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AQA BIOL5 Biology Unit 5 Exam - 22nd June 2011 watch

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    (Original post by BackDoorEntry)
    I think the second probe was meant to be 'primer'
    Yep thanks for the correction
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    (Original post by Aiboz)
    Well how I remember is it that we have two ways - increase of a heartbeat and slowing of a heartbeat.

    So when we exercise there is an increase in metabolic/muscular activity, this increases the rate of respiration and thereby increase the level of carbon dioxide in the blood. When carbon dioxide is dissolved in solution it becomes acidic. So this increased level of carbon dioxide lowers the pH level. The chemoreceptors in the walls of the carotid arteries (the arteries that serve the brain) detect this and send signals to the medualla oblongata in the brain. The centre in the medulla oblongata that increases heart rate increases the frequency of impulses to the sinoatrial node via the sympathetic system. The sinoatrial node increases the heart beat. This causes increased blood flow, which removes the carbon dioxide from the lungs faster. This means carbon dioxide levels decrease back to normal.

    If this helps, quote me. I will then explain the control in slowing down the heartbeat and pressure receptors.
    And the medulla oblongata also increases the rate of muscular activity by sending impulses to the intercostal muscles around the lungs which increase the breathing rate, to decrease the pH in the blood back to core levels.

    :cool:
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    Right I just don't understand In-Vivo cloning...

    Edit: Well I don't understand many things but one of them is in-vivo cloning
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    (Original post by xelaman)
    Has anybody thought about what extra content they will include-outside of the syllabus for the essay?
    Oh **** I completely forgot about that part of the essay!

    As a matter of fact I completely forgot about revising about the essay!
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    (Original post by xelaman)
    Has anybody thought about what extra content they will include-outside of the syllabus for the essay?
    Nothing, not really bothered about it tbh. I'm too busy revising the things we need to know without worrying about anything else just to get that one extra mark for scientific content
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    do you think we can safely say taxes and kinese and that stuff wont come up because they asked so much about it in the practical
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    Does anyone have OCR S2 on tomorrow as well?
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    (Original post by percy93)
    don't think you use primers, you use probes
    nooooo honest it is primers! probes are only used in genetic fingerprinting and when locating genes. primers are used in DNA sequencing
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    ****, feel so underprepared for this exam :'(.
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    (Original post by Stratos)
    Oh **** I completely forgot about that part of the essay!

    As a matter of fact I completely forgot about revising about the essay!
    The outside material is worth two marks at most. I wouldn't be too worried.
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    how is recombinant dna in genetic fingerprinting????????

    also does pcr copy all the dna in one cell??? how i thought it only copies small fragment of dna from each cell??? and if it does copy small fragments of dna from each cell, isnt the dna in the form of chromosomes, or is it all linked up in that one cell?? woudnt you need to take dna from different chromosomes in that one cell??? so that parents can be determined
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    Could someone explain to me how to do Q9b on the specimen paper please?
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    (Original post by angel1992)
    how is recombinant dna in genetic fingerprinting????????

    also does pcr copy all the dna in one cell??? how i thought it only copies small fragment of dna from each cell??? and if it does copy small fragments of dna from each cell, isnt the dna in the form of chromosomes, or is it all linked up in that one cell?? woudnt you need to take dna from different chromosomes in that one cell??? so that parents can be determined


    is recombinant dna in genetic finger printing??? i dont think it is
    and yeah you can copy unlimited amounts of dna in pcr so that wouldnt be a problem
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    (Original post by *QueenBeee)
    you my friend are a life saviour!! Amazzzing!
    I understand it now - could you help me on muscles?? Its just the sliding filament theory - if youre busy then its fine
    but seriously big big thanks!!!
    You're welcome! Typing stuff up like this helps me too.

    Sliding filament theory: When an action potential stimulates a muscle cell (i.e. after a neuromuscular junction, it depolarises the sarcolemma (membrane of the muscle) and this depolarisation is carried down the T-tubules (formed by folds in the sarcolemma) to the sarcoplasmic reticulum. This causes the sarcoplasmic reticulum to release calcium ions into the sarcoplasm. The ions then bind to troponin, which changes its shape and so pulls the tropomyosin it is attached to out of the way. This exposes the actin-myosin binding site.

    The globular myosin head on the myosin protein has an ADP molecule attached. This allows the myosin head to bind to the actin and form a cross-bridge. The myosin head then changes its angle, causing the actin to move (or slide), and the ADP molecule is released. In its place an ATP molecule attaches, which then breaks the cross bridge. The calcium ions activate the enzyme ATPase, which hydrolyses the ATP to ADP and inorganic phosphate (so you have an ADP molecule attached to the myosin head again!), and the energy released allows the myosin head to return to its original angle, so the process can continue. It does this until nervous stimulation stops.

    When this happens, the energy released from the ATP is used to return the calcium ions to the sarcoplasmic reticulum (so this is an example of active transport). Without the calcium ions, the tropomyosin moves back into position and the binding site is no longer exposed, so the myosin heads can no longer form cross-bridges.

    http://i56.tinypic.com/if0bo3.png

    So, if that's our relaxed sarcomere, when it is contracted the actin filaments slide over the myosin.

    http://i51.tinypic.com/o0eclx.png

    The sarcomere itself is contracted, but the actin and myosin remain the same size. The actin filaments have just moved closer together. Normally when describing this contraction from diagrams, it gets split into different parts.

    http://i51.tinypic.com/izz2mg.png

    The A-band is where you have myosin and some actin, the H-zone is entirely myosin and the I-bands are entirely actin. When the actin slides over, the A-bands stay the same (because the myosin doesn't move, only the actin!), the H-zone gets smaller and the I-bands get smaller.

    http://i52.tinypic.com/npexau.png

    If you can stand the excitement, sometimes they don't label it and instead just use different light levels. Now, because myosin is thicker than actin, areas with myosin are darker than with actin - but because combined they're denser still, the darkest area has both myosin and actin. When the sarcomere contracts, the darkest area gets wider, and the light and medium-dark areas get narrower.

    ... So you know, like an hour later you get a response. Sorry!
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    (Original post by Abcdcba)
    Could someone explain to me how to do Q9b on the specimen paper please?
    basically you count how many fragments are produced in the TOTAL digest and then work out how many time the restriction enzyme would have to cut the DNA in order to produce that many fragments, if that makes any more sense to you???? lol
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    (Original post by Aiboz)
    Right I just don't understand In-Vivo cloning...

    Edit: Well I don't understand many things but one of them is in-vivo cloning
    'In vivo' cloning refers to cloning genes in an organism. The process begins with using restriction endonucleases to cut a plasmid, and cutting a gene out of another organisms' genome using the same restriction endonuclease. The gene is then inserted into the plasmid by mixing the fragments and the plasmid together, and using DNA ligase to join the two sections. Once this is done, the plasmids must be reintroduced back into host cells; the bacteria and plasmids are mixed in a medium containing calcium ions; these calcium ions, and changes in temperature, make the bacterial cells permeable to the plasmids, and this means that the bacteria can take up the plasmids containing the new gene.
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    Do neurotransmitter have to be hormones?

    Also, can someone explain restriction mapping, is it meant to give you a base sequence?

    (Please quote me when you reply, otherwise i never see the answer) x
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    need help, can someone explain the refractory period for me? i'll rep your ass?
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    (Original post by angel1992)
    how is recombinant dna in genetic fingerprinting????????

    also does pcr copy all the dna in one cell??? how i thought it only copies small fragment of dna from each cell??? and if it does copy small fragments of dna from each cell, isnt the dna in the form of chromosomes, or is it all linked up in that one cell?? woudnt you need to take dna from different chromosomes in that one cell??? so that parents can be determined
    Yes, it appears to copy all the DNA. That's one of the disadvantages of PCR compared to in vivo, in that it just copies the DNA. As for the second question, I assume linked? And as for the third question, I have no idea, I presume we don't need to know that-however, given the idea of maternal and paternal chromosomes, I would assume yes, you do.
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    (Original post by stressedatschool)
    Do neurotransmitter have to be hormones?

    Also, can someone explain restriction mapping, is it meant to give you a base sequence?

    (Please quote me when you reply, otherwise i never see the answer) x
    No, they don't-are they ever hormones? Dopamine, and serotonin aren't? :confused:

    Restriction mapping is meant to give you the sequence of the DNA fragments; basically the genome is usually too big to sequence in one go, so you use restriction endonucleases to to cut the genome; but, after sequencing these separate fragments, you need to put the genome back together; by using pairs of restriction endonucleases and looking at where they cut, one can determine the sequence of genes....
 
 
 
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