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OCR BIOLOGY UNIT 2 F212 8TH JUNE - revision thread

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Acta Non Verba

Hey,

I've attatched my personal notes on the biology specification. There's a lot of spelling and grammar errors which I can't be asked to fix, but hopefully it might be of some use.

thank you so much :biggrin:

Reply 21

amyyy24

Can anyone help me understand B & T Cells better?
In the OCR textbook, it says 'Pathogens must be detected by specific T-lymphocytes and B-lymphocytes for the immune response to begin'

If a B-lymphocyte detects an antigen, does it mean T-helper cells aren't needed? :/

Reply 22

BeekieBoo

amyyy24

Oooh interesting, I guess a B-cell could produce antibodies and job done the antigens are dealt with. But don't T-cells release cytokines that stimulate the B-cells? Won't the B-cells just "be hanging around" until stimulated by the T-cells? Not sure on this! Sorry :frown:

Reply 23

786girl

the following is all the revision i have done for 2moro, i thought it would help some people aswell as my self :frown:

PLEASE EXCUSE THE SPELLING I CBA.

list the 4 macromolecules found in living things and give e.g.

polysacharides/carbs-starch
proteins-haemoglobin
lipids-tricgyclerdies
nucleic acids-DNA

how is a peptide bond formed?
between an amine and carboxylic acid group. water molecules is eliminated in a condesation reaction.
broken by hydrolisis. 2 amini acids join by a peptide bond 2 form a DIPEPTIDE

explain what is meant by primary, secondary and tertiary
1-sequence of A.A
2-polypeptide folded in2 alpha helix or beta pleated sheets
3-complex folding of seocndary to give a 3D

explain how the teritaury stuctutre of a polypeptide is stabilised
bonds between R
-hydrogen bonds
-ionic
-disulhide hydrophobic
these give specific shape

what is denaturation
bonds thats stabilise tertiary strcutures are broken struure changes

why is haemoglobin quaternary??
made up up of FOUR polypeptide

define globular and fibrous protein and e.g.
glob-complex 3D-soluble e.g. haemoglobin
fibrous-linear structure-insoluble in water e.g. collagen

structure of collagen ideal for ligaments and tendons
-triple helices with loads of H-bonds between polypeptides
strong covalent bonds hold it together
molecules overlap

compare haemoglobin and collagen
haemoglobin:
`. glubular
4 polypeptides
comples 3d
function is 2 trsnaport o2 and co2

collagen:
fibrous
3 polypeptieds
triple helix
strnegthn tissues

define MONOSCACHS. DISCHAS. POLYSACHS. GLYCOSIDIC BONDS
MONO-simple sugar cant b broken down
DI-complex sugar foemed by 2 monos joined by glycosidid bonds
POLYSACHS-polymer of monos joined by glyc bonds
GLYC BONDS-covalent bonds btween 2 suagrs by condesation

how is a glycosidic bond formed between 2 molecules of alpha glucos and broken

OH on carbon 1 4 water is foremd leaveing oxygen "bridge" between the 2 glucose units.
glycosid bond is BROKEN by hydrolisis

why are starch and glycogen good stores of energy?

insoluble, compact and can b broken donw in2 many glucos

why is cellulose "ideal" for plant cell wall (this is getting so boring)
many OH groups. which form H-bonds-strneght-resistant 2 pressure blabla

strcuture of TRIGLYCERIDE
3 FATTY ACIDS AND ONE GLYCEROL JOINED BY ESTER BONDS ESTER ESTER ETSERRRRRRRRRRRRRRR

how can they differ
coz they can have difff fatty acidss which can be staturated mono sat or poly sat

phospholipds are diff coz?
coz they have 1 phsophate group instead of 3 fatty acids! and anothr hydrophillic group

importance of cholestErol in human mmetabolism?
components of cell membrane, synthesis steroids
liver conrols prod of cholesterol
can be deposited in2 artey walls and lead 2 artherosclerosiss or cardiovascular disease :frown:

TESSTS FOR BIO MOLECULES :angry:

STARCH- IODINE - BROWN TO BLUE

REDUCING SUGAR - BENEDICTS 80*C WAER BATHS- BLUE TO ORANGE/RED

NON REDUCING - IF ABOVE IS NEGATIVE THEN USE HCL - NETARLISE USING NaOH- REPEAT BENEDICTS - BLUE 2 ORANGE-

PROTEIN-BIURET-BLUE TO LILAC/PURPLE - REMEBER PP PROTEIN PURPLE

LIPID-ETAHNOL-WHITE EMULSION ON TOP

FUNCTION OF DNA AND RNA
dna-long term info storage
rna- 3 finctions:
prtein synthes
carryin amino acid 2 ribosomes
being part of the ribisome

what happens when dna is replciated (doubt that will come up as it was an 8 marker in the 2010 :s ohwell
1. double helix unwinds
2.existng polynucleotides act as templaytes
3.free nucleotides move 2 exposed bases of dna
4. base pairing happens
5. enzyme dna polymerase formcovalent bonds btween nucleotides attached 2 each template
6. 2 daughter dna molecules form :biggrin:

ROLE OF DNA IN PROTEIN SYNTHESIS
provides sequence of basesthat code for polypeptides primary strcuutre

IM GOING TO SKIP THE ENZYMES PART ITS SIMPLE IMO

WHAT IS MALNUTRITION?
eating less that required

why is cholestErol tranported in the form of lipoproteins??
COZ ITS NOT WATER SOLUBLE !!!!! SO CANT MOVE IN PLASMA! DUH

ways 2 preserve food
remeber:
FISH-P
FREEZE
IRRADIATE
SALT
HEAT
PICKLING

TUBERCULOSIS....
CAUSED-mycobacterium tuberculosis
trabsported in droplets breathes coughed-tranmission in MILK :redface:

from cattle with mycobaterium BOVIS

how can spread of HIV/ADIS/TB/MALARIA BE CONTROLLED?
self explanotery except tb
tb-antibiotics-BCG vaccine

thats it so far brb i need a break :frown:

ACTION OF B AND T LYMPHS

B LYMPH
Specific binding-lymph with antbody binds 2 complementary antigen
Clonal selection-stimulated lymph DIVIDIES INTO :
1.Memory cells- later memory
2.Plasma cells - secrete anti bodies

T LYMPH
Antigen presenting cells present antigen and say "ITS HERE"
Specific binding
Clonal selection
Killer - binds 2 cells-make memory or kills cell
Helper - secerte cytokines which stimulate pahgocutisis - and also make moeory cells

structure of antibody
variable region- antigen bindng site
constanst region-
heavy polypeptide
light polypeptide
disulphde bonds

WHAT IS A VAAACCINNEE??
conatin antifens 2 stimulate active imunity

smoking :cool:

jk

Tar- destroy cilia-goblet cells secrete mucus-CHRNIC BRNCHITIS AND EMPHYSEMA

Carbon Monoxide- in blood-comibens wih haemoglobin 2 form carboxyhaemolglbin -starves heart muscle of o2

Nicotine-in blood-increases BP-blood clots-damages artery walls

chronic bronchitis-iflamed lining-smooth muscle layer thickens
symtoms-shortness of breath-wheeeeezing-persistant cough

emphysema-alveoli overstetch, lose elasticity, fewer elastic fibres-smaller Surface area
sumtoms-shortnes of breath
hard to breath OUT OUT OUT not in!! OUTTTT
use a mask 2 breathe

lung cancer-bronchi bkocked by cancerois growth
sumtoms- coughingg up BLOOD, WEIGHT LOSS, PERISSTANT COUGH

now all the BORING BORINGG BORINGG stuff starts :frown:

DEFINE BIODIVERSITY
variety of habitats,communities,species in an area. GENETIC VARATION WITHIN A POPULATION

DEFINE: TAXONOMY, PHYLOGENY, CLASSIFICATION
TAXONOMY-science of clasifying organisms
PHYLOGENY-evolutionary history of a group of organism
CLASSIFICATION-grouping organisms in2 groups accorind to their similarited and differences.

HIERACHY OF TAXA
Kingdom-smallest number of similarities -largest group-distantly shared ancestors
Phylum
Class
Order
Family
Genus
Species-largest number of similarites-smllest group-share a common ancestpr increadingly recently

characteristic features of kingdoms
REMEMBER FAPPP
FUNGI-chitin cell wall-non-photosynthetic-have absorbitve methods of feeding :s
e.g. mushroom

ANIMLAIA-multi cellular, non-photosnthtic- have nervous conditions
e.g. us! :smile:

fish reptiles worms etc

PROKAARYOTAE-lack nuclei-membrane bound oragnelles-DNA is circular
e.g. bacteriaaaa

PROTOCTISTA-eukaryotes- onecelled- some r autotrophic (does not require organic nutrients)- and some r heterotrophs (requires organic nutrients)

PLANTAE- eukaryotic- photosynthetic autrophs -cellulose walls-non motile
e.g. mosees, ferns, ROSES :smile:

3 domain classification
ARCHEA, BACTERIA, EUKARYOTA
domain above kingdom, introd. coz bactera can be divided into 2 large groups coz of features such as ribsomal rna , flagella

define : VARIATION
diffs between organisms. btween species and withing
between species- CAUSED BY DIFFS IN GENES
wothin speices- CAUSED BY DIFFS IN ALLELES OF THAT GENE OF THAT SPECIES

define SPECIATION
production of a new species.

Reply 24

Dr Acula

Mariyah

My friend sent the January paper to me yesterday.
I've just uploaded it here;

http://www.4shared.com/document/j3hWoyf_/4_AS_Bio_F212_Exam_Paper_Jan10.html

http://www.4shared.com/document/bICHxTrr/6_AS_Bio_F212_Mark_Schemes_Jan.html

btw thanks so much to the person posting the notes over the spec, huge help :smile:

Ahhhh you actual legend, have been looking for this paper!, thank you muchos!

Reply 25

Dr Acula

786girl

the following is all the revision i have done for 2moro, i thought it would help some people aswell as my self :frown:

Wow, this is helpful! Thanks for putting it up, shall rep asap :yep:

Reply 26

Hoomz

Describe the structure and mode of action of T lymphocytes and B lymphocytes, including the significance of cell signalling and the role of memory cells.

Does anyone have a way to remember this? It just doesn't seem to stick in my mind :frown:

Reply 27

Acta Non Verba

Thanks for all the comments, hopefully the notes do help you in your exams.

BUT, I noticed a huge error that you should be careful of. I think it's on page two, that there's something along the lines of 'compare the structure/function of glucose and cellulose'

It shouldn't say glucose, it should say starch

As for the mode of action of T and B cells:

1) A phagocyte will detect a pathogen within the body. Now a few things will take place.
- The phagocyte will move towards the pathogen via a process called chemotaxis. (Basically, pathogens give off certain chemicals and the phagocyte can detect them)
- The phagocyte sticks the pathogen onto its membrane
- Then endocytosis takes place. The pathogen is now within the phagocyte inside a phagocytic vacuole.
- The phagocyte may release enzymes or free radicals which will kill the pathogen.
- Now lysosomes will digest the pathogen.
- the phagocyte will now present the antigens of the pathogen, this is an example of cell signaling and triggers the immune response

2)This will active T cells. The first process that takes place is clonal selection

- Clonal selection is the process by which a suitible T cell is found. (i.e, one that has a complementary antigen receptor to that of the pathogen which the phagocyte detected in 1) )

- Once we've found the right T cell we need to make more of them. This process is called clonal expansion, by which the T cells divide by mitosis.

- The next relevent thing that happens is that T helper cells active B lymphocytes via cell signaling

- These B cells will go under the same processes as the T cells, i.e clonal selection and clonal expansion.

- And now, once all that is done, the B cells differentiate into memory cells and plasma cells. Plasma cells secrete antibodies into the blood.
So too do memory cells, but these memory cells stay around a lot longer and provide an immunological memory.

Reply 28

DR_X

Do anybody have OCR F212 Biology Jan 2010 Mark scheme?.......rep?....

Reply 29

volvicstar

what is neutralisation and aggultination?

i know its to do with antibodies but why does this process happen instead of the t and b lymphocyets?

Reply 30

volvicstar

what is neutralisation and aggultination?

i know its to do with antibodies but why does this process happen instead of the t and b lymphocyets?

Reply 31

Acta Non Verba

volvicstar

what is neutralisation and aggultination?

i know its to do with antibodies but why does this process happen instead of the t and b lymphocyets?

It's the antibodies that bring the pathogens to these cells so that they may be digested or gotten rid of in whatever way.

Antibodies are able to get together multiple pathogens and bring them to the cells, which speeds up the process of getting rid of the pathogen.

EDIT:

Didn't really explain it well.

Neutralisaton is when multiple antibodies will bind to the viral binding sites of pathogens, blocking them from emitting toxins.

Aggulation on the other hand is when antigens bind to multiple pathogens.

http://scienceaid.co.uk/biology/micro/images/antibodyantigen.png

Reply 32

volvicstar

Acta Non Verba