocrine pancreas. The goal of the present study was to elucidate the pathogenic mechanisms underlying pancreatic autoimmunity in a murine disease model.
    Methods: A transgenic mouse with an S100A4/fibroblast-specific protein 1 (FSP1) Cre-mediated conditional knockout of the transforming growth factor beta (TGFbeta) type II receptor, termed Tgfbr2(fspKO), was used to determine the direct role of TGFbeta in S100A4(+) cells. Immunohistochemical studies suggested that Tgfbr2(fspKO) mice develop mouse AIP (mAIP) characterised by interlobular ductal inflammatory infiltrates and pancreatic autoantibody production. Fluorescence-activated cell sorting (FACS)-isolated dendritic cells (DCs) from diseased pancreata were verified to have S100A4-Cre-mediated DNA recombination.
    Results: The Tgfbr2(fspKO) mice spontaneously developed mAIP by 6 weeks of age. DCs were confirmed to express S100A4, a previously reported protein expressed by fibroblasts. Adoptive transfer of bone marrow-derived DCs from Tgfbr2(fspKO) mice into 2-week-old syngenic wild-type C57BL/6 mice resulted in reproduction of pancreatitis within 6 weeks. Similar adoptive transfer of wild-type DCs had no effect on pancreas pathology of the host mice. The inability to induce pancreatitis by adoptive transfer of Tgfbr2(fspKO) DCs in adult mice suggested a developmental event in mAIP pathogenesis. Tgfbr2(fspKO) DCs undergo elevated maturation in response to antigen and increased activation of naïve CD4-positive T cells.
    Conclusion: The development of mAIP in the Tgfbr2(fspKO) mouse model illustrates the role of TGFbeta in maintaining myeloid DC immune tolerance. The loss of immune tolerance in myeloid S100A4(+) DCs can mediate mAIP and may explain some aspects of AIP disease pathogenesis.
    MeSH term(s) Adoptive Transfer ; Animals ; Autoantibodies/analysis ; Autoimmune Diseases/immunology ; Biomarkers/analysis ; Cell Proliferation ; Chimera ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Flow Cytometry ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Animal ; Pancreatitis/immunology ; Protein-Serine-Threonine Kinases/genetics ; Receptor, Transforming Growth Factor-beta Type II ; Receptors, Transforming Growth Factor beta/genetics ; S100 Calcium-Binding Protein A4 ; S100 Proteins/metabolism ; Signal Transduction/physiology ; T-Lymphocytes/immunology ; Transforming Growth Factor beta/metabolism ; beta-Galactosidase/analysis
    Chemical Substances Autoantibodies ; Biomarkers ; Receptors, Transforming Growth Factor beta ; S100 Calcium-Binding Protein A4 ; S100 Proteins ; S100a4 protein, mouse ; Transforming Growth Factor beta ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Receptor, Transforming Growth Factor-beta Type II (EC 2.7.11.30) ; beta-Galactosidase (EC 3.2.1.23)
    Language English
    Publishing date 2009-07-21
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gut.2008.170779
    Database MEDical Literature Analysis and Retrieval System OnLINE

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