特別講演会のお知らせ 2017.6.27
北海道支部 支部長 土谷 浩昭
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記
日 時 ： 2017年 7月 7日（金） 16：30〜18：00
場 所 ： 北海道大学工学部 アカデミックラウンジ3 （札幌市北区北１３条西８丁目）
講 演 ： 16:30〜17:15
Prof. Masaaki Sato, Professor, Director
of Frontier Research Institute for Interdisciplinary Sciences, Tohoku
University, Japan
Arterial bifurcations are known to be common sites for development of cerebral aneurysms, where the combination of high shear stress (SS) and
high spatial SS gradient (SSG) may induce some damages or dysfunction
of endothelial cells (EC). However, the details of the relationship
between the hemodynamic environment and EC responses remain unclear.
We have developed two types of flow chamber to apply simultaneously SS and SSG to ECs. One is T-shaped flow section in a chamber and
the flow velocity and SSG are not constant depending on the location.
The other is designed to be SSG constant in the some flow section.
Confluent ECs were exposed to various levels of SS and SSG for 24 h using both flow chambers.
Although ECs exposed to lower levels of SS/SSG were not oriented
or elongated in the direction of flow,
they responded under the conditions of SS with an SSG when the
SS exceeded a threshold value depending on the magnitude of SSG.
Using a simplified computational model, we found that the presence of an SSG affects the strain field in ECs, resulting in a morphological response.
SS combined with an SSG can alter the localization of SS mechano-sensing
proteins along the strain field as a result of shear flow.
The results suggest that the magnitude of the relationship between
SS and SSG plays an important role in regulating EC polarity and
the resulting morphological changes in response to fluid flow.
17:15〜18:00
Prof. Dan Bader, Professor, Faculty of Health Sciences, University of Southampton,
UK and Department of Biomedical Engineering,
Eindhoven University of Technology, the Netherlands
A few researchers have adopted an hierarchical approach, involving multi -scale models, to examine various aspects of soft tissue damage,
in the form of pressure ulcers (PUs). These have identified several
physiological mechanisms each of which play a role in concert in the aetio-pathogenesis
of PUs. These include, mechanical-induced ischaemia, ischaemia-reperfusion
injury, impaired lymphatic and interstitial fluid flows and direct cell
damage.
Translation to human models involves monitoring conditions at the loaded soft tissue interface and developing early screening methods to identify individuals
at risk of developing PUs. A recent focus involves the potential
damage caused by medical devices, designed to support functional activities
in patients with
vulnerable tissues. Devices include respiratory masks in both paediatric
and adult intensive care units, the prosthetic socket-stump interface of
amputees,
as well as support surfaces associated with sitting and lying.
The experimental approach adopts both biomechanical (pressure and
shear) and microclimate (temperature and humidity) measures,
and the use of biomarkers to assess the skin response to mechanical-induced irritation caused by prolonged use of medical devices.
The resulting parameters can provide input in the form of boundary
conditions at the device-skin interface into computational models to predict
conditions
at which soft tissue damage can occur.
共催 ： 日本機械学会北海道支部バイオメカニクス懇話会
日本機械学会バイオエンジニアリング部門（「計測と力学−生体への応用」研究会）
問い合わせ先：
Tel&Fax: 011-706-6424, Email: ohashi@eng.hokudai.ac.jp