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    (Original post by gildartz)
    :confused:
    I thought recombinant bacteria had nothing to do with altering the human cell DNA, you're probably thinking about gene therapy and using viral vectors
    it doesnt :/
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    Im off to bed now guys. Goood luccckk!!! Here's a little (arguably) comic relief related to biology

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    Yer, recombinant bacteria is basically the GMO stuff...
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    (Original post by darkiee)
    mUCH APPRECIATED :d
    De rien n.p
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    when are we alowed to discuss post exam?
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    (Original post by Meesta)
    when are we alowed to discuss post exam?
    because it's a morning edexcel exam, we can talk about it from midnight ie thursday 00:01 kinda thing x
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    ok now im getting nervous. still havent finished topic 8, still havent looked at the article, aiming for an A*
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    (Original post by nikki_aiyana)
    because it's a morning edexcel exam, we can talk about it from midnight ie thursday 00:01 kinda thing x
    ahhh nice
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    (Original post by bertstare)
    ok now im getting nervous. still havent finished topic 8, still havent looked at the article, aiming for an A*
    i think everyone is NERVE-ous
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    (Original post by Meesta)
    when are we alowed to discuss post exam?
    For Edexcel: morning exams may not be discussed until 12:00 midnight (BST)
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    Well thats the article done for me! I hope epo questions come up and like the risks of epo and all that, that seems easiest. Now just gonna go over revision guide...
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    someone help me please...mantyrantas abnormal genes
    -Ok has he got abnormal gene in the kidney cells that keep making more epo? Or
    abnormal genes that code for the EPO receptor in the bone marrow cells? the epo receptors always turned on, so epo circulating activates red blood cell production so never switching off?
    Which one is it? Help meeeee please...im confused
    1)epo constantly being made by mutation in the kidney cells or the receptors in the cells of bone marrow?
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    (Original post by ballroomboy)
    Me and you both
    a transcription factor turns on or off genes FOXO, turns ON atrogenes causing atrophy in skeletal muscles so blocking foxo prevents atrophy
    Did someone shout on me?
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    Hey all, just a quick post to seek some advice for answering Question 7...

    I've not actually done any past papers on Unit 5 - I'm doing June 2010 shortly, but I'm not going to have time to read the article and do the questions relating to it. I've read through the questions, and looked at the mark scheme, so I've got an idea of what to expect.

    However, I just want some advice on ways to go about answering these bigger questions. Obviously, a 7 mark question is quite intimidating, so I just want some advice as to how to go about these questions. Especially when referring to the article. Is using quotes and statistics from the article advisable? I need to pick up some marks here, so any help will be greatly appreciated!
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    (Original post by bertstare)
    ok now im getting nervous. still havent finished topic 8, still havent looked at the article, aiming for an A*
    same aha were so going to fail xD
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    (Original post by hey-hey-hey)
    someone help me please...mantyrantas abnormal genes
    -Ok has he got abnormal gene in the kidney cells that keep making more epo? Or
    abnormal genes that code for the EPO receptor in the bone marrow cells? the epo receptors always turned on, so epo circulating activates red blood cell production so never switching off?
    Which one is it? Help meeeee please...im confused
    1)epo constantly being made by mutation in the kidney cells or the receptors in the cells of bone marrow?
    Its the feedback mechanism thats not present.. so the body doesnt realise that theres enough EPO there already, so it just keeps pumping them outtt
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    can someone explain how epo works?

    ok so peptide hormones in general bind to receptions, causes adenyl cyclase release, causes ATP to cyclic AMP which then activates transcription factors

    but for Epo, does this happen to bone marrow cells? this is what i dont get. and surely red blood cells cant just be produced from another cell, they happen through stem cell differation right? so how does epo cause this?
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    (Original post by VetApplicant2011)
    same aha were so going to fail xD
    iF YOU SAY YOU WILL FAIL, then SURE YOU WILL FAIL.
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    I am soooooooooo worried good luck guys! xx
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    (Original post by bertstare)
    can someone explain how epo works?

    ok so peptide hormones in general bind to receptions, causes adenyl cyclase release, causes ATP to cyclic AMP which then activates transcription factors

    but for Epo, does this happen to bone marrow cells? this is what i dont get. and surely red blood cells cant just be produced from another cell, they happen through stem cell differation right? so how does epo cause this?
    wut O_o

    please explain everything you just said to me? pleasepleaseplease? God Im so ****ed
 
 
 
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