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

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    (Original post by FristyKino)
    I'd guess ATPase breaks ATP down into ADP and inorganic P.
    While ATPsynthase makes ATP by joining ADP with an inorganic P
    This definition is spot on.

    Unfortunately, Edexcel calls the ATPsynthatase enzyme in the mitrochondrial membrane the ATPase, hence the source of confusion. ATPase breaks down ATP whereas ATP synthetase makes new ATP.
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    hi can someone help with question 5 on the specimen paper, i dont understand why they wrote sodium ions move out, when its depolarisation and dont sodium ions move in making it more positive inside than out.
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    (Original post by JJ 91)
    hi can someone help with question 5 on the specimen paper, i dont understand why they wrote sodium ions move out, when its depolarisation and dont sodium ions move in making it more positive inside than out.
    The specimen paper is POO!
    You are right, the Na+ ions move INTO the axon membrane.
    Never trust what the specimen paper says - the people who make the specimen papers are half drunk when they make them
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    thanks , was worrying a bit there, ur right absolutely hate this spec paper.
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    (Original post by FristyKino)
    Well i googled it and came across this website and read through the first paragraph. It kinda says that ATPsynthase makes ATP.... but then i saw part of the enzyme structure at the bottom and i saw 'woo enzyme structure - lets scroll down the page and see the whole structure' - one look at the full picture and instantly i thought 'TRANSFORMER!!!'..... totally off-topic but im sure it looks a transformer :/

    (Original post by flowerscat)
    This definition is spot on.

    Unfortunately, Edexcel calls the ATPsynthatase enzyme in the mitrochondrial membrane the ATPase, hence the source of confusion. ATPase breaks down ATP whereas ATP synthetase makes new ATP.
    Thanks! And wooooo transformers! WHERE?!
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    Im kinda struggling with all the gene technology stuff :/ anyone got any tips?
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    hey guys
    if you look on page 263 of NT text book, the germ line bit is what I don't get :|
    it says 'replacing or suppleenting defective gene in fertilised egg' - that means it can only happen in females right?
    or is it done in-vitro?
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    and also, if the fertilized egg is implanted into females, the female is not treated . it is the embryo developing that is treated right? argh
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    (Original post by Flux_Pav)
    hey guys
    if you look on page 263 of NT text book, the germ line bit is what I don't get :|
    it says 'replacing or suppleenting defective gene in fertilised egg' - that means it can only happen in females right?
    or is it done in-vitro?
    Germ line therapy = fertilise the eggs in vitro (in the laboratory) (IVF) = test the zygote (very early stage of embryo) for defective gene = if positive replace the defective gene with new gene.

    Implant the fertilised egg into the female, where it will develop into a foetus.

    The cells in the zygote are totipotent, hence all the cells of the foetus will carry the modified gene. Any offspring of this child will now also inherit the modified gene.
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    (Original post by flowerscat)
    Germ line therapy = fertilise the eggs in vitro (in the laboratory) (IVF) = test the zygote (very early stage of embryo) for defective gene = if positive replace the defective gene with new gene.

    Implant the fertilised egg into the female, where it will develop into a foetus.

    The cells in the zygote are totipotent, hence all the cells of the foetus will carry the modified gene. Any offspring of this child will now also inherit the modified gene.
    omg thank you so much
    all makes perfect sense
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    AHHH starting to have a nervous breakdown about this exam!!!
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    (Original post by flowerscat)
    Muscle contraction: Sliding filament theory:

    An impulse arriving at the neuromuscular junction causes the release of achetylcholine into the space between the neurone and the muscle cells.

    This causes depolarisation at the muscle cells, resulting in release of calcium ions (*from the sarcoplasum reticulum, which is a special type of endoplasmic reticulum found in muscle cells). This calcium travels rapidly down the muscle cells (*via transverse tubules)

    Calcium binds to troponin. Troponin causes tropomyosin to change shape, revealing the myosin-binding sites on actin.

    Mysoin binds to actin, forming a "cross-bridge".

    ADP (which is attached to the myosin head) now detaches, providing the energy for the myosin head to "nod" forwards.

    This causes the actin filament to slide over myosin. The muscles shorten (contract). * this is called the power stroke.

    ATP now binds to the myosin head, causing it to detach from actin.

    ATP is hydrolysed, providing the energy for the myosin head to return to its upright position.

    Myosin head now binds further along the actin filament and the whole process is repeated.

    When an impulse is no longer received, calcium ions are mopped up (into the sarcoplasmic reticulum) and the tropomyosin once again blocks the myosin-binding sites on actin.

    * a single power stroke only contracts muscles by 1%, whereas 35% contraction is need to actually perform work - therefore a powerstroke must be repeated several times in one muscle contraction.

    Information marked with an * does not form part of the AQA syllabus, have included it here to make the explanation clearer.
    Thank you!!
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    can anyone help me with a few of these please
    1) when histamine is release from WBC's, how does dilation of the aterioles/arteries help injured or infected cells?

    2)does the breakdown of the pigment in rod/cone cells cause the production of a generator potential?

    3) what is the second messenger model of adrenaline and glucagon action?

    4) how does positive feedback result in a breakdown of control systems?

    5) in the DNA technology bit, which order does restriction mapping, PCR, DNA sequencing and gel electrophoresis come?

    6) why would scientists use genetic fingerprints for deciding what animal and plants breed?

    some of these answers are probably really obvious and i'm just being stupid..but if anyone could help me out i'd be mega grateful
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    Just finished looking over all of the AS textbook... Pretty biologied out now!
    Anyone want to help me make a list of synpotic topics?
    To start off:
    DNA, structure and function. Protein synthesis, inheritance, selection.
    How cells are adapted to their function- this bit seems to come up in every section.
    Polymers
    Diffusion and osmosis
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    (Original post by vickidougal)
    can anyone help me with a few of these please
    1) when histamine is release from WBC's, how does dilation of the aterioles/arteries help injured or infected cells?

    2)does the breakdown of the pigment in rod/cone cells cause the production of a generator potential? Yes

    3) what is the second messenger model of adrenaline and glucagon action?

    4) how does positive feedback result in a breakdown of control systems?

    5) in the DNA technology bit, which order does restriction mapping, PCR, DNA sequencing and gel electrophoresis come? Pcr to make more dna to sample, then retsriction enzymes to make fragments. Gel electrophoresis separates the fragments. What kind of dna sequencing do you mean?

    6) why would scientists use genetic fingerprints for deciding what animal and plants breed? Organisms with similar genetic fingerprints have similar genotypes. To prevent inbreeding, you should breed organisms with the most different fingerprints.

    some of these answers are probably really obvious and i'm just being stupid..but if anyone could help me out i'd be mega grateful
    Answers to some questions above. These are just off the top of my head
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    [QUOTE=vickidougal;32320195]can anyone help me with a few of these please
    1) when histamine is release from WBC's, how does dilation of the aterioles/arteries help injured or infected cells?


    It allows the white blood cells (mostly macrophages) to travel to the site of infection and ingest the pathogens.


    2)does the breakdown of the pigment in rod/cone cells cause the production of a generator potential?

    Pigment in rod cells = rhodopsin = breaks down into retinal and opsin. Opsin binds to sodium ions channels in the upper part of the rod cell, causing it to close. This decreases the membrane potential in the rod cell (hyperpolarisation). It stops secreting neurotransmitter. The neurotransmitter, glutamate, is an inhibitory neurotransmitter. As soon as glutamate secretion stops, the bipolar cell becomes depolarised (generator potential) and sends an impulse down the optic nerve.

    None of this is required for the AQA syllabus.

    3) what is the second messenger model of adrenaline and glucagon action?

    Adrenaline (first messenger) binds to its receptor on the cell memberane forming a receptor-substrate complex. This activates enzymes located on the inside of the membrane, which result in ATP being converted to cyclic AMP (cAMP). cAMP is the second messenger, and activates enzymes responsible for converting glycogen to glucose. *It also stimulates the production of glucagon by the alpha-cells in the pancreas (*info not in AQA textbook)

    Adrenaline is produced during times of stress, when the muscles need a quick burst of energy.

    Glucagon is not an enzyme, it is an hormone that binds to the receptors on liver cells and results in the activation of enzymes that convert glycogen to glucose.
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    look at the spec 3.5.7

    'evaluate the use of stem cells in treating human disorders'
    someone explain ?
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    Could someone explain in vivo to me please.
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    4) how does positive feedback result in a breakdown of control systems?

    Body temp, blood pH, etc are regulated by certain "set points". Negative feedback loops work to ensure that these parameters stay with a certain range of the set point.ie.body temp stays 37+/- 0.5.

    Positive feedback results when a change results in even more deviation from the set point - hence there are very few examples (depolarisation being one). In certain infections, the negative feeback loop does not operate well, and this results in positive feeback. eg. during typhoid fever, the body is not able to control the body temperature and it goes beyond set point and keep increasing.

    5) in the DNA technology bit, which order does restriction mapping, PCR, DNA sequencing and gel electrophoresis come?

    First isolate the DNA from source (or from mRNA - mRNA converted to DNA via reverse transcriptase).

    If the amount of DNA is very low, amplify by PCR.

    If you want to produce recombinant DNA, then cut the source DNA and vector DNA by restriction enzymes, and ligate. Transform into bacteria, which will start producing the new DNA.

    If you want to identify DNA fragments, then digest the source DNA (or after PCR) with restriction enzymes. Then run it on an agarose gel (restriction mapping). If you want to identify the fragment further, transfer the DNA onto a nitrocellulose membrane (southern blot) and add probes.

    DNA sequencing can be done on DNA directly from the source, but works best if you have sufficient sample, and small fragments (ie. after PCR and restriction digest). It is essential that you have a primer for DNA sequencing, so you would have to know at least a few bases at the start of your gene.



    6) why would scientists use genetic fingerprints for deciding what animal and plants breed?

    can you clarify the question?
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    (Original post by Master.K)
    Could someone explain in vivo to me please.
    In vivo = within the body
    In vitro = outside the body (ie. in the laboratory)
 
 
 
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