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    In the spec it says 'describe, using one example, the advantages of social behaviour in primates'

    in the book it has the advantages, such as how they only give birth to one (or few) at one time so the care is concentrated. But what do they mean about examples?
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    (Original post by aiden1234)
    In the spec it says 'describe, using one example, the advantages of social behaviour in primates'

    in the book it has the advantages, such as how they only give birth to one (or few) at one time so the care is concentrated. But what do they mean about examples?
    The example just means give an example of the situation of which species of primates, i think...
    the easiest is that gorrilas live in a group called a Troop, in which there is one silverback male which protects the rest which are females. this provides a few advantages such as, protection of the young, better spotting of predators, extended care of the young (as you said) and sharing of found resources.

    Other primates live in groups too such as chimps so you could say the same for them.
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    (Original post by Falcon91)
    The example just means give an example of the situation of which species of primates, i think...
    the easiest is that gorrilas live in a group called a Troop, in which there is one silverback male which protects the rest which are females. this provides a few advantages such as, protection of the young, better spotting of predators, extended care of the young (as you said) and sharing of found resources.

    Other primates live in groups too such as chimps so you could say the same for them.
    ahh good so you think that we can use our own example in the exam? or do you think that they'll give us an example that we'll have to suggest the advantages of? either way that seems pretty simple though...:rolleyes:
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    also does anyone reckon we need to know about CRF or ACTH when we are talking about how the body is stimulated into the fight or flight response....i swear this book goes into ALOT of detail...the heinemann OCR one
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    (Original post by aiden1234)
    also does anyone reckon we need to know about CRF or ACTH when we are talking about how the body is stimulated into the fight or flight response....i swear this book goes into ALOT of detail...the heinemann OCR one
    I think you just need to understand there is a release of hormones caused by the hyopthalamus. The specification makes no reference to CRF/ACTH directly but it might be helpful to learn it to help your understanding (the little diagram on the top right of the page on the Flight or Fight response).
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    (Original post by Falcon91)
    I think you just need to understand there is a release of hormones caused by the hyopthalamus. The specification makes no reference to CRF/ACTH directly but it might be helpful to learn it to help your understanding (the little diagram on the top right of the page on the Flight or Fight response).
    ace thanks falcon 91!!
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    (Original post by MG.GULED)
    Ok this is the simplest way :

    1) cut of the tips of two shoots , to one of the shoots apply sythetic auxin 1AA and the shoot will continue to grow with the lateral buds inhibited and apical dominance is maintained. However to the other shoot where no auxin had been aplied we see that side branches grow and later buds can grow since supply of auxin has been cut off.

    2) When a plant is grown upside down apical dominance is lifted and doesnt occur , this is because auxin cannot be transported up against gravity and therefore can not reach the internodes beside the lateral buds , hence these buds can grow sideways.

    And also its auxi which acts on the lateral bud , inhibits the later buds from growing , so experiments follow the method by preventing auxin being transported down the stem of a plant.
    Hope that helps.
    makes sense, thanks bro.
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    What are peoples predictions on topics to come up on this exam?
    I think it'll be a lot of genetics, one question on brain and nervous system/ muscles,
    and a lot of biodiversity stuff which will tie into being part of the synoptic part of the paper..
    .its all just way too much...too broad a subject and sucks cos it'll be a synoptic paper
    So even hating this module will make it harder......arghhhhhh
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    (Original post by Falcon91)
    Im completely stressed. I believe im getting nowhere and i keep forgetting small things, its really irking me and i feel like im wasting my time.
    Maybe i should take a break from this...

    try to not stress yourself out, lol stress is bad :P
    maybe switch to another subject?, when i start to get frustrated i usually switch to chemistry or maths then come back, it works for me
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    Jeez I havent slept for over r23 hours straight and about to start Biology... :/
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    What are peoples predictions on topics to come up on this exam?
    I think it'll be a lot of genetics, one question on brain and nervous system/ muscles,
    and a lot of biodiversity stuff which will tie into being part of the synoptic part of the paper..
    .its all just way too much...too broad a subject and sucks cos it'll be a synoptic paper
    So even hating this module will make it harder......arghhhhhh
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    (Original post by ibysaiyan)
    Jeez I havent slept for over r23 hours straight and about to start Biology... :/
    :O:O
    lol
    how can you stay up???
    tonight im pulling an all nighter though for biology to finish the plant responses stuff, been doing too much maths lately -.-
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    (Original post by chuck111)
    :O:O
    lol
    how can you stay up???
    tonight im pulling an all nighter though for biology to finish the plant responses stuff, been doing too much maths lately -.-
    Good good make sure to hang around TSR (here)
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    Come on peeps remember quitters never win and winners never quit

    Was feeling like poop yesterday night but popped some caffeine tabs, watched some michael jordan, tiger woods nike commercials and a bit of rocky and al pacino inch by inch speech and i managed to work til 3 in morning.

    http://www.youtube.com/watch?v=UTuk5Uloyjg TIGER

    http://www.youtube.com/watch?v=f4eUUVbpXtk JORDAN

    http://www.youtube.com/watch?v=BirIE...eature=related JORDAN

    http://www.youtube.com/watch?v=TEpO8AUqHm0 ALI

    http://www.youtube.com/watch?v=GEkz1XK75XE MELEE
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    (Original post by afhussain)
    Come on peeps remember quitters never win and winners never quit

    Was feeling like poop yesterday night but popped some caffeine tabs, watched some michael jordan, tiger woods nike commercials and a bit of rocky and al pacino inch by inch speech and i managed to work til 3 in morning.

    http://www.youtube.com/watch?v=UTuk5Uloyjg TIGER

    http://www.youtube.com/watch?v=f4eUUVbpXtk JORDAN

    http://www.youtube.com/watch?v=BirIE...eature=related JORDAN

    http://www.youtube.com/watch?v=TEpO8AUqHm0 ALI

    http://www.youtube.com/watch?v=GEkz1XK75XE MELEE
    LMAO what an inspirational sportsmen : WOODS! thanks for the much needed motivation. :ninja2:
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    I've been over everything at least three times, it doesn't want to stick.
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    Anyone care to summarise the whole of muscle contraction for me, from the neuromuscular juntion right way through the the contraction and the role of ATP.. it just doesn't seem to want to agree with me.
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    (Original post by ibysaiyan)
    Good good make sure to hang around TSR (here)
    will do
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    (Original post by skatealexia)
    Anyone care to summarise the whole of muscle contraction for me, from the neuromuscular juntion right way through the the contraction and the role of ATP.. it just doesn't seem to want to agree with me.
    Ill do it before i go to bed for the night. Btw thanks chuck for the advice (and the cards, using them for synoptic stuff from next week, theyre great).

    Okay Neuromuscular junctions:

    -These are motor end plates to muscles (i.e. a synapse between a muscle and an effector is a simple way to think of it)

    Step 1 - An action potential arrives at the presynoptic knob

    Step 2 - this causes the voltage-gated calcium ion channels on the presynaptic membrane to open and Ca2+ ions move into the presynpatic knob

    Step 3 - this causes active movement of vesicles containing neurotransmitter, Acetylcholine, to fuse to the presynaptic membrane and release the neurotransmitter into the neuromuscular cleft/junction by exocytosis

    Step 4 - The acetylcholine diffuses across the cleft/gap to bind to nicotonic cholinerginc receptors on the cell surface membrane of the muscle fibre/cell called the Sarcolemma on the postsynpatic membrane

    Step 5 - This causes an opening of ligand gated (sodium) channels which causes depolarisation of the muscle fibre. The depolarisation spreads through muscle fibres via foldings of the sarcolemma which stick into the sarcoplasm of the muscle fibres called Transverse (T) Tubules

    Step 6 - This causes a release of Ca2+ ions from the sarcoplasmic reticulum which bind to myofilaments to cause contraction

    Contraction theory

    Myosin has globular heads which has binding sites for ATP and Actin filaments.
    Actin has binding sites for Myosin, called the Actin-Myosin Binding Site, it also has two proteins attached to it. In the actin-myosin binding site there is tropomyosin which is bound to another protein called troponin. Tropomyosin is said to be blocking the A-M binding site.

    Step 1 - An action potential at a neuromuscular junction causes depolarisation of the muscle fibre, which causes release of Ca2+ ions from Sarcoplasmic reticulum. The Ca2+ ions diffuse through the cytoplasm to bind to TROPONIN

    Step 2 - The binding to troponin, causes it to change shape. This pulls TROPOMYOSIN out of the Actin-Myosin binding site

    Step 3 - The globular Myosin heads can then bind to the exposed the Actin-Myosin binding site on the Actin filament. This forms an Actin-Myosin Cross-Bridge

    Step 4 - The Ca2+ ions also activate ATPase enzymes on the myosin head. After an actin-myosin cross bridge has formed, the myosin head hydrolyses an ATP to pull the actin filament along. This is called the Power Stroke.

    Step 5- Another ATP is hydrolysed into ADP + Pi, this then breaks the actin-myosin cross bridge and resets the myosin head so it can now bind to another actin-myosin binding site furthur along the actin filament.

    Step 6 - Many actin-myosin cross bridges are formed and broken simultaneously, which causes contraction of the sarcomere. The simultaneous contraction of many sarcomeres causes contraction of the muscle fibres and thus contraction of muscles.

    the sarcomere will go back to relaxation length

    Step 7 - Acetylcholinesterase present in clefts on the postsynaptic membrane (back @ the Neuromuscular Junction), break down the Acetylcholine in the postsynaptic receptors so that the muscle only contracts when action potentials/impulses arrive continuously

    Step 8 - The Ca2+ stop binding to troponin which returns to its original shape, this means tropomyosin can now fit back and block the Actin-Myosin Binding site. Thus stopping any actin-myosin cross bridges forming and so the sarcomere cannot contract.

    Lastly, the Ca2+ ions are actively transported using ATP back into the Sarcoplasmic Reticulum and so can be used for muscle contraction again.

    Maintenance of the ATP supply

    3 ways

    1) Aerobic Resp - This produces many ATP (around 30) via Oxidative phosphorylation in the mitochondria of the muscle fibres (on the cristae/stalked particles). This is dependant upon the bloody supply and amount of respiratory substrate (glucose). So its used for low-intensity exercise such as Jogging or Walking

    2) Anaerobic Resp - this produces few ATP but very rapidly. However this causes lactate fermentation and this is toxic and builds up in the muscle causing it to fatigue. This is transported away in the blood stimulating increased blood flow to this area (its held without affecting pH due to buffers in the blood HCO3- ions). This is used for high intensity exercise such as sprinting. This takes place in the sarcoplasm of a muscle fibre.

    3) ATP-Phosphocreatine System - you have a small amount of a substance called Phosphocreatine stored in cells such as muscle fibres. In the sarcoplasm of muscle fibres, as ADP needs to be phosphorylated to form ATP, phosphocreatine can transfer its phosphate to ADP to form ATP using an enzyme called Creatine Phosphotransferase. This is very rapid but due to only a small amount sotred it can only provide enough energy to allow muscle contraction for 2-4 seconds. So is used for short bursts of vigorous exercise, such as a tennis serve.

    There you go, i hope that helps. 766 words O.o
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    ^^ good post, think i summarised it in my notes in about 60 words though

    anyone know why stimulation from the sympathetic nervous system and endocrine system (adrenaline) causes relaxation of anal and urethra sphincter muscles??
 
 
 
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