728 research outputs found
The NLO contributions to the scalar pion form factors and the annihilation corrections to the decays
In this paper, by employing the factorization theorem, we made the
first calculation for the space-like scalar pion form factor at
the leading order (LO) and the next-to-leading order (NLO) level, and then
found the time-like scalar pion form factor by analytic
continuation from the space-like one. From the analytical evaluations and the
numerical results, we found the following points: (a) the NLO correction to the
space-like scalar pion form factor has an opposite sign with the LO one but is
very small in magnitude, can produce at most decrease to LO result in
the considered region; (b) the NLO time-like scalar pion form factor
describes the contribution to the
factorizable annihilation diagrams of the considered decays,
i.e. the NLO annihilation correction; (c) the NLO part of the form factor
is very small in size, and is almost independent with the
variation of cutoff scale , but this form factor has a large strong
phase around and may play an important role in producing large CP
violation for decays; and (d) for and decays, the newly known NLO annihilation correction can produce
only a very small enhancement to their branching ratios, less than in
magnitude, and therefore we could not interpret the well-known -puzzle
by the inclusion of this NLO correction to the factorizable annihilation
diagrams.Comment: 26 pages, 12 figures, 1 Table; Minor correction
Down-Regulation of Platelet Surface CD47 Expression in Escherichia coli O157:H7 Infection-Induced Thrombocytopenia
BACKGROUND: Platelet depletion is a key feature of hemolytic uremic syndrome (HUS) caused by Shiga toxin-producing Escherichia coli (STEC) infection. The mechanism underlying STEC-induced platelet depletion, however, is not completely understood. METHODOLOGY/PRINCIPAL FINDINGS: Here we demonstrated for the first time that platelet surface expression of CD47 was significantly decreased in C57BL6 mice treated with concentrated culture filtrates (CCF) from STEC O157:H7. STEC O157:H7 CCF treatment also led to a sharp drop of platelet counts. The reduction of cell surface CD47 was specific for platelets but not for neutrophil, monocytes and red blood cells. Down-regulation of platelet surface CD47 was also observed in isolated human platelets treated with O157:H7 CCF. Platelet surface CD47 reduction by O157:H7 CCF could be blocked by anti-TLR4 antibody but not anti-CD62 antibody. Down-regulation of platelet surface CD47 was positively correlated with platelet activation and phagocytosis by human monocyte-derived macrophages. Furthermore, the enhanced phagocytosis process of O157:H7 CCF-treated platelets was abolished by addition of soluble CD47 recombinants. CONCLUSIONS/SIGNIFICANCE: Our results suggest that platelet CD47 down-regulation may be a novel mechanism underneath STEC-induced platelet depletion, and that the interactions between CD47 and its receptor, signal regulatory protein alpha (SIRPalpha), play an essential role in modulating platelet homeostasis
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