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Biology subjects

Higgins, C. A.

Publications and source records attributed to Higgins, C. A..

2 recordsLinked to original sources

Pressure equalisation as a principle for designing support surfaces to prevent deep tissue pressure ulcers

When immobile or neuropathic patients are supported by beds or chairs, their soft tissues undergo deformations that can cause pressure ulcers. Current support surfaces that redistribute under-body pressures at vulnerable body sites have not succeeded in reducing pressure ulcer prevalence. Here we show that adding a supporting lateral pressure can counter-act the deformations induced by under-body pressure, and that this pressure equalisation approach is a more effective way to reduce ulcer-inducing deformations than current approaches based on redistributing under-body pressure.\n\nA finite element model of the seated pelvis predicts that applying a lateral pressure to the soft tissue reduces peak von Mises stress in the deep tissue by a factor of 2.4 relative to a standard cushion -- a greater effect than that achieved by using a more conformable cushion. The ratio of peak lateral pressure to peak under-body pressure was shown to regulate deep tissue stress better than under-body pressure alone. By optimising the magnitude and position of lateral pressure, tissue deformations can be reduced to that induced when suspended in a fluid.\n\nOur results explain the lack of efficacy in current support surfaces, and suggest a new approach to designing and evaluating support surfaces: ensuring sufficient lateral pressure is applied to counter-act under-body pressure.

bioengineering

EPS8 facilitates uncoating of influenza A virus

All viruses balance interactions between cellular machinery co-opted to support replication and host factors deployed to halt the infection. We used gene correlation analysis to perform an unbiased screen for host factors involved in influenza A virus (FLUAV) infection. Our screen identified the cellular factor epidermal growth factor receptor pathway substrate 8 (EPS8) as the highest confidence pro-viral candidate. Knockout and overexpression of EPS8 confirmed its importance in enhancing FLUAV infection and titers. Loss of EPS8 did not affect virion attachment, uptake, or fusion. Rather, our data show that EPS8 specifically functions during virion uncoating. EPS8 physically associated with incoming virion components, and subsequent nuclear import of released ribonucleoprotein complexes was significantly delayed in the absence of EPS8. Our study identified EPS8 as a host factor important for uncoating, a crucial step of FLUAV infection during which the interface between the virus and host is still being discovered.

microbiology