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    Will we ever be tested on the HSW (how science works) boxes??

    Does anyone revise/note-take on them?
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    (Original post by Zanny17)
    First you need to be aware of the reaction that takes place

    RED LIGHT - Day
    FAR RED LIGHT - Night
    So in red light/DAY Pr is changed to Pfr
    and in far red light/NIGHT Pfr is is changed to Pr

    You need to be aware of two types of plants:
    • LDP (long day plants)
    • SDP (short day plants)


    LDP can be referred to as SNP 'short night plants' for better understanding but do not call them this during the exam!

    • Pfr STIMULATES flowering
    • Requires MAXIMUM hours of darkness, any longer and Pfr will be changed into Pr so no flowering.


    SDP 'Long night plants'
    • Pfr INHIBITS flowering
    • requires MINIMUM length of darkness - requires enough far red light to change sufficient amount of Pfr to remove the inhibition


    Remember its the length of DARKNESS that determines whether a plant flowers. This can be demonstrated by:
    Placing a SDP 'long night plant' and exposing it to say 3 hours of day and 9 hours of darkness. The result is flowering. However if you distrub this single period of darkness by flashing red light (day - changes Pr to Pfr) there is NO flowering.
    Therefore the conclusion is that the period of darkness is the CRITICAL FACTOR in inducing flowering.
    Hope that helps!

    Thanks a lot.. cheers !
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    (Original post by idiotone)
    Thanks a lot.. cheers !
    But i still dont get how Pr stimulates germination if it is converted to Pfr..? If you look at the last 2 lines on page 22 on the orange text book, it says that Pr stimulates germination and Pfr inhibits germination. Thats whats confusing me
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    (Original post by idiotone)
    But i still dont get how Pr stimulates germination if it is converted to Pfr..? If you look at the last 2 lines on page 22 on the orange text book, it says that Pr stimulates germination and Pfr inhibits germination. Thats whats confusing me
    me too... i'd just argue that pfr is biologically active, whereas the books says pr is just more 'stable'
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    (Original post by IGotAQuestion)
    me too... i'd just argue that pfr is biologically active, whereas the books says pr is just more 'stable'
    yeahh probably so
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    (Original post by Zanny17)
    You forgot the main part of oxidative phosphorylation ^^ which is oxygen acting as the terminal electron acceptor forming h20 in the process Without O2, the electrons in the ETC can't be 'disposed' of (which is done by combining with oxygen and forming water) and so the ETC stops functioning as all the carriers are loaded with an electron - ETC stops so no ATP formation
    another question on the ETC.
    My teacher keeps on saying when a molecule accepts hydrogen it is the same as accepting an electron. For some reason it doesnt seem right to me. Can you please explain this?
    thanks
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    (Original post by IGotAQuestion)
    Will we ever be tested on the HSW (how science works) boxes??

    Does anyone revise/note-take on them?
    Theres always hsw questions in the exam but they do tell you what the case is about in the exam. It is better to familiarise yourself with the hsw boxes so you dont have to spend loads of time thinking about it in the exam
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    (Original post by idiotone)
    But i still dont get how Pr stimulates germination if it is converted to Pfr..? If you look at the last 2 lines on page 22 on the orange text book, it says that Pr stimulates germination and Pfr inhibits germination. Thats whats confusing me
    Ok think of it like this: seeds don't require sunlight to germinate, right? Therefore it makes sense that Pfr will inhibit germination (as Pr is changed to Pfr in the DAY). In other words the best conditions for germination will be dark where there is plenty of Pr I hope that's cleared things up..:s
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    (Original post by tkoki1993)
    another question on the ETC.
    My teacher keeps on saying when a molecule accepts hydrogen it is the same as accepting an electron. For some reason it doesnt seem right to me. Can you please explain this?
    thanks
    Your teacher is kind of right Basically H breaks down to form H+ and e-
    Reduction is the gain of electrons so when NAD accepts a H atom, its basically taking up a H+ AND an e- which is why some books may refer to redNADP as NADPH+
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    (Original post by Zanny17)
    Your teacher is kind of right Basically H breaks down to form H+ and e-
    Reduction is the gain of electrons so when NAD accepts a H atom, its basically taking up a H+ AND an e- which is why some books may refer to redNADP as NADPH+
    thanks
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    (Original post by tkoki1993)
    thanks
    Not sure if you do Chem or not but the thinking about it is this:
    Hydrogen is the least electronegative element there is, so when it is in a covalent bond with anything, the electrons are distributed towards the other atom, therefore the gain of hydrogen is known as reduction- gain of electrons.
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    (Original post by tkoki1993)
    Can anyone explain oxidative phophorylation. I have a general idea of what it is and I know it happens in the inner membrane of the cristae but i'm not entirely sure of what I should write if it comes up in the exam. Thanks
    Okay I've seen the other post; not meaning to be a pedant. However, it's not called oxidative phosphorylation because it is dependent on Oxygen, of course it is dependent on Oxygen. It's oxidative because the energy required to synthesize the ATP comes from the Oxidation of the Co-enzymes

    NAD + FAD both give up H+ and 2e-: Oxidation

    If you wonder where the energy comes from, it comes from the idea that in the co-enzymes the electrons are in a really excited state, as they pass through the electron transport chain through a series of redox reactions their energy state is lowered, and of course energy is never lost, it is transferred, and the energy goes towards moving the H+ across into the inter membrane space and creating the electrochemical gradient.

    Hope everyone understands this, I tried to make the chemistry quite basic.
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    (Original post by haydyb123)
    Okay I've seen the other post; not meaning to be a pedant. However, it's not called oxidative phosphorylation because it is dependent on Oxygen, of course it is dependent on Oxygen. It's oxidative because the energy required to synthesize the ATP comes from the Oxidation of the Co-enzymes

    NAD + FAD both give up H+ and 2e-: Oxidation

    If you wonder where the energy comes from, it comes from the idea that in the co-enzymes the electrons are in a really excited state, as they pass through the electron transport chain through a series of redox reactions their energy state is lowered, and of course energy is never lost, it is transferred, and the energy goes towards moving the H+ across into the inter membrane space and creating the electrochemical gradient.

    Hope everyone understands this, I tried to make the chemistry quite basic.
    thanks
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    Some possible Q's our teacher gave us for section 1, to have a go at. We might be given more but im not sure. Just thought i'd share them.

    Muscles, genes and gym in a bottle.

    1.Why does bolstering the delivery of oxygen to labouring tissues increase performance?
    2.Describe how Mantyranta's genetic mutation could have altered the receptor for the the hormone EPO.
    3.Explain the feedback mechanism involved in maintaining red blood cell production.
    4.Explain how EPO could be produced by recombinant bacteria.
    5.Explain how gene therapy could be used to 'aquire the equivalent of Mantyranta's super-gene with a single shot'.
    6.Why are viruses used to 'carry EPO genes into cells?
    7.Why are Adenoviruses 'easily recognised by the immune system'.
    8.What safety issues are involved with gene therapy?
    9.Outline the stages that would be involved in the EPO gene therapy clinical trials.
    10.One side effect of EPO gene therapy is likely to be high blood pressure. Why does high BP increase the risk of atherosclerosis and how can this lead to a heart attack or a stroke?
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    (Original post by blush.ox)
    Some possible Q's our teacher gave us for section 1, to have a go at. We might be given more but im not sure. Just thought i'd share them.

    Muscles, genes and gym in a bottle.

    1.Why does bolstering the delivery of oxygen to labouring tissues increase performance?
    2.Describe how Mantyranta's genetic mutation could have altered the receptor for the the hormone EPO.
    3.Explain the feedback mechanism involved in maintaining red blood cell production.
    4.Explain how EPO could be produced by recombinant bacteria.
    5.Explain how gene therapy could be used to 'aquire the equivalent of Mantyranta's super-gene with a single shot'.
    6.Why are viruses used to 'carry EPO genes into cells?
    7.Why are Adenoviruses 'easily recognised by the immune system'.
    8.What safety issues are involved with gene therapy?
    9.Outline the stages that would be involved in the EPO gene therapy clinical trials.
    10.One side effect of EPO gene therapy is likely to be high blood pressure. Why does high BP increase the risk of atherosclerosis and how can this lead to a heart attack or a stroke?
    cn u provide the answers ?
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    (Original post by dush_2)
    cn u provide the answers ?
    im not sure yet, i'll try
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    Hi Everyone,

    Really great thread here. Im hoping someone can just explain to me what Unit 5 is all about - ie the format! Im doing Edexcel Biology as a distant student, and to be honest the college don't want to know once they have your money! - It seems any question I ask them the tutor says that's not her job! (Oxford College by the way!).

    Anyways, I get that there is an article, which I have read through. Im just wandering where this fits into the exam? Is it an exam based solely on this article, or is this just part of the exam? Also, what kind of stuff can they ask, and how does this relate to the article?

    Thanks in advance for anyone that can make this a little clearer for me!
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    If anyone needs help with respiration, I highly recommend you watch this video on youtube, it's so good! In the textbook the whole process is so simplified especially the electron transport chain and oxidative phosphorylation:

    http://www.youtube.com/watch?v=mfgCc...feature=relmfu
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    Has anyone got any notes on the core practicals?
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    Lets all post some notes on some chapters we have covered..that way we would have covered almost every chapters on the book
 
 
 
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