biology
The standard of care for ischemic stroke is:steroids (cortisone/prednisone), to prevent edemarecombinant tissue plasminogen activator (tPA), aka alteplase (Activase) within three hours of onset, to dissolve the clotHemodilution (replacement of some whole blood with plasma/saline), to reduce whole blood viscosity and improve perfusionHemicraniectomy (cutting a hole in the), to relieve pressure10 pointsQUESTION 2What are neural progenitor cells? What populations of cells to they give rise to? Are they only present in early development or do they persist in the adult brain (in rodents and/or humans)?10 pointsQUESTION 3What does it mean that a drug is an “agonist” of a receptor or pathway? What about an antagonist?10 pointsQUESTION 4What is angiogenesis? What secreted substances are mainly responsible for angiogenesis in the brain?10 pointsQUESTION 5What sort of markers do the authors rely on to (a) identify and (b) assess differentiation potential of neural progenitor cells?10 pointsQUESTION 6Describe the MCAO. What processes are typically responsible for the actual lesion formed in the brain following MCAO?10 pointsQUESTION 7Choose one (1) neurological or motor function test from figure 1, and describe it. Also, look at those p-values! 1.776×10^-15, what do you think that even means?10 pointsQUESTION 8Figure 2: What are “sham”, “vehicle”, and “sova”? What can you say about the expression of doublecortin in the fore/midbrain of rats that experienced an ischemic attack (both those treated with vehicle and those that received the drug)?10 pointsQUESTION 9In case it’s not clear, I’d like to point out that in figure 3B (and others) the p values are between the bars on the left and right sides of the line. For example, p=0.128 represents the difference between Sham_RH and Veh_RH.Questions:What pair(s) of groups show a statistically significant difference in the expression of HuC/HuD?What are HuC/HuD?10 pointsQUESTION 10Figure 4 A and B show that the mature neuron marker NeuroD1 is very significantly upregulated post-injury in sovateltide-treated brains. What is the experiment shown in 4C and 4D?10 pointsQUESTION 11Figure 5, why do you think the authors looked at Drp1 and Mfn2? What results are shown? What could those results mean?10 pointsQUESTION 12Figures 6 and 7 show mitochondria (the powerhouse of the cell) responding to model stroke and sovateltide. Are mitochondria only important because of their critical role in energy homeostasis? If not (obviously the answer to that last question is “no”), what are some consequences of mitochondrial dysfunction following ischemia/reperfusion? That is, what’s the mechanism by which damage to the mitochondria causes/worsens the lesion in the brain
