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    pls... why would the heart rate drop when a person is diving into a deep water region and it will increase when get back to the surface?
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    Mornig guys.. do we havr 2 know all practicals or only ones for unit 5
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    (Original post by sadbuttrue92)
    pls... why would the heart rate drop when a person is diving into a deep water region and it will increase when get back to the surface?
    as u godown pressure increase and so less o2 availble.. thats the main cause i guess
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    undr the water he respired anaerobically,he builds up lots of lactate so on the surface more oxygen is requried to convert lactate back into pyruvate!so heart rate rises to supply the tissues with oxygen faster?
    (Original post by sadbuttrue92)
    pls... why would the heart rate drop when a person is diving into a deep water region and it will increase when get back to the surface?
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    what is thedifference between dimlight?and brightlight
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    (Original post by USERUSER)
    hi i dont understand why when light hits a rod cell, no neurotransmitter being released would lead to depolarization of the bipolar cell ? I thought it was the neurotransmitter which caused the opening of the Na+ channels on the post synaptic membrane ?

    Also what does the bipolar cell depolarizing actually do because can't rod cells provide vision in dim light conditions (even when the bipolar cell isnt depolarized?)
    The neurotransmitters in rod cells are inhibitory neurotransmitters so stop an action potential from forming.
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    (Original post by Maria1234)
    what is thedifference between dimlight?and brightlight
    Low light intensity and high light intensity.
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    (Original post by Maria1234)
    what is thedifference between dimlight?and brightlight
    dim light is low light intensity (like almost in dark) bright light is high light intensity which is at morning for example
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    can anybody tell me how this antibody therapy for mysotatin works?
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    thnsx
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    Clearly differentiate between adaptation and habituation?
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    (Original post by Parthenon93)
    Clearly differentiate between adaptation and habituation?
    This has been answered so many times:

    1) Adaptation ... or sensory adaptation involves a decreased response due to the neurotransmitters not being synthesised fast enough to keep up with a repeated stimulus

    2) Habituation is a type of LEARNING where there is a gradual loss of response to a repeated harmless stimuli that fails to bring about any sort of reiinforcement... it is due to lack of responsiveness of the calcium ion channels in the synaptic knob....
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    why does blocking myostatin not solve the underlying problems with muscle dystrophy?
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    (Original post by chemdweeb1234)
    This has been answered so many times:

    1) Adaptation ... or sensory adaptation involves a decreased response due to the neurotransmitters not being synthesised fast enough to keep up with a repeated stimulus
    That is accommodation. :e
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    (Original post by Parthenon93)
    That is accommodation. :e
    My bad, apologies.... the adaptation in sensory organs / receptors is due to decreased permeability of the membrane to Na+ ions, therefore less likely that the generator potential will reach threshold potential
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    (Original post by Maria1234)
    [COLOR="DarkRed"]why does blocking myostatin not solve the underlying problems with muscle dystrophy?[/COLOR]
    The article says so clearly... blocking myostatin stops the inhibition of the satellite stem cells... and thus more of these stem cells can proliferate. However, it may not SOLVE the underlying problem because:
    1) Muscular dystrophy is a genetic condition involving death of muscle cells... using myostatin has basically just treated the symptoms by increasing the muscle growth.... i.e. muscle synthesis outweighing muscle death
    2) and once all the satellite stem cells store has been replenished, the muscle breakdown/ death will once again outweigh the growth.... and there is overall decrease in muscle cells.....

    its only a temporary repreive
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    Is there a 2010 January paper? If so, does anyone have it? Thank you!
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    (Original post by Maria1234)
    why does blocking myostatin not solve the underlying problems with muscle dystrophy?
    it does not increase the blood supply to the muscles and doesn't increase the number of mitochondria :confused: i think... also if muscle stem cells are allowed to differentiate continuously then the supply might run out.. :/


    edit: ...just saw what chemdweeb1234 posted and i agree
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    (Original post by Hibz93)
    Is there a 2010 January paper? If so, does anyone have it? Thank you!
    The first paper was in June 2010.
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    ohhanks I hope you will get an A star!!but how does then the antibody therapy help to prevent loss of muscles?
    (Original post by chemdweeb1234)
    The article says so clearly... blocking myostatin stops the inhibition of the satellite stem cells... and thus more of these stem cells can proliferate. However, it may not SOLVE the underlying problem because:
    1) Muscular dystrophy is a genetic condition involving death of muscle cells... using myostatin has basically just treated the symptoms by increasing the muscle growth.... i.e. muscle synthesis outweighing muscle death
    2) and once all the satellite stem cells store has been replenished, the muscle breakdown/ death will once again outweigh the growth.... and there is overall decrease in muscle cells.....

    its only a temporary repreive
 
 
 
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