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    Hi. Seeing as I've seen quite a few threads about how to deal with the Edexcel Biology AS coursework I thought I'd make this to help out. I got 39/40 raw marks which equated to 58/60 UMS. I will post the main body of the report but not include images or references. This is because the main idea here is to give people ideas on how to structure it and what kind of things to include in each section.

    One thing to note is your referencing. You should use Harvard Referencing (Google how to do this). You also need to include one or two non-web based sources which I believe gains you one mark. This can be done by taking a source from a scientific journal and referencing it in such a way that it looks like a non-web based source. For example, I found a paper from the British Medical Journal website and referenced it as a non-web based source as follows :

    Name of author,Title of paper, (name of journal) 2003; 326:1423 (random numbers from the abstract), page 3, Published 23 June 2003

    For the web based references:

    Name of website, author, date accessed by you(Don't forget that part!)


    More things to consider:


    • Reference absolutely everything.
    • Make sure any biological processes/mechanisms are written to and beyond A-Level standard, don't be afraid to go quite in depth.
    • Explain why your chosen solution is better than the alternatives, using data to support the statement.


    Spoiler:
    Show
    What’s the best solution for CVD?
    So, what’s the problem…?
    The NHS have stated that over 2.6 million people in the UK currently suffer from chronic heart disease and is responsible for over 88,000 deaths. Heart attacks are the most prominent cause of death, with over 124,000 heart attacks per year [1]. Angina pectoris has a prevalence of 13.3% across the UK (2006) [2] for both male and females.
    The NHS claims that “Angina is a common condition among older adults, In England it is estimated that 1 in every 12 men and 1 in every 30 women between 55 and 64 years of age have angina. This figure rises to 1 in every 7 men and 1 in every 12 women who are over 65 years of age.” [3] Another quote says “Coronary heart disease (CHD) is the UK's biggest killer, causing around 82,000 deaths each year. About one in five men and one in eight women die from the disease.” [4] Both these quotes and data exemplify the widespread of the issue and vast number of people suffering from it. A statement from the BHF (British Heart Foundation) also says “CHD is responsible for over 74,000 deaths each year” [32]. Therefore it is imperative that everything is done to reduce the effects of CVDs/CHD and reduce the likelihood of people developing them. Instinctively this data is also trustworthy as the NHS is the leading healthcare provider in the UK and not only collects all the data itself, but would also not publish any falsified data. The World Health Organization (WHO) also quotes from a study by -------- published in 2006 that “The number of people who die from CVDs, mainly from heart disease and stroke, will increase to reach 23.3 million by 2030” [27], suggesting more and more people are being affected by it each year. This is a serious cause for concern among doctors and scientists.
    Coronary heart disease (CHD) falls under a category of diseases known as cardiovascular disease. It is the main cause of myocardial infarction. Cardiovascular disease is a class of diseases which affect the heart and blood vessels. There are various causes of cardiovascular disease (CVD) however the most common are atherosclerosis and hypertension. Atherosclerosis is a condition in which the walls of blood vessels thicken and harden. This is due to the damaging of the endothelial lining within them. The damage is often caused by hypertension (high blood pressure) or toxins within the blood, often due to smoking habits. The damage invokes an inflammatory response; white blood cells (mostly macrophages) move into the site of damage. The white blood cells and lipids such as cholesterol clump together under the endothelium to form a fatty streak. Over time as more white blood cells, lipids and calcium ions build up, a hard plaque forms, known as an atheromatous plaque. This is called an atheroma and reduces the size of the blood vessel, restricting blood flow. The hardening of arteries caused by atheromas is known as atherosclerosis. An atheroma can actually rupture the endothelial lining and damage it further, leaving a rough surface. This triggers the formation of a thrombis (blood clotting). Both atheroma and thrombosis inhibit blood flow through the blood vessel leading to a decreased volume of oxygen reaching the heart – this can lead to myocardial infarction (heart attack), cerebrovascular accident, coronary heart disease (CHD) and angina pectoris; pain in the chest caused by hypoxia of the heart.
    There are also several risk factors (things which increase the chance of developing the disease) which are associated with CVD. Risk factors can be separated into two categories, lifestyle factors and genetic factors. Lifestyle factors are ones which one has control over, for example; diet, high blood pressure, smoking and inactivity. A diet consisting of excessive saturated fat can increase the risk of developing CVD because it increases the blood cholesterol level. This in turn leads to atheroma formation. As mentioned before, high blood pressure will also increase atheroma formation and alcohol/saturated fats intake along with stress can increase blood pressure, as indicated by one with a type A personality. Smoking is also another risk factor; it increases the toxins within the blood and again, increases the chances of atheroma forming. Carbon monoxide combines with haemoglobin and reduces the amount of oxygen transported in the blood. Nicotine makes the platelets sticky, leading to blood clotting. Nicotine also activates the sympathetic nervous system which increases blood pressure.
    Genetic factors are ones that one cannot control; these include age, genetics and gender. As age increases, so does the risk of CVD. Men are also more likely to develop CVD (compared with premenopausal women) [5]. After menopause, the levels of oestrogen decline, therefore the risk of CVD increases. However, in certain areas of the world, it must be emphasised that both environmental and genetic factors can increase the risk of CVD. For example, afro Caribbean individuals are genetically predisposed to hypertension (polymorphism of the ATP2B1 gene), but also consume a large amount of salt.
    What are the possible solutions?
    A study published in October 2013 states that the statins are the most effective treatment, with an odds ratio of reducing mortality of 0.82 (credible interval 95%), as oppose to 0.83, 0.85 and 0.89 to that of antiplatelet drugs, beta-blockers and exercise alone, respectively -----------) [6]. The WHO (World Health Organisation) also states that “Treatment with statins is recommended for all patients with established CHD.” [7] Within this article, the other available drugs are reviewed however each one is only recommended following more specific events, for example, for antihypersensitives, “Blood pressure reduction should be considered in all patients with established CHD, particularly with a blood pressure level above 140/90 mmHg” [7] This is an indication that statins are holistically the best drug for treating CHD and other CVD as it is recommended (by the world’s leading health organisation) for all patients. A study published in the Lancet medical journal, carried out at the University of Oxford and University of Sydney and funded by the UK Medical Research Council, British Heart Foundation (and several others) also state that statins are an effective treatment. The results concluded “an overall further reduction of 15% in first major vascular events and a 13% reduction in coronary death or non-fatal heart attack” Another quote from the NHS website, from the same study, concludes the evidence that statins are largely effective “Across all 26 trials, deaths from all causes were reduced by 10% for every 1.0 mmol/L reduction in LDL (RR 0.90, 95% CI 0.87 to 0.93), largely reflecting a drop in deaths from cardiac causes.” [15] This study is particularly valid due to the fact it was carried out at two world renowned universities, and also funded by the world’s leading medical councils; it would not make sense to release falsified data as millions of people already trust them and also other data supports the findings.
    The effectiveness of stain drugs can be classed into two categories; primary and secondary prevention. Primary prevention is when a patient shows risk factors of developing CVD, for example being overweight, eating excessive amounts of fat and smoking habits however have not shown symptoms, and are prescribed drugs as a prophylaxis in order to prevent myocardial infarction or atherosclerosis. Secondary prevention occurs after a patient has experienced a reciprocate of CVD, for example the patient may have suffered from an acute myocardial infarction or stable angina, and are prescribed drugs in order to prevent any further problems. A study in 2013, on the effect of statins in primary prevention, concluded that statins “significantly reduced the risk of major coronary events” [10]. Carried out by ----------one study showed Rosuvastatin to lower mean LDL cholesterol by 50% [11]. This study is also incredibly reliable as it was carried out with 17,802 people. Even though it was sponsored by a drug company the results are still trust worthy as other studies also found similar results; Rosuvastatin reduced the mean LDL cholesterol by 60% [12] (------ 2003). As briefly stated by the NHS, “It is estimated that statins save 7,000 lives a year in the UK” [13]. Again, like stated before, the data from the NHS is trustworthy however; this particular quote is fairly vague, not indicating what these people actually suffer from and what particular statin they take, etc.
    On a molecular level; how do statins work?
    Statins are known as HMG - CoA reductase (3-hydroxy-3-methylglutaryl-coenzyme - A reductase) inhibitors. HMG-CoA reductase is a rate controlling enzyme of the mevalonate pathway; this pathway is used in the production of cholesterol in the liver. Statins work buy a mechanism known as competitive inhibition. The HMG-CoA reductase has an active site, as it is an enzyme. Only a specific shaped substrate can attach to it and thus allow the HMG – CoA to catalyse its reaction; statins have similar shapes to the substrate and are able to bind to the active site of the enzyme. This means that the normal substrate (mevalonate) can no longer bind to it and thus cannot be metabolised. As cholesterol is derived from mevalonate, the inhibition of production of it will hence decrease the amount of mean LDL cholesterol produced in the liver and consequently the levels in the blood. Less cholesterol in the blood means that atherosclerosis is less likely to develop.

    Above shows the mevalonate pathway, the pathway in which cholesterol is synthesised. At the top, the reaction of HMG – CoA forming mevalonate is shown to be catalysed by HMG – CoA reductase as indicated by the text. If mevalonate is not metabolised, cholesterol cannot be metabolised.


    Figure 11 on the left shows a simple diagram illustrating the mechanism of competitive inhibition, the mechanism used by statin drugs in order to prevent metabolism of mevalonate. Part a) shows a normal reaction occurring; a substrate binding to the enzyme forming an enzyme-substrate complex and then forming the products. Part b) shows the competitive inhibitor in blue, binding with the active site and preventing the normal substrate (yellow) from binding. Notice how the inhibitor does not metabolise into anything; this suggests that the inhibition does not form any products. It is also reversible as the inhibitor can detach from the active site. This means that one the inhibitor detaches, more must be introduced into the system to continue inhibition. This is why statins are not a permanent solution, however this can be advantageous as we can control how much cholesterol is produced and alter dosages according to the patient’s needs.
    Risks
    The main risks of using statins and any other drug for that matter would be the side effects. The common ones for statins would include: headache, nosebleed, muscle and joint pain and insomnia however reports suggest that only 1 in 10,000 people will experience a dangerous side effect [14]. Statins have also be found to reduce bone mineral density (BMD); a study by -------- published in 2001 stated that the use of statins the use of several named statins (Simvastatin, Atorvastatin and Pravastatin, with 20mg doses decreasing to 1mg ) “resulted in significant reductions of BMD when compared with control groups” [17]. Why is this important? Having low BMD is known as osteoporosis, meaning that your bones are more susceptible to fracture. Loss of memory has also been associated with statin use; A study by --------- (July 2003) states “Of the 60 patients identified who had memory loss associated with statins, 36 received simvastatin, 23 atorvastatin, and 1 pravastatin. About 50% of the patients noted cognitive adverse effects within 2 months of therapy.” [18].This data is not the most reliable as there are only 60 patients included in the study. Also we cannot put a measure on “cognitive adverse” i.e. how much the patients memory deteriorated/improved, therefore there is no indication as to how much of a risk exists when using statin drugs.
    Myopathy is a disease in which muscle fibres do not function properly [19] and rhabdomyolysis is a condition in which damaged skeletal muscle breaks down [20]. Statin associated myopathy has been observed by -------------- (2005); “Resolution of muscle pain occurred a mean (SD) of 2.3 (3.0) months after discontinuation of statin therapy.” [21] – i.e. an observation in cessation of muscle pain was only made once statin therapy had stopped. This data is valid as It was carried out by a certified doctor (has M.D in their name) however is slightly unreliable as only 45 patients were included in the study. Also, much like statin associated memory loss, there is no measurement for pain sensation, thus, again there is no numerical indication to the extent to which the side effect has on the patient.

    Benefits:
    Statin drugs actually work. As outlined above they reduce LDL cholesterol by up to 60%. Another reason as to why statin drugs are an effective solution to preventing/reducing the effects of CVD is because they are cost effective. Put simply this means the treatment is affordable over long periods of use. Taking into account other possible solutions (which will be discussed later on) the cost effectiveness of reducing cholesterol levels using statins shows that they are the most effective solution.

    The image on the left shows standard simvastatin tablets. As you can see they are packaged in high quantity and are small, making them easy to consume. The high volume per pack means that the patient will not need to make regular trips to the pharmacy (or online) to purchase them.
    Statins have also been shown to increase HDL. HDL or high density lipoprotein is another lipoprotein, like LDL. However, unlike LDL, HDL is known as the “good cholesterol”. Conducted by---------- (2010) a study exemplifies this increase of HDL among statin users; those taking varied doses of Rosuvastatin were observed to have an increase of between 5.5% to 7.9% of HDL blood concentration [16] . Although these data can be considered reliable they may not shed complete light on the benefits of statins as they only represent the increase of LDL for one named statin whereas in reality many different ones are used.
    As with any drug solution to a disease, there will be benefits and risks. However in the case of statins, the benefits outweigh the risks, meaning they are the most effective solution for CVD/CHD. The studies showing that statins are linked with reduced BMD (-------------) only represent the effects of using statins of 20mg dosage; as many patients may be prescribed a lower dosage the resulting side effects may be less extreme than outlined in the study. This leads onto another benefit, as there are different strengths of statins, and each one can be differed in dosage, even if the patient does experience side effects they can be minimized by adjusting what statin they take and what dosage; they can still experience the benefits of using statins even if the side effects are present. Regarding the study by ------------ (July 2003), “Fourteen of 25 patients noted improvement (of memory) when the statin was discontinued” [18]. This piece of data suggests that neurological side effects are not always permanent and can be reversed given the termination of use of the statin. Again, doctors can prescribe different dosages to allow a “compromise” between effectiveness of the treatment and side effect; once again the fact statins are so flexible in terms of dosage and strength in order to allow such compromises (even if the given side effect is rare) means that they are the most effective solution.
    Implications
    Five out of the nine common statins are synthetic meaning they do not occur in nature and need to be chemically produced. The following four are derived from various fungi and yeasts. The fact that the majority of statins are chemically synthesised means that the use of these drugs will have both economic and environmental implications. The nature of the disposal of these drugs also raises issues. As shown in figure 6, statins are packaged in cardboard boxes and plastic/foil. The production of the packaging itself will have major environmental implications; oil is needed for the production of plastic and we all know that this resource is depleting faster than we’d like. The cardboard box will lead to deforestation, not only will this significantly reduce the amount of trees, it will also cause all kinds of problems for the vast number of organisms living within forests. The extent to which the rate of deforestation can be summarized by this quote from Wikipedia – “Some scientists have predicted that unless significant measures (such as seeking out and protecting old growth forests that have not been disturbed) are taken on a worldwide basis, by 2030 there will only be 10% remaining, with another 10% in a degraded condition.” [22] This quote is reliable as on the Wikipedia page itself it contains citations from where the actual data came from, these citations are referenced in the bibliography, not the Wikipedia page. Also, it is displayed on one of the largest sources on the internet, therefore thousands, if not millions of people will read it, meaning if there was something false about it, it would be changed due to the nature of Wikipedia (certain users are allowed to change certain data on Wikipedia). This large scale deforestation leads to diminishing of habitats and ultimately reduces biodiversity. This will lead to areas of the food chain being affected and leads onto even larger implications such as loss of entire species due to their habitat being destroyed. Figure 8 continues to exemplify the extent to which forests are being destroyed.
    However production of packaging isn’t the only environmental implication of using drugs, incorrect disposal of unused medication also brings rise to concern. Due to the nature of the composition of chemically synthesized drugs, incorrect disposal can cause massive problems within the environment. When disposed improperly drugs can find their way easily into the water system. This will affect many marine ecosystems. Impurities within water systems leads to them being present in human drinking water; a study by -------- (2011, France) suggests that for 20 different human pharmaceuticals, “16 were quantified in both the surface water and drinking water, with 22% of the values above the limit of quantification for surface water and 14% for drinking water)” [23], i.e. 16 of 20 were found in water samples.
    The two implications discussed above outline the wider effects of using statin drugs. However the data doesn’t represent solely the use of statins alone; although statins do contribute to the given statistics they are not wholly responsible for the entirety of the implications. One must also consider that statins are an effective drug and do save lives, and again do not wholly contribute to all the environmental issues. Having said that, it is still important to consider the wider implications of using statin drugs.


    Are there any other solutions to reducing CVD?
    Although as outlined throughout this article, statins are the most effective solution to lowering high cholesterol levels, they are not the only way to do so. Lifestyle changes such as increasing the amount of exercise one partakes in or controlling one’s diet can also be an effective way to control LDL cholesterol. These are both risk factors which can contribute to CVD, meaning if the risk factor is lowered; the chances of developing CVD are also lowered. These are also the lifestyle solutions that the NHS advertises [24]. Like stated before the NHS is a trustworthy service and will only provide reliable advice as thousands, if not millions of people will seek advice from it.
    A bad diet can lead to high cholesterol, one containing many saturated fats and oils will almost certainly increase the amount of LDL cholesterol in the blood. Examples of these foods include red meats, fried foods such as fast food and crisps and sugary foods such as deserts. Hence reducing the amount of fats in one’s diet will reduce the mean LDL levels. A study conducted by---------- suggests that a low fat vegetarian diet (one consisting of no meats and low fats) will reduce LDL cholesterol by up to 16.9% [25]. Although this data is valid, it is not 100% reliable as the study was only carried out on healthy premenopausal women, suggesting the results aren’t representative of the entire population. However this does not mean that changing diet will not be effective to anybody outside the group who were tested in the study. Another issue regarding changing diets is that some people may find it difficult to make such a change. It is also difficult to measure what the actual fat intake is as some people may consume more/less, however the results still show that a holistic reduction in fat intake (via vegetarian diet) suggest it is an effective alternative. Another study (-------------(October 200)) illustrates this, stating “On average, Ornish's patients lost 24 lbs in a year and had a 37% reduction in LDL cholesterol levels” [26]. Ornish simply refers to the type of diet, “This vegetarian diet consists of fruits, vegetables, soybean products, non-fat milk, and yogurt with no oils or animal products. Roughly 7% of calories are from fat, 15% to 20% from protein, and the remainder from complex carbohydrates. Only 12 mg of cholesterol per day is allowed.” [26]
    Partaking in exercise has also been proven to lower mean LDL cholesterol, especially when combined with altering one’s diet. A study by ---------(July 1998) concludes that “The serum level of LDL cholesterol was significantly reduced among women (a decrease of 14.5±22.2 mg per deciliter) and men (a decrease of 20.0±17.3 mg per deciliter) in the diet-plus-exercise group.” [28].
    Another common risk factor for CVD is whether or not somebody smokes. Smoking increases the chances of one developing CVD due to the nature of the chemicals within the cigarette; chemicals such as tar can get into the bloodstream. Tar is known as a toxin, and can lead to the damaging on the endothelial lining in blood vessels. As explained before and in figure 1, damage to the endothelial lining causes an inflammatory response and leads to the formation of atherosclerosis and thus CVD. Therefore quitting smoking will be an effective solution to preventing such eventualities. One study was conducted to measure the levels of HDL (good cholesterol) compared with whether or not the subjects smoked; (---------) “Men and women who were smokers had significantly (p < 0.01) lower HDL cholesterol levels than non-smokers, and heavier smokers had lower HDL cholesterol levels than lighter smokers.” [29].To summarize the study, smokers had both higher LDL cholesterol and lower HDL cholesterol. So smoking has three detrimental effects on health; introducing toxins into the blood stream, lowering HDL cholesterol and raising LDL cholesterol. A quote from a study by S Heyden states “Low-density lipoprotein (LDL) cholesterol levels were significantly higher among persons who smoked cigarettes” [33] exemplifies that smoking has a negative effect on the body. As stated before, high concentrations of the toxins and LDL cholesterol will undoubtedly increase the likelihood of atherosclerosis. Due to these effects, it is obvious that quitting smoking will supress them and thus reduce the chances of atherosclerosis arising.
    Cigarettes also contain the infamous chemical known as nicotine. Although it isn’t harmful (unless in excessive dosages), it is incredibly addictive and is the reason why people become addicted to smoking. Therefore, for some, it will be difficult to quit smoking. When deprived of something someone is addicted to, they may begin to show withdrawn symptoms and may eventually relapse and begin smoking again. Similar to changing one’s diet, quitting smoking also requires a certain level of perseverance to be effective and many people may fail in doing so. However, with the development of nicotine patches and other cigarette substitutes, quitting smoking is becoming easier as time progresses, meaning that it is an ever improving alternative solution to preventing CVD.
    High blood pressure (hypertension) is also a risk factor for CVD. Hypertension contributes to the damaging of the endothelial lining. Currently there is on-going research into how we can treat hypertension. The most recent treatment that has been under much investigation is the idea of renal denervation. This involves quite simply trying to remove some of the innervation to the kidney with the intention of therefore reducing hypertension. Up until the 1960s medical professionals used to surgically denervate kidneys in order to try and reduce muscle sympathetic activity however this was abandoned as major side effects, such as postural hypotension and impotence became apparent, it was also abandoned due to the introduction of modern anti-hypertensive medication.
    This idea is now being revisited for people who have resistant hypertension. The procedure involves ablation of both afferent and efferent renal sympathetic nerves with a radio-frequency emitting catheter [30] which is inserted percutaneously into the renal artery. The back end of the catheter handle connects to a radio-frequency generator that supplies power. The procedure is performed under local anaesthesia and sedation. Four to six - two minute treatments are delivered at different locations longitudinally and rotationally in order to achieve a helical pattern of ablation within each renal artery [31]. It is important to note that the patient will also receive anti-coagulation and IV nitro-glycerine before the procedure. The most important feature about this new medication is that if it is successful, there would be absolutely no need for any anti-hypertensive drugs.


    I've also not included the evaluation of references or name of authors throughout (the idea is to find these for yourself) or images/diagrams in order to stop people from taking too much "inspiration" from this. There's a mark for having an image on each page I believe. I'll make a post later on, on how to evaluate your references. A lot of this can be literally made up on the spot in my opinion, like writing things like "it's reliable because a Doctor carried out the study, we can see this because the have M.D in their name" or some other rubbish like that.

    Please don't copy and past any of this. You'll be flagged for plagiarism.

    Good luck
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    Sorry you've not had any responses about this. Are you sure you’ve posted in the right place? Posting in the specific Study Help forum should help get more responses. Hopefully someone will be able to get back to you
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    Thank you for this I was literally about to drop out of college because I thought I'd fail lol.
    Do you have anymore tips? Like key things/points to include? My teacher didn't really offer much help so I don't even know what I'm supposed to write.
    By the way what is meant by biological processes of the solution to the problem?
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    (Original post by Pine3278)
    Thank you for this I was literally about to drop out of college because I thought I'd fail lol.
    Do you have anymore tips? Like key things/points to include? My teacher didn't really offer much help so I don't even know what I'm supposed to write.
    By the way what is meant by biological processes of the solution to the problem?
    So I wrote about the biochemistry behind drugs, and how they work. For example things like how statins (my chosen solution) block certain metabolic pathways and prevent an enzyme from being synthesized etc
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    (Original post by TajwarC)
    So I wrote about the biochemistry behind drugs, and how they work. For example things like how statins (my chosen solution) block certain metabolic pathways and prevent an enzyme from being synthesized etc
    Oh thank you that was really helpful in writing about epilepsy and the use of anti epileptic drugs as my main treatment but I wasn't sure if I should write about how exactly the drugs work but now I will thanks
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    Hello there, sorry to be of nuisance but I have a few questions if you wouldn't mind answering please.

    For the "Describe the biological methods and processes involved in producing data or solutions to problems or questions relevant to a visit made or issue researched" do we have to describe research into the solution? How long should this be and how should we be doing this?

    What an absolute struggle, thanks for your thread by the way!
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    (Original post by Romanoff)
    Hello there, sorry to be of nuisance but I have a few questions if you wouldn't mind answering please.

    For the "Describe the biological methods and processes involved in producing data or solutions to problems or questions relevant to a visit made or issue researched" do we have to describe research into the solution? How long should this be and how should we be doing this?

    What an absolute struggle, thanks for your thread by the way!
    I think that point is in terms of your chosen solution (the methods and processes involved in solutions to problems). You need to be able to talk about it in quite a bit of detail, at least to A-Level standard. So for example with my statins I talked about how they block certain metabolic pathways and all the names of the enzymes and how they work, etc. Make sure to include diagrams where possible.

    Talking about the research is useful when you're evaluating the references. For example research done with more trials is going to me more reliable (obviously go into more detail, stating figures you've found). Also talking about who does the research is important, basically whose research/data would be most reliable, and why.

    In terms of length I can't really comment because the chosen solution will be different to mine therefore may require more or less explanation, just make sure you go into enough detail

    Hope this helps
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    (Original post by TajwarC)
    Hi. Seeing as I've seen quite a few threads about how to deal with the Edexcel Biology AS coursework I thought I'd make this to help out. I got 39/40 raw marks which equated to 58/60 UMS. I will post the main body of the report but not include images or references. This is because the main idea here is to give people ideas on how to structure it and what kind of things to include in each section.

    One thing to note is your referencing. You should use Harvard Referencing (Google how to do this). You also need to include one or two non-web based sources which I believe gains you one mark. This can be done by taking a source from a scientific journal and referencing it in such a way that it looks like a non-web based source. For example, I found a paper from the British Medical Journal website and referenced it as a non-web based source as follows :

    Name of author,Title of paper, (name of journal) 2003; 326:1423 (random numbers from the abstract), page 3, Published 23 June 2003

    For the web based references:

    Name of website, author, date accessed by youPlease don't copy and past any of this. You'll be flagged for plagiarism.

    Good luck
    Hi, sorry to revive an old thread. I'm doing the AS coursework on the same topic as yours but when in the specification it says "Discuss alternative views or solutions for implications ofthe biology encountered within the context of the visit orissue" Could you talk about other drugs that work similar to Statins such as antihypertensive, antiplatelet drugs etc?
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    (Original post by TrewKazim)
    Hi, sorry to revive an old thread. I'm doing the AS coursework on the same topic as yours but when in the specification it says "Discuss alternative views or solutions for implications ofthe biology encountered within the context of the visit orissue" Could you talk about other drugs that work similar to Statins such as antihypertensive, antiplatelet drugs etc?
    Exactly that, yes. If you can find data to suggest that your chosen solution is better than the alternatives that would be great; my teacher emphasized that we do that as there's marks for it (it's been over 2 years however so I don't really remember much!)
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    (Original post by TajwarC)
    Exactly that, yes. If you can find data to suggest that your chosen solution is better than the alternatives that would be great; my teacher emphasized that we do that as there's marks for it (it's been over 2 years however so I don't really remember much!)
    Okay thanks bro
 
 
 
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