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    can someone make a summary from each topic of the article?
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    (Original post by InItToWinItGetIt?)
    Regarding the article: Pg 3 paragraph 4
    Why are Adeno-associated virus less likely to stimulate immune response?

    Is it just the fact they are smaller, and maybe less antigens, so less likely to come into contact with immune sytem cells.
    Not sure, the Wikipedia entry says AAV's do not cause disease, so I guess there isn't much of an immune response as the body maybe doesn't recognise the AAV as being pathogenic?
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    Can anyone help? I am a bit confused with calculating marks and stuff. If for Jan 2011 I got 68 UMS marks and I calculated like 68/120 * 90. I got 51 marks in total and now I am so lost because the boundaries say that 51 is a high C. How can I work it out?
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    (Original post by katelv)
    Can anyone help? I am a bit confused with calculating marks and stuff. If for Jan 2011 I got 68 UMS marks and I calculated like 68/120 * 90. I got 51 marks in total and now I am so lost because the boundaries say that 51 is a high C. How can I work it out?
    The UMS marks you receive aren't directly proportional to your exam mark They're standardised so your raw mark is given a UMS value which reflects how you performed relative to everyone else taking that exam
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    (Original post by smiffy_83)
    Not sure, the Wikipedia entry says AAV's do not cause disease, so I guess there isn't much of an immune response as the body maybe doesn't recognise the AAV as being pathogenic?
    The immune system I would assume does recognise it as pathogenic (since according to wiki anyway(, cause a mild response. But the response is not as big as usual as the AAVs are not as pathogenic. But it doesn't seem to say why they're less pathogenic. At least I can't find it.

    EDIT: According to my dad, the AAVs' antigens have low specificity, meaning they are less easily recognised by the immune response, hence less reaction.
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    wait do we get the article again in the exam? Also how do you revise for the synoptic unit? Do you revise the article or just the information that will relate to it?oh dear somebody please help, it would be appreciate
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    (Original post by guichiguichi)
    wait do we get the article again in the exam? Also how do you revise for the synoptic unit? Do you revise the article or just the information that will relate to it?oh dear somebody please help, it would be appreciate
    The article would be included in the exam paper and of course, we do not have to revise it. but still, for some important sections, I would try to memorize a little bit.

    btw, could anyone tell me the difference between muscular dystrophy and muscle atrophy?? :confused::confused:
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    (Original post by sadbuttrue92)
    The article would be included in the exam paper and of course, we do not have to revise it. but still, for some important sections, I would try to memorize a little bit.

    btw, could anyone tell me the difference between muscular dystrophy and muscle atrophy?? :confused::confused:

    Muscle atrophy is a wasting away of muscle from n0n-use or poor nutrition, while muscle dystrophy is a degeneration of the muscles or any organ caused by a disease process. Dystrophy can also be caused by malnourishment.
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    need the topic 8 specification notes.....URGENT GUYS..............!!!!!!!!!!!!!! !!!!!
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    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
    (Original post by law-RAH)
    The UMS marks you receive aren't directly proportional to your exam mark They're standardised so your raw mark is given a UMS value which reflects how you performed relative to everyone else taking that exam
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    It says this occurs due to a mutation in the gene that codes for EpoR, but if the receptor is malformed then Epo wouldn't bind to it so it shouldn't keep producing RBCs.

    Then the article is talking about how Mantyranta's mutation turns off the feedback system, so his body keeps making more RBCs.

    I don't get it
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    you know in a person without mutation ,once oxgygen has gained its normal level, the kidneys shut down to not produce any red blood cell. They shut down by producing a repressor molecue which binds in the promote region that inhibits the formation of the transcrition initiation complex. In the mutated person this repressor molecule is not formed ,so it keeps producing a redblood cells ,becuase EPO is acting as a transcrption factor. This is a negative feedback,becuase once the level of blood is set on a specific set point. transctriopn stoprs
    (Original post by InItToWinItGetIt?)
    It says this occurs due to a mutation in the gene that codes for EpoR, but if the receptor is malformed then Epo wouldn't bind to it so it shouldn't keep producing RBCs.

    Then the article is talking about how Mantyranta's mutation turns off the feedback system, so his body keeps making more RBCs.

    I don't get it
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    (Original post by Maria1234)
    you know in a person without mutation ,once oxgygen has gained its normal level, the kidneys shut down to not produce any red blood cell. They shut down by producing a repressor molecue which binds in the promote region that inhibits the formation of the transcrition initiation complex. In the mutated person this repressor molecule is not formed ,so it keeps producing a redblood cells ,becuase EPO is acting as a transcrption factor. This is a negative feedback,becuase once the level of blood is set on a specific set point. transctriopn stoprs
    Yes but where does the mutation in the EpoR (epo receptor) gene come into that? What you described is the mutation in the gene that produces this repressor molecule in the kidneys.

    The EpoR is in the bone marrow as that's where EPO binds to EpoR to synthesise RBCs. While the synthesis of EPO is in the kidneys and this is where the repressor molecule works.

    The article seems to be contradicting itself by saying the mutation is in the EpoR and then saying the mutation turns off the feedback mechanism.
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    more han confused
    (Original post by InItToWinItGetIt?)
    Yes but where does the mutation in the EpoR (epo receptor) gene come into that? What you described is the mutation in the gene that produces this repressor molecule in the kidneys.

    The EpoR is in the bone marrow as that's where EPO binds to EpoR to synthesise RBCs. While the synthesis of EPO is in the kidneys and this is where the repressor molecule works.

    The article seems to be contradicting itself by saying the mutation is in the EpoR and then saying the mutation turns off the feedback mechanism.
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    (Original post by Maria1234)
    more han confused
    Same - Can anyone else shed any light on this?
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    (Original post by phetylheminthes)
    need the topic 8 specification notes.....URGENT GUYS..............!!!!!!!!!!!!!! !!!!!
    I have some but it wont let me attach
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    (Original post by bashx)
    I have some but it wont let me attach
    where did u get it?can u please give me the adress?
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    any1 got topic8 specification based notes??i got topic7 but i need the topic8 URGENTLYYYYYYY!!!!!!!!!
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    I've got some topic 8 notes I made from the SNAB textbook if anyone wants them:

    http://www.mediafire.com/?75xe7r25a4j72lx

    But, I've also included some extra images from the internet/some diagrams and powerpoint printscreens for my own understanding, so you don't have to learn that stuff in the notes, you'll able to recognise the content that's not needed.
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    Unit 4 & 5 Notes.....

    http://www.mediafire.com/?djtr8cyl979b751
 
 
 
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