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    When the epo level is high in a normal person, enough binds to Epo receptors to reach a threshold that stops epo production. Mantyranta has a mutation in the receptor so i assume the epo can no longer bind to the receptor, so the body doesn't know how much epo is knocking about (what is meant by the 'crucial feedback') so just keeps producing it (i guess).
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    Can somebody PLEASE tell me where to find the JAN 11 Mark Scheme?!!! A PDF link would be great!!
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    (Original post by bashx)
    I have some but it wont let me attach
    Bash, email them me!!! xo
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    (Original post by Maria1234)
    Hey I see you have done january paper!could you please explain it to me question 5 c!the investigation which was carried on the ability of the bacteria to use different substrate. Suggest the exaplantion for the diiference in oxugen uptake!I do not under stand the question neither the markscheme !please thnsx
    Sorry, I haven't seen the jan'11 paper since sitting it and I really don't remember this question sorry
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    (Original post by PHOLIO)
    When the epo level is high in a normal person, enough binds to Epo receptors to reach a threshold that stops epo production. Mantyranta has a mutation in the receptor so i assume the epo can no longer bind to the receptor, so the body doesn't know how much epo is knocking about (what is meant by the 'crucial feedback') so just keeps producing it (i guess).
    Thinking about it, my original point was wrong I think.

    If the EPO doesn't bind to the receptor then you shouldn't get RBC production anyway. So how did he get abnormally high levels of RBCs? Hence I don't think it's a mutation that affects the binding of EPO, to the EPO receptor.

    But I don't get how the receptor mutation affects the feedback system though The article doesn't really explain what exactly the actual mutation of the EPO receptor does - i.e. how does it change the receptor to stop the feedback mechanism work like it should.
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    (Original post by InItToWinItGetIt?)
    Thinking about it, my original point was wrong I think.

    If the EPO doesn't bind to the receptor then you shouldn't get RBC production anyway. So how did he get abnormally high levels of RBCs? Hence I don't think it's a mutation that affects the binding of EPO, to the EPO receptor.

    But I don't get how the receptor mutation affects the feedback system though The article doesn't really explain what exactly the actual mutation of the EPO receptor does - i.e. how does it change the receptor to stop the feedback mechanism work like it should.
    Honestly, i think you are wasting you are time worrying about the details... focus on the things relevant to the specification....

    i was curious... but i read up on it earlier... if you are interested, here is the name of his condition: primary familial and congenital polycythemia
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    People going for grade A's, in terms of revision, where are you at ...


    I understand most of topic 7, but need to do a little more on transcription factors and genes.

    I understand little of topic 8, but I think it is mainly just understanding the nervous system.

    I have not yet read the scientific article, but apparently its not too bad.


    I should have done more but had a chem exam that used most of my time.
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    (Original post by chemdweeb1234)
    Honestly, i think you are wasting you are time worrying about the details... focus on the things relevant to the specification....

    i was curious... but i read up on it earlier... if you are interested, here is the name of his condition: primary familial and congenital polycythemia
    I know I'm wasting time. It's just that I'm really stressed right now after the flop that was Unit 4.
    How would you go about answering the following:

    Describe how Mantyranta's mutation could have altered the epo receptor and how this mutation affected its function.

    - Mutation is change in base sequence of a DNA molecule (e.g. caused by deletion, substitution or insertion a base)
    - a mutation leads to a different mRNA strand being produced
    - hence different primary structure as different amino acids are coded for
    - different secondary and tertiary as bonds are different due to different R groups present
    - hence 3d shape of EPO receptor different

    How it affects the function what would you say?
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    (Original post by InItToWinItGetIt?)
    How would you go about answering the following:

    Describe how Mantyranta's mutation could have altered the epo receptor and how this mutation affected its function.
    1) The Epo receptor is a protein, whose structure is determined by the sequence of DNA nucleotides on the gene that codes for the receptor
    2) Mantyranta's mutation could mean there was a change in the sequence of DNA nucelotides (addition, deletion or substitution) which could lead to a different mRNA strand being produced
    3) This would lead to a different sequence of amino acids and since the sequence of amino acids determines the final 3D shape of the receptor, the shape would be different... there may be incorrect bonding (such as hydrogen bonding, ionic bonding, or disulfide bridging) or incorrect hydrophic interactions between R groups
    4) The epo receptor is essential in controlling the feedback of epo.... the incorrect shape may prevent epo from binding to the receptor... leading to the negative feedback not being switched off... and thus more epo would be continued to be produced by the kidneys.... depsite O2 levels being at the norm value
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    (Original post by chemdweeb1234)
    1) The Epo receptor is a protein, whose structure is determined by the sequence of DNA nucleotides on the gene that codes for the receptor
    2) Mantyranta's mutation could mean there was a change in the sequence of DNA nucelotides (addition, deletion or substitution) which could lead to a different mRNA strand being produced
    3) This would lead to a different sequence of amino acids and since the sequence of amino acids determines the final 3D shape of the receptor, the shape would be different... there may be incorrect bonding (such as hydrogen bonding, ionic bonding, or disulfide bridging) or incorrect hydrophic interactions between R groups
    4) The epo receptor is essential in controlling the feedback of epo.... the incorrect shape may prevent epo from binding to the receptor... leading to the negative feedback not being switched off... and thus more epo would be continued to be produced by the kidneys.... depsite O2 levels being at the norm value
    See this is what I don't get. His condition leads to an increase in RBCs in the blood, which is caused by the continued EPO production.

    However, if the mutation prevented the EPO binding to the epo receptor there would be no RBC production and hence, RBC levels should drop in him, which they don't. So the mutation affect something else that is involved in the feedback mechanism.
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    (Original post by InItToWinItGetIt?)
    See this is what I don't get. His condition leads to an increase in RBCs in the blood, which is caused by the continued EPO production.

    However, if the mutation prevented the EPO binding to the epo receptor there would be no RBC production and hence, RBC levels should drop in him, which they don't. So the mutation affect something else that is involved in the feedback mechanism.
    Dont look for zebras when you hear hooves ... or so the saying goes

    There may be two types of epo receptors all we know? The epo receptor that is found on the cell surface membrane of the heamopoietic stem cells in the bone marrow, or epo receptors in other parts of the body that detect the levels of the epo in blood... sorta like chemo receptors.... could be a mutation in the second one which prevents epo levels being ever recognized as being low... and thus the epo is kept being produced and the epo binds to the receptors on the haemopoietic stem cells... causing differential gene expression

    OR, alternatively, perhaps more INplausibly, (cosidering oxygen is actually used?)

    there is only one epo receptor on the haemopoietic stem cells

    it could be that epo receptor has two sites... one for oxygen and one for epo... in a normal human, when the oxygen levels reach normal levels, the epo receptors will be saturated with oxygen, and this leads to allosteric site changes - the active site for epo changes, and thus epo will no longer be able to bind to the receptors and thus no more differential gene expression to produce more RBC's.... in the case of Mantyranta's polycythemia, there could be the case of a change in the binding site for oxygen, which prevents oxygen from binding to these receptors, which prevents any allosteric inhibition of the epo active site, and thus epo can continue to bind to these cell surface membranes and cause differential gene expression....

    why complicate it? Just say epo cant bind to the freaking receptors sorted
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    (Original post by chemdweeb1234)
    Dont look for zebras when you hear hooves ... or so the saying goes

    There may be two types of epo receptors all we know? The epo receptor that is found on the cell surface membrane of the heamopoietic stem cells in the bone marrow, or epo receptors in other parts of the body that detect the levels of the epo in blood... sorta like chemo receptors.... could be a mutation in the second one which prevents epo levels being ever recognized as being low... and thus the epo is kept being produced and the epo binds to the receptors on the haemopoietic stem cells... causing differential gene expression

    OR, alternatively, perhaps more INplausibly, (cosidering oxygen is actually used?)

    there is only one epo receptor on the haemopoietic stem cells

    it could be that epo receptor has two sites... one for oxygen and one for epo... in a normal human, when the oxygen levels reach normal levels, the epo receptors will be saturated with oxygen, and this leads to allosteric site changes - the active site for epo changes, and thus epo will no longer be able to bind to the receptors and thus no more differential gene expression to produce more RBC's.... in the case of Mantyranta's polycythemia, there could be the case of a change in the binding site for oxygen, which prevents oxygen from binding to these receptors, which prevents any allosteric inhibition of the epo active site, and thus epo can continue to bind to these cell surface membranes and cause differential gene expression....

    why complicate it? Just say epo cant bind to the freaking receptors sorted
    You had me all until the final final bit. Because you said can't bind to receptors there and can bind to receptors in the bit just above it lol -

    Are you saying as a possible reason (as obviously we wouldn't be expected to know the exact reasons):

    normally when the body regains its normal oxygen levels, which is caused by the increase in RBCs, which is caused by epo, the epo receptor should prevent the epo binding to it and this would raise blood epo levels. This would then detected by the kidneys which would STOP producing more epo, therefore no more RBC production.

    Since mantyranta has a problem with the epo receptors, the return of oxygen levels to the norm is NOT detected by the receptors and hence can't undergo a conformational change to prevent binding to epo and so the receptor(s) is continuously 'on'. Hence the kidney is not stimulated to cease epo production.
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    Anyone has the topic 8 spec note and can a nice person explain Auxin and IAA and everyting we need to knw about it. Thanks
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    (Original post by sam_xo)
    Can somebody PLEASE tell me where to find the JAN 11 Mark Scheme?!!! A PDF link would be great!!
    BABE i have the mark shcmeemeehegwej!!!!
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    (Original post by bashx)
    BABE i have the mark shcmeemeehegwej!!!!
    Here you go
    ill email you the notes they wont attach
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  1. File Type: pdf BIO UNIT 5 - JAN 11 MS.pdf (132.9 KB, 73 views)
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    (Original post by darkiee)
    Anyone has the topic 8 spec note and can a nice person explain Auxin and IAA and everyting we need to knw about it. Thanks

    - IAA is an important Auxin ( which is a plant growth substance)
    - produced in the tips of shoots of flowering plants
    - IAA moves around the plants controlling tropism( by diffusun and ATP via the phloem)

    whats tropism?
    tropism is the response of a plant to a DRECTIONAL stimulus so in turn the plants regulates its growth as a response.

    - different parts of the plant have different amount of IAA
    - if you have uneven growth in IAA - you have an uneven plant!

    - IAA is also water soluble chemical

    STEPS:
    1) IAA produced in coleptile
    2) IAA moves away from light
    3) IAA diffuses to meristem cells
    4) IAA bind to all membrane receptors
    5) causes H+ ions to be pumped into cell (provides a lower PH for enzymes to break bonds between cellulose microfibrils)


    does this help?
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    Ive attached the topic 8 teaching scheme if it helps as a spec.
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  2. File Type: pdf snab-t8-tchg-scheme-09-9679.pdf (120.4 KB, 677 views)
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    (Original post by darkiee)
    Anyone has the topic 8 spec note and can a nice person explain Auxin and IAA and everyting we need to knw about it. Thanks
    yap..i alsoo need the notes....ANYONE HAVING TOPIC 8 SPEC NOTE PLEASE UPLOAD IT....hwvr...auxin is a plant hormone that causes phototrophic response of plant to light...it is effective even at very low concentration.The first auxin discovered was IAA.
    How Auxin works?
    Auxin is made at the apical meristem in shoot tip.Once stimulated by unilateral light,auxin moves down and binds to receptor site in cell surface membrane of the cell over there...it causes activation of active Hydrogen ion pumping and so Hydrogen ion pumped into cell cytoplasm.It lowers the PH,breaks down the bond between cellulose microfibrils and makes the cell wall flexible by absorbing water by osmosis and thus causes cell elongation.
    Once unilluminated,the auxins move back to the shoot tip.Ph of the cell membrane decreases.As a result,bonds between microfibril forms,cell stretches and elongation is ceased.
    Additional
    However,auxin moves to the cell elongation site of the shaded part of the plant-so cell growth occurs at the darker side causing the illuminated side to bed over towards the light.
    hope it works for u.......
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    (Original post by bashx)
    here you go
    ill email you the notes they wont attach
    yay. Love you bash xoxo
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    does anyone know whether the article questions in the real exam will have details of where in the article each question is related to? (e.g. page 4, paragraph 5 or whatever..)
    thanks))
 
 
 
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