Predicting Threats on Electric Health Record Systems

Security is a key concern in the development of electronic health record (EHR) systems. This paper considers Neutralization Theory and the Fear Appeals Model in proposing a conceptual model for use in predicting breach behaviors within EHR systems. The goal of the model is to determine which factors influence security breach intent on the part of the offender. Specifically, perceived penalty, perceived evasiveness, awareness of opportunity, enforcement, and user participation are proposed to act as antecedents to security breach intent, a surrogate for actual breach behavior

Project Report No. 62, Site Index Equations for Loblolly and Slash Pine Plantations in East Texas, Update: Fall 1998

This update utilizes height-age pairs measured from 1982 - 1998. As a result, the number of observations available for analysis is 1,814 loblolly and 788 slash. It is anticipated that the equations in this Fall 1998 update may quantify the productivity of East Texas loblolly and slash pine plantations in a more accurate and reliable manner than the seven previous sets of equations

T-bet–dependent S1P5 expression in NK cells promotes egress from lymph nodes and bone marrow

During a screen for ethylnitrosourea-induced mutations in mice affecting blood natural killer (NK) cells, we identified a strain, designated Duane, in which NK cells were reduced in blood and spleen but increased in lymph nodes (LNs) and bone marrow (BM). The accumulation of NK cells in LNs reflected a decreased ability to exit into lymph. This strain carries a point mutation within Tbx21 (T-bet), which generates a defective protein. Duane NK cells have a 30-fold deficiency in sphingosine-1-phosphate receptor 5 (S1P(5)) transcript levels, and S1P(5)-deficient mice exhibit an egress defect similar to Duane. Chromatin immunoprecipitation confirms binding of T-bet to the S1pr5 locus. S1P-deficient mice exhibit a more severe NK cell egress block, and the FTY720-sensitive S1P(1) also plays a role in NK cell egress from LNs. S1P(5) is not inhibited by CD69, a property that may facilitate trafficking of activated NK cells to effector sites. Finally, the accumulation of NK cells within BM of S1P-deficient mice was associated with reduced numbers in BM sinusoids, suggesting a role for S1P in BM egress. In summary, these findings identify S1P(5) as a T-bet–induced gene that is required for NK cell egress from LNs and BM