53 research outputs found
New Mechanics of Traumatic Brain Injury
The prediction and prevention of traumatic brain injury is a very important
aspect of preventive medical science. This paper proposes a new coupled
loading-rate hypothesis for the traumatic brain injury (TBI), which states that
the main cause of the TBI is an external Euclidean jolt, or SE(3)-jolt, an
impulsive loading that strikes the head in several coupled degrees-of-freedom
simultaneously. To show this, based on the previously defined covariant force
law, we formulate the coupled Newton-Euler dynamics of brain's micro-motions
within the cerebrospinal fluid and derive from it the coupled SE(3)-jolt
dynamics. The SE(3)-jolt is a cause of the TBI in two forms of brain's rapid
discontinuous deformations: translational dislocations and rotational
disclinations. Brain's dislocations and disclinations, caused by the
SE(3)-jolt, are described using the Cosserat multipolar viscoelastic continuum
brain model.
Keywords: Traumatic brain injuries, coupled loading-rate hypothesis,
Euclidean jolt, coupled Newton-Euler dynamics, brain's dislocations and
disclinationsComment: 18 pages, 1 figure, Late
Shear Forces during Blast, Not Abrupt Changes in Pressure Alone, Generate Calcium Activity in Human Brain Cells
Blast-Induced Traumatic Brain Injury (bTBI) describes a spectrum of injuries caused by an explosive force that results in changes in brain function. The mechanism responsible for primary bTBI following a blast shockwave remains unknown. We have developed a pneumatic device that delivers shockwaves, similar to those known to induce bTBI, within a chamber optimal for fluorescence microscopy. Abrupt changes in pressure can be created with and without the presence of shear forces at the surface of cells. In primary cultures of human central nervous system cells, the cellular calcium response to shockwaves alone was negligible. Even when the applied pressure reached 15 atm, there was no damage or excitation, unless concomitant shear forces, peaking between 0.3 to 0.7 Pa, were present at the cell surface. The probability of cellular injury in response to a shockwave was low and cell survival was unaffected 20 hours after shockwave exposure
Computational neurotrauma—design, simulation, and analysis of controlled cortical impact model
Microvascular endothelial cells-derived microvesicles imply in ischemic stroke by modulating astrocyte and blood brain barrier function and cerebral blood flow
Pomalidomide mitigates neuronal loss, neuroinflammation, and behavioral impairments induced by traumatic brain injury in rat
Increased Intracranial Pressure after Diffuse Traumatic Brain Injury Exacerbates Neuronal Somatic Membrane Poration but not Axonal Injury: Evidence for Primary Intracranial Pressure-Induced Neuronal Perturbation
Quantification of Poly(ADP-Ribose)-Modified Proteins in Cerebrospinal Fluid from Infants and Children after Traumatic Brain Injury
Reduction of Cognitive and Motor Deficits after Traumatic Brain Injury in Mice Deficient in Poly(ADP-Ribose) Polymerase
Monitoring neuron and astrocyte interactions with a 3D cell culture system
Methods are described for the generation and analysis of 3D co-culture models in which astrocyte and neuronal behavior can be studied. Cells may be obtained from a variety of sources, then cultured within collagen hydrogels to explore cellular responses and interactions in response to substances under test or under conditions that mimic physiological or pathological environments. Cell populations are labelled then either mixed within gels or arranged as separate adjacent populations, with further options including directing the self-alignment of cells to form anisotropic 3D cultures. Immunofluorescence staining and confocal microscopy can be used to capture image data from 3D structures and detailed protocols are provided for obtaining reliable results. Finally, 3D image analysis of confocal microscopy data is discussed, providing guidance on how astrocyte and neuronal features can be quantified
Poly(adenosine diphosphate—ribose) polymerase expression in human traumatic brain injury
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