Surviving a delayed trans-diaphragmatic hepatic rupture complicated by an acute superior vena cava and thoracic compartment syndromes.

We describe the first reported survivor of a delayed trans-diaphragmatic hepatic rupture complicated by acute superior vena cava (SVCS) and thoracic compartment syndromes (TCS). A thirty one year old male was involved in a boating accident. The patient was diagnosed with a grade IV liver laceration, which was initially managed with both angio-embolization and open surgical repair. Exactly one month from admission, the patient presented with an abrupt cardiac arrest, which was further complicated by a SVCS and TCS. The SVCS was managed with bilateral thoracostomies which revealed a delayed trans-diaphragmatic hepatic rupture into the right chest cavity. The TCS was managed with a decompressive thoraco-abdominal incision. The patient survived and is now leading a normal life. Our success was largely due to an integrated trauma system of physicians, nurses and technicians that prompted the early recognition of two potentially life threatening complications of a delayed trans-diaphragmatic hepatic rupture.

Calcineurin activation is only one calcium-dependent step in cytotoxic T lymphocyte granule exocytosis.

We have tested the idea that calcineurin, a calcium-dependent phosphatase that is critical for activating cytokine gene expression in helper T cells, plays a role in lytic granule exocytosis in cytotoxic T lymphocytes (CTLs). We used TALL-104 human leukemic CTLs as a model. Our results confirm an earlier report (Dutz, J. P., Fruman, D. A., Burakoff, S. J., and Bierer, B. E. (1993) J. Immunol. 150, 2591-2598) that immunosuppressive drugs inhibit exocytosis in CTLs stimulated either via the T cell receptor (TCR) or via TCR-independent soluble agents. Of the two recently reported alternate targets of immunosuppressive drugs (Matsuda, S., Shibasaki, F., Takehana, K., Mori, H., Nishida, E., and Koyasu, S. (2000) EMBO Rep. 1, 428-434 and Matsuda, S., and Koyasu, S. (2000) Immunopharmacology 47, 119-125), JNK is not required for lytic granule exocytosis, but we were not able to exclude a role for P38. Exocytosis could be inhibited by expressing GFP fused to a C-terminal fragment of CAIN (cabin 1), but not by expressing VIVIT-GFP. Finally, expressing either full-length or truncated constitutively active mutant calcineurin A enhanced lytic granule exocytosis. However, the mutant calcineurin was unable to support exocytosis when cells were stimulated in the absence of Ca2+ influx. Taken together, our results support the idea that activation of calcineurin is required for lytic granule exocytosis but suggest that it is not the sole Ca2+-dependent step.