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

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    (Original post by kingsmod1)
    guys for chap 13 i dont understand it says fsh stimulates oestrogen to be prodcued but then oestrogen inhibits fsh?

    for up to day 10 oestrogen stimulaes rise in fsh, wtf though it inhibits it?????

    MANY THANKSSSSSSSSSSSSS
    It's an example of negative and positive feedback! At first, oestrogen inhibits the release of FSH (so negative feedback), but when it reaches a certain level it stimulates the production of FSH and LH (and that surge of LH causes ovulation). (It's positive feedback because the increase in oestrogen stimulates the release of LH, and the LH then stimulates the ovary to release more oestrogen, and then oestrogen further stimulates the release of LH - and so on until ovulation occurs.) It's a little odd, but you just need to remember that oestrogen inhibits FSH release until there's a high level of it.
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    in the nt it says that genetic fingerprinting pcr is used to amplify the dna sample, does it amplify all the dna sample, and if so how, i though all the dna sample couldnt be amplified in pcr, which only amplifies small amounts?
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    (Original post by tehsponge)
    Well you could still get an A even if you left the essay, lol. You'd be able to get a max of 75% without even touching the essay, but you'd have to be a HSW god.
    im not really a hsw god but i did manage to get a B in jan 2011 i even amazed myself on that one
    but i thought unit 5 was normal like unit1 and only one question was hsw
    if alot more than one question is hsw then i will need to do the essay
    thanks
    i just cant wait for this exam to be over cant be bothered revising anymore want to revise for chem5
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    (Original post by appleschnapps)
    Probes: first of all, the definition for probes that seems to come across most often is short, single strands of DNA that have a base sequence complementary to the base sequence of part of the target gene. The probe can then bind to (or hybridise with) the target gene. Probes are labelled, usually radioactively (so to see where the probes have attached, it's exposed onto x-ray or photographic film) or with a fluorescent label (so the target gene will fluoresce under UV light). In a practical sense, this is used with restriction endonucleases to break the DNA sample into fragments, and then transferred to a nylon membrane (southern blotting) and incubated with the probe. If the gene is present, it will be labelled and can be detected. (To carry on this idea, if a disease causing gene/gene mutation has been identified, the best course of treatment can be decided.)

    On a large scale, probes are used for genetic screening for mutated genes as a part of a DNA microarray, where DNA is washed over an array of different DNA probes (for different mutated genes) and if the DNA binds to a specific probe, the mutation can be identified. [Note: in the specification, you're supposed to understand that scientific methods are constantly updated. This is an example, as DNA microarrays are much faster and cost-effective than using DNA probes on a smaller scale.] This again lets you consider treatments, and you can also bring up genetic counselling (e.g. whether or not to screen embryos if parents are a carrier for a mutated gene).

    Restriction mapping, meanwhile, is kind of horrible. First of all, restriction mapping is used for putting DNA fragments back in the right order, because in order for DNA sequencing to take place, the (labelled, this is important) DNA sample must first be cut into fragments using restriction endonucleases, and then separate the fragments by length using electrophoresis.

    You then get a nice little (haha, no) diagram:



    This is a pretty simplified version; it's possible you can get one with more than one restriction enzyme, but for let's keep it simple for now. Your total digest fragments are ones that have been completely cut by the enzyme (which I'm going to call enzyme A). Your partial digest fragments occur when the enzymes haven't been left long enough, so you can also get fragments of different lengths (in this instance, there isn't a cut after the 3kb fragment, so you have a fragment of 8kb because 3+5=8 - and in the mark schemes, they do apparently like to see you can add 3+5). The radioactive fragment is important, as this gives you your starting point - this is because the radioactive fragment is the one with the probe attached - so in this instance, because we have a partial fragment of 8 and not 7 (and so not 2+5), there are two recognition sequences and so the recognition map is...



    (Concise posts - this is how not to do it. )
    Well I did give you +ve rating but still wanted to thanxs. That post covers all the "ermm" moment I had while doing june 2010.
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    how the hell did anyone get 69 marks in the june 10 paper its impossible they must have been a hsw god
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    Don't suppose any kind soul would give me a quick rundown of the second messenger model of adrenaline and glucagon action? pwetty please..
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    (Original post by Sly Racoon)
    Don't suppose any kind soul would give me a quick rundown of the second messenger model of adrenaline and glucagon action? pwetty please..
    Second messenger model is one of the two models of hormone action. This model involves peptide hormones that aren't soluble in the lipid bilayer but are soluble in water. What happens is:

    1) The hormone binds to a receptor protein on the cell surface membrane, forming a hormone - receptor complex.
    2) This activates an enzyme - adenyl cyclase - which converts ATP into cyclic AMP, or cAMP for short. The cAMP is a second messenger with the hormone being the first.
    3) The cAMP can go on to cause a cascade of chemical reactions. In the case of glucagon, it can go on to cause glycogenolysis and gluconeogenesis. In the case of adrenaline it activates enzymes involved in glycogenolysis and deactivates enzymes involved in glycogenesis.

    Hope that helped
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    (Original post by flf)
    ok, Here's an essay question from an old Human bio 08 paper.

    discuss 'The biological importance of plants to humans.'

    I'm gonna put my essay plan up, can ppl add topics/points to it that I haven't thought of? Breadth is a bit of a problem for me, I can't really 'think outside the box' very well!

    Plan:

    -plants used in photosynthesis which gives humans glucose (and then a brief description of the stages of photosynthesis)
    -so we can respire (brief respiration description)
    -needed for ATP. uses of ATP: metabolism, reactions, active transport, e.g. in muscle contractions (brief description of its role in moving calcium ions)

    I'm not sure whether these points are relevant for 'biological importance'. What does that even mean???!!!
    -Plants, when prevented for decay, gives fossil fuels
    -the nitrogen cycle (the leguminous plants) which give us ammonium ions


    I'm a bit stuck now. plus it says 'biological' -so can we even talk about fossil fuels?
    you can talk about stuff like making medicines(herbs) , agriculture, plants are needed to remove CO2 so less global warming effect, needed for stable food chain, maintain constant climate (like transpiration), they provide shelter....i am not sure about some of the points but i would suggest you to try and relate as much as u can.
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    (Original post by Sly Racoon)
    Don't suppose any kind soul would give me a quick rundown of the second messenger model of adrenaline and glucagon action? pwetty please..
    I suspect you don't need to know any more than 'they activate an enzyme, which then causes glycogenolysis to take place', but just in case...

    When glucagon and adrenaline bind to their specific receptors, they activate the enzyme adenylate cyclase. When this is activated, it converts ATP into a 'second messenger' called cyclic AMP (or cAMP), which then activates a chain of reactions that make up glycogenolysis.

    EDIT: l4ith put it better, and more quickly.
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    in the nt it says that genetic fingerprinting pcr is used to amplify the dna sample, does it amplify all the dna sample, and if so how, i though all the dna sample couldnt be amplified in pcr, which only amplifies small amounts?
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    (Original post by l4ith)
    Second messenger model is one of the two models of hormone action. This model involves peptide hormones that aren't soluble in the lipid bilayer but are soluble in water. What happens is:

    1) The hormone binds to a receptor protein on the cell surface membrane, forming a hormone - receptor complex.
    2) This activates an enzyme - adenyl cyclase - which converts ATP into cyclic AMP, or cAMP for short. The cAMP is a second messenger with the hormone being the first.
    3) The cAMP can go on to cause a cascade of chemical reactions. In the case of glucagon, it can go on to cause glycogenolysis and gluconeogenesis. In the case of adrenaline it activates enzymes involved in glycogenolysis and deactivates enzymes involved in glycogenesis.

    Hope that helped
    Awesome, thanks, you're a saint
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    (Original post by Sly Racoon)
    Don't suppose any kind soul would give me a quick rundown of the second messenger model of adrenaline and glucagon action? pwetty please..

    Basically, adrenaline is the first messenger, it binds to a receptor site of target cells (these are usually muscle cells). This causes an enzyme on the inside of the cell to become active, which converts ATP to cyclic AMP (cAMP). cAMP is the second messenger. It activates other enzymes that perform glycogenolysis. (Glycogen to glucose)
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    (Original post by appleschnapps)
    It's an example of negative and positive feedback! At first, oestrogen inhibits the release of FSH (so negative feedback), but when it reaches a certain level it stimulates the production of FSH and LH (and that surge of LH causes ovulation). (It's positive feedback because the increase in oestrogen stimulates the release of LH, and the LH then stimulates the ovary to release more oestrogen, and then oestrogen further stimulates the release of LH - and so on until ovulation occurs.) It's a little odd, but you just need to remember that oestrogen inhibits FSH release until there's a high level of it.
    thank u and also chap 16 do ui have to remember all those stages about antibiotics coz i look at past papers and theres nnot many big marker Qs?
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    (Original post by Sly Racoon)
    Don't suppose any kind soul would give me a quick rundown of the second messenger model of adrenaline and glucagon action? pwetty please..
    - adrenaline binds to receptors and activate the enxyme adenylate cyclase
    - andenylate cyclase converts ATP into a chemical signal called a second messenger known as cAMP
    - cAMP activates a chain of reactions that break down glycogen into glucose (glycogenlysis)



    - glucagon binds to receptors on the cells membranes of liver cells
    - glucagon activates thebreaking down of glycogen into glucose (glycogenlysis)
    - glucagon also promotes the formation of glucose from fatty acids and amino acids


    hope this helps
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    Question!!!
    Some organisms are adapted for living in hot, dry environments.
    Explain what causes the activity of reptiles living in a desert to vary greatly over a twenty-four hour period.
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    (Original post by tehsponge)
    Glucagon isn't involved in the second messenger model.
    Basically, adrenaline is the first messenger, it binds to a receptor site of target cells (these are usually muscle cells). This causes an enzyme on the inside of the cell to become active, which converts ATP to cyclic AMP (cAMP). cAMP is the second messenger. It activates other enzymes that perform glycogenolysis. (Glycogen to glucose)
    The specification says 'The second messenger model of adrenalin and glucagon action'
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    (Original post by Sly Racoon)
    The specification says 'The second messenger model of adrenalin and glucagon action'
    Yeah I just saw that. The textbook doesn't go into the detail of the glucagon mechanism at all...
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    (Original post by hahaff)
    how the hell did anyone get 69 marks in the june 10 paper its impossible they must have been a hsw god
    I got 65 without really revising (I was expecting an epic fail) when I did it as a mock under exam conditions so it can easily be done
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    (Original post by tehsponge)
    Yeah I just saw that. The textbook doesn't go into the detail of the glucagon mechanism at all...
    Yeah just goes on about 'the hormone' :| my hatred of AQA grows every single day
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    (Original post by kingsmod1)
    thank u and also chap 16 do ui have to remember all those stages about antibiotics coz i look at past papers and theres nnot many big marker Qs?
    Er, I'm assuming you're talking about the genetic modification bit? If so, you should be safe - the spec says 'The use of recombinant DNA technology to produce transformed organisms that benefit humans', and because it doesn't go in depth there I'd be surprised if you need to remember them in too much detail. Just try and remember some examples, and memorise the arguments for and against genetic modification if you have difficulty thinking of them off the top of your head.

    If you were talking about something else, please tell me what because I've completely missed it.
 
 
 
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