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    (Original post by InItToWinItGetIt?)
    i always say ''restriction enzymes (also called restriction endonucleases)'' just to be sure
    ahhh okay well hopefully restriction enzymes would award me with a mark as that's all i've seen in the 2 books i'm using! lol
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    The pre release is a b*****
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    k thanks!for reply
    (Original post by InItToWinItGetIt?)
    i always say ''restriction enzymes (also called restriction endonucleases)'' just to be sure



    antigens don't get recognised as easily on AAVs. i don't know why they don't recognised as much, as that is going in way beyond A2 knowledge. Might be something to do with affinity but who knows.
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    page 5 para 4 from the artcile

    ''these issues are big and unknown becuase no one really know whtat extent people turn over their muscles cells.............true to ther muscles''
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    hey does anyone have any practise questions and answers for topic 8? would be much appreciated
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    Could anyone help me with this question:

    Bungaratoxin can be isolated from the venom of the Prugasti krait. In minute amounts, it can cause paralysis of the diaphragm and intercostal muscles by its effects at synapses. Suggest how bungaratoxin causes these effects.

    MS answer:
    1. ref to prevention of release of neurotransmitter from presynaptic membrane;
    2. similar shape (to neurotransmitter);
    3. {binds / blocks / fits into} receptor on postsynaptic membrane;
    4. ref to {sodium ion / Na+ / cation} channels / hyperpolarisation / permanent depolarisation} of postsynaptic membrane;
    5. no nerve impulses / action potentials / continuous action potential / eq;
    6. inhibits acetylcholinesterase / breakdown enzyme / (bungarotoxin) not affected by breakdown enzyme;

    I don't get it as if the Bungaratoxin has a similar shape to the neurotransmitter, then it would do the same effect as that neurotransmitter, or no?

    I put that it's complementary to the the neurotransmitter, so binds to it and prevents as many binding to receptors on the post-synaptic membrane.
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    (Original post by Jsmalley1)
    hey does anyone have any practise questions and answers for topic 8? would be much appreciated
    http://www.mediafire.com/?mhuznkz3njt
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    (Original post by InItToWinItGetIt?)
    Could anyone help me with this question:

    Bungaratoxin can be isolated from the venom of the Prugasti krait. In minute amounts, it can cause paralysis of the diaphragm and intercostal muscles by its effects at synapses. Suggest how bungaratoxin causes these effects.

    MS answer:
    1. ref to prevention of release of neurotransmitter from presynaptic membrane;
    2. similar shape (to neurotransmitter);
    3. {binds / blocks / fits into} receptor on postsynaptic membrane;
    4. ref to {sodium ion / Na+ / cation} channels / hyperpolarisation / permanent depolarisation} of postsynaptic membrane;
    5. no nerve impulses / action potentials / continuous action potential / eq;
    6. inhibits acetylcholinesterase / breakdown enzyme / (bungarotoxin) not affected by breakdown enzyme;

    I don't get it as if the Bungaratoxin has a similar shape to the neurotransmitter, then it would do the same effect as that neurotransmitter, or no?

    I put that it's complementary to the the neurotransmitter, so binds to it and prevents as many binding to receptors on the post-synaptic membrane.
    i think the idea is that it has a similar stucture to the neurotransmitter and it binds to the receptors and either has no effect but also prevents the neurotransmitter binding. OR the toxin has an inhibitory effect on the post synaptic neurone and allows Cl- channels to open, hyperpolarising the neurone making it less likely a action potential will occur.
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    (Original post by Meesta)
    i think the idea is that it has a similar stucture to the neurotransmitter and it binds to the receptors and either has no effect but also prevents the neurotransmitter binding. OR the toxin has an inhibitory effect on the post synaptic neurone and allows Cl- channels to open, hyperpolarising the neurone making it less likely a action potential will occur.
    I see. Cheers
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    Pleasee please help!
    Whats the difference between ventilation rate, breathing rate and respiration rate? Or are they the same thing :/
    sooo confused!
    xxx
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    (Original post by claire4095)
    Pleasee please help!
    Whats the difference between ventilation rate, breathing rate and respiration rate? Or are they the same thing :/
    sooo confused!
    xxx
    Ventilation rate is the volume of air inhaled or exhaled per minute (or per unit time)
    Breathing rate is the number of breaths taken per minute (or per unit time)
    Respiration rate is the rate of respiration? u can measure that using a respirometer and the volume of oxygen consumed per unit time
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    thanks! how do i open it? its .rar?
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    (Original post by Jsmalley1)
    thanks! how do i open it? its .rar?
    just extract it using win zip or something.
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    so screwed for this unit do you guys know how much we'll need to know of the article /from memory/? i know we get it in the exam but i can imagine there are specifics we should learn?

    oh and can anyone recommend page/line numbers? i'll post some up too
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    learn this and you should ace the article.http://www.scribd.com/doc/54265374/Q...icle-June-2011
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    What's the function of the 3-way tap in a respirometer?
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    (Original post by InItToWinItGetIt?)
    What's the function of the 3-way tap in a respirometer?
    allows you to equilibrate the apparatus with the atmospheric pressure before the experiment begins
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    (Original post by Scheeps)
    Thank you that clears a lot up!
    there's one final thing though, you wouldn't be able to describe how to get HR from an ECG for me could you? doing a pract. question and i have no idea how they got the answer once i looked it up in the mark scheme.
    So, you know that a heartbeat on an ECG is made up of peaks and dips, P, QRS, and T.
    The P wave is a small peak (caused by contraction of the atria)
    The 'QRS complex' is the main peak and the two dips either side (caused by contraction of the ventricles)
    The T wave is another small peak after this (caused by relaxation of the ventricles)
    ..and then it all starts again.

    One full heartbeat is the interval between one P wave and the next P wave on an ECG, so to calculate heart rate you look to see how many of these happen within one minute. (e.g. if you're given 5 seconds of an ECG you would multiply the number of heart beats within that graph by 12 to get the number in 60 seconds.) The units for your answer are bpm.
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    hows article revision???
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    (Original post by chemdweeb1234)
    allows you to equilibrate the apparatus with the atmospheric pressure before the experiment begins
    thanks
 
 
 

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