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Full NameProfessor Laoise McNamara

Biomedical Engineering

National University of Ireland Galway

Webpage:mechanobiology.ie

Email Address:Email hidden; Javascript is required.

Research Fields
  • cell and developmental biology/regenerative medicine
  • bioengineering/medical devices
Postgrad Medical Specialties
  • Medicine
  • Surgery
  • Pathology
  • Radiology
  • Sports and Exercise Medicine
Medical Subspecialties
  • Cardiac Surgery
  • Endocrinology
  • Orthopaedic surgery
  • Rheumatology
My Work

Biomechanical interactions of self-expanding valves:
We have developed experimental and computational models to simulate implantation of Transcatheter Aortic Valve Implants (TAVI). In collaboration with Medtronic we investigated how non-concentric stent deployment influenced (1) the fluid mechanics and haemolytic potential of the device and (2) leaflet mechanics and deformation (Gunning et al., 2015, Gunning et al., 2014a, Gunning et al., 2014b). In collaboration with Boston Scientific we experimentally and computationally investigated stent-root interaction for calcified aortic valves (McGee et al., 2018a, McGee et al.b). These studies inform design of next-generation TAVI devices.

Biological consequences of thermal elevations during surgical cutting:
In collaboration with Stryker Instruments, experimental and computational methods were employed to predict thermal elevations to bone cells due to orthopaedic surgical cutting (Dolan et al., 2014). The effects of such thermal elevations on cell damage, regeneration and signalling responses by bone cells to initiate remodelling were uncovered in vivo and in vitro (Dolan et al., 2016, Dolan et al., 2015, Dolan et al., 2012).

The role of mechanobiology in the aetiology osteoporosis and metastatic bone disease:
Our research was the first to show that bone tissue composition is also altered at the microscopic level (McNamara et al., 2006, Brennan et al., 2011a, Brennan et al., 2011b, Brennan et al., 2012b), which is undetectable by conventional diagnostic techniques (DEXA) but may contribute to bone fracture. We have found that such changes likely arise due to (a) disrupted mechanosensory proteins (Voisin and McNamara, 2015), (b) altered biochemical responses (Brennan et al., 2014, Brennan et al., 2012 , Brennan et al., 2012a, Deepak et al., 2017) and (c) changes in mechanical stimuli (Verbruggen et al., 2015, Vaughan et al., 2015, Verbruggen et al., 2016) to bone cells following estrogen deficiency. These findings uncover fundamental changes in mechanobiology, a crucial process in healthy bone, not previously understood during osteoporosis. We are currently applying these methods and techniques to understand the role of mechanobiology in bone metastasis.