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Flavor versus mass eigenstates in neutrino asymmetries: implications for cosmology
Barenboim, Gabriela,Kinney, William H.,Park, Wan-Il Springer 2017 European Physical Journal C Vol.77 No.9
<P>We show that, if they exist, lepton number asymmetries (L-alpha) of neutrino flavors should be distinguished from the ones (L-i) of mass eigenstates, since Big Bang Nucleosynthesis (BBN) bounds on the flavor eigenstates cannot be directly applied to the mass eigenstates. Similarly, Cosmic Microwave Background (CMB) constraints on the mass eigenstates do not directly constrain flavor asymmetries. Due to the difference of mass and flavor eigenstates, the cosmological constraint on the asymmetries of neutrino flavors can be much stronger than the conventional expectation, but they are not uniquely determined unless at least the asymmetry of the heaviest neutrino is well constrained. The cosmological constraint on L-i for a specific case is presented as an illustration.</P>
WHY WE SHARE IT – AN INVESTIGATION ABOUT REASONS FOR ACCOUNT SHARING OF ONLINE CONTENT PROVIDERS
Gerrit Cziehso,Monika Kukar-Kinney,Joel Mier,Dennis Tann 글로벌지식마케팅경영학회 2018 Global Marketing Conference Vol.2018 No.07
To remain competitive in the realm of the Internet, developers of new business models not only have to take into account the behavior of online consumers, but also their misbehavior. Today, companies are faced with special challenges regarding consumer misbehavior, particularly in the segment of online content providers (e.g. Netflix, Amazon Prime Video, etc.), where it has become a common practice to share an account with multiple persons, while only one of them is the rightful owner. Such misbehavior may lead to negative consequences, such as direct and indirect financial performance implications, increased workload to deal with dysfunctional customer behavior, underestimated membership, and a lack of understanding the true customer base (Harris & Raynolds, 2003; Hwang et al., 2009). Therefore this study investigates account sharing as a part of customer misbehavior with a qualitative approach to identify customers’ reasons for account sharing. Thereby this investigation makes meaningful implications for companies (e.g., Netflix) and research alike.
Bai, Xiyuan,Shang, Shaobin,Henao-Tamayo, Marcela,Basaraba, Randall J.,Ovrutsky, Alida R.,Matsuda, Jennifer L.,Takeda, Katsuyuki,Chan, Mallory M.,Dakhama, Azzeddine,Kinney, William H.,Trostel, Jessica National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.16
<P><B>Significance</B></P><P>Interleukin-32 (IL-32) is induced by IL-1β, Toll-like receptor agonists, and nucleotide oligomerization domain as well as by <I>Mycobacterium tuberculosis</I> (<I>MTB</I>). Expression of human IL-32γ in the lungs of mice reduced the burden of <I>MTB</I> in both the lungs but also in the spleen and was associated with increased survival. Mechanistically, increased numbers of host-protective innate and adaptive immune cells were present in the IL-32 transgenic mice. Alveolar macrophages from the transgenic mice were also better able to control <I>MTB</I> infection and had increased colocalization of <I>MTB</I> with lysosomes. IL-32 expression was increased in the surgically resected lungs of tuberculosis patients, particularly in macrophages, airway epithelial cells, B cells, and T cells. Thus, IL-32 enhances host immunity against <I>MTB</I>.</P><P>Silencing of interleukin-32 (IL-32) in a differentiated human promonocytic cell line impairs killing of <I>Mycobacterium tuberculosis</I> (<I>MTB</I>) but the role of IL-32 in vivo against <I>MTB</I> remains unknown. To study the effects of IL-32 in vivo, a transgenic mouse was generated in which the human <I>IL-32γ</I> gene is expressed using the surfactant protein C promoter (SPC-IL-32γTg). Wild-type and SPC-IL-32γTg mice were infected with a low-dose aerosol of a hypervirulent strain of <I>MTB</I> (W-Beijing HN878). At 30 and 60 d after infection, the transgenic mice had 66% and 85% fewer <I>MTB</I> in the lungs and 49% and 68% fewer <I>MTB</I> in the spleens, respectively; the transgenic mice also exhibited greater survival. Increased numbers of host-protective innate and adaptive immune cells were present in SPC-IL-32γTg mice, including tumor necrosis factor-alpha (TNFα) positive lung macrophages and dendritic cells, and IFN-gamma (IFNγ) and TNFα positive CD4<SUP>+</SUP> and CD8<SUP>+</SUP> T cells in the lungs and mediastinal lymph nodes. Alveolar macrophages from transgenic mice infected with <I>MTB</I> ex vivo had reduced bacterial burden and increased colocalization of green fluorescent protein-labeled <I>MTB</I> with lysosomes. Furthermore, mouse macrophages made to express IL-32γ but not the splice variant IL-32β were better able to limit <I>MTB</I> growth than macrophages capable of producing both. The lungs of patients with tuberculosis showed increased IL-32 expression, particularly in macrophages of granulomas and airway epithelial cells but also B cells and T cells. We conclude that IL-32γ enhances host immunity to <I>MTB</I>.</P>