Anti-PIV type 3 Monoclonal antibody, Clone O0402409

We have recently proposed a new method to extract the three-dimensional (3D) velocity vector data from double-exposure holographic particle image velocimetry (HPIV), which we call the digital shearing method. In contrast to the full 3D correlation, it has been shown that all three components (3Cs) of particle image displacement can be retrieved using six two-dimensional fast Fourier transform operations and appropriate coordinate transformations. In this paper we demonstrate the capabilities of this approach on actual HPIV data. The holographic recording method described uses an imaging system to record a hologram of high numerical aperture using a conventional 35 mm film. The holograms are digitized and particle images are reconstructed numerically. From particle images reconstructed from separate holograms, we illustrate the analysis process by computing the 3Cs of particle image displacement in a step-by-step manner.

Sendai virus (SeV) and human parainfluenza virus type I (hPIV 1) are highly homologous but have distinct host ranges, murine versus human. To identify the factors that affect the host specificity of parainfluenza viruses, we determined the infectivity and anti-IFN activities of SeV and hPIV1 in human and murine culture cells. SeV infected normal human lung MRC-5 and murine lung MM14.Lu or MLg2908 cells efficiently. Infection with SeV induced the release of IFN-beta into culture medium in MRC-5 cells at similar levels with that of cells infected with hPIV1. SeV or hPIV1 infections, as well as expression of SeV or hPIV I C proteins, inhibited the nuclear localization of STAT I induced by IFN-beta, suggesting that both SeV and hPIV I C proteins block the IFN Jak/STAT pathway in MRC-5 cells. Pretreatment of MRC-5 cells with IFN suppressed replication of SeV and hPIV1 at an early stage of infection. However, hPIV1 overcame this suppression while SeV did not. SeV replication was restored in IFN-beta pretreated murine MM14. Lu cells, suggesting SeV anti-IFN activity is species specific. These results suggest that SeV is less effective than hPIV1 in overcoming antiviral activity in human cells, which could be one of the factors that restrict the host range of SeV. (c) 2006 Elsevier B.V. All rights reserved.