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AQA BIOL1 ~ 14 May 2012 ~ AS Biology

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    (Original post by AAA_)
    Does any 1 have a PDF version of a biology book preferably the Nelson Thornes 1, because i lost mine :facepalm: and don't wanna have to buy it?
    https://www.google.co.uk/search?q=aq...&tbo=1&oq=aqa+

    Not sure if it will help, but there might be something on there for you.
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    (Original post by AlligatorSky)
    Can anyone explain 'Absorption in the small intestine' ?
    For how the small intestine is ADAPTED for absorption in the small intestine:
    - Lots of microvilli, increases surface area
    - Many mitochondria in cells are site of aerobic respiration, they respire and produce ATP for active transport
    - You have carrier proteins for active transport
    - Channel proteins for facilitated diffusion
    - Also you have co-transport of sodium and glucose, therefore also the sodium/potassium pump, that causes a concentration gradient between the cell and the lumen, so then the co-transport takes place
    - Membrane-bound organelles (not sure of this point, but its on the mark scheme.....)

    Then this is the processes involed in the absorption of the products of starch digestion in the small intestion:
    (you would first do your starch to maltose via amylase produced from salivary glands, it passes to stomach where acidic conditions stop further hydrolysis.. then the pancreas produces pancreatic juice containing pancreatic amylase that breaks the remainging starch to maltose. then the small intestine produces maltase that hydrolyses the maltose to glucose..) then....
    - Glucose moves in with sodium to the cell via a protein channel
    - Sodium is removed from the cell to the blood by the sodium/potassium pump
    - This creates a concentration gradient (a low concentration of sodium in the cell) and maintains a sodium concentration gradient between the lumen and the epithelial cell
    - Finally glucose moves into the blood via diffusion.

    If you get 'How is the cell-surface membrane adapted for absorption of products':
    Then you talk about the phospholipid bilayer, the fluid mosaic model (How its fluid due to the phospholipids that can move relative to one another and mosaic due to the different shapes and sizes of proteins scattered throughout the bilayer)
    Talk about the hydrophillic heads all point outwards.
    Intrinsic and Extrinsic proteins
    How water-soluble substances move throughout the intrinsic proteins and ion channels
    And the lipid soluble substances move directly through the phospholipid bilayer
    Osmosis of water here from high water potential to low water potential..
    Active transport against a concentration gradient using carrier proteins


    Hope this helped. x
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    Thank you guys.
    It makes so much more sense when someone explains it.
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    sorry guys, i can't be bothered to trail through the thread but does anyone have the unit 1 specimen paper? it's no longer on the aqa website... thanks
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    hi can someone be kind enough to give me the "mark-scheme" notes for these please:

    the role of plasma cells and memory cells in producing a secondary response


    the effects of antigenic variability in the influenza virus and other pathogens on immunity

    thank you!
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    (Original post by shybrowngirl)
    hi can someone be kind enough to give me the "mark-scheme" notes for these please:

    the role of plasma cells and memory cells in producing a secondary response


    the effects of antigenic variability in the influenza virus and other pathogens on immunity

    thank you!
    Cant do the second one of you..
    but the first one I can have a go.

    Right. Well
    When your infected with a pathogen for the first time..
    You have ONE B cell that is complementary to the antigen.
    More of this B cell is produced via mitosis to form cloned B cells
    The B cells produce B plasma cells that make antibodies and these anitbodies destroy the pathogen. This is your Primary Immune Response.
    The B cells ALSO produce B memory cells and these are stored.
    When you are next infected with the antigen again, a much more RAPID response is produced. The B memory cells develop into B plasma cells and more B memory cells. The B plasma cells produce the antibodies needed to destroy the pathogen. This is your secondary immune response.

    Literally just remember.
    1st immune response - you have only 1 B cell. This does mitosis so you have tons of clones. Some go to B plasma cells. Some to B memory cells. The B plasma cells make antibodies. The B memory cells are stored. The antibodies get rid of the antigen (because they are cloned they are complementary and antigen-specific)
    2nd immune response - Your B memory cells quickly recognise your infected with the same antigen. These develop to B plasma cells and more B memory cells. So you have lots and more antibodies that quickly destroy the anitgen. This is MUCH faster.

    Hope that helps. It took me forever to understand this topic, but now it seems easy to me x
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    Ok dw thanks.
    I'm just really stresses about bio. Itslike one subject that has ne'erending revision
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    I'm focusing on BIOL 1 most at the moment compared to BIOL 2. When's the best time after BIOL 1 to star focusing on BIOL 2. The weekend before? As in Fri, Sat, Sun the days before the BIOL 2 exams.

    Also, I'm just going to tank some past papers tomorrow and revise as much as possible for BIOL 1.
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    (Original post by George_)
    I'm focusing on BIOL 1 most at the moment compared to BIOL 2. When's the best time after BIOL 1 to star focusing on BIOL 2. The weekend before? As in Fri, Sat, Sun the days before the BIOL 2 exams.

    Also, I'm just going to tank some past papers tomorrow and revise as much as possible for BIOL 1.
    I'm starting biology 2 after my religious studies exams (which are ridiculously solid).. so thursday morning for me.
    But I've got chemistry as well.. so biology 2 is a bit of a worry for me.
    I know i've left revision for that far too late, so i'll just have to do my best :3
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    (Original post by dinosaretoocool)
    sorry guys, i can't be bothered to trail through the thread but does anyone have the unit 1 specimen paper? it's no longer on the aqa website... thanks
    Still on AQA

    Question Paper
    http://store.aqa.org.uk/qual/gce/pdf...IOL1-W-SQP.PDF

    Mark Scheme
    http://store.aqa.org.uk/qual/gce/pdf...IOL1-W-SMS.PDF
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    (Original post by britash)
    I'm starting biology 2 after my religious studies exams (which are ridiculously solid).. so thursday morning for me.
    But I've got chemistry as well.. so biology 2 is a bit of a worry for me.
    I know i've left revision for that far too late, so i'll just have to do my best :3
    I have Chem. Salters B as well, which is tough. When did you properly start revising OTHER than at school? I suppose I started a week & a bit ago :/

    Sure I'll do OK though.
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    Right list for tonight:
    definitions of magnification, resolution, diffusion, osmosis, active transport, fluid mosaic model.
    equations for ficks law, pulomary ventilation and cardiac output
    mark scheme answers for - roles of proteins, roles of lipids, systole, diastole, inspiration, expiration.
    graphs - heart, valves

    That should take me 30 minutes, then finally done ALL my notes and revised everything
    Tomorrow - past papers and questions :elmo:
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    (Original post by George_)
    I have Chem. Salters B as well, which is tough. When did you properly start revising OTHER than at school? I suppose I started a week & a bit ago :/

    Sure I'll do OK though.
    *properly*?? Well the half term holidays we had about 4/3-ish weeks ago..
    I do AQA chemistry. I can afford to get a middle/high B to get an A overall on that, so I guess I could revise the night before, like I did in january

    I have maths as well.. and I'm failing stats, so I dont really care about that one
    What else do you do? x
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    (Original post by barzy_j)
    i think..

    upon second infection:

    memory cells from 1st infection already present:

    divide rapidly to develop into plasma cells and more memory cells

    plasma cells produce greater number off antibodies/ more quickly

    for antigenic variability

    change in antigens;

    due to mutations

    antigens no longer complementary to surface receptors of memory cells

    no secondary response
    thank you!
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    (Original post by britash)
    *properly*?? Well the half term holidays we had about 4/3-ish weeks ago..
    I do AQA chemistry. I can afford to get a middle/high B to get an A overall on that, so I guess I could revise the night before, like I did in january

    I have maths as well.. and I'm failing stats, so I dont really care about that one
    What else do you do? x
    Ive got Chemistry and Math too.
    What board are you doing?
    And are you resitting any?
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    (Original post by britash)
    *properly*?? Well the half term holidays we had about 4/3-ish weeks ago..
    I do AQA chemistry. I can afford to get a middle/high B to get an A overall on that, so I guess I could revise the night before, like I did in january

    I have maths as well.. and I'm failing stats, so I dont really care about that one
    What else do you do? x
    I do Maths, (hate stats too!), Chemistry Salters B, Biology AQA and Physics AQA.

    I'm good at Core 1 and Core 2 though, so they're OK. And Physics is just pretty easy :P
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    (Original post by britash)
    Cant do the second one of you..
    but the first one I can have a go.

    Right. Well
    When your infected with a pathogen for the first time..
    You have ONE B cell that is complementary to the antigen.
    More of this B cell is produced via mitosis to form cloned B cells
    The B cells produce B plasma cells that make antibodies and these anitbodies destroy the pathogen. This is your Primary Immune Response.
    The B cells ALSO produce B memory cells and these are stored.
    When you are next infected with the antigen again, a much more RAPID response is produced. The B memory cells develop into B plasma cells and more B memory cells. The B plasma cells produce the antibodies needed to destroy the pathogen. This is your secondary immune response.

    Literally just remember.
    1st immune response - you have only 1 B cell. This does mitosis so you have tons of clones. Some go to B plasma cells. Some to B memory cells. The B plasma cells make antibodies. The B memory cells are stored. The antibodies get rid of the antigen (because they are cloned they are complementary and antigen-specific)
    2nd immune response - Your B memory cells quickly recognise your infected with the same antigen. These develop to B plasma cells and more B memory cells. So you have lots and more antibodies that quickly destroy the anitgen. This is MUCH faster.

    Hope that helps. It took me forever to understand this topic, but now it seems easy to me x
    thank you! i hope you get your A - yeah i was reading through the thread

    sorry i hope i'm not annoying you! but can you answer these as well please, i like your answers they're so detailed

    - pressure and volume changes and associated valve movements during the cardian cycle

    - myogenic stimulation of the heart and transmission of a subsequent wave of electrical activity

    - roles of the SAN, AVN and the bundle of His
    these are from the spec, i understand it but the book just confused me
    and i don't know how to answer it the mark scheme way
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    Aw thanks! I couldn't find these
    Yay more papers for tomorrow :elmo:
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    What does everyone expect to come up on Monday? Of course, I'm not going to take your suggestions and just revise those - I just like to know what people are thinking.
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    (Original post by shybrowngirl)
    thank you! i hope you get your A - yeah i was reading through the thread

    sorry i hope i'm not annoying you! but can you answer these as well please, i like your answers they're so detailed

    - pressure and volume changes and associated valve movements during the cardian cycle

    - myogenic stimulation of the heart and transmission of a subsequent wave of electrical activity

    - roles of the SAN, AVN and the bundle of His
    these are from the spec, i understand it but the book just confused me
    and i don't know how to answer it the mark scheme way
    Aw thank-you. So do I!!!

    I'll do the one I like the best first so number 3.
    Roles of SAN, AVN and bundles of His.

    SAN (Sino-Atrial Node)
    This is called also the pacemaker. It inititates the electrical impulses across the atria causing them to contract
    AVN (atrioventricular node)
    This receives the electrical impulse from the SAN and delays it from carrying on (the importance of this delay is to allow the venticles to fill up with blood before they contract).
    After the short delay, the AVN sends the electrical impulse between the venticles down the septum, down the bundles of His to the purkyne fibres.
    The electrical impulse reaches the base of the ventricles where both venticles contract upwards pushing blood out of the venticles.

    I think of it in a few stages
    1. SAN, pacemaker. Initiates heartbeat and electrical impulses. Contraction of atria.
    2. AVN receives impulse and DELAYS (this is important!!!) to allow the ventricles to fill with blood before they contract
    3. AVN sends impulse down septum to bundles of His
    4. Impulse reaches bottom of venticles where it causes both walls of the venticles to contract upwards.
    (this is literally all there is to it) All they could ask questions on is the importance of the delay. What the SAN is, where is it situated etc. xx

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