I'll be doing this, good luck to you too. Honestly, I'm way too behind with biolgoy and will start pretty hardcore revision tomorrow after my chemistry exam.

The A mark last year was 67%, do you think it'll be even lower than last year? I think it was much harder!!

i messed the most basic question up.. how do you test for starch? ! im so gna fail :(

What is pyruvate?

I got confused because when I google Adrenaline it says it's a hormone while my revision guide says that Noradrenaline is a neurotransmitter... It feels strange but is this correct? There's still not much difference (since they have the same function more or less) in general but here it seems kind of relevant since I'm looking at heart rate control in A2 biology

(ok not really relevant... But I'm curious and extra info like this makes me understand it better if that makes sense)

Your blood type is determined by ONE gene, and ONE gene only.

Your height is determined by MULTIPLE genes (it is no way a monogenic trait), and is affected by the environment.

Yes you are correct relating your first sentence. However NADh2 is the same chemical as NAD+. Fortunatley they are not on the syllabus.

There basically coenzymes found in all living cells.NAD+ is involved in redox reactions, carrying electrons from one reaction to another. The coenzyme is, therefore, found in two forms in cells: NAD+ is an oxidizing agent – it accepts electrons from other molecules and becomes reduced. This reaction forms NADH, which can then be used as a reducing agent to donate electrons. These electron transfer reactions are the main function of NAD+.

Again way out of our spec:D

Is it bad that I don't even know what that is? All i could think of was the internal organs needing protecting more, seemed like it would make sense o.o

What topics are included in biology gcse and a level. I would like to find out what's involved in it as I'm interested in it.


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Hi,
Does anyone have a link to the f212 January 2013 mark scheme??

Thanks

When we done a similar experiment, we got given a sample gel with the respective weights (in your case, kbp) labeling each of the coloured bands. We then used this to plot the log graph and used this graph to work out the size of our bands on the gel we run.

It would be impossible to work out the kbp on your gel without a graph already plotted. Did you get given sample results so you could plot this? Gels can be run for different lengths of time, and at different voltages, therefore the bands will move different distances depending on these factors.

Seeds are less viable to disease because they have resistance features. Firstly, bacteria can't get inside them. Secondly, they can stay dormant if unfavorable conditions ensue.

It says SOME of the offspring were salt-tolerant. Meaning some weren't.

Seeing as the plant self polinated you can do punnet tables for the gene being hetreozygous, or homozygous for the dominant or recessive allele.

If they were homozygous, and self polinated, ALL offspring must be salt-resistant if their parent was.

However if you draw the punnet table for a hetrozygous Hh, you'd get HH, Hh, Hh and hh. 75% Having the dominant allele.

"How do we conclude that exactly 50% of gametes will have this gene?"

If we've deduced the parent is hetrozygous, then through meiosis, each gamete will contain one copy of the honolygous parents of its parent. 50/50

I thought the two 5 mark questions on the heart were fairly straight forward though.

I suppose that plants that can be polyploid are more likely to become useful to humans and then domesticated.
so we know more about them

It's A2 and I don't mind going into detail, as long as I understand it. :p

Did you only do this at degree level or something? It's OCR by the way... so that's probably why :p

I think I got 2 A's in the EMPA and today's unit 1 exam, but if worst comes to worst and I got B's, would I still be able to get an A if I do really well in the Biol2 exam?


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Is receptor an organelle ?

This may get confusing for OP, though, as the post synaptic membrane has receptors embedded into it.


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Can anyone remember the question on marman grasses or something? I hate how they had to overcomplicate everything.

anyway, for that question it asked why it was good the leaves uncurled when it was moist in the second bit

I said something about It would be able to increase uptake of CO2 for increased photosynthesis as RUBP requires co2 to make GP in the calvin cycle

It's ridiculous how biology examinations are so tough to imagine, out of all the sciences, it's the hardest to figure out what to write that would satisfy the mark-scheme.

I understand what you're trying to say and it makes sense, but the book says something different. Basically before the table it talks about how meiosis causes a different combination of alleles to be present and the expected phenotypic ratio we'd expect is 9 : 3: 3 : 1. But if the observed value is different we apparently have to use this equation to see if the difference was due to chance and isn't significant, but if the difference is significant i.e. the percentage that the results were due to chance alone was below 5% then we have to re-think our current biological theory. But what I'm confused about is: if we're 5% certain that the deviation from the expected value is due to chance alone, then that would mean that we're 95% certain that our theory is wrong

http://www.thestudentroom.co.uk/show....php?t=2347119

Link at the bottom !

Yes sorry Light first activates the photoreceptors (rods or cones) which then stimulate bipolar cells which stiumlate the ganglion cells.

So that flow chart is backwards, except for the lens.

I think for AQA you only need to know bipolar cells send impuleses to the optic nerve, which sends impulses to the brain, ganglion cells are not in the syllabus.

This is all correct yes.

You seem to be confusing where the light goes and where the action potential goes. The ganglion and bipolar cells are on top of the rods and cones. The light therefore goes through the lens, through the bipolar and ganglion cells to the light-sensing cells. These cells then detect the light, sending impulses back in the direction the light came from to the bipolar and ganglion cells, then out to the optic nerve.

Well you mentioned it in your post but it wasn't clear if you were aware so I was just bringing it to your attention. Calm down :)

I think you might be getting some of your terminology a bit confused-water potential doesn't contribute to hydrostatic pressure, but rather hydrostatic pressure contributes to water potential. I'm honestly not surprised, because that textbook passage is one of the most confusing/unhelpful things I've ever read, and you've probably been misled on what water potential actually means (I've explained later).

The rate of filtration from capillary is dependent on three things: the "holey-ness" of the filtration barrier, the hydrostatic pressure and the colloid osmotic pressure. The "holey-ness" normally stays roughly the same (assuming the kidney is healthy), so we don't need to talk about that here.

The hydrostatic pressure is the sort of pressure you're most familiar with. It's the same sort of "mechanical" pressure that keeps water running through your taps or shoots water out of a water gun. The hydrostatic pressure in the glomerular capillaries is due to the blood being pushed through them by your heartbeat; the hydrostatic pressure in Bowman's capsule is due to the build up of filtered fluid that's just been pushed through the filtration barrier. The hydrostatic pressure is normally much higher in the capillary than in the capsule, so hydrostatic pressure encourages fluid to go from the capillary into the capsule.

Colloid osmotic pressure is the result of differences in osmotic potential due to protein. When plasma is filtered in the nephron, the proteins in the blood are too big to fit through the holes in the filtration barrier, but pretty much all the ions can pass through, so the ionic concentrations of the fluid either side of the barrier will be almost identical (my lecturers compared this to putting orange juice and rice in a sieve: the rice (protein) cannot pass through, but the orange juice (rest of the plasma) will pass through without becoming any more or less concentrated). Given that there's no real ionic differences between capillary plasma and capsule fluid, any osmotic pressure across the barrier must result from the difference in protein content. As the protein content is far greater in the capillary plasma compared to the capsule fluid (because no protein should have passed through the filtration barrier), colloid osmotic pressure is lower in the capillary, so colloid osmotic potential encourages fluid to pass from the capsule into the capillary.

The overall fluid movement is the result of the combined effects of hydrostatic pressure, pushing fluid out of the capillary, and colloid osmotic pressure, pulling fluid into the capillary. The hydrostatic pressure is bigger than colloid osmotic pressure, so the is an overall movement of fluid out of the capillary and into the capsule.

I know that at A level, I was taught that water potential was basically the same concept as osmotic potential, but a quick google has shown me that it actually refers to the tendency of water to move from one place to another due to the combined effects of osmosis, gravity, pressure etc. (http://www.biology-online.org/dictio...ater_potential). As such, the water potential is technically higher in the capillary than the capsule, even though the osmotic potential is higher in the capsule. I'd be careful about using the water potential terminology in an exam, because the textbooks (and therefore possibly the marking schemes) seem to operate on the basis of a dodgy definition, so you may actually be marked down for writing something that's technically correct.

What did you think structure 'x' was then?

Thanks a lot, I too couldn't find it anywhere. You wouldn't happen to have the mark scheme?

That is an example of directional selection; the change is working in one direction i.e. favouring those who are resistant

Stabilising selection is where the change is towards the average, so all plants having similar sized leaves instead of some having massive leaves and some having smaller leaves, for example

Anyone?

Hi WoopWoop,

That method would be used to produce a pyramid of energy. To calculate the energy released multiplly the mass of water by the temperature change by the specific heat capacity of water (4.18). This will give you the energy released in joules.

Your Friend, Mr Medicine

Creating a selection pressure? Maybe humans were more likely to kill mice with certain features, ie bigger ones? Or houses, roads etc meant that certain mice survived better - mice who were darker in colour? Leading to a direction shift in the population phenotype


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By negative pressure im guessing you mean hydrostatic pressure? If so ill explain:
Water is drawn up the xylem under tension in the process of transpiration pull.As water is lost by evaporation from the aerial parts of a plant it is replaced.Because of the cohesion between water molecules that form a long continuous column it causes the water to be drawn up under tension to replace this lost water.It is due to the presence of lignin lining the walls of the xylem that allows the xylem to withstand this tension.Therefore we call this the "cohesion tension theory".

I understand that hydrostatic pressure is part of a separate theory: Another method of water being transported up the xylem is root pressure.Due to the active transport of nitrate ions from the surrounding cells into the xylem this lowers the water potential of the xylem.Therefore water moves down the water potential gradient and into the xylem by osmosis.This creates a high hydrostatic pressure and therefore forces water up the xylem.

I hope ive helped :)

For a start, don't forget that there's glucose in the cell as well-I just did a cheeky google, and whilst I can't find a figure to put on [intracellular glucose], I did see that glucose moves from cell to blood via GLUT2 transporters (which mediate facilitated diffusion)-this shows glucose concentration is higher in the cell than the bloodstream.

That aside, let's remember that the luminal glucose concentration will fall gradually as more and more glucose is absorbed. Even if luminal glucose starts off higher than intracellular glucose, eventually you'll reach a point where enough has been absorbed from the lumen that glucose concentration is equal across the cell membrane; to keep absorbing past this point, you need some sort of active process.

Oh so there wasn't really a specific reason why the book didn't mention that we can synthesise carbohydrates (from the monomers)

Thanks for the reply :) I really appreciate it

I'm not entirely sure but is it to ensure that a surplus of product isn't produced? Please quote me if you have any ideas. :)

What is the material to which T cells respond because it is genetically different from other body tissues?

I was asked this question in a crossword, apparently it has 12 letters!!


And the letter clues are:

_ _ _ _ _ _ L _ N _ E _

Thank you!

As always, Wikipedia explains it pretty well: http://en.wikipedia.org/wiki/Respiratory_quotient.

Also, welcome to TSR :)

yes, ive got the methods, the graphs and the tables all completed, he said to me add a hypothesis, but when i asked him for help he walked of, he does this with most of the class so i'm not the only one. he also wanted me to conclude how this experiment went. which i have also done.

In animal cells, the result of telophase II is 4 sperm or egg cells. I don't know about plant cells; A level biology was 4 years ago for me.

i can give them to you as we have done this as a mock

http://biofort.files.wordpress.com/2...2-qp-jan13.pdf

and the marking scheme: http://biofort.files.wordpress.com/2...ms-jan13-1.pdf

I have some good revision tips for this biology unit if anyone wants me to share?

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I don't know exactly why they are not used but I would assume that the energy required to move them in to the IM space isn't there but the FAD is still required to bring electrons that enable the protons from the NADH to move in to the IM space.

My book first describes atheroma, thrombosis, aneurysms and myocardial infarction. Then is describes which factors increase the chance of coronary heart disease.

Are atheroma, thrombosis, aneurysms and heart attacks all included in coronary heart disease or is it a seperate disease altogether. Ive looked on the internet but its making me more confused

any help will be appreciated

Because they're an extra layer of regulation. Think of it like watchdog organisations which are independent from the companies that they regulate. Does that make sense?

sigh
*books* eh?

You still Can't trust the content.

im not wrong but ill leave :E

What book are you looking at? if I read that somewhere I would disregard it as wrong tbh, but depends what book it is. The inducer I believe is a separate entity, coding for a distinct entity. It was a while since I did the lac operon, remember it confusing the hell out of me :(.

NO. NO. NO.

Many non-coding regions do have functions; some do not. Of the ones that do not have a function, they might have a function that we haven't found yet.

There's a list of functions here.

Non-coding DNA isn't one homogenous entity. Lots of different parts have lots of different functions - some don't have any function at all. We can't talk about "non-coding DNA" as if it's all the same thing.



The ENCODE project suggests that >80% of our DNA is functional.

It doesn't mention that the chemoreceptors detect the pH returning back to normal and then sending action potentials down the vagus nerve. It just says that the chemoreceptors detect a low pH of blood and then send action potentials down the accelerator nerve.

Oh I see, thank you :)

Can I ask you something? How would a mutation not cause change to an organism if it's in a non coding region of the DNA? Don't non-coding regions of DNA have regulatory functions? Or do some regions of DNA have no function?

I see what you mean but they mentioned in the book that the photolysis of water is affected: 'increasing the temperature will have little effect upon the rate of the light dependent reaction as apart from photolysis of water it is not dependent upon enzymes'.

I'm still revising this stuff for my finals, so I'm not 100% sure, but as far as I understand it:

If you cut up an old-but-otherwise-healthy brain and stick it under a microscope, you'll typically see some big, insoluble lumps of protein outside the cells, known as amyloid (or senile) plaques. If you do the same thing with an Alzheimer's affected brain, there will be lots more of these extracellular plaques in certain brain regions, and you may also see neurofibrillary tangles inside some cells.

There's a protein, amyloid precursor protein, which gets enzymatically cut up to form beta-amyloid protein (Aβ). There is a misfolded form of Aβ protein which has a final structure with more β-sheet motifs (= a commonly seen way a chain of amino acids will fold to form a flat sheet), and this β-sheet rich form is more likely to aggregate and form amyloid plaques. Heritable, early-onset forms of Alzheimer's have been linked to three genes-the APP gene, and two others which encode enzymes responsible for cutting APP up; the Alzheimer's-promoting forms of these genes tend to encourage this misfolding.

Tau protein is normally responsible for stabilising a cell's microtubules (which act as a kind of intracellular scaffold). If tau protein gets hyper-phosphorylated (=gets lots of phosphate groups attached to it), it aggregates in a similar way to Aβ, but this time to form the neurofibrillary tangles rather than the amyloid plaques.

There's been lots of argument as to which of these aggregates is more important in Alzheimer's, and whether these aggregates are harmful or helpful to the progress of the disease. One idea that's gaining support is that smaller, soluble aggregates of Aβ may cause the harmful effects-these smaller aggregates are sometimes known as ADDLs.

Oh so even though the inner membrane and thylakoid membrane are connected the thylakoid space is not part of the intermembrane space?

There's still a layer of oil between the cells and the air so the Na ions are not always lost. This process is tightly regulated to prevent unnecessary loss. I think it's 3 Na ions to 2 K ions which is what causes a gradient. But other ions like Ca, Cl and H ions are also involved in polarisation and depolarisation.

Your book's description of growing "from the 3' end" is ambiguous, and could be taken in one of two ways. I suspect you're thinking of the way they don't mean-not your fault, just the sloppy wording of the book. What they mean is this:

If I have a growing strand of DNA bases (B):

5'.........3'
BBBBBB

And I add new bases (N) to it:

5'.........3'
BBBBBBNNNN

The new bases get added to the 3' end, or to put it another way, the strand grows from the three prime end. It's also growing in the 5' to 3' direction.

I don't know about this specific reaction.
This may well be because the activation energy for the reaction is high, so that the energy released is not greater than the energy released.
Also the construction of a larger molecule from smaller ones may well mean the loss of bonds.
This may be worth a look. :)

Tumour suppressor genes regulate cell growth by stopping mitosis, oncogenes are the genes that have the potential to develop into cancerous cells (ergo a tumour)

A mututation is a change in a base sequence so say there is a mutation on the tumour suppressor gene the gene would no longer be functional and therefore stop cell division leading to the development of cancer via uncontrollable cell growth

Just as an add-on to this, typically tumour suppressor genes will require a mutation in both copies of the gene to cause a cancer, as one functional copy will prevent the cell cycle from going into overdrive. On the other hand, oncogenes cause cancer when they are mutated (often they're part of a signalling pathway that tells the cell to divide and when mutated constantly give that signal) and therefore a mutation is only required in one copy of it.

There are exceptions to this, but that's a good general rule and is a nice example that helps you remember the difference between the two.

If you have, please can you put it up as a reply please. Thanks a lot!!!
new spec (60marks)
Tuesday 12 june 2012

so to cut a long story short, I got banned on my account so I created another account and TSR permenantly banned it. What is the ****ing point when I could simply use a proxy?? Anyways this goes out to the mods, if any of you are reading this then .... **** YOU WITH A SLICK D*ck