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    People are getting too confused:
    -The concentration gradient is generated by the Na/K pumps
    -The electrical gradient is set up because of the K diffusion
    Look at the diagram on page 203 in the orange textbook!
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    Im confused again. It says on the first page of article on the 5th paragraph line 5 that 'epo receptor should shut down epo production.' istnt it the kidneys that produce epo and arent epo receptors on the bone marrow?? soo confusedd
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    Can someone help me answer these questions?

    1)Why might AAVs be less vulnerable to attack from the immune system?
    2) Why is the fact that IGF-1 doesn't alter blood sugar an important consideration for tennis players?
    3)How might muscle wastage be controlled by a complex genetic pathway?
    4) How may proteasome be compared to lysosomes?
    5) Why might myostatin keep the satellite cells in check and stop the developing into new muscle cells?

    Thank youuuuuu to whoever helps me out with this
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    Restoring resting potential:

    1)Membrane is highly permeable to potassium ions, and more ions move out than occurs at resting potential, making potential difference more negative than normal resting potential

    2) This is HYPERPOLARISATION of the membrane

    3) Resting potential is re-established by closing of the voltage-dependent k+ channels and potassium ion diffusion into the axon via the potassium channels
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    (Original post by yagmurainie)
    Im confused again. It says on the first page of article on the 5th paragraph line 5 that 'epo receptor should shut down epo production.' istnt it the kidneys that produce epo and arent epo receptors on the bone marrow?? soo confusedd
    epo receptors aren't in the bone marrow. Bone marrow produces red blood cells.
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    (Original post by k256_93)
    Can someone help me answer these questions?

    1)Why might AAVs be less vulnerable to attack from the immune system?
    2) Why is the fact that IGF-1 doesn't alter blood sugar an important consideration for tennis players?
    3)How might muscle wastage be controlled by a complex genetic pathway?
    4) How may proteasome be compared to lysosomes?
    5) Why might myostatin keep the satellite cells in check and stop the developing into new muscle cells?

    Thank youuuuuu to whoever helps me out with this
    I know 1.) Because they are smaller (AAV's are smaller than adenoviruses)

    Also, do you know what topic viruses being used as vectors was it, and what do we need to know for it (details)
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    (Original post by k256_93)
    epo receptors aren't in the bone marrow. Bone marrow produces red blood cells.
    ok, thanks rof reply.so how does epo stimulate production of rbc?
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    (Original post by Adam9)
    I know 1.) Because they are smaller (AAV's are smaller than adenoviruses)

    Also, do you know what topic viruses being used as vectors was it, and what do we need to know for it (details)
    Well viruses are smaller than bacteria and some of them don't get detected less by the immune system?
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    Does anybody have the markscheme for the January 2011 paper?
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    do we need to know things about oprant conditioning or insightful learning ect?
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    (Original post by k256_93)
    Can someone help me answer these questions?

    1)Why might AAVs be less vulnerable to attack from the immune system?
    2) Why is the fact that IGF-1 doesn't alter blood sugar an important consideration for tennis players?
    3)How might muscle wastage be controlled by a complex genetic pathway?
    4) How may proteasome be compared to lysosomes?
    5) Why might myostatin keep the satellite cells in check and stop the developing into new muscle cells?

    Thank youuuuuu to whoever helps me out with this
    I'll answer them as best as I can, as I'm not sure we'll be expected to know some of them:

    1) It says in the text that AAVs are smaller than adenoviruses, being small decreases the likelihood that a macrophage or other non-specific immune cells will recognise the antigen as being non-self. (just because of size)

    2) I guess it would be important in the sense that the fact it doesn't alter blood sugar levels is that you can continue to play with enhanced performance without the fear of suffering symptoms of a diabetic etc.

    3) The pathway is the ubiquitin-ligase pathway,
    ubiquitin tags are placed onto muscle cells, labelling them for destruction the complex formed binds to the proteosome and the protein starts to be hydrolyzed into its component amino acids, ubiquitin is released.

    4) They can be compared similarly as they both involved with programmed destruction, the differences however is that a lysosome releases digestive enzyme that is involved with apoptosis of a cell, whereas a proteosome is only involved with the destruction of proteins, so it's on a smaller scale

    5) Perhaps myostatin is a repressor molecule, in its presence the gene that codes for new satellite cells cannot be expressed, therefore when it is blocked this allows the synthesis of the satellite cells and results in more muscles.
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    (Original post by yagmurainie)
    ok, thanks rof reply.so how does epo stimulate production of rbc?
    Epo binds to the receptors on a target cell (on bone marrow). This activates a secondary messenger which activates transcription factors and switches the gene for producing red blood cells on. So the gene for manufacturing red blood cells is expressed. Hope that makes sense
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    (Original post by avig613)
    Hi, I just double checked in the mark scheme for june 2010, and you are both wrong! Actually, it is the idea that the potassium ions re-enter the axon through the membrane which is still permeable to them. this removes the + from the outside- restores the equilibrium between the diffusion gradient and the potential difference.

    okayyy, so what happens to Na+ then?
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    (Original post by haydyb123)
    I'll answer them as best as I can, as I'm not sure we'll be expected to know some of them:

    1) It says in the text that AAVs are smaller than adenoviruses, being small decreases the likelihood that a macrophage or other non-specific immune cells will recognise the antigen as being non-self. (just because of size)

    2) I guess it would be important in the sense that the fact it doesn't alter blood sugar levels is that you can continue to play with enhanced performance without the fear of suffering symptoms of a diabetic etc.

    3) The pathway is the ubiquitin-ligase pathway,
    ubiquitin tags are placed onto muscle cells, labelling them for destruction the complex formed binds to the proteosome and the protein starts to be hydrolyzed into its component amino acids, ubiquitin is released.

    4) They can be compared similarly as they both involved with programmed destruction, the differences however is that a lysosome releases digestive enzyme that is involved with apoptosis of a cell, whereas a proteosome is only involved with the destruction of proteins, so it's on a smaller scale

    5) Perhaps myostatin is a repressor molecule, in its presence the gene that codes for new satellite cells cannot be expressed, therefore when it is blocked this allows the synthesis of the satellite cells and results in more muscles.
    You are actually amazing! Thank you so much
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    (Original post by haydyb123)
    I'll answer them as best as I can, as I'm not sure we'll be expected to know some of them:

    1) It says in the text that AAVs are smaller than adenoviruses, being small decreases the likelihood that a macrophage or other non-specific immune cells will recognise the antigen as being non-self. (just because of size)
    But then all viruses must have a less chance of being detected than bacteria by that reasoning. Surely how detectable they are varies from virus to virus and bacteria to bacteria?
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    (Original post by InItToWinItGetIt?)
    But then all viruses must have a less chance of being detected than bacteria by that reasoning. Surely how detectable they are varies from virus to virus and bacteria to bacteria?
    but you see the question isn't asking you to compare between bacteria and a virus, it's asking you to compare between AAV and an adenovirus, and on given evidence that's the most plausible answer. I have a strong feeling this might come up too!
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    (Original post by k256_93)
    You are actually amazing! Thank you so much
    No worries, I don't suppose you have any notes on the core practicals do you?
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    ******************************** ******
    How are viruses used to insert genes into cells ?
    ******************************** ******

    Are there any specific things (like enzymes) we need to know about
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    (Original post by Adam9)
    ******************************** ******
    How are viruses used to insert genes into cells ?
    ******************************** ******

    Are there any specific things (like enzymes) we need to know about
    It's things like on the HIV virus i.e. Glycoprotein 120, that was complementary to receptors on the t-helper cells. It will differ slightly virus to virus

    but inserting genes, they have enzymes like integrase, which will incorporate Viral RNA/DNA into host cell genome.
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    It might be to do with the fact that we may have encountered the Adeno (common cold) virus in the past so have developed antibodies against it. therefore, the immune system will detect and destroy it faster than say the AAV, which perhaps has different surface antigens?

    JP
 
 
 
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