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Traumatic Brain Injury (TBI) Modeling attempts to replicate certain aspects of TBI in order better understand what is physically happening to the brain. A variety of models can be used for this process with different models able to replicate certain aspects of TBI while also producing their own limitations. There are an estimated 1.7 million cases of TBI per year,〔(【引用サイトリンク】url=http://www.cdc.gov/traumaticbraininjury/statistics.html )〕 not taking into account the lasting affects that TBI may cause. TBI is also reported to be a contributing factor in about 30% of all injury related death.〔 Given how prevalent TBI is, preventing or minimizing its effects would benefit many people worldwide. In order to better understand what is happening during TBI, models are used to approximate the damage. Models bring both advantages and disadvantages to TBI research; on one hand brain models are very good at representing one aspect that can be observed, while on the other, aspects of the whole system must be ignored. For example, when studying blunt impacts, a neuronal cell culture model can be created that is the depth of the cortical layer. This is then subjected to different impact sizes, shapes, and forces in order to see how the cells react and what cytokines are released. This model works very well for the cortical layer, but deeper cell layers must be ignored due to the inability to oxygenate a deeper cell culture effectively. In this experiment, the disadvantage and limitation of this model is cell depth; any interactions that might occur below the cortical layer are ignored in order to gather accurate information within the cortical layer itself.〔 ==Damage on a cellular level== TBI occurs when neurons in the brain experience stresses and strains that exceed their threshold for elastic deformation.〔 Diffuse Axonal Injury (DAI) has been found to occur when strain exceeds 10%, and strain rates exceed 10 meters per second.〔 Once this threshold is passed, cells begin to die due to apoptosis, or simply from the rupturing of cell membranes. The death of neurons is compounded by the fact that neurons do not undergo mitosis unless very specific conditions are met; not only are the cells removed, but they are also not replaced by new neurons. This, in turn, means that a person experiencing multiple TBIs in a similar area will suffer the culmination of all previous injuries, possibly up to four times the initial damage. In addition to the physical stresses and strains that neurons experience during TBI, cell-cell interactions also contribute to the damage, primarily due to the formation of a glial scar. Neurons release cytokines during TBI that have a variety of effects, including summoning astrocytes to the afflicted area. Once they arrive, the astrocytes begin to generate more cytoskeletal structures until the damaged region is completely sealed. While this does create chemical and physical stability in the area, this scarring prevents any self-healing processes from occurring.〔 These processes are part of the natural damage response mechanisms which also include the brain experiencing a pro-inflammatory response at the location of damage that is regulated by an anti-inflammatory response that is farther away from the damaged area. In addition to this response, there is also a general haemodynamic response function that follows TBI.〔 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Traumatic brain injury modeling」の詳細全文を読む スポンサード リンク
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