Time-domain seismic simulation can form the basis of reverse time depth migration and full-waveform inversion. These applications need to temporally crosscorrelate a forward simulation state with an adjoint simulation state and therefore need to be able to access each time step of a forward simulation in time-reverse order. This requires saving all forward states for all times (which can require more memory than is typically available on a computer system for many problems of interest), or the ability to checkpoint information and rapidly recompute forward simulation states as needed. Prior work has suggested how to do the latter by optimally choosing which forward simulation time steps to checkpoint, thereby enabling the most efficient reuse of memory buffers and minimizing recomputation. The optimal trade-off between memory usage and recomputation can be further improved under the assumption that the information needed to do temporal crosscorrelation is smaller than the information required to restart a simulation from a given time step. This assumption is true for many geophysical problems of interest. The modification can yield a reduction in the memory requirement and recomputation time. The tested examples applied to isotropic elastic reverse time migration and anisotropic viscoelastic full-waveform inversion.
The expression of CD5 can be induced on murine B-2 cells by anti-IgM, a recognized analog of thymus-independent 2 type (TI-2) antigen. Given that cyclosporin A (CsA) sensitivity is a distinguishing feature of TI-2 type B cell activation, we asked whether the in vitro induction of CD5 on B cells by anti-mu is CsA sensitive. We report that anti-mu induced CD5 expression on B-2 cells was inhibited by CsA as well as FK-520 and rapamycin. When L-685,818, a FK-520 and rapamycin antagonist, was added to anti-mu stimulated B cell cultures containing FK-520 or rapamycin, but not CsA, suppression was abrogated and complete induction of CD5 was seen. When we used either CD4+CD8+ thymocytes or peripheral T cells activated by phorbol ester and ionomycin, the cell surface induction of CD5 was also partially blocked by CsA, FK-520 and rapamycin. Moreover, in both B and T cells, the same immunosuppressive drugs did not affect constitutive CD5 expression but only blocked de novo induction. To determine the level of CD5 regulation, we activated T cells using phorbol myristate acetate (PMA)/ionomycin and report that CD5 induction was sensitive to actinomycin D (AcD). Similarly, the induction of CD5 on anti-mu activated B cells was blocked by AcD. In addition, T cells that were activated by PMA/ionomycin expressed more abundant CD5 mRNA than CsA or FK-520 treated cells. Based on the CsA-sensitive regulation of CD5 we thought that the CsA-sensitive nuclear factor of activated T cells (NFAT) might be involved in CD5 regulation. We report evidence by Western blot analysis that NFATp is expressed by both resting and TI activated B cells but apparently not CD4+CD8+CD5+ thymocytes. We conclude that in both B and T cells the induction of CD5 requires transcriptional regulation, and that the inhibition of CD5 expression by the immunosuppressive drugs CsA, FK-520 and rapamycin requires drug-immunophilin complex formation.
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