Essay On Biomeltration

Traumatic brain injury (TBI) is a type of injury that is a critical public health and socio-economic problem. TBI is a leading cause of death and disability in both children and adults [5]. The Centers for Disease Control and

Although these models were reported to produce graded severities of brain injury with similar morphology to the clinical condition, they present their own limitation. The severity of injury induced by an acceleration injury (weight drop) is often highly variable. Mild CCI cause focal contusion and subrachnoid hemorrhage are not commensurate with the typical concussion in humans. CCI and FPI require craniotomy/ craniectomy which are not clinically relevant. While blast injury is more controversial model with little standardization in blast modeling with regard to the duration of exposure and measurement of peak overpressure. An updated concussive animal model is necessary to replicate the important features of the injury in patients with mTBI as closely as

The review study written by Barkhoudarian et al explored the pathophysiology of concussive brain injury in young athletes. Sport-related concussions cause diffuse axonal injury (DAI) or white matter shearing injury (Barkhoudarian et al., 2011; Wozniak et al., 2007). They disrupt the axonal membrane leading to a disrupted normal ionic crossing and increased calcium influx. This flow of calcium not only causes mitochondrial-swelling leading to possible apoptosis but also prevents microtubular function (Halstead et al., 2010; Barkhoudarian et al., 2011). All these factors together can prevent axonal transport and form axonal blebs (Figure 6), hence altering the

Apoptosis, programmed cell death, has also been found to play a role in traumatic brain injury. This has been demonstrated in an early, but commonly acknowledged study involving the effects of TBIs on the brains of male Wistar rats. A craniotomy took place in each of the rats within the experimental group, which results in effects similar to a significant TBI. Four of the rats died within 10 to 15 minutes after the impact took place. All of the rats within the experimental group experienced a persistent cell loss in neurons, up to weeks after the experiment. Neurons at the center of the impact area were no longer structurally intact and did not recover at any time (Kaya). This study has proven that concussions and other significant TBIs lead to irreversible cell death.

Traumatic Brain injury (TBI) is projected to be a significant cause of global disease burden by 2020; with an estimated 10 million people affected by TBI annually worldwide. A concussion is the most common form of TBI and is particularly prevalent among children and young adults. The U.S. Centers for Disease Control (CDC) reported an annual estimated 1.6-3.8 million sports related TBI,

Traumatic Brain injury (TBI) is projected to be the third largest cause of global disease burden by 2020; with an estimated 10 million people affected by TBI annually worldwide.[endnoteRef:1] A concussion is the most common form of TBI and is particularly prevalent among children and young adults. The U.S. Centers for Disease Control (CDC) reported an annual estimated

Fruitvale was a perfect town. There was a nice creek (Strawberry Creek) that dogs and children could play in and a very good diner that families could eat out at. Fruitvale was a mini fairy-tale land, until they hit reality. Fruitvale was recently contaminated by a No-Bug Pesticide that farmers had been using to get rid of the bugs eating their crops. Twelve wells were tested and the No-Bug Pesticide had not contaminated the Fruitvale Municipal Water Well yet. After one year, we tested all of the wells again to see how far the contaminant has spread. We have found that Fruitvale has approximately three years to get Fruitvale de-contaminated. We want to keep the cost at a minimum and all of the Fruitvale residents safe. To meet these goals, we hypothesize that bioremediation would be the most efficient way to accomplish the following task of making Fruitvale a safe

TBI termed as Traumatic Brain Injury is an intracranial injury that often occurs when an external force is applied to the brain. TBI survivors encounter changes in cognition, sensorimotor function and personality. Incidents caused by rapid change in acceleration, blast waves, crush or penetration by a projectile. This could result in temporary or permanent impairment of cognitive, physical and psychological functions. In TBI, the primary injury is an external force, that induces mechanical tissue deformation, resulting in necrotic cell death, shearing and tearing of the vessels, neurons, glial and initiation of secondary injury. A primary injury would basically result in the immediate rupture of the brain tissue. A secondary injury involves

GM1 is a ganglioside that impacts neuronal plasticity, repair mechanisms, and the release of neurotrophins in the brain. GM1 promotes neuronal growth and survival by modulating tyrosine kinase receptors for neurotrophic factors. GM1’s neurotrophic action is exerted on dopaminergic neurons by interacting with the GDNF receptor complex, Ret tyrosine kinase, and GFR alpha-1

1. TBI is a complex injury with a broad spectrum of symptoms and disabilities. The clinical situation is various, sometimes unpredictable and out of control. However, in the experimental models of TBI, the type and severity of injury can be manipulated and standardized. So there is a gap between the basic research and clinical treatment.

BDNF, and other neurotrophins, play a major role in development by assisting with the migration, proliferation, and differentiation of growing cells (Dwivedi, 2009). While in the adult brain, neurotrophins have been implicated in neuronal maintenance and neurogenesis (Dwivedi, 2009). BDNF in particular has been shown to be involved in synaptic plasticity, learning and memory, and in promoting the survival of serotonergic neurons (Allen and Dawbarn, 2006). Altered synaptic plasticity has been shown to correlate with depression, especially with respect to learning and memory, and altered connections between areas such as the amygdala and pre-frontal cortex (Marsden, 2013). This altered circuitry would then in turn cause a decreased control of emotions and an increase in negative responses to events, symptoms easily observed in depression (Marsden, 2013). The role of BDNF in enhancing neuron function and neuroplasticity, as well as the observed correlation between BDNF levels and the action of antidepressants, forms the basis of the neurotrophin hypothesis of

Astrocytes perform a multitude of important functions, such as, in supporting the endothelial cells that form the blood-brain barrier, provide maintenance of extracellular ion balance and play a role in the repair and scarring process of the brain and spinal cord following traumatic injuries. When astrocytes become affected by the build-up of plaque they become unable to provide all of these necessary bodily functions to an individual. The presence of this plaque also makes it more difficult for the BBB to restrict and mediate the substances that pass

The overall goal of this proposal is to develop a composite scaffold that integrates growth factors to overcome neuron growth-preventing factors attributed to glial scarring in injuries to the central nervous system (CNS). The environment formed from glial scarring is inhibitory to the development and survival of cells that are implanted at the site of injury, chiefly due to the inability of axons to extend through glial scars. However, glial scarring is necessary to protect brain tissue from infection and to prevent additional cell damage. Hence, tissue engineering and regenerative medicine approaches for effective treatment of CNS injuries are subject to extensive investigation, but an optimal method is yet to be established due to difficulties in overcoming the glial scar barrier. Therefore, this proposal aims to establish such a method and take a large step towards an effective CNS injury treatment.

How is the “biovalue” of kidneys driven by market forces of supply and demand? Is this sustainable? Why or why not?

Several mechanisms explaining the mechanism by which MSCs exert their therapeutic effect in neurological disorders have been proposed. Currently, the must accepted hypothesis is that MSCs exert their neuroprotective action mainly through a paracrine-mediated mechanism. In fact, MSCs have the capacity to secret a plethora bioactive factors (secretome), including neurotrophic growth factors, chemokines, interleukins or cytokines, extracellular proteins and extracellular vesicles, which promote injured tissues repair and regeneration (Caplan and Correa, 2011; Maltman, Hardy and Przyborski, 2011; Paul and Anisimov, 2013).