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

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    this is my final exam and my hardest one this exam season
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    does anyone have a copy of the June 2011 specimen paper? i was away for the mock and because some classes have still not done it my teacher says i have to come collect the paper in the next month if i want it! and i kind of need it now to get my bio revision done!. anyone?
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    hey, does anyone know if there was a jan 2011 BIOL5 paper??
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    (Original post by neverhide)
    hey, does anyone know if there was a jan 2011 BIOL5 paper??
    there wasn't one.
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    Anyone else failed to start revision for this so far? :P

    I really need to get going with this, sort of ignoring it because it's my last exam. Probably will start properly in the next few days...
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    hi can someone help me with this essay question
    describe how mammals maitain internal conditions despite external environmental conditions

    i knw this is bout homeostasis and stuff
    so ive thought
    homeostasis
    why mammals need to maintain internal temperature
    how they maintain body temp
    by hormonal control(blood glucose levels)
    and temperature control by the autonomic nervous system(hypothalamus gland)

    can anyone think of anything else
    my teacher sed if this was written as a proper essay i wud probably get about 17/25 but thats as a proper essay im not that good at writing is properly
    thanks guys
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    Hi, i'm really confused with a chapter 15 exam style question in the nelson thornes text book. Its question 4a

    It asks about how oestrogen stimulates some breast cancers, and how tamoxifen is a drug to treat it by binding to oestrogen receptors, and therefore prevents the cancer from dividing.

    But i thought cancer was caused by uncontrolled cell division, and is completely unrelated to protein synthesis, but the mark scheme talks about protein synthesis by saying:

    less / no oestrogen binds to receptor;
    less / no receptors change shape;
    fewer / no transcriptional factors;
    less protein synthesis;

    so obviously cancer is related to protein synthesis, but how????
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    (Original post by cws121)
    Hi, i'm really confused with a chapter 15 exam style question in the nelson thornes text book. Its question 4a

    It asks about how oestrogen stimulates some breast cancers, and how tamoxifen is a drug to treat it by binding to oestrogen receptors, and therefore prevents the cancer from dividing.

    But i thought cancer was caused by uncontrolled cell division, and is completely unrelated to protein synthesis, but the mark scheme talks about protein synthesis by saying:

    less / no oestrogen binds to receptor;
    less / no receptors change shape;
    fewer / no transcriptional factors;
    less protein synthesis;

    so obviously cancer is related to protein synthesis, but how????
    well you know there are sequences of bases coding for oncogenes and tumour suppressor genes, basically if protein synthesis does not occur OR something goes wrong during transcription/translation, a tumour supressor gene may not be coded for. this means tumour supressor genes will either not function properly or not be made at all, therefore cancer can occur as cells will divide uncontrollably without these tumour supressor genes.
    hope that helps, thats all i could think of for cancer caused by protein synthesis.. i probably would have said caused by mutagens or something :/
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    (Original post by emmaaa65)
    well you know there are sequences of bases coding for oncogenes and tumour suppressor genes, basically if protein synthesis does not occur OR something goes wrong during transcription/translation, a tumour supressor gene may not be coded for. this means tumour supressor genes will either not function properly or not be made at all, therefore cancer can occur as cells will divide uncontrollably without these tumour supressor genes.
    hope that helps, thats all i could think of for cancer caused by protein synthesis.. i probably would have said caused by mutagens or something :/
    omg i'm so stupid! its so obvious now you've said it!!! Thanksss !!!!
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    Physics 5 is my last exam, both that and biology 5 are an utter pain.

    Questions:

    Describe what a vector is in terms of DNA technology.

    Describe the process of translation of DNA into a polypeptide in full, and adaptations that can increase the rate of synthesis of polypeptides.
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    aaaah this exam is getting so close going to start properly properly revising today!!
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    (Original post by TlanTlan)
    Physics 5 is my last exam, both that and biology 5 are an utter pain.

    Questions:

    Describe what a vector is in terms of DNA technology.

    Describe the process of translation of DNA into a polypeptide in full, and adaptations that can increase the rate of synthesis of polypeptides.
    Vector: A carrier.The term may refer to something such as a plasmid, which carries DNA into a cell, or to an organism that carries that carries a parasite to its host.
    Plasmids are circular circular lengths of DNA, found in bacteria. An example of there use is with the synthesis of insulin. The desired gene/DNA fragment is cut out using a specific restriction endonuclease, a plasmid is also cut with the same restriction endonuclease to ensure that the 'sticky ends' are complimentary to each other. The DNA fragments are mixed with the plasmids and become incorporated into them, the join is made permenant by DNA ligase. These plasmids are then transferred into bacteria and the insulin is cultured.

    Translation of DNA occurs outside the nuclear membrane, a mRNA starting codon attaches to a ribosome and tRNA molecules carry complimentary anticodons to the ribosome to bind with the mRNA. Each triplet base corrosponds to a specific amino acid, as the triplet bases bond, so a polypeptide is synthesised. The amino acids form peptide bonds by condensation reactions.
    The rate of synthesis can be increased through the increase in presence of related enzymes and corresponding tRNA molecules. The alteration of temperature, pressure, water potential and pH to optimum levels.

    Gd Questions-Hope thats covered it.

    QS: Explain the transmission of an action potential across a neuromuscular junction.

    QS: Explain how a muscle contracts.
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    (Original post by xelaman)
    Vector: A carrier.The term may refer to something such as a plasmid, which carries DNA into a cell, or to an organism that carries that carries a parasite to its host.
    Plasmids are circular circular lengths of DNA, found in bacteria. An example of there use is with the synthesis of insulin. The desired gene/DNA fragment is cut out using a specific restriction endonuclease, a plasmid is also cut with the same restriction endonuclease to ensure that the 'sticky ends' are complimentary to each other. The DNA fragments are mixed with the plasmids and become incorporated into them, the join is made permenant by DNA ligase. These plasmids are then transferred into bacteria and the insulin is cultured.

    Translation of DNA occurs outside the nuclear membrane, a mRNA starting codon attaches to a ribosome and tRNA molecules carry complimentary anticodons to the ribosome to bind with the mRNA. Each triplet base corrosponds to a specific amino acid, as the triplet bases bond, so a polypeptide is synthesised. The amino acids form peptide bonds by condensation reactions.
    The rate of synthesis can be increased through the increase in presence of related enzymes and corresponding tRNA molecules. The alteration of temperature, pressure, water potential and pH to optimum levels.

    Gd Questions-Hope thats covered it.

    QS: Explain the transmission of an action potential across a neuromuscular junction.

    QS: Explain how a muscle contracts.

    An action potential is transmitted through a neuromuscular junction through the action of neurotransmitters. Acetylchloline is broken down by acetylcholinase and the remaining acetyl and choline diffuse in to the neurone and are combined again by energy from mitochondria.

    The tropomysoin molecule prevents myosin head from attaching to actin binding site is pulled away as calcium ions released from the sarcoplasmic reticulum. The myosin head can now attach to the binding site on actin and when the myosin head changes angle it moves the actin filament along. ATP fixes to myosin head causing it to detach from actin. Hydroylsis of ATP to ADP by ADPase gives energy for myosin head to go back to its normal position.

    Compare rod cells and cone cells
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    (Original post by INeedToRevise)

    Compare rod cells and cone cells

    Rod cells and cone cells are the photosensitive cells in the retina of the eye. Cone cells can perceive colour by having pigments for red, blue and green, whereas rod cells can not perceive colour. Both types of cell are connected to bipolar neurones. However 3 rod cells are connected to every bipolar neurone compared to only one cone cell per bipolar neurone. This allows rod cells to perceive very low intensity light, as when photons of light cause the breakdown of pigment in the rod(and cone cells) a generator potential is created. In low intensity light a smaller generator potential is created but with multiple rod cells per bipolar neurone the generator potential accumulates. This means a smaller generator potential per light sensitive cell is required to reach the threshhold frequency in the bipolar neurone and cause an action potential to the brain. The disadvantage of this however is that rod cells have a lower resolution and visual acuity as a result.

    Also, the distribution of rod cells puts the majority of them at the edges of the retina, whereas the highest concentration of cone cells are at the fovea of the retina.
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    (Original post by TlanTlan)
    Rod cells and cone cells are the photosensitive cells in the retina of the eye. Cone cells can perceive colour by having pigments for red, blue and green, whereas rod cells can not perceive colour. Both types of cell are connected to bipolar neurones. However 3 rod cells are connected to every bipolar neurone compared to only one cone cell per bipolar neurone. This allows rod cells to perceive very low intensity light, as when photons of light cause the breakdown of pigment in the rod(and cone cells) a generator potential is created. In low intensity light a smaller generator potential is created but with multiple rod cells per bipolar neurone the generator potential accumulates. This means a smaller generator potential per light sensitive cell is required to reach the threshhold frequency in the bipolar neurone and cause an action potential to the brain. The disadvantage of this however is that rod cells have a lower resolution and visual acuity as a result.

    Also, the distribution of rod cells puts the majority of them at the edges of the retina, whereas the highest concentration of cone cells are at the fovea of the retina.
    Thats good You could also mention the pigments are called rhodopsin and iodopsin...
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    Could someone explain the oestrus cycle in a way we could get asked in an exam question?
    Also, in the transmission across a synapse, the book says some drugs cause receptors on the postsyanptic region to remain open, allowing sodium ions to continue diffusing in, causing repeated action potentials in the postsynapstic region, resulting in tetanus. This wouldn't really happen would it, surely you would run out of sodium ions because they wouldn't be replaced fast enough?
    To the above poster, do we have to know about photoreceptors in such depth, mentioning rhodopsin and iodopsin? I'm not sure how much to mention in exam answers.
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    reading all of the comments on this thread makes me feel sooooo unprepared!! usually i start doing revision months before an exam... but it feels like ive left this one really late... and i have two more exams on top of this one! omgomgomgomgomgomgomgomgomggmogm gogomgmogmomg!! panicking! :O
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    So much prep needed for BIOL5, it's almost driving me insane. And boy, do genetics suck
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    (Original post by janet9)
    So much prep needed for BIOL5, it's almost driving me insane. And boy, do genetics suck
    I take it your talking about chapter 16 in the textbook :ahhhhh:, I know the feeling
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    basically am stuck on genetics part. If a gene codes for a specific polypeptide chain how can you have different alleles which are the same gene because different alelles have different polypeptide chains( they usually have one amino acid thats different) and that would therefore make them different genes

    Is it that the differences are so small, i.e. one amino acid difference still makes it the same polypeptide chain?

    very confused
    any ideas or explanation would be helpful?
 
 
 
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