Edexcel A2 Biology Unit 5 (6BIO5) - 22/06/2011- OFFICIAL THREAD !

dear anybody that can help (:

does anyone understand the process of bleaching of the photopigment rhodopsin. what happens when the molecule is split, i know that the events that follow bleaching arnt the same as an action potential in which Na channels open --> depolarisation occurs. in bleaching, it causes Na channels close and hyperpolarisation occus?... little confused about this how does this work. if anyone could clear this up for me would be grateful

Reply 2221

abuelzouz

Original post by darkiee

you havent read anything have you? Its in the freaking article, you better start your revision

noo i did read article long time ago.. now i just finished going through expected questions...feeling much confident..

Reply 2222

BustyLaRouge

Original post by ethiokid

what would you write for that question? I sounds hard.....

I'll find my mock, she wrote one up for us. I'll find the answers for you

Reply 2223

abuelzouz

Original post by care3ash

dear anybody that can help (:

does anyone understand the process of bleaching of the photopigment rhodopsin. what happens when the molecule is split, i know that the events that follow bleaching arnt the same as an action potential in which Na channels open --> depolarisation occurs. in bleaching, it causes Na channels close and hyperpolarisation occus?... little confused about this how does this work. if anyone could clear this up for me would be grateful

this ispretty easy because you just have to memorize steps
1) a photon of light hits a molecule of rhodopsin
2)rhodopsin is broken down to retinal and opsin
(retinal which is a derivative of Vitamin A and opsin which is a lipoprotein)
3)retinal changes form form cis to rans (this changes shape of retinal)
this is bleaching
4) bleaching cause a change in permeability of cell membrane of rod to Na ions so Na channel closes (hyperpolarisation)
5) Bipolar cells become depolarised
6)Action potential formed in ganglion cell

hope this helped

Reply 2224

abuelzouz

dear bio peeps,
as i might be lucky and u might see this (&reply) , i am going to post all my questions regarding nervous system/brain part (as I just finished revising it)
i really hope you help.. even if only 1 question..
:smile:

1)Do we have to know excitory/inhibitory post synaptic potential ??
2) Do we have to knowo effect of each drug on neurotransmitters, such as table in page 209 if you have green book..???
3) There is a difference between accommodation and habituation.. can you plz simplify it for me??
4) what about primary/secondary receptors? do we need to know them?
5) Last thing: page 239 green book; (habituation, conditional reflexes, tiral and error learing and imprinting... do we have to know these ALSO???

thank u a lot :smile:

Reply 2225

care3ash

Original post by abuelzouz

this ispretty easy because you just have to memorize steps
1) a photon of light hits a molecule of rhodopsin
2)rhodopsin is broken down to retinal and opsin
(retinal which is a derivative of Vitamin A and opsin which is a lipoprotein)
3)retinal changes form form cis to rans (this changes shape of retinal)
this is bleaching
4) bleaching cause a change in permeability of cell membrane of rod to Na ions so Na channel closes (hyperpolarisation)
5) Bipolar cells become depolarised
6)Action potential formed in ganglion cell

hope this helped

cheers for replying bro. i got up to step 4, but how does hyperpolarisation of the cell make the bipolar cells depolarised? i dnt get that bit. or do we not have to explain that? if not, then its kl

Reply 2226

yagmurainie

In salters nuffield book on page 183 about vigarous exercise it says that inflammatory response occurs in muscles due to damage to muscle fibers caused by heavy exercise,this may reduce the available non-spesific immune response against URT infections. How does inflammation reduce non-spesific immune response? I'm confused :confused:

Reply 2227

abuelzouz

Original post by care3ash

cheers for replying bro. i got up to step 4, but how does hyperpolarisation of the cell make the bipolar cells depolarised? i dnt get that bit. or do we not have to explain that? if not, then its kl

i mean when neurotransmitter substances are released into synapse with the bipolar cell

hyperpolarization occur when Na ions chain close, fewer Na ions in rod cell,interior becomes more negative than usual

:smile:

cheers bro

Reply 2228

BustyLaRouge

Original post by ethiokid

what would you write for that question? I sounds hard.....

"Gym in a bottle discusses the solutions of three different research groups to solve the problem of muscular atrophy. Scientists often propose different solutions to the same problem ad then evaluate the evidence before exploring the most effective. Evaluate the three solutions suggested, considering the similarities and differences in their approaches"
Was the question we got given in our mock: idiot me didn't write down all the answers so i'll just pick out some sentences I got marks for.
"Goldberg and the Regeneron team associate their focus with turning on and off genes"
"Similarly to the purdue team, Goldberg has identified erg1a as a source of atrophy, but in combination with Foxo"
"Wyeth of Madison, have different findings that both Goldberg and the Purdue teanm. They feel to stop atrophy is not to prevent it, but to coax muscle growth. Therefore instead of the risk of creating long QT syndrome, like the purdue team, the wyeth of madison company has avoided this risk"
"wyeth of madison are doing human trials, whereas both Goldberg and the Purdue team are still working with mice"

Hope this helped with ideas of what could come up and how to answer it. But don't just like take it on my word, could be wrong, but is a good place to start

(edited 12 years ago)

Reply 2229

care3ash

Original post by abuelzouz

dear bio peeps,
as i might be lucky and u might see this (&reply) , i am going to post all my questions regarding nervous system/brain part (as I just finished revising it)
i really hope you help.. even if only 1 question..
:smile:

1)Do we have to know excitory/inhibitory post synaptic potential ??
2) Do we have to knowo effect of each drug on neurotransmitters, such as table in page 209 if you have green book..???
3) There is a difference between accommodation and habituation.. can you plz simplify it for me??
4) what about primary/secondary receptors? do we need to know them?
5) Last thing: page 239 green book; (habituation, conditional reflexes, tiral and error learing and imprinting... do we have to know these ALSO???

thank u a lot :smile:

1) its not that hard to remember, you know it now lool. just remember that the neruotransmitters bind to specific receptors which change the permeability of Na ions to the post synaptic membrane, this creates an EPSP. if EPSP is greater than threshold, an action potential is initiated.

3) accomodation is when the rate at which impulses arrive at the presynaptic knob is greater than the rate at which the vesicles containing neurotransmitters can be resynthesised- the neurone becomes fatigued or accomodated.

habituation is when the calcium channels become less responsive due to repeated stimulation. therefore less neruotransmitter is released

4) primary receptors are just neurones with dendrites specific to particular stimulus. secondary receptors are specialised cells its not too hard to remember, id remember it anyway just in case.

5) this chapter is alot of bull**** so dnt worry about it u can waffle ur way through it, id be more concerned about respiration and nervous system which are the hardcore chapters lol

Reply 2230

chemdweeb1234

Original post by yagmurainie

In salters nuffield book on page 183 about vigarous exercise it says that inflammatory response occurs in muscles due to damage to muscle fibers caused by heavy exercise,this may reduce the available non-spesific immune response against URT infections. How does inflammation reduce non-spesific immune response? I'm confused :confused:

Releasing hormones like adrenaline and cortisol that could chemically prevent the action of cytokines? im guessing here

Reply 2231

Parthenon93

7

I remember doing something about how transcription factors all need to be present to get a gene to translate ... and how transcription factors attach to a region adjacent to the gene ...

Now I can't find where I read it! :eek:

Help anyone?

Reply 2232

BustyLaRouge

Original post by abuelzouz

dear bio peeps,
as i might be lucky and u might see this (&reply) , i am going to post all my questions regarding nervous system/brain part (as I just finished revising it)
i really hope you help.. even if only 1 question..
:smile:

1)Do we have to know excitory/inhibitory post synaptic potential ??
2) Do we have to knowo effect of each drug on neurotransmitters, such as table in page 209 if you have green book..???
3) There is a difference between accommodation and habituation.. can you plz simplify it for me??
4) what about primary/secondary receptors? do we need to know them?
5) Last thing: page 239 green book; (habituation, conditional reflexes, tiral and error learing and imprinting... do we have to know these ALSO???

thank u a lot :smile:

1) Think you should know this, it's only a tiny bit I wrote down :smile:

2) No i don't think so, I drew the diagram on page 242 which shows how a drug could effect neurotransmitters
3) It's similar - habituation (See diagram on 240) is when Ca2+ channels become less responsive so less ca2+ crosses presynaptic membrane. Accommodation is when the vesicles can't be remade fast enough to send an impulse.
4)Know the difference between the two
5) Asked my teacher about this today, she said it's good to know the definitions of them, but other than that no.

Hope this helped

Reply 2233

yagmurainie

Original post by chemdweeb1234

Releasing hormones like adrenaline and cortisol that could chemically prevent the action of cytokines? im guessing here

Yeap you're right but it says inflammatory response too.. whats the point of that?

Reply 2234

TheBigI

Original post by Parthenon93

I remember doing something about how transcription factors all need to be present to get a gene to translate ... and how transcription factors attach to a region adjacent to the gene ...

Now I can't find where I read it! :eek:

Help anyone?

In the salters nuffield book it is page 190-191 :smile:

Reply 2235

abuelzouz

Original post by care3ash

1) its not that hard to remember, you know it now lool. just remember that the neruotransmitters bind to specific receptors which change the permeability of Na ions to the post synaptic membrane, this creates an EPSP. if EPSP is greater than threshold, an action potential is initiated.

3) accomodation is when the rate at which impulses arrive at the presynaptic knob is greater than the rate at which the vesicles containing neurotransmitters can be resynthesised- the neurone becomes fatigued or accomodated.

habituation is when the calcium channels become less responsive due to repeated stimulation. therefore less neruotransmitter is released

4) primary receptors are just neurones with dendrites specific to particular stimulus. secondary receptors are specialised cells its not too hard to remember, id remember it anyway just in case.

5) this chapter is alot of bull**** so dnt worry about it u can waffle ur way through it, id be more concerned about respiration and nervous system which are the hardcore chapters lol

thnx bro for replying!

Reply 2236

sangeen yahya

to be honest id me more worried bout the supposed bull **** airy fairy stuff, it seems to be more hsw generally and as of late edexcel, they seem to love hsw lol

Reply 2237

rf1993

1

Original post by yagmurainie

Yeap you're right but it says inflammatory response too.. whats the point of that?

Basically, the non-specific response requires certain resources like neutrophils etc. There's only limited amounts so if there's an inflammatory response in muscles, it reduces the amount of white blood cells available to other areas (I think :colondollar: