Targeting The Mitochondrial Transition Pore In Acute SCI Essay

Additionally, having these precautions will save more lives. With constant, damaging effects to the brain, people start to develop tumors and other injuries.

Evidence is mounting that a correlation exists between TBI and the likelihood of the development of a neurodegenerative disease such as AD (Weiner et al, 2013). The conflicts in Iraq and Afghanistan have produced countless cases of TBI. It is estimated that since 2003 more than 200,000 of the men and women deployed to Iraq and Afghanistan have been exposed to concussive events that have resulted in a diagnosis of TBI (DOD,

Brain injury is a general term referring to any injury to the brain. Brain injury is stimulated by a number of factors such as bike and a car accident, assault, as fall, or a blow to the head, but these example of brain injuries which occur in nature. They are types of brain injuries such as, the brain injury that occur after birth, the traumatic brain injury (TBI) which is caused by an object such as stabbing or gun shots entering the brain causing widespread damage (Brain Injury Support(BIS), 2015; Volpe,2012). Apart from these types of brain injuries, the brain can be damaged due to lack of enough oxygen to the brain as a result to heart attack, internal bleeding like a stroke (ABI, 2015; Volpe, 2012). ABI (acquired brain injury) rehabilitation is an agency that specialises in rehabilitation after a traumatic brain injury and a stroke. But this paper will focus on brain injury only because it is an area of interest. Max Cavit is the manager director of ABI who came to an agreement with ACC to develop rehabilitation service in New Zealand (NZ), Max 's ideas evolve around how people living with brain injury were mostly garaged without access to rehabilitation service in 1996 NZ (ABI, 2015). After fifteen years, ABI has stood alone with its own facilities in Auckland and Wellington. ABI has about 200 medical specialist across all regions, and these specialists have a background whether in nursing or therapy, but they all have experience across all ages

Mild traumatic brain injury (mTBI) is becoming more prevalent every year, “with an incidence of about 100 to 300 per 100 000” (Konrad et al 2010). Mild traumatic brain injury or concussion can be the result of any minor trauma to the head from accident, sports related injury, blast injury, or fall. “Possible acute symptoms of mTBI comprise short-time unconsciousness, headache, dizziness, irritability, anxiety and impaired neuropsychological functions such as reduced attention, concentration or memory problems” (Evans, 1992; Hall et al. 2005 as cited by Konrad et al 2010). Some people who sustain a mTBI return to base level of function within hours and some take up to two months, there are even those that years later have not fully

Traumatic Brain Injury (TBI) is one of the leading causes of death and disability among children, adolescents, and adults (Trudel, Scherer, & Elias, 2009, p.41). There are close to 1.4 million individuals a year who are treated with a TBI. Out of this 50,000 of them die. That is 1 out of every 28 people treated for a TBI dies every year. Another 6 out of 28 people are admitted into medical facilities for longer-term care. These number do not take in account the number of people each year with TBI’s who go untreated. However, TBI’s had received little to no support publicly or policy wise until recent years. This increase in attention was due to the increase in TBI’s among military personnel returning home from the wars in Afghanistan and Iraq.

Traumatic brain injuries, or TBI, are the leading cause of death in children and young adults globally. Of the people who survive, most live a drastically

I am conducting biomedical research in the laboratory of cardiac physiology under the mentorship of Dr. Elizabeth Murphy. Cardiovascular disease is the major cause of death in the US; therefore, a better understanding of the mechanisms regulating cardiomyocyte death in ischemia and reperfusion injury are important. Mitochondrial calcium plays a crucial role in the normal functioning of many processes, including the regulation of cardiac biochemical pathways and mediating ischemia-reperfusion injury. The uptake of calcium into the mitochondrial matrix is regulated by the mitochondrial calcium uniporter (MCU). An endogenous enzyme, Ca2+ Calmodulin Dependent Kinase II (CaMKII) has shown to regulate cell death and have increased activity during

Mild traumatic brain injuries (mTBI) are amongst the most common injuries affecting approximately 42 million individuals annually (Gardner & Yaffe, 2015). This incidence rate is inaccurate as many mTBI are not reported (Gardner & Yaffe, 2015). Such injuries are thought to increase susceptibility to neurodegenerative diseases including Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS) (Gardner & Yaffe, 2015). AD accounts for up to 80% of all senile dementia and is characterized by cognitive deficits that progressively manifest into severe cognitive and behavioral impairment (Elder et al., 2010). Such symptoms are causally associated with amyloid plaques and neurofibrillary tangles

The literature is outdated; publishing dates ranged from 1997 to 2006. This article was published in 2009; only one of the articles used for research was within five years, all others were older. The literature would be more relevant if it was more recent. The literature that was used although it may have been outdated, did support the problem researched; using hypothermia as a means of treatment for a traumatic brain injury.

Such neuroprotective effect was long-lasting and was still observed when thiorphan was administered 12 h after the insult, suggesting a remarkable window for therapeutic intervention

The amyloid precursor protein (APP) is long associated with Alzheimer’s disease (AD). It is a single-pass transmembrane protein and is responsible for producing the neurotoxic Aβ plaque which accumulates within the brain (O’Brien et al. 2011). This accumulation of Aβ is what characterises AD. However, in spite of APP’s detrimental role in the pathogenesis of AD, it has been recently shown that APP can act as a neuroprotective molecule following traumatic brain injury (TBI). Approximately 10 million people worldwide are affected by this disease every year and it is projected that by 2020, TBI will surpass various diseases and become a major disease of burden (Hyder et al. 2007). Thus, due to this increase in morbidity and burden, TBI is an urgent medical and public problem.

In the military setting, wide decompression carries the benefit of reducing malignant brain edema and elevations in ICP in the first several hours after the TBI (intro 15,16). However, the patients with large cranial defects and complex brain injuries remain as a challenge, and the outcome at severe primary or secondary blast injuries of children varies from adult one. Therefore, conclusive evidence of whether it has a beneficial or adverse effect on outcome is lacking (Intro4, trat 9). Children have more shearing and diffuse damage than adults. Even the definition of normal ICP and CPP varies with age (intro19). The differences in bio-structure of children’s brain from adult including more edema, hypotension, cardiac output, and less antioxidative capacity and basement membrane glycoproteins. Better outcome in children would be explained by several factors such as low level of chondrotin sulfate proteoglycan glycoproteins, which is responsible for rigidity and support of parenchyme (intro18,

Colton et al. (2014) research looked at 117 clients who experienced increase intracranial pressure as a result of severe traumatic brain injury. Their research looked at client’s respond to pharmacological interventions and these pharmacological interventions include hypertonic saline, mannitol, propofol, fentanyl, and barbiturate. In their research Colton et al., (2014) found “all treatment resulted in significant intracranial pressure changes after 1 hour or 2 hours except for mannitol and barbiturate administration” (Colton at el., 2014). This finding is significant given that mannitol is used as a first line treatment for management of increased intracranial pressure. The chart below demonstrates how each of these pharmacological interventions decreased intracranial pressure and it allows us to compare each pharmacological intervention to each other. (Colton et al., 2014)

The response to a SCI can be separated into three discrete, partially overlapping phases: acute (seconds to minutes after SCI), sub-acute (minutes to weeks after SCI), and chronic (months to years after SCI). The acute phase centers around the primary SCI damage resulting from the trauma, resulting in immediate physical and biochemical cellular changes. These include direct cell death, vasospasms (leads to vasoconstriction, ischemia, and tissue death), plasma membrane compromise, disruption of ionic homeostasis, and accumulation of neurotransmitters (26, 27). Many local immune cells such as microglia, neutrophils, and astrocytes respond instantly. While some acute events continue into the sub-acute phase (such as neurotransmitter and ionic dysregulation), the sub-acute and chronic phases are defined by the

Currently, there are no effective treatments that actively promote tissue repair and regeneration post moderate-to-severe TBIs. While there have been efforts to mitigate the secondary damage post-TBI, these measures have been proven clinically unsuccessful. At present, there is no cure for neither the initial damage nor the secondary loss of tissue post the biomechanical insult. In this study, we sought to devise a mechanism that would provide neuroprotective factors and facilitate tissue repair post moderate-to-severe TBIs. We developed a sulfated CS-GAG matrix, a biomaterial native to the brain’s ECM, capable of regulating NSC behavior.29 As part of this study, we acutely delivered these sulfated CS-GAG matrices into the rat cortex after