BIOL6890 Traumatic Brain Injury and Loss of ATP Production Consequences Exam

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This exam has a total of 13 points. Each point corresponds to a numbered question. The numbered question is to be answered. The correct answer to a numbered question will give you one point. If the answer is partially correct, partial credit will be given as a decimal value. If the answer is incorrect, no credit will be given. If the question is unanswered, no credit will be given so it is better to guess than to leave a question blank. The number of points earned will be divided by the total number of points on the exam and multiplied by 100 to get your grade. Good luck!

1. In the introduction section the authors wrote “Subsequent to an acute lack of oxygen, such as that caused by a stroke or traumatic brain injury (TBI), is the potential for further damage to surviving neuronal tissues due to hyper-activation of inflammatory and various stress or damage-induced cell death pathways long after initial insult has been resolved [2-4].” Why does a stroke cause an acute lack of oxygen? (1 point)

1. In the introduction section the authors wrote “In addition to this loss of ATP production, extreme changes to the Δψ_m, for example hyperpolarization as reported with stroke and TBI [15], have been shown to increase ROS production and subsequently trigger formation of the mitochondrial permeability transition pore (mPTP), an opening within the inner mitochrondrial membrane that allows for the leakage of ions and other mitochondrial nutrients/proteins.” Why is there hyperpolarization due to stroke TBI? (1 point)

1. In the introduction section the authors wrote “We have previously noted CoCl₂’s ability to cause oxidative damage through increased ROS production and hyperpolarization of the mitochondrial member in HT22 cell [37].” Why does CoCl₂’s oxidative damage cause hyperpolarization? (1 point)

1. In the exposure to CoCl₂ significantly reduces HT22 cell viability, while treatment with rapamycin increases viability during exposure section of the results section the authors wrote “Assessment of resultant cell viability was through the resazurin blue assay which revealed a dose-dependent response causing significant decreases in viability at all doses tested (p ≤ 0.001).” What is a dose dependent response? (1 point)

1. In the exposure to CoCl₂ significantly reduces HT22 cell viability, while treatment with rapamycin increases viability during exposure section of the results section the authors wrote “DMSO only became significantly toxic at the two highest doses tested (p ≤ 0.01) and, even then, rapamycin further decreased viability in comparison by 24% (p < 0.001).” What concentration did DMSO become significantly toxic? (1 point)

1. In the Assay for measurement of the mitochondrial membrane potential (Δψ_m) section of the methods section the authors wrote “Measurement of Δψ_m was performed essentially as previously described [31].” What was done to measure Δψ_m? In other words what was Δψ_m measured with? (1 point)

1. Quote something from the article as evidence that your answer to question 6 is correct. (1 point)

1. In the Rapamycin treatment restores the Δψ_m and decrease the production of ROS in CoCl₂ –exposed cells to limit hypoxia-induced damage section of the results section the authors wrote “On the other and, CoCl₂ exposure for 24 h had significantly upregulated the TMRM fluorescent signal, increasing it by 680% (p ≤0.001). This nearly sevenfold increase indicated severe hyperpolarization of the mitochondrial membrane.” Why was there no depolarization? (1 point)

1. In the Rapamycin treatment restores the Δψ_m and decrease the production of ROS in CoCl₂ –exposed cells to limit hypoxia-induced damage section of the results section the authors wrote “When rapamycin was added together with CoCl₂, this hyperpolarization was markedly inhibited (85% reduction) compared to CoCl₂ alone (p ≤0.001) and fluorescence remained only slightly elevated when compared to control (38%; p ≤ 0.01).” Why was hyperpolarization inhibited? (1 point)

1. In the Rapamycin treatment enhances autophagy to protect cells during CoCl₂ exposure section of the results section the authors wrote “We observe that untreated cells had low levels of autophagy induction as the ratio of LC3-II/LC3-I was around 0.5. With CoCl₂ exposure LC3-II to LC3-I expression was observed at a 1:1 ratio (p ≤ 0.0.1). Finally, when rapamycin was added during CoCl₂ exposure, the LC3-II/LC3-I ratio increased to 2 (p ≤ 0.05).” Did: (1) untreated cells; (2) cells with CoCl₂; or (3) cells with CoCl₂ and rapamycin have the most conversion of LC3-I to LC3-II? (1 point)

1. How to do you know that your answer to question 10 is correct? (1 point)

1. In the Rapamycin treatment reduces the Bax/Bcl-2 ratio and increases pMARK protein expression to promote survival during CoCl₂ exposure section of the results section the authors wrote “Furthermore, the activation of MAPK through phosphorylation has also been related to detoxification of ROS [46-48] and we hypothesized it could play a role in our CoCl₂ –simulated hypoxia model.” Is their hypothesis a null hypothesis or an alternate/alterative hypothesis? (1 point)

1. How do you know that your answer to question 12 is correct? (1 point)

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