Optimizing usability and signal capture: a proactive risk assessment for the implementation of a wireless vital sign monitoring system.

Wearable vital sign monitors are a promising step towards optimal patient surveillance, providing continuous data to allow for early detection and treatment of patient deterioration. However, as wearable monitors become more widely adopted in healthcare, there is a corresponding need to carefully design the implementation of these tools to promote their integration into clinical workflows and defend against potential misuse and patient harm. Prior to the roll-out of these monitors, our multidisciplinary team of clinicians, clinical engineers, information technologists and research investigators conducted a modified Healthcare Failure Mode and Effect Analysis (HFMEA), a proactive evaluation of potential problems which could be encountered in the use of a wireless vital signs monitoring system. This evaluation was accomplished by focussing on the identification of procedures and actions that would be required during the devices' regular usage, as well as the implementation of the system as a comprehensive process. Using this method, the team identified challenges that would arise throughout the lifecycle of the device and developed recommendations to address them. This proactive risk assessment can guide the implementation of wearable patient monitors, optimising the use of innovative health information technology.

DNMT1 is regulated by ATP-citrate lyase and maintains methylation patterns during adipocyte differentiation.

During adipocyte differentiation, significant epigenomic changes occur in association with the implementation of the adipogenic program. We have previously shown that histone acetylation increases during differentiation in a manner dependent on acetyl coenzyme A (acetyl-CoA) production by the enzyme ATP-citrate lyase (ACL). Whether ACL regulates nuclear targets in addition to histones during differentiation is not clear. In this study, we report that DNA methyltransferase 1 (DNMT1) levels in adipocytes are controlled in part by ACL and that silencing of DNMT1 can accelerate adipocyte differentiation. DNMT1 gene expression is induced early in 3T3-L1 adipocyte differentiation during mitotic clonal expansion and is critical for maintenance of DNA and histone H3K9 methylation patterns during this period. In the absence of DNMT1, adipocyte-specific gene expression and lipid accumulation occur precociously. Later in differentiation, DNMT1 levels decline in an ACL-dependent manner. ACL-mediated suppression of DNMT1 occurs at least in part by promoting expression of microRNA 148a (miR-148a), which represses DNMT1. Ectopic expression of miR-148a accelerates differentiation under standard conditions and can partially rescue a hypermethylation-mediated differentiation block. The data suggest a role for DNMT1 in modulating the timing of differentiation and describe a novel ACL-miR-148a-dependent mechanism for regulating DNMT1 during adipogenesis.