The design of decisions: Matching clinical decision support recommendations to Nielsen's design heuristics.

Objective: While general design heuristics exist for graphic user interfaces, it remains a challenge to facilitate the implementation of these heuristics for the design of clinical decision support. Our goals were to map a set of recommendations for clinical decision support design found in current literature to Jakob Nielsen's traditional usability heuristics and to suggest usability areas that need more investigation.

Materials And Methods: Using a modified nominal group process, the research team discussed, classified, and mapped recommendations, organized as interface, information, and interaction, to design heuristics.

Interface, information, interaction: a narrative review of design and functional requirements for clinical decision support.

Objective: Provider acceptance and associated patient outcomes are widely discussed in the evaluation of clinical decision support systems (CDSSs), but critical design criteria for tools have generally been overlooked. The objective of this work is to inform electronic health record alert optimization and clinical practice workflow by identifying, compiling, and reporting design recommendations for CDSS to support the efficient, effective, and timely delivery of high-quality care.

Material And Methods: A narrative review was conducted from 2000 to 2016 in PubMed and The Journal of Human Factors and Ergonomics Society to identify papers that discussed/recommended design features of CDSSs that are associated with the success of these systems.

p53 and hTERT determine sensitivity to viral apoptosis.

Apoptosis is a potent host defense against microbes. Most viruses have adapted strategies to counteract this response. Herpes simplex virus (HSV) produces a balance between pro- and antiapoptotic processes during infection.

Susceptibility of cancer cells to herpes simplex virus-dependent apoptosis.

Apoptosis has recently been associated with herpes simplex virus 1 (HSV-1) latency and disease severity. There is an intricate balance between pro- and anti-apoptotic processes during HSV-1 infection. When anti-apoptotic pathways are suppressed, this balance is upset and the cells die by apoptosis, referred to here as HSV-1-dependent apoptosis (HDAP).

Caspase 3 activation during herpes simplex virus 1 infection.

During herpes simplex virus 1 (HSV-1) infection, apoptosis is initiated by immediate early gene transcription and is later modulated by proteins synthesized in infected cells. We have previously shown that procaspase 3 levels are reduced during HSV-1 replication. We now demonstrate that a replication-defective HSV-1 recombinant virus which is incapable of packaging viral DNA into capsids activated caspase 3 but retained the ability to prevent the apoptotic process from killing the infected cells.

African green monkey kidney Vero cells require de novo protein synthesis for efficient herpes simplex virus 1-dependent apoptosis.

During HSV-1 infection, IE gene expression triggers apoptosis, but subsequent synthesis of infected cell proteins blocks apoptotic death from ensuing. This "HSV-1-dependent" apoptosis was identified in HEp-2/HeLa cells infected with wild-type HSV-1 in the presence of an inhibitor of protein synthesis or a virus lacking ICP27 {HSV-1(vBSDelta27)}. Unlike HEp-2/HeLa cells, vBSDelta27-infected Vero cells fail to exhibit dramatic apoptotic morphologies at times prior to 24 hpi.