In organelle function and its biochemical responses, it

In order to foresee the post-TBI outcomes of organelle function and its biochemical
responses, it became apparent to investigate the biomechanical effects on
junctions where blood vessels and cellular networks meet 4, 5. This region is
classified as the blood-brain barrier
which is just one of the primary pathways that will ultimately lead to calcium
overload and cell-death cascades, if mechanically injured 4, 5. This is a
result of microvascular stenosis or
blood that is restricted to the microcirculatory systems at the barrier due to
a narrowing of the vessels, which cause the latched feet of astrocytes to swell
and avoid glutamate intake 4. Therefore, the group of Ellis et al. prepared a
population of astroglial cell monolayers (from neonatal rat pups) to study the homeostatic
alterations of a mechanical insult 4, 9, 10. Their experiment setup is
depicted in Fig. 1.2 with the main component being the 94A Cell Injury
Controller (Commonwealth Biotechnology, Richmond, VA, USA) 10. Furthermore,
the well (Flexcell® culture plates, Dow Corning® corp.,
Midland, MI, USA) is a circular, collagen-coated silicone elastomer (Silastic®)
membrane which is readily flexible and assumed to be sufficiently adherent to
the cultured cells so that in the presence of a pressurized force, both will
stretch in a similar manner 9-11. The advantage this device presents is that
the user can control the duration and magnitude of the pulse 10. Moreover,
astrocytes are particularly responsive to a focalized mechanical pulse,
allowing the pressure waves to traverse their entire intercellular network 4.
Overall, their goal was to create a reliable model that could inflict voluntary
insults that are representable to forces experienced in vivo 10. Simply, the experiment was meant to demonstrate a
rapid application of force to induce in
vitro cell deformation and strain, rather than just uniformly compressing
the cells 10.