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    (Original post by iesians)
    i have a question

    why do muscles work in antagonistic pairs ..!? (4 marks) .?!?!
    antagonistic means when one muscle gives action its antagonistic pair gives the opposite action, this arrangement is important in many muscle activities like fine skillful alternative movement of the fingers like typing and playing on piano.
    In walking and when the two muscles contract at the same time can fix the body in any needed position like lifting weight and posture.

    gd luck
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    I found this for those who are having trouble learning the sliding filament theory like how I did:
    Here is a quick reminder of all the structures involved:

    Myofibril: A cylindrical organelle running the length of the muscle fibre, containing Actin and Myosin filaments.
    Sarcomere: The functional unit of the Myofibril, divided into I, A and H bands.
    Actin: A thin, contractile protein filament, containing 'active' or 'binding' sites.
    Myosin: A thick, contractile protein filament, with protusions known as Myosin Heads.
    Tropomyosin: An actin-binding protein which regulates muscle contraction.
    Troponin: A complex of three proteins, attached to Tropomyosin.
    Here is what happens in detail. The process of a muscle contracting can be divided into 5 sections:

    A nervous impulse arrives at the neuromuscular junction, which causes a release of a chemical called Acetylcholine. The presence of Acetylcholine causes the depolarisation of the motor end plate which travels throughout the muscle by the transverse tubules, causing Calcium (Ca+) to be released from the sarcoplasmic reticulum.

    In the presence of high concentrations of Ca+, the Ca+ binds to Troponin, changing its shape and so moving Tropomyosin from the active site of the Actin. The Myosin filaments can now attach to the Actin, forming a cross-bridge.

    The breakdown of ATP releases energy which enables the Myosin to pull the Actin filaments inwards and so shortening the muscle. This occurs along the entire length of every myofibril in the muscle cell.

    The Myosin detaches from the Actin and the cross-bridge is broken when an ATP molecule binds to the Myosin head. When the ATP is then broken down the Myosin head can again attach to an Actin binding site further along the Actin filament and repeat the 'power stroke'. This repeated pulling of the Actin over the myosin is often known as the ratchet mechanism.

    This process of muscular contraction can last for as long as there is adequate ATP and Ca+ stores. Once the impulse stops the Ca+ is pumped back to the Sarcoplasmic Reticulum and the Actin returns to its resting position causing the muscle to lengthen and relax.
    It is important to realise that a single power stroke results in only a shortening of approximately 1% of the entire muscle. Therefore to achieve an overall shortening of up to 35% the whole process must be repeated many times. It is thought that whilst half of the cross-bridges are active in pulling the Actin over the Myosin, the other half are looking for their next binding site.
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    Introduction

    What is Cellular Respiration?

    Cellular respiration allows organisms to use (release) energy stored in the chemical bonds of glucose (C6H12O6). The energy in glucose is used to produce ATP. Cells use ATP to supply their energy needs. Cellular respiration is therefore a process in which the energy in glucose is transferred to ATP.



    In respiration, glucose is oxidized and thus releases energy. Oxygen is reduced to form water.

    The carbon atoms of the sugar molecule are released as carbon dioxide (CO2).

    The complete breakdown of glucose to carbon dioxide and water requires two major steps: 1) glycolysis and 2) aerobic respiration.* Glycolysis produces two ATP. Thirty-four more ATP are produced by aerobic pathways if oxygen is present.

    In the absence of oxygen, fermentation reactions produce alcohol or lactic acid but no additional ATP.
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    Summary for cellular respiration

    Glycolysis

    During glycolysis, glucose (C6) is converted to two pyruvates (C3).

    C-C-C-C-C-C ? C-C-C + C-C-C

    Formation of Acetyl CoA

    One acetyl CoA is formed for each pyruvate produced by glycolysis (see the step above).

    C-C-C ? C-C + CO2

    pyruvate ? acetyl CoA + CO2

    Krebs Cycle

    C-C ? 2 CO2

    The Krebs Cycle produces NADH, FADH2, and ATP.

    NADH and FADH2 carry electrons to the electron transport system.

    Electron Transport System

    In the electron transport system, NADH and FADH2 are oxidized and the energy is used to produce ATP.

    Total ATP yield per glucose

    Conversions

    NADH produced in the cytoplasm produces two to three ATP by the electron transport system.

    NADH produced in the mitochondria produces approximately three ATP.

    FADH2 adds its electrons to the electron transport system at a lower level than NADH, so it produces approximately two ATP.

    Glycolysis

    2 ATP

    2 NADH (= 4 ATP; these are converted to ATP in the mitochondria during cellular respiration)

    Formation of Acetyl CoA

    2 NADH (= 6ATP)

    Krebs Cycle

    6 NADH (= 18 ATP)

    2 FADH2 (= 4 ATP)

    2 ATP
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    (Original post by sammy_93)
    Summary for cellular respiration

    Glycolysis

    During glycolysis, glucose (C6) is converted to two pyruvates (C3).

    C-C-C-C-C-C ? C-C-C + C-C-C

    Formation of Acetyl CoA

    One acetyl CoA is formed for each pyruvate produced by glycolysis (see the step above).

    C-C-C ? C-C + CO2

    pyruvate ? acetyl CoA + CO2

    Krebs Cycle

    C-C ? 2 CO2

    The Krebs Cycle produces NADH, FADH2, and ATP.

    NADH and FADH2 carry electrons to the electron transport system.

    Electron Transport System

    In the electron transport system, NADH and FADH2 are oxidized and the energy is used to produce ATP.

    Total ATP yield per glucose

    Conversions

    NADH produced in the cytoplasm produces two to three ATP by the electron transport system.

    NADH produced in the mitochondria produces approximately three ATP.

    FADH2 adds its electrons to the electron transport system at a lower level than NADH, so it produces approximately two ATP.

    Glycolysis

    2 ATP

    2 NADH (= 4 ATP; these are converted to ATP in the mitochondria during cellular respiration)

    Formation of Acetyl CoA

    2 NADH (= 6ATP)

    Krebs Cycle

    6 NADH (= 18 ATP)

    2 FADH2 (= 4 ATP)

    2 ATP
    Thank u
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    Ur very welcome
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    How are you guys revising for this thing? I always find biology exams hard, not only because of the content but because of the way these edexcel exams are worded and laid out
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    (Original post by Dentistry:))
    How are you guys revising for this thing? I always find biology exams hard, not only because of the content but because of the way these edexcel exams are worded and laid out
    U R tooootally ryt
    but the gd thing is that its my LAAAAST examination session
    thats GREAT is it?!!!:cool:
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    Has anyone got advice on how to tackle exam questions? I know the stuff but the points that I write down are not on the mark scheme, as they are waaayyy more specific than AS.
    Please help!
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    (Original post by ghogho)
    com on pple no one is taking unit 5 this session???!!!!:dontknow:
    i truely need help in the article any
    any suggested questions ?????
    plzzzzz HELP!!!
    :zomg:


    Q-define obesity?
    Q-how many kinds of adipose tissue have been identified and where are they located?
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    Can anyone please explain me the differences between accomodation, adaptation and habituation in details?
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    (Original post by ghogho)
    com on pple no one is taking unit 5 this session???!!!!:dontknow:
    i truely need help in the article any
    any suggested questions ?????
    plzzzzz HELP!!!
    :zomg:
    i'm not sure if this will help..but i just found this website now and i'm planning to use their service..so here it is: http://edexcelbiosolutions.com/index...?view=document

    it includes a set of predicted questions with detailed answers...i thought that the sample was pretty good..
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    (Original post by desertautumn)
    i'm not sure if this will help..but i just found this website now and i'm planning to use their service..so here it is: http://edexcelbiosolutions.com/index...?view=document

    it includes a set of predicted questions with detailed answers...i thought that the sample was pretty good..
    Hey so ure purchasing? could u PM us what you get or upload it??
    We all cant purchase it ://
    anyway asking only if u wish to do that! no force
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    hey ppl that is a sample of the expected questions that might come

    wish that will help and truely hope that we can all discuss together the topic of the article

    gd luck for everyone
    Attached Files
  1. File Type: doc expected qu.doc (224.5 KB, 636 views)
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    (Original post by sammy_93)
    I found this for those who are having trouble learning the sliding filament theory like how I did:
    Here is a quick reminder of all the structures involved:

    Myofibril: A cylindrical organelle running the length of the muscle fibre, containing Actin and Myosin filaments.
    Sarcomere: The functional unit of the Myofibril, divided into I, A and H bands.
    Actin: A thin, contractile protein filament, containing 'active' or 'binding' sites.
    Myosin: A thick, contractile protein filament, with protusions known as Myosin Heads.
    Tropomyosin: An actin-binding protein which regulates muscle contraction.
    Troponin: A complex of three proteins, attached to Tropomyosin.
    Here is what happens in detail. The process of a muscle contracting can be divided into 5 sections:

    A nervous impulse arrives at the neuromuscular junction, which causes a release of a chemical called Acetylcholine. The presence of Acetylcholine causes the depolarisation of the motor end plate which travels throughout the muscle by the transverse tubules, causing Calcium (Ca+) to be released from the sarcoplasmic reticulum.

    In the presence of high concentrations of Ca+, the Ca+ binds to Troponin, changing its shape and so moving Tropomyosin from the active site of the Actin. The Myosin filaments can now attach to the Actin, forming a cross-bridge.

    The breakdown of ATP releases energy which enables the Myosin to pull the Actin filaments inwards and so shortening the muscle. This occurs along the entire length of every myofibril in the muscle cell.

    The Myosin detaches from the Actin and the cross-bridge is broken when an ATP molecule binds to the Myosin head. When the ATP is then broken down the Myosin head can again attach to an Actin binding site further along the Actin filament and repeat the 'power stroke'. This repeated pulling of the Actin over the myosin is often known as the ratchet mechanism.

    This process of muscular contraction can last for as long as there is adequate ATP and Ca+ stores. Once the impulse stops the Ca+ is pumped back to the Sarcoplasmic Reticulum and the Actin returns to its resting position causing the muscle to lengthen and relax.
    It is important to realise that a single power stroke results in only a shortening of approximately 1% of the entire muscle. Therefore to achieve an overall shortening of up to 35% the whole process must be repeated many times. It is thought that whilst half of the cross-bridges are active in pulling the Actin over the Myosin, the other half are looking for their next binding site.
    hey, i thought ATP only attaches to the myosin head, toward the end of the process. Just before the myosin head detaches from the binding site.
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    (Original post by i_luv_basky)
    Can anyone please explain me the differences between accomodation, adaptation and habituation in details?
    Habituation is due to less responsive Calcium ion channel. So, there is less influx of calcium ion into the presynaptic neurone. So, there is less neurotransmitter released into the synapse. The post synaptic neurone is not depolarised enough to generate action potential.

    Accomodation happens when the rate of synthesis of neurotransmitter cannot keep up with the rate of release of neurotransmitter into the synapse.

    Adaptation occurs when there is decline in generator potential leading to no action potential..
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    can someone help me with this question..its a unit 5 one

    Explain how chemical levels in the brain may change, resulting in illnesses such as parkinsons and depression???
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    Hey, sorry if what I ask has already been answered, but does anybody have a file of revision notes for unit 5 that they could link please? Would really help!


    This was posted from The Student Room's iPhone/iPad App
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    [QUOTE=19941994;37923031]Hey, sorry if what I ask has already been answered, but does anybody have a file of revision notes for unit 5 that they could link please? Would really help!


    This was posted from The Student Room's iPhone/iPad App[/QUOTEgo over the cgp revision guide. Its amazing:-)
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    [QUOTE=aqua05;37927642]
    (Original post by 19941994)
    Hey, sorry if what I ask has already been answered, but does anybody have a file of revision notes for unit 5 that they could link please? Would really help!


    This was posted from The Student Room's iPhone/iPad App[/QUOTEgo over the cgp revision guide. Its amazing:-)
    ok thanks would there be a copy online of that guide?
 
 
 
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