AQA BIOL1 ~ 14 May 2012 ~ AS Biology

What does everyone expect to come up on Monday? Of course, I'm not going to take your suggestions and just revise those - I just like to know what people are thinking.

Random Tips for this papers 2/3 Mark questions and how to answer them.

If it asks you a question on how an (competitive) inhibitor slows down an enzyme catalyzed reaction always mention:




Questions stating why an enzyme is specific normally follows this route:




Question regarding Antibodies and why they are specific follow this route:





Questions about what an antigen is always follows this route:






questions regarding emphysema always want you to mention these sort of things when it talks about reducing gas exchange efficiency:





I'm not saying these are correct but they tend to follow this pattern, there are more that i know of but these are the most common, if there are any errors tell me and sorry for any spelling/grammar mistakes.

Aw thank-you. So do I!!!

I'll do the one I like the best first so number 3.
Roles of SAN, AVN and bundles of His.

SAN (Sino-Atrial Node)
This is called also the pacemaker. It inititates the electrical impulses across the atria causing them to contract
AVN (atrioventricular node)
This receives the electrical impulse from the SAN and delays it from carrying on (the importance of this delay is to allow the venticles to fill up with blood before they contract).
After the short delay, the AVN sends the electrical impulse between the venticles down the septum, down the bundles of His to the purkyne fibres.
The electrical impulse reaches the base of the ventricles where both venticles contract upwards pushing blood out of the venticles.

I think of it in a few stages
1. SAN, pacemaker. Initiates heartbeat and electrical impulses. Contraction of atria.
2. AVN receives impulse and DELAYS (this is important!!!) to allow the ventricles to fill with blood before they contract
3. AVN sends impulse down septum to bundles of His
4. Impulse reaches bottom of venticles where it causes both walls of the venticles to contract upwards.
(this is literally all there is to it) All they could ask questions on is the importance of the delay. What the SAN is, where is it situated etc. xx

let's say the 5 marker did come up on cell fractionation or Ultracentrifugation... what do we actually write to gain 5 marks - by the "mark scheme" way ??

I have a feeling Fluid mosaic model would come up!
But what are they going to ask?
What are peripheral proteins?
integral proteins?
What is able to pass the bilayer?
What are glycoproteins are what are they used for?
Where are glycoproteins situated?

Anymore anyone could think of?
What is a fluid mosaic model? =p

I think the best way to set out this question is by using bullet points, this is how I would answer a question like this:-

- Homogenize the cells in an Ice Cold, Isotonic Buffer solution

- The ice-cold solution reduces the activity of the enzymes significantly preventing them from destroying the organelles.

- The solution is isotonic to prevent osmosis and to prevent organelles becoming damaged.

- The buffer solution is used at a known pH to keep the pH constant.

- The homogenized solution is then spun in a centrifuge at low speed
- The sediment contains nuclei

- It is then spun at medium speed
- The sediment contains mitochondria & chloroplasts

- It is then spun at high speed
- The sediment contains endoplasmic reticulum, golgi apparatus & membrane fragments

- It is then spun at very high speed
- The sediment contains ribosomes

You are then left with the cytoplasm.

Hope this helps and good luck for tomorrow

Can someone run over the main facts in non-competitive inhibition in ezymes, and monoclonal antibodies? Thanks! Good luck with rev today, can't believe it's tomorrow!!

Why are glycoproteins? I mean I've learnt about their existence but not to any detail?

What do SER do i know RER allow large surface are for protein synthesis because of the ribosomes on their surface but what do SER do then?

Erm what?
If elastin is broken and they cannot recoil, then air can't be expelled well, so low conc of oxygen affect rate of diffusion by reducing it = correct like you said.
But, they don't have a larger surface area, their surface area actually gets reduced because the alveoli walls are destroyed THIS reduction in surface area also reduces the rate of diffusion.