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    hi, can some one link me to the specimen?
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    What sort of 'synoptic' topics or material are you guys looking at for this unit? If any at all? At the moment i've looked at everything on the spec but nothing else, as in specifics from AS. Any ideas or recommendations for the synoptic topics they might throw in? .
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    (Original post by blush.ox)
    What sort of 'synoptic' topics or material are you guys looking at for this unit? If any at all? At the moment i've looked at everything on the spec but nothing else, as in specifics from AS. Any ideas or recommendations for the synoptic topics they might throw in? .
    Anything is fair game.
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    (Original post by Iron&Wine)
    Anything is fair game.
    :grumble:
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    (Original post by blush.ox)
    :grumble:
    They can ask you to describe the structure of cellulose microfibrils, xylem vessels, describe how a mutation leads to cystic fibrosis, how atheromas form, reliability of studies, drug trials... pretty much anything. They probably won't require much detail and specific answers though (but you never know!).
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    (Original post by touran22)
    hi, can some one link me to the specimen?
    Did you mean specification?
    http://www.edexcel.com/quals/gce/gce...s/default.aspx
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    hey guys can predict what kind of question we will get this time if we go through the papers
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    Really good resourses on this scribd page.
    thought of sharing it with you all.




    http://www.scribd.com/Raaga92



    All the best for your exams!!!


    including the edxcel physcics A2 text book
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    good stuff thanks (though dont know why the font has to be so big?)
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    When electrons get excited by light in PSII, they leave the chlorophyll but where do they go?

    Some places say they are used to form reduced NADP but other places say they go to PSI.
    And then electrons excited in PSI go and reduce NADP.
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    (Original post by InItToWinItGetIt?)
    Macrophages engulf the pathogens and then display the foreign (or non-self) antigens on their surface. When any cell in the human body displays foreign antigens in this way it is known as an antigen-presenting cell (APC).

    Macrophages are part of the non-specific and specific immune response. They are non-specific in that when they come across any foreign antigen pathogen they try and engulf and digest them off. They don't know what type of organism they are digesting (i.e. they can't say ooo this is Virus 'X', bad!! - kill it!). They say.. hey.. I don't know if you are Virus X or Y but I do know you're not meant to be part of the body let me kill you.

    Then once they present the antigens, this activates the specific immune response (T-cells and B-cells etc. etc.), which have complementary receptors that are specific to that antigen and bind to the antigens via these receptors.

    I've put my notes on the immune system response in the spoiler

    Spoiler:
    Show

    • Viruses/bacteria have antigens which are recognised as ‘non-self’ and this recognition activates the non-specific and specific immune responses
    • Phagocytes engulf virus/bacterium
    - pathogen now contained in a vesicle in the phagocyte
    - Vesicle containing pathogen fuses with a lysosome and enzymes in lysosome break down the pathogen
    - Phagocyte then presents the pathogen’s antigens on it’s surface ? activates other immune system cells
    • Phagocyte presents the antigen to a T-helper cell.
    - T-helper cell binds onto the antigen via complementary surface receptors
    - This activates the T-helper cell and it then divides to make, active T-helper cells and T-memory cells
    • B-cells have antibodies on their surface and these binds to a pathogen with complimentary antigen. NOTE: Each B-cell will bind to a different antigen
    - This antigen-antibody complex along with T helper cell activate the B-cell
    - The B-cell then divides and differentiates into plasma cells and B-memory cells
    - Plasma cells produce antibodies which are bind to the antigens of the pathogen that triggered the response in the first place which helps destroy the pathogen.

    CELL-MEDIATED RESPONSE
    Bacterium/virus infects a host cell ? Host cell displays antigens ? T-killer cells with complimentary receptor bind to the antigens ?If exposed to cytokines by T-helper cells the T-killer cells divide and differentiates into active T-killer cells and T-memory cells ? Activated T-killer cells bind to infected cells which are presenting the complementary antigen ? Release enzymes and chemicals that cause pores to form in the infected cell’s membrane which leads to cell lysis and cell death.


    NOTE: Phagocyte ^ is a general term for any WBC which engulfs and digests stuff. A macrophage is a type of phagocyte.

    Antibodies kill a pathogen in many ways:

    1) reduce the pathogens' ability to infect cells (don't ask me how coz book doesn't say so and I doubt we need to know)

    2) bind to the foreign antigens to make an antigen-antibody complex - which is readily digested by macrophages

    3) antigen-antibody complex causes pathogens to clump together preventing them spreading to other parts of the body (don't ask me how again )
    Thank you so much InIt..... : )

    One question:
    So, does this mean that in the NON-SPECIFIC / INNATE Immune response, B cells produce antibodies which bind to antigens as labels, for enhanced binding to receptors on macrophages? In that case, are the receptors on macrophages specific?

    In the Edexcel Unit 4 Biology June 2010 paper, Q4, it states that antibodies and B-cells are involved in the NON-SPECIFIC response. I thought antibodies and B-cells are only part of the SPECIFIC immune response.

    Could you please shed some light on this matter? THANK YOU SO MUCH! : )
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    (Original post by InItToWinItGetIt?)
    When electrons get excited by light in PSII, they leave the chlorophyll but where do they go?

    Some places say they are used to form reduced NADP but other places say they go to PSI.
    And then electrons excited in PSI go and reduce NADP.
    The electron goes into PS1 TO replace the ones that keep leaving to make reduced NADP
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    Please any1 have the past paper and mark schem for the JAN 2011? AND ALSO MARK SCHEME FOR JUNE10 AND JAN10
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    what core practicals are we tested on? apparently we don't need to know them all
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    (Original post by sarahcsm)
    Thank you so much InIt..... : )

    One question:
    So, does this mean that in the NON-SPECIFIC / INNATE Immune response, B cells produce antibodies which bind to antigens as labels, for enhanced binding to receptors on macrophages? In that case, are the receptors on macrophages specific?

    In the Edexcel Unit 4 Biology June 2010 paper, Q4, it states that antibodies and B-cells are involved in the NON-SPECIFIC response. I thought antibodies and B-cells are only part of the SPECIFIC immune response.

    Could you please shed some light on this matter? THANK YOU SO MUCH! : )
    I think we need to realise that immune system response is probably WAY more complex than what we are taught.

    I did that ques yesterday and it probably meant non-specific as macrophages were involved. The B-cells and antibodies are part of the specific AND non-specific response as each B-cell and antibody bind only to specific (complementary) antigens.
    Non-specific because the antigen-antibody complex leads to the pathogen/antigen more readily engulfed by Macrophages, and macrophages just engulf anything that is non-self, without recognising what it is they are engulfing.

    (Original post by darkiee)
    The electron goes into PS1 TO replace the ones that keep leaving to make reduced NADP
    That's what I thought, but some sources such as Khan academy and the specimen paper (Q1b i), state that the electrons lost from PSII go and reduce NADP.
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    (Original post by InItToWinItGetIt?)
    .



    That's what I thought, but some sources such as Khan academy and the specimen paper (Q1b i), state that the electrons lost from PSII go and reduce NADP.
    wELL i THINK THEY ARE PREPARED TO FAIL, if they keep getting mixed up, it states clearly on the diagram and in words that the electron that leave ps2 is picked up by the electron transport chain and makes ATP in the process and the electron goes into PS1. I think they must have gotten it wrong somewherre, you are right dont let some sources make you fail.
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    (Original post by darkiee)
    Please any1 have the past paper and mark schem for the JAN 2011? AND ALSO MARK SCHEME FOR JUNE10 AND JAN10
    Attached every paper for Unit 4. Sorry don't have a PDF version of June 10 MS but you can dload/view it from the link below.

    June 10 MS: http://www.scribd.com/doc/46124422/B...-Scheme-Unit-4

    (Original post by darkiee)
    wELL i THINK THEY ARE PREPARED TO FAIL, if they keep getting mixed up, it states clearly on the diagram and in words thats the electron that leave ps2 is picked ur by the electron transport chain and makes ATP in the process and they electron goes into PS1. I think the must have gotten it wrong somewherre, you are right dont let some sources make you fail.
    Ok thanks. I'm just going to stick with my notes.

    e- from PSII --> PSI
    e- from PSI --> NADP + (H+) --> NADPH
    e- from photolysis --> PSII
    Attached Images
  1. File Type: pdf Edexcel-Biology-Unit-4-6BI04-January-2010-QP.pdf (285.5 KB, 191 views)
  2. File Type: pdf 6BI04 Official January 2010 Markscheme.pdf.pdf (136.8 KB, 153 views)
  3. File Type: pdf 6BIO4 JUNE 10 QP.pdf (534.2 KB, 153 views)
  4. File Type: pdf BIO UNIT 4 JAN 11 QP.pdf (607.0 KB, 231 views)
  5. File Type: pdf BIO UNIT 4 JAN 11 MS.pdf (184.3 KB, 210 views)
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    (Original post by inittowinitgetit?)
    attached every paper for unit 4. Sorry don't have a pdf version of june 10 ms but you can dload/view it from the link below.

    june 10 ms: http://www.scribd.com/doc/46124422/b...-scheme-unit-4



    ok thanks. I'm just going to stick with my notes.

    E- from psii --> psi
    e- from psi --> nadp + (h+) --> nadph
    e- from photolysis --> psii
    thanks man much appreciated
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    (Original post by darkiee)
    thanks man much appreciated
    You're welcome
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    Is it me, or was the Januray 2011 paper a *****? I think it was the hardest so far? Am i right?
 
 
 
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