Reasoning about Cardinal Directions between Extended Objects

Direction relations between extended spatial objects are important commonsense knowledge. Recently, Goyal and Egenhofer proposed a formal model, known as Cardinal Direction Calculus (CDC), for representing direction relations between connected plane regions. CDC is perhaps the most expressive qualitative calculus for directional information, and has attracted increasing interest from areas such as artificial intelligence, geographical information science, and image retrieval. Given a network of CDC constraints, the consistency problem is deciding if the network is realizable by connected regions in the real plane. This paper provides a cubic algorithm for checking consistency of basic CDC constraint networks, and proves that reasoning with CDC is in general an NP-Complete problem. For a consistent network of basic CDC constraints, our algorithm also returns a 'canonical' solution in cubic time. This cubic algorithm is also adapted to cope with cardinal directions between possibly disconnected regions, in which case currently the best algorithm is of time complexity O(n^5)

Pathogenetic role of tissue factor in graft-versus-host disease

Graft-versus-host disease (GVHD) is a serious complication after allogeneic stem cell transplantation, the mechanism of it is still not elucidated. Recent findings suggest that host endothelial cells are a target of alloreactive donor cytotoxic T lymphocytes in GVHD and tissue factor (TF) plays an important role not only in coagulation-inflammation cycle, but also in transplant immunology. We postulate TF expression in vascular endothelial cells(VEC) may play an pivotal role in the pathogenesis of GVHD. TF gene andprotein expression in target organs of GVHD in aGVHD mice was significantly elevated compared to that of controls as determined by real-time PCR and Western blotting. Allogeneic CD4^+^T cell and CD8^+^T cells enhanced TF, VCAM-1, TNF-[alpha], IFN-[gamma] and IL-6 expression in TNF-[alpha] prestimulated HUVECs compared to controls as determined by flowcytometry and real-time PCR. JNK and p38MAPK mediated allogeneic T cells-induced TF expression in HUVECs. These effects were largely prevented by monoclonal antibody against TF, SB203580 and SP600125. In concert, these data provide strong evidence that upregulated TF expression is related to tissue damage caused by GVHD, TF isthe key factor in GVHD mediated by endothelial cells and allogeneic T cells-induced TF and consecutive proinflammatory cytokines expression in VEC contribute to the pathogenesis of GVHD