Edexcel A2 Biology Unit 5 (6BIO5) - 22/06/2011- OFFICIAL THREAD !
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Original post by sheep_go_baa
Anyone have any notes on the respiration and spirometer practicals? I don't even remember doing them 
A2_BIOLOGY_CORE_PRACTICAL_SUMMARY[1].pdf
hope this helps
Original post by amnah_70
You sir/madame are AWESOME
Spoiler
Original post by appleitunes
amnah_70 i cant open your link, anyway you could send it to me?
ive attached it agian hopefuly should work ?
54265374-Questions-and-Answers-for-Scientific-Article-June-2011.pdf
Outline how gene expression may play a part in the day-by-day regulation of conditions in
the body. (5)
Any ideas????
the body. (5)
Any ideas????
Original post by sheep_go_baa
You sir/madame are AWESOME
Spoiler
hahahahahaahaha soo many thanks loll
no problem hope ur exam goes reallllllllllllly well for u
I was taking a short break from revising on iSketch and it's like my mum could sense it. She walked past my room and gave me a dirty look lol!
Original post by voices1
HOw gene therapy works?
Viruses are inactivated and inserted into the body. The viruses contain the DNA for the gene to be inserted. Firstly they then attach onto the particles of the receptor cells and the DNA combines with the host cell DNA to form the recombinant DNA which is transcribed and translated producing the appropriate protein.
is this correct?
how is this different from recombinant bacteria?
Viruses are inactivated and inserted into the body. The viruses contain the DNA for the gene to be inserted. Firstly they then attach onto the particles of the receptor cells and the DNA combines with the host cell DNA to form the recombinant DNA which is transcribed and translated producing the appropriate protein.
is this correct?
how is this different from recombinant bacteria?
With gene therapy, the protein is being made by the actual cell. With recombinant bacteria, firstly the plasmid is used instead, secondly the bacteria makes the substance not the cell itself, also the person's DNA is not altered as a result hence cannot go on to manufacture more of the substance themselves, and finally a vector isn't used for recombinant bacteria, heat shock is used instead to reinsert the plasmid
Original post by sheep_go_baa
I was taking a short break from revising on iSketch and it's like my mum could sense it. She walked past my room and gave me a dirty look lol!
iSketch is brilliant, I love that site! Same with my mum, every time she chooses to come upstairs I'm either playing angry birds or reading a book! And every time she gets the answer "I'm on a break!!" so I can see where she is coming from when she nags me for not revising!
Original post by e11
hey guys does anyone know how to answer this:
Explain how antibody therapy could help treat muscular dystrophy?
Explain how antibody therapy could help treat muscular dystrophy?
Do you mean using the virus as a vector to insert genes that block the ubiquitin pathway and that so muscle cells aren't destroyed?! But then you can't do that over and over again because the body builds up antibodies to the virus you use as a vector...
Original post by Kayak
iSketch is brilliant, I love that site! Same with my mum, every time she chooses to come upstairs I'm either playing angry birds or reading a book! And every time she gets the answer "I'm on a break!!" so I can see where she is coming from when she nags me for not revising!
And that's why you hide your phone/book behind the bio textbook. Alt + tab has been so unbelievably useful during exam periods
Not sure how useful this is now, but I made these paragraph summaries ages ago, so thought might as well post it!
Page 2 – paragraph 2
?Alter genes to help athletes excel at sport
?officials aware of gene doping but practice is undetectable
Page 2 – paragraph 4
?If athletes do turn to gene therapy, genetically enhanced athletes risk with heart disease/strokes/early death
Page 2 – paragraph 5
?Mantyranta born with genetic mutation that loaded his blood with more red blood cell than average man’s. More oxygen delivered from lungs to body tissues, got more oxygen they needed for aerobic exercise
Page 2 – paragraph 6
?Mantyranta got extra red blood cells because of mutation in gene that produces receptor for hormone erythropoietin [epo]
?kidneys make epo when oxygen levels drop
?epo commands body to manufacture new red cells which raises blood’s capacity to carry oxygen
?Once oxygen back to normal level – epo receptor shuts down epo production
?mutation turned off this feedback, so body keeps making more red cells
Page 2- paragraph 7
?Mutation rare
?Anyone can boost their red cells by adding more epo to bloodstream
?Injectable form of epo produced by recombinant bacteria, as a treatment for severe anaemia
Page 3 – paragraph 2
?problem becomes bigger if athletes can insert gene that makes bodies produce extra doses of hormone
?instead of injecting themselves with epo several times a week, athletes could use ‘’gene therapy’’ to acquire ‘’super gene’’
Page 3 – paragraph 3
?Gene therapy techniques: e.g. use viruses to carry epo gene into cells
?remove the genes that make a disease-causing virus harmful and insert epo gene in their place
Page 3 – paragraph 4
?Adenoviruses e.g. like the ones that cause a common cold – good delivery system for gene therapy
?because they are large/carry big genes in their payload
?however, they are easily recognised and destroyed by immune system
?To evade body’s defences, Avigen has patented use of Adeno-associated viruses [AAVs] for delivering epo
?AAVs smaller than adenoviruses, an AAV can’t carry as much cargo but is less vulnerable to attack from immune system
Page 3 – paragraph 5
?Result of using adenovirus: adenovirus to deliver epo gene to mice and monkeys
?After scientists injected virus into animals’ muscles, it infiltrated their cells, inserting epo gene and spurring the cells to pump out protein
?Boosted hematocrits [volume of blood made up of red blood cells]
?AAVs also increased hematocrits
Page 4 – paragraph 1
?Elevating red blood cell count is risky: blood thickens when packed with so many red blood cells, high risk for high blood pressure and stroke
Page 4 – paragraph 2
?Successful gene therapy problems: because no way to turn gene off once it’s been inserted
?Healthy athletes that take epo gene therapy: require frequent bleedings to keep haematocrit low enough to prevent strokes – still have risk of high blood pressure and atherosclerosis
Page 4 – paragraph 3
?Scientists believe hard exercise, the kind that leaves you sore next day, builds muscle by inducing microscopic damage to muscle fibres
?”micro tears” are repaired by beefing up fibres with extra proteins so they will be adapted to exercise next time
?Protein called insulin-growth-factor 1 [IGF-1] which is turned on by mechanical signals e.g. stretch/exercise overload plays a role in repair process
?IGF-1 exists in at least five different forms, whose parts are spliced together in different ways. All forms produced by a single gene.
Pumping genes – page 4 –paragraph 4
?Gene therapy – uses form of IGF-1 called mechano growth factor [MGF] to treat muscle wasting diseases e.g. muscular dystrophy
?MGF made in muscle tissue so doesn’t circulate in blood, its effects are localised to muscle
?Group tested MGF gene therapy in mice, a single injection of MGF gene: two weeks later injected muscles had grown by 20%
page 4 – paragraph 5
?Another form of IGF-1, made in liver and muscle
?when circulates in blood, IGF-1 raises blood sugar levels
?But when in muscle tissue – IGF-1 mainly involved in repairing and building muscles
page 4 – paragraph 6
?Used an adenovirus to deliver IGF-1 gene to leg muscles of mice
?After 3 months, mouse leg muscles injected with IGF-1 gene had grown by 15% without any special exercise
Page 5 – paragraph 1
?When mice injected with IGF-1, they are expressing IGF-1 gene as if they had been exercising hard
?May be that some people naturally make more IGF-1 thus some people can build more muscle easily than others
Page 5 – paragraph 2
?IGF-1 gene therapy is thought to be relatively safe because protein produced by newly added gene seems to stay in muscle that receives an injection
?IGF-1 not found circulating in animals’ bloodstream, so suggests it was being made and used locally in muscle
?this means IGF-1 injected won’t lead to an enlarged heart nor will it alter blood sugar levels
Page 5 – paragraph 3
?Ability to target IGF-1 therapy to specific muscles attracts athletes
?Because the effects are local, you could just inject IGF-1 gene directly into muscle you want to enlarge
page 5 – paragraph 4
?Not tested on humans, may require completely different protocol for larger animals because it’s harder to access the inside of a large muscle
page 5 – paragraph 5
?No guarantee IGF-1 therapy will work over long period time
?Might wear more quickly in athletes because they damage the muscle more often
?when you damage muscle through exercise, there is a risk of losing genes that you’ve put in there
?Unknown issues: no one knows to what extent people turn over their muscle cells, every cell that’s in your heart when you’re born is there when you die, not sure if that’s true of other muscles
page 5 – paragraph 6
?if athlete’s gene therapy stop working: no guarantee second dose will have same effect as first one
?problem with repeated dosing: body will build antibodies against virus that inserts the gene into cells
?so another injection with same virus, body’s immune system may wipe out virus before it can deliver its genes
?thus alternative viruses might instead be used to deliver illicit genes
catching cheaters – page 6 – paragraph 1
?detecting abuse not easy
?problem is protein made by engineered genes look identical to ones the body makes naturally
?scientists detecting gene therapy by: find traces of virus that delivered the gene
?If looking for MGF-1 or IGF-1: biopsy from muscle and look for viral DNA
?But have to know exactly where it was put in
?same method could be used to detect epo therapy i.e. where gene was injected
page 6 – paragraph 2
?not feasible for athletes to line up for muscle biopsies before Olympics
?so less invasive strategy needs to be found
?one method: look for abnormally high levels of gene’s product
?have to get athlete inactive for 12 hours and then test for MGF
?If levels still high, indication: gene has been switched on all the time instead of being induced by natural activity
?not feasible because athletes unlikely to remain inactive for 12 hours or longer
page 6 – paragraph 3
?Approach might be useful for detecting epo gene doping
?people with plenty of red blood cells should have little or no epo circulating in their blood
?testing could not separate illegal gene dopers from athletes who carry natural mutations
page 6 – paragraph
?researchers studying how muscles build up and break down – are close to creating a drug to stop body dismantling when we stop using it
?aim to tackle weakness in sick and elderly and to make long space flights feasible for humans
page 6 – paragraph 7
?muscle-challenging exercises: muscle cells expand to take strain
?rest and muscle proteins start breaking down as soon as you stop moving.
?idle muscle is an unnecessary metabolic expense
page 6 – paragraph 8
?Muscle growth and breakdown exist in a balance – unless diet or exercise regime changes
?injury to bones, muscles on their nerve supply puts part of body out of action/body becomes starved of food, balance shifts and muscle breakdown outweighs synthesis
page 6 – paragraph 9
?for people confined to bed for long periods of time, or for astronauts in microgravity, muscle wasting is a serious problem
?wasting/atrophy is a symptom of disuse/injury/but of many diseases e.g. kidney failure/cancer/AIDS
?once enough muscle lost, exercise becomes difficult which in turn leads to disuse and further atrophy
page 7 – paragraph 1
?Only way to stop patients losing muscle is long course of physiotherapy involving weight-bearing exercise
page 7 – paragraph 2
?use of anabolic steroids – these compounds have huge effects on body besides promoting muscle growth, some of which are undesirable
?only appear to work well in conjunction with exercise
Active atrophy – page 7 – paragraph 2
?passive side effect of disuse/disease, muscle wasting is an active process controlled by complex genetic pathway
?would be possible to turn it off
page 7 – paragraph 4
?process involves ubiquitin-proteasome pathway [UPP]
?disposal machinery used to break down unwanted proteins in the cell
?once system activated , ubiquitin ‘’destroy me’’ labels added to muscle proteins
?tagged proteins fed into proteasome [a multi-protein complex that breaks down proteins into their component amino acids for reuse]
?breaks down muscle filaments within cells, but does not change number of muscle cells
?instead they become thinner and weaker
?studies showed that at least 90 genes involved in atrophy called atrogenes
page 7 – paragraph 5
?still unknown which genes trigger atrophy, but become clear that two of them are: Atrogin1 and muRF1 – are the only two atrogenes active during muscle atrophy
?they code for ubiquitin ligases, enzymes that attach the ‘’destroy me’’ labels to proteins
?the genes are barely active in normal muscle but expression level shoots up in sick animals
page 7 – paragraph 7
? more atrogenes found every year
?a switch for muscle atrophy had been found, an existing drug could turn the switch off
Gym in a bottle – page 8 – paragraph 1
?Has been found that in mice when muscle atrophy sets in, there is increased activity of gene erg1
?erg1 codes for potassium channel protein found in both skeletal and cardiac muscle tissue
?in heart muscle, channel consists of two variants of protein, erg1a and erg1b which helps heart keep its rhythm by letting muscle repolarise after each beat
?a mutation in erg1 gene causes ‘’long QT syndrome’’ – in which heart muscle cannot repolarise fast enough can lead to sudden death
page 8 – paragraph 2
?erg1a variant stimulates atrophy in skeletal muscle
?in muscles, that were wasting due to disuse or cancer, found high levels of expression of erg1a
?when they increased the number of erg1a potassium channels on surface of muscle cells in mice by adding an extra gene coding for this protein, atrophy set in
?adding a gene for erg1b version of the protein did not trigger atrophy
page 8 – paragraph 3
?an existing drug, an antihistamine called astemizole blocks erg1a channels
?when given to mice, it prevented atrophy in muscles not being used
page 8 –paragraph 4
?team thinks erg1a protein stimulates ubiquitin-proteasome-pathway
?problem: astemizole not only blocks erg1 channels in skeletal muscle, it also blocks them in heart, potentially causing long QT syndrome
?because of this risk, astemizole was withdrawn
?if approach is to work, need to find a way to target erg1a in skeletal muscle without blocking erg1 channels in heart which consist of both erg1a and erg1b sub-units
page 8 – paragraph 5
?team is also investigating possibility of blocking erg1a expression using gene-silencing technique – RNA interference
page 8 – paragraph 6
?focusing on proteins called transcription factors that can turn other genes on or off
?Foxo has been identified that controls activity of many atrogenes
?Disabling Foxo blocks atophy
page 8 – paragraph 7
?E.g. insulin and related hormone insulin-like growth factor [IGF-1] is involved in muscle synthesis but also prevents muscle breakdown by suppressing foxo and turning off atrogin1 gene
?Can’t see Foxo in normal muscle because insulin and IGF-1 supress it
?but don’t know how inactivity or disease activates Foxo transcription factor
page 8 – paragraph 8
?Foxo could be involved in erg1a-mediated atrophy
?erg1a protein is known to bind to transcription factors like Foxo, so increased erg1a activity might trigger atrophy through interaction with Foxo
?companies looking for drugs that block the atrogin1 protein
?team is looking into whether proteasome inhibitors e.g. Velcade used to treat cancer might slow muscle breakdown
page 9 – paragraph 1
?company began trials in people with muscular dystrophy of an antibody therapy designed to stimulate muscle growth rather than prevent atrophy
?produce more muscle tissue is different to attempting to turn off wasting, but end result could be same
page 9 – paragraph 2
?Patients confined to bed for more than a few days could be given drug to prevent muscle loss
?could take patients of respirators would become easier as doctors could prevent muscle wasting of diaphragm
?wouldn’t need painful physiotheraphy sessions to rebuild muscle strength
?anti-wasting drug could keep older people on their feet
page 9 – paragraph 3
?preventing atrophy: interest to NASA because astronauts lose their muscle mass
page 9 – paragraph 4
?valid medical and space applications for anti-wasting drugs, as a safer alternative to steroids, they will be tempting to athletes
page 9 – paragraph 5
?muscle size is not everything
?endurance training: better blood supply to muscles/more energy-supplying mitochondria in muscle cells
?drugs that maintain muscle size will keep people strong, but not fitter
page 9 – paragraph 6
?maintaining more muscle will help use up extra calories
page 9 – paragraph 7
?two tried and tested ways to lower Foxo levels and prevent muscle atrophy
?one is to increase your IGF-1 and to stimulate insulin production
Pump up the volume – page 10 – paragraph 1
?the boy had mutation in both copies of gene coding for muscle growth inhibitor myostatin
?mother had mutation in one copy of gene giving her unusual strength
?the boy didn’t have any myostatin at all
page 10 – paragraph 2
?blocking myostain in mice makes them twice as muscular as usual
?clinical trial – to see if blocking myostatin with an antibody therapy to prevent further muscle loss in people with muscular dystrophy
page 10 – paragraph 3
?muscular dystrophy causes different kind of muscle wasting from that seen in disuse or disease, muscle cells do not shrink, they die
?myostatin is thought to keep muscle stem cells called satellite cells in check and in its absence the satellite cells give rise to new muscle cells
?blocking myostatin will not solve causes of muscular dystrophy but by boosting muscle growth might compensate for lost tissue
?however, possible that treatment might exhaust supply of satellite cells thus only temporary
page 10 – paragraph 4
?antibody trial has started
?hoped that myostatin blockers could help treat other kinds of muscle wasting and the elderly
Page 2 – paragraph 2
?Alter genes to help athletes excel at sport
?officials aware of gene doping but practice is undetectable
Page 2 – paragraph 4
?If athletes do turn to gene therapy, genetically enhanced athletes risk with heart disease/strokes/early death
Page 2 – paragraph 5
?Mantyranta born with genetic mutation that loaded his blood with more red blood cell than average man’s. More oxygen delivered from lungs to body tissues, got more oxygen they needed for aerobic exercise
Page 2 – paragraph 6
?Mantyranta got extra red blood cells because of mutation in gene that produces receptor for hormone erythropoietin [epo]
?kidneys make epo when oxygen levels drop
?epo commands body to manufacture new red cells which raises blood’s capacity to carry oxygen
?Once oxygen back to normal level – epo receptor shuts down epo production
?mutation turned off this feedback, so body keeps making more red cells
Page 2- paragraph 7
?Mutation rare
?Anyone can boost their red cells by adding more epo to bloodstream
?Injectable form of epo produced by recombinant bacteria, as a treatment for severe anaemia
Page 3 – paragraph 2
?problem becomes bigger if athletes can insert gene that makes bodies produce extra doses of hormone
?instead of injecting themselves with epo several times a week, athletes could use ‘’gene therapy’’ to acquire ‘’super gene’’
Page 3 – paragraph 3
?Gene therapy techniques: e.g. use viruses to carry epo gene into cells
?remove the genes that make a disease-causing virus harmful and insert epo gene in their place
Page 3 – paragraph 4
?Adenoviruses e.g. like the ones that cause a common cold – good delivery system for gene therapy
?because they are large/carry big genes in their payload
?however, they are easily recognised and destroyed by immune system
?To evade body’s defences, Avigen has patented use of Adeno-associated viruses [AAVs] for delivering epo
?AAVs smaller than adenoviruses, an AAV can’t carry as much cargo but is less vulnerable to attack from immune system
Page 3 – paragraph 5
?Result of using adenovirus: adenovirus to deliver epo gene to mice and monkeys
?After scientists injected virus into animals’ muscles, it infiltrated their cells, inserting epo gene and spurring the cells to pump out protein
?Boosted hematocrits [volume of blood made up of red blood cells]
?AAVs also increased hematocrits
Page 4 – paragraph 1
?Elevating red blood cell count is risky: blood thickens when packed with so many red blood cells, high risk for high blood pressure and stroke
Page 4 – paragraph 2
?Successful gene therapy problems: because no way to turn gene off once it’s been inserted
?Healthy athletes that take epo gene therapy: require frequent bleedings to keep haematocrit low enough to prevent strokes – still have risk of high blood pressure and atherosclerosis
Page 4 – paragraph 3
?Scientists believe hard exercise, the kind that leaves you sore next day, builds muscle by inducing microscopic damage to muscle fibres
?”micro tears” are repaired by beefing up fibres with extra proteins so they will be adapted to exercise next time
?Protein called insulin-growth-factor 1 [IGF-1] which is turned on by mechanical signals e.g. stretch/exercise overload plays a role in repair process
?IGF-1 exists in at least five different forms, whose parts are spliced together in different ways. All forms produced by a single gene.
Pumping genes – page 4 –paragraph 4
?Gene therapy – uses form of IGF-1 called mechano growth factor [MGF] to treat muscle wasting diseases e.g. muscular dystrophy
?MGF made in muscle tissue so doesn’t circulate in blood, its effects are localised to muscle
?Group tested MGF gene therapy in mice, a single injection of MGF gene: two weeks later injected muscles had grown by 20%
page 4 – paragraph 5
?Another form of IGF-1, made in liver and muscle
?when circulates in blood, IGF-1 raises blood sugar levels
?But when in muscle tissue – IGF-1 mainly involved in repairing and building muscles
page 4 – paragraph 6
?Used an adenovirus to deliver IGF-1 gene to leg muscles of mice
?After 3 months, mouse leg muscles injected with IGF-1 gene had grown by 15% without any special exercise
Page 5 – paragraph 1
?When mice injected with IGF-1, they are expressing IGF-1 gene as if they had been exercising hard
?May be that some people naturally make more IGF-1 thus some people can build more muscle easily than others
Page 5 – paragraph 2
?IGF-1 gene therapy is thought to be relatively safe because protein produced by newly added gene seems to stay in muscle that receives an injection
?IGF-1 not found circulating in animals’ bloodstream, so suggests it was being made and used locally in muscle
?this means IGF-1 injected won’t lead to an enlarged heart nor will it alter blood sugar levels
Page 5 – paragraph 3
?Ability to target IGF-1 therapy to specific muscles attracts athletes
?Because the effects are local, you could just inject IGF-1 gene directly into muscle you want to enlarge
page 5 – paragraph 4
?Not tested on humans, may require completely different protocol for larger animals because it’s harder to access the inside of a large muscle
page 5 – paragraph 5
?No guarantee IGF-1 therapy will work over long period time
?Might wear more quickly in athletes because they damage the muscle more often
?when you damage muscle through exercise, there is a risk of losing genes that you’ve put in there
?Unknown issues: no one knows to what extent people turn over their muscle cells, every cell that’s in your heart when you’re born is there when you die, not sure if that’s true of other muscles
page 5 – paragraph 6
?if athlete’s gene therapy stop working: no guarantee second dose will have same effect as first one
?problem with repeated dosing: body will build antibodies against virus that inserts the gene into cells
?so another injection with same virus, body’s immune system may wipe out virus before it can deliver its genes
?thus alternative viruses might instead be used to deliver illicit genes
catching cheaters – page 6 – paragraph 1
?detecting abuse not easy
?problem is protein made by engineered genes look identical to ones the body makes naturally
?scientists detecting gene therapy by: find traces of virus that delivered the gene
?If looking for MGF-1 or IGF-1: biopsy from muscle and look for viral DNA
?But have to know exactly where it was put in
?same method could be used to detect epo therapy i.e. where gene was injected
page 6 – paragraph 2
?not feasible for athletes to line up for muscle biopsies before Olympics
?so less invasive strategy needs to be found
?one method: look for abnormally high levels of gene’s product
?have to get athlete inactive for 12 hours and then test for MGF
?If levels still high, indication: gene has been switched on all the time instead of being induced by natural activity
?not feasible because athletes unlikely to remain inactive for 12 hours or longer
page 6 – paragraph 3
?Approach might be useful for detecting epo gene doping
?people with plenty of red blood cells should have little or no epo circulating in their blood
?testing could not separate illegal gene dopers from athletes who carry natural mutations
page 6 – paragraph
?researchers studying how muscles build up and break down – are close to creating a drug to stop body dismantling when we stop using it
?aim to tackle weakness in sick and elderly and to make long space flights feasible for humans
page 6 – paragraph 7
?muscle-challenging exercises: muscle cells expand to take strain
?rest and muscle proteins start breaking down as soon as you stop moving.
?idle muscle is an unnecessary metabolic expense
page 6 – paragraph 8
?Muscle growth and breakdown exist in a balance – unless diet or exercise regime changes
?injury to bones, muscles on their nerve supply puts part of body out of action/body becomes starved of food, balance shifts and muscle breakdown outweighs synthesis
page 6 – paragraph 9
?for people confined to bed for long periods of time, or for astronauts in microgravity, muscle wasting is a serious problem
?wasting/atrophy is a symptom of disuse/injury/but of many diseases e.g. kidney failure/cancer/AIDS
?once enough muscle lost, exercise becomes difficult which in turn leads to disuse and further atrophy
page 7 – paragraph 1
?Only way to stop patients losing muscle is long course of physiotherapy involving weight-bearing exercise
page 7 – paragraph 2
?use of anabolic steroids – these compounds have huge effects on body besides promoting muscle growth, some of which are undesirable
?only appear to work well in conjunction with exercise
Active atrophy – page 7 – paragraph 2
?passive side effect of disuse/disease, muscle wasting is an active process controlled by complex genetic pathway
?would be possible to turn it off
page 7 – paragraph 4
?process involves ubiquitin-proteasome pathway [UPP]
?disposal machinery used to break down unwanted proteins in the cell
?once system activated , ubiquitin ‘’destroy me’’ labels added to muscle proteins
?tagged proteins fed into proteasome [a multi-protein complex that breaks down proteins into their component amino acids for reuse]
?breaks down muscle filaments within cells, but does not change number of muscle cells
?instead they become thinner and weaker
?studies showed that at least 90 genes involved in atrophy called atrogenes
page 7 – paragraph 5
?still unknown which genes trigger atrophy, but become clear that two of them are: Atrogin1 and muRF1 – are the only two atrogenes active during muscle atrophy
?they code for ubiquitin ligases, enzymes that attach the ‘’destroy me’’ labels to proteins
?the genes are barely active in normal muscle but expression level shoots up in sick animals
page 7 – paragraph 7
? more atrogenes found every year
?a switch for muscle atrophy had been found, an existing drug could turn the switch off
Gym in a bottle – page 8 – paragraph 1
?Has been found that in mice when muscle atrophy sets in, there is increased activity of gene erg1
?erg1 codes for potassium channel protein found in both skeletal and cardiac muscle tissue
?in heart muscle, channel consists of two variants of protein, erg1a and erg1b which helps heart keep its rhythm by letting muscle repolarise after each beat
?a mutation in erg1 gene causes ‘’long QT syndrome’’ – in which heart muscle cannot repolarise fast enough can lead to sudden death
page 8 – paragraph 2
?erg1a variant stimulates atrophy in skeletal muscle
?in muscles, that were wasting due to disuse or cancer, found high levels of expression of erg1a
?when they increased the number of erg1a potassium channels on surface of muscle cells in mice by adding an extra gene coding for this protein, atrophy set in
?adding a gene for erg1b version of the protein did not trigger atrophy
page 8 – paragraph 3
?an existing drug, an antihistamine called astemizole blocks erg1a channels
?when given to mice, it prevented atrophy in muscles not being used
page 8 –paragraph 4
?team thinks erg1a protein stimulates ubiquitin-proteasome-pathway
?problem: astemizole not only blocks erg1 channels in skeletal muscle, it also blocks them in heart, potentially causing long QT syndrome
?because of this risk, astemizole was withdrawn
?if approach is to work, need to find a way to target erg1a in skeletal muscle without blocking erg1 channels in heart which consist of both erg1a and erg1b sub-units
page 8 – paragraph 5
?team is also investigating possibility of blocking erg1a expression using gene-silencing technique – RNA interference
page 8 – paragraph 6
?focusing on proteins called transcription factors that can turn other genes on or off
?Foxo has been identified that controls activity of many atrogenes
?Disabling Foxo blocks atophy
page 8 – paragraph 7
?E.g. insulin and related hormone insulin-like growth factor [IGF-1] is involved in muscle synthesis but also prevents muscle breakdown by suppressing foxo and turning off atrogin1 gene
?Can’t see Foxo in normal muscle because insulin and IGF-1 supress it
?but don’t know how inactivity or disease activates Foxo transcription factor
page 8 – paragraph 8
?Foxo could be involved in erg1a-mediated atrophy
?erg1a protein is known to bind to transcription factors like Foxo, so increased erg1a activity might trigger atrophy through interaction with Foxo
?companies looking for drugs that block the atrogin1 protein
?team is looking into whether proteasome inhibitors e.g. Velcade used to treat cancer might slow muscle breakdown
page 9 – paragraph 1
?company began trials in people with muscular dystrophy of an antibody therapy designed to stimulate muscle growth rather than prevent atrophy
?produce more muscle tissue is different to attempting to turn off wasting, but end result could be same
page 9 – paragraph 2
?Patients confined to bed for more than a few days could be given drug to prevent muscle loss
?could take patients of respirators would become easier as doctors could prevent muscle wasting of diaphragm
?wouldn’t need painful physiotheraphy sessions to rebuild muscle strength
?anti-wasting drug could keep older people on their feet
page 9 – paragraph 3
?preventing atrophy: interest to NASA because astronauts lose their muscle mass
page 9 – paragraph 4
?valid medical and space applications for anti-wasting drugs, as a safer alternative to steroids, they will be tempting to athletes
page 9 – paragraph 5
?muscle size is not everything
?endurance training: better blood supply to muscles/more energy-supplying mitochondria in muscle cells
?drugs that maintain muscle size will keep people strong, but not fitter
page 9 – paragraph 6
?maintaining more muscle will help use up extra calories
page 9 – paragraph 7
?two tried and tested ways to lower Foxo levels and prevent muscle atrophy
?one is to increase your IGF-1 and to stimulate insulin production
Pump up the volume – page 10 – paragraph 1
?the boy had mutation in both copies of gene coding for muscle growth inhibitor myostatin
?mother had mutation in one copy of gene giving her unusual strength
?the boy didn’t have any myostatin at all
page 10 – paragraph 2
?blocking myostain in mice makes them twice as muscular as usual
?clinical trial – to see if blocking myostatin with an antibody therapy to prevent further muscle loss in people with muscular dystrophy
page 10 – paragraph 3
?muscular dystrophy causes different kind of muscle wasting from that seen in disuse or disease, muscle cells do not shrink, they die
?myostatin is thought to keep muscle stem cells called satellite cells in check and in its absence the satellite cells give rise to new muscle cells
?blocking myostatin will not solve causes of muscular dystrophy but by boosting muscle growth might compensate for lost tissue
?however, possible that treatment might exhaust supply of satellite cells thus only temporary
page 10 – paragraph 4
?antibody trial has started
?hoped that myostatin blockers could help treat other kinds of muscle wasting and the elderly
I know this is cheeky but i literally just got back from hospital after having my appendix out and so havent revised for the last few days can someone help me please? does anyone have any revision notes they can email me PLEASE??
for some reason the core practicals just wont stick HELP!!
for some reason the core practicals just wont stick HELP!!
topic 8 sucks :/
i keep forgetting stuff from this topic! UGH! :/
i keep forgetting stuff from this topic! UGH! :/
can anyone define Summation for me please?
Original post by Rizam
Original post by Rizam
can anyone define Summation for me please?
http://www.interactive-biology.com/1660/what-is-summation-2-types-%E2%80%93-episode-19/
Original post by Rizam
can anyone define Summation for me please?
Summation is the fact that each impulse adds to the effect of the others and then you get spatial summation and temporal summation
Original post by Phenylethylamine_
Summation is the fact that each impulse adds to the effect of the others and then you get spatial summation and temporal summation
Thanksss
What topic was 'viruses being used as vectors' in.
Also, could anyone explain it in the detail we have to know it in.
Also, could anyone explain it in the detail we have to know it in.
Original post by Rizam
Thanksss
You live in Kuwait?? So you're doing this syllabus from there?! wow
Original post by chemdweeb1234
Original post by chemdweeb1234
i love the fact that the mark schemes are taken as being always right... edexcel obviously messed that one up.... sodium potassium pump has to be involved in restoring the resting membrane potential.... most sources say that... i have no idea why they didnt credit that
Actually, I just checked a university textbook which says that the recovery from hyperpolarisation is diffusion, not pumping!
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