Biochemistry, cell biology, and genetics question thread

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Nutmeg

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All users may post questions about MCAT, DAT, OAT, or PCAT cell/molecular biology, genetics, and biochemistry here. Anatomy, physiology, development, embryology, and evolution questions should be posted in the other biology thread. We will answer the questions as soon as we reasonably can. If you would like to know what biology topics appear on the MCAT, you should check the MCAT Student Manual (http://www.aamc.org/students/mcat/s...anual/start.htm)

Acceptable topics:
-general, MCAT-level biology.
-particular MCAT-level biology problems, whether your own or from study material
-what you need to know about biology for the MCAT
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-how best to tackle the MCAT biological sciences section

Unacceptable topics:
-actual MCAT questions or passages, or close paraphrasings thereof
-anything you know to be beyond the scope of the MCAT

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If you really know your cell/molecular biology, I can use your help. If you are willing to help answer questions on this thread, please let me know. Here are the current members of the Cell/Molecular Biology Team:

-Nutmeg (thread moderator): My background is in neurobiology. Please note that I am nocturnal, and generally only post between the hours of 10pm and 8am PST.

I'm going to make this thread a bit different than the others, because the material covered in the BS section is a bit different. With o-chem, gen-chem, and physics, there are a number of core concepts to understand. While there is also a lot of that in the BS, there is also a great deal of specific knowledge involved in this section (relative to the others). Test questions often introduce an experimental set-up, asking for either expected results or the interpretation of results. As such, passages might relate to advanced concepts that you are not expected to know coming into the test, and that they will explain in the passages. Any familiarity that you have with these concepts will make the test easier.

While in general this forum is designed for people studying for the MCAT, I welcome any questions relating to molecular biology, even though they might be beyond the scope of the MCAT. I know some people also like to use these threads to get help on homework questions, and I welcome that, too.

-LT2: LT2 is finishing her MS in microbiology.

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hi:)

just confused by why unsaturated fats would be considered to lower the melting temp., and increase membrane fluidity since they're the ones with the double bonds. I've always been under the impression that double bonds meant more stability, hence higher melting points...etc...

thanks in advance:)
 
hi:)

just confused by why unsaturated fats would be considered to lower the melting temp., and increase membrane fluidity since they're the ones with the double bonds. I've always been under the impression that double bonds meant more stability, hence higher melting points...etc...

thanks in advance:)
Think about the 3d structure... because of the double bond there is a "kink" in the fatty acid. The kink means it takes up more space and the fats aren't able to pack as tightly. This increases membrane fluidity (is that a word? You know what I mean ;) )

As far as melting point, same logic applies. Unable to pack at tightly, so less organized structure, disrupting intermolecular bonds and meaning less energy is required to break those forces and a lower melting point.

Does that make sense?
 
Think about the 3d structure... because of the double bond there is a "kink" in the fatty acid. The kink means it takes up more space and the fats aren't able to pack as tightly. This increases membrane fluidity (is that a word? You know what I mean ;) )

As far as melting point, same logic applies. Unable to pack at tightly, so less organized structure, disrupting intermolecular bonds and meaning less energy is required to break those forces and a lower melting point.

Does that make sense?

yep, very much so...thank you:):luck:
 
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Think about the 3d structure... because of the double bond there is a "kink" in the fatty acid. The kink means it takes up more space and the fats aren't able to pack as tightly. This increases membrane fluidity (is that a word? You know what I mean ;) )

As far as melting point, same logic applies. Unable to pack at tightly, so less organized structure, disrupting intermolecular bonds and meaning less energy is required to break those forces and a lower melting point.

Does that make sense?

you might know this, but I was just curious. I was messing around on google looking for some concepts when I ran across this:

"In many viruses, the capsid is the virion. Such virions are called "naked" virions. In such virions, the capsid proteins must contain the virus receptors capable of recognizing receptors on the surface of the cell for adsorption, penetration, and entry to occur. "

Do you have any idea what they mean when they say the capsid is the virion? isn't it like this in all cases? Or am I just confused about something?

Thank you so much for being patient with me, you're the best!:love:
 
you might know this, but I was just curious. I was messing around on google looking for some concepts when I ran across this:

"In many viruses, the capsid is the virion. Such virions are called "naked" virions. In such virions, the capsid proteins must contain the virus receptors capable of recognizing receptors on the surface of the cell for adsorption, penetration, and entry to occur. "

Do you have any idea what they mean when they say the capsid is the virion? isn't it like this in all cases? Or am I just confused about something?

Thank you so much for being patient with me, you're the best!:love:
That's oddly worded but what I think they mean is that some viruses will have another membrane (often made of modified pieces of the host's cell membrane)...

from Wikipedia:
Enveloped viruses
In addition to a capsid some viruses are able to hijack a modified form of the cell membrane surrounding an infected host cell, thus gaining an outer lipid layer known as a viral envelope. This extra membrane is studded with proteins coded for by the viral genome and host genome, however the lipid membrane itself and any carbohydrates present are entirely host-coded. The common Influenza virus uses this strategy.

The viral envelope can give a virion a few distinct advantages over other capsid-only virions, such as protection from enzymes and chemicals. The proteins studded upon it can include glycoproteins functioning as receptor molecules, allowing healthy cells to recognise these virions as "friendly", resulting in the possible uptake of the virion into the cell. Some viruses are so dependent upon their viral envelope that they fail to function if it is removed.
 
hello,
i encountered a question about blood's buffering capacity in relation to bicarbonate buffering system in one of the kaplan;s exams.
here's the quick recap of the idea:

*Increasing the total volume of blood will increase blood's buffering capacity.
*Increasing only bicarbonate will no do anything to the buffering capacity, but it will increase the basicity of blood.
*The same is with H+, it will not affect the capacity, just will increase the acidity of blood.

I realize that the more volume there is the more difficult it is to change the pH by adding acid or base. But Are there any other factors that effect blood's buffering capacity??????
I also think that increasing both absolute concentration of buffer A- (conj acid) and HA (buffer acid) will increase buffering capacity. Is this true?


thank you very much in advance :)


To affect the buffering capacity the blood needs carbonic acid, not just one if its components (bicarbonate or H+). Also more blood = more carbonic acid hence the more buffering capacity. In theory you could add more buffer to blood to increase its capacity too....just make sure you add carbonic acid. A good buffer needs to give and take. A conjugate Base, A- as you put it, has no free hydrogens so it can't help lower pH. Only the actual acid itself will both donate and accept hydrogens at the desired pHs.
 
What is the difference between Kinetochore and centromere? Centromere is a repeated dna seq in the middle zone of the dna that allows attachment of kinetochore (protein?)? Is kinetochore protein? my genetics book says its combo of prot and dna but i don't understand because centromere is the dna. and also it says that kinetochore has motor proteins that moves chromosome to the end pole. but i thought it was mitotic spindle that fastens to the kinetochore and pulls toward both ends, thereby separating sister chromatids during mitosis. any help would be greatly appreciated!
 
What is the difference between Kinetochore and centromere? Centromere is a repeated dna seq in the middle zone of the dna that allows attachment of kinetochore (protein?)? Is kinetochore protein? my genetics book says its combo of prot and dna but i don't understand because centromere is the dna. and also it says that kinetochore has motor proteins that moves chromosome to the end pole. but i thought it was mitotic spindle that fastens to the kinetochore and pulls toward both ends, thereby separating sister chromatids during mitosis. any help would be greatly appreciated!
The kinetochore does have motor proteins... think of the mitotic spindle as an anchor with a rope (the rope being the microtubules). The kinetochore is like a man climbing up the rope - he's actually putting force on the rope to move himself along. (the kinetochore also breaks down the microtubule as it goes along).

It was explained in my genetics class that the kinetochore is defined as the proteins and the associated centromere DNA (so the definition encompasses both). But this is according to my professor and I haven't validated that with an outside source. As it is, it's a pretty semantic distinction and I doubt it would turn up on the MCAT.

The concept that the kinetochore is actually responsible for the movement of the chromosomes is a concept you should have down though. I can see that possibly being tested.
 
Just 2 quick questions:)

If we disable the Na/K pump, Na will build up in the cell, and it will eventually depolarize on its own, since it's not being thrown out of the cell through that pump. The K on the other hand will build up outside the cell, since it's not being taken into the cell, obviously.

My questions. That Na building up in the cell, where is it coming from? That K outside of the cell that has to be taken into the cell, where is it coming from?

Thanks in advance.
 
Just 2 quick questions:)

If we disable the Na/K pump, Na will build up in the cell, and it will eventually depolarize on its own, since it's not being thrown out of the cell through that pump. The K on the other hand will build up outside the cell, since it's not being taken into the cell, obviously.

My questions. That Na building up in the cell, where is it coming from? That K outside of the cell that has to be taken into the cell, where is it coming from?

Thanks in advance.

Na and K are both diffusing down their electrochemical gradients. The sodium that is entering the cell is coming from the extracellular space and the potassium leaving the cell is coming from the inside of the cell, going to the outside.

The Na/K pump simply works to maintain electrochemical potential accross the cell.

I'm a little confused by your question. Does this answer it at all?
 
Na and K are both diffusing down their electrochemical gradients. The sodium that is entering the cell is coming from the extracellular space and the potassium leaving the cell is coming from the inside of the cell, going to the outside.

The Na/K pump simply works to maintain electrochemical potential accross the cell.

I'm a little confused by your question. Does this answer it at all?

thanks for the reply:)

I guess I didn't word the question too well...i'm sorry...

what you're saying is right...that's why we have the pump, so it can take the Na and K against their gradients.

You just said that the Na diffusing into the cell, i.e. going from the extracellular to inside, and that the K is going from inside to outside, assuming that the pump isn't working of course.

Now my question is this: WHERE is that Na coming from? The cell seems to be producing a lot of Na outside the cell, where is that Na coming from? The second question is where is that K coming from? The cell seems to have a lot of K inside it that its producing constantly, where is it coming from?

Thank you so much for your time...
 
thanks for the reply:)

I guess I didn't word the question too well...i'm sorry...

what you're saying is right...that's why we have the pump, so it can take the Na and K against their gradients.

You just said that the Na diffusing into the cell, i.e. going from the extracellular to inside, and that the K is going from inside to outside, assuming that the pump isn't working of course.

Now my question is this: WHERE is that Na coming from? The cell seems to be producing a lot of Na outside the cell, where is that Na coming from? The second question is where is that K coming from? The cell seems to have a lot of K inside it that its producing constantly, where is it coming from?

Thank you so much for your time...

So where does the Na and K originate? From your diet... the cell isn't creating Na or K out of nothing, it is ingested by you. Your body is in a constant state of osmoregulation, where it excretes salt (NaCl and KCl, primarily) and consumes salt, maintaining the ideal extracellular concentrations. Your cell then utilizes the fact that Na and K are in your extracellular fluid to store energy via its Na/K pump..well you know the rest.

The very nature of cellular function depends in a large part on having salts in the internal/surrounding fluids. Your question is almost philosophical- to me, at least).

Somehow I don't think this is the answer you are looking for...
 
So where does the Na and K originate? From your diet... the cell isn't creating Na or K out of nothing, it is ingested by you. Your body is in a constant state of osmoregulation, where it excretes salt (NaCl and KCl, primarily) and consumes salt, maintaining the ideal extracellular concentrations. Your cell then utilizes the fact that Na and K are in your extracellular fluid to store energy via its Na/K pump..well you know the rest.

The very nature of cellular function depends in a large part on having salts in the internal/surrounding fluids. Your question is almost philosophical- to me, at least).

Somehow I don't think this is the answer you are looking for...

thanks!:)

haha, I didn't think it would be percieved as philosophical... i just finished studying for the bio, and I was asking myself why there's excess Na inside the cell and excess K outside the cell, and not the other way around. I guess I was just making sure there wasn't some cycle/pathway i'm missing, etc.

I guess you did answer the question though, thank you:)
 
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thanks!:)

haha, I didn't think it would be percieved as philosophical... i just finished studying for the bio, and I was asking myself why there's excess Na inside the cell and excess K outside the cell, and not the other way around. I guess I was just making sure there wasn't some cycle/pathway i'm missing, etc.

I guess you did answer the question though, thank you:)

No problem. I think it's also important to point out that if all chemical species were allowed to move freely across the membrane, they would do so until there were equal concentrations of all species on each side and no electric potential difference across the membrane. This is characteristic of a dead cell.

Your question of why the cell excludes Na and pulls in K and not the other way around has a better answer, or at least a good insight. I think I read something about it in my MCB textbook. Maybe someone else can provide a little info.

What you know about the Na/K pump should be fine for any undergrad bio class and the MCAT.
 
this is the reason why NaK pumps are selective

this is taught in inorganic chemistry :) so MCAT probably won't need you to know it.

Na is smaller than K, right? not really, if you were to meet Na+ in person.

Na+ is stuck to 6 water molecules in real life

the hole in the K+ transporter protein is just big enough to admit K+, which is completely dehydrated to be admitted through the channel.

but Na+ (H2O)6 is too big

so Na+ does not get through.
 
I am looking at a picture of chromosomes just after meiosis I+II and they have one single sister chromatid each homologue. But autosomes and sex chromosomes show X and Y which are two sister chrmatids connected by centromeres, right? I dont understand how we go from homologous chromosomes, each of which consists of two sister chromatids (like X and Y), to homologous chromosomes consisting of one chromatid (like | instead of X).... I am so...confused...please enlighten me......thank you!:confused:
 
this is the reason why NaK pumps are selective

this is taught in inorganic chemistry :) so MCAT probably won't need you to know it.

Na is smaller than K, right? not really, if you were to meet Na+ in person.

Na+ is stuck to 6 water molecules in real life

the hole in the K+ transporter protein is just big enough to admit K+, which is completely dehydrated to be admitted through the channel.

but Na+ (H2O)6 is too big

so Na+ does not get through.

Na is smaller than K, and this poses and interesting question: how is the K channel (this is facilitated diffusion we're talking about here) selective?

It's not that hydrated Na is too big, it's that once it's dehydrated, it's not big enough. It takes energy to dehydrate both K and Na, but since K is a little bigger, it interacts with the amino acid side chain/backbone residues that form the inside of the channel protein more efficiently than Na does. This is simply due to the size difference.

The more efficient K interaction results in a negative delta G for its dehydration and movement through the channel protein, whereas with sodium, this is not true.

This is how the K channel is selective for only potasium.

You won't need to know this for the MCAT, but you will undoubtedly learn about it in your medical school biochemistry class.
 
I am looking at a picture of chromosomes just after meiosis I+II and they have one single sister chromatid each homologue. But autosomes and sex chromosomes show X and Y which are two sister chrmatids connected by centromeres, right? I dont understand how we go from homologous chromosomes, each of which consists of two sister chromatids (like X and Y), to homologous chromosomes consisting of one chromatid (like | instead of X).... I am so...confused...please enlighten me......thank you!:confused:

nobody can pull you over and give you a ticket for saying that a chromosome with 1 chromatid and a chromosome with two chromatids are the same thing :) it is legal to say that.

it is helpful to think in terms of what meiosis and mitosis must accomplish.

Mitosis must create two cells each with the same amount of DNA as the original cell.

Meiosis must create 4 cells each with half the amount of DNA as the original cell.

therefore - both procedures must initially double the amount of DNA.

in humans, haploid number = 23, diploid number = 46

So, to create two diploid cells from 1 diploid cells you must make 2 copies of each of the 46 chromosomes - 46*2 = 92. At this point, you see each chromosome contains 2 chromatids. At the end of mitosis, each chromosome is split in two - creating 2N = 46 again.

To create four haploid cells from 1 diploid cell you must make 2 copies of each of the 46 chromosomes - 46*2 = 92 as well. At this point, you see each chromosome contains 2 chromatids. At the end of meiosis, each chromosome is split in two TWICE - creating 92/2 = 46, 46/2 = 23. Now you see each chromosome contains 1 chromatid. However, you ALSO see that each cell only has 1 allele of each of the genes.

happy to explain you more if you would like more :)
 
Hi there, there’s something renal confusing me I was hoping you could help me with. Thanks in advance:)

Amino Acids are absorbed in the proximal tubule by a secondary active transport mechanism down the concentration gradient of sodium. A high protein diet would most likely lead to…
Answer: An increase in glomerular filtration rate and renal blood flow.

It’s question 131 on page 219 in the EK bio book. Although it’s passage-based, I would really like to know the reasoning behind it.

To increase the glomerular filtration rate, we’d have to increase the systemic pressure. How would an elevated level of proteins in our diet induce the elevation in systemic pressure (or the oncotic pressure for that matter)?

Another question I had was more of a general one. When we’re talking about secondary transport of something like, let’s say amino acids hitching a ride on sodium who’s going down its concentration gradient; now if we didn’t have any amino acids, the sodium is still going to be going to the other side. In this case, whether we increase or decrease the rate of amino acids, it’s not going to affect the rate of sodium transfer, right? So for example, sodium can be transferred alone to the other side, OR if amino acids are present, they can bind to it, and hitch a ride to the other side. If my reasoning valid?

Again, many thanks in advance for your time.

:)
 
this is the reason why NaK pumps are selective

this is taught in inorganic chemistry :) so MCAT probably won't need you to know it.

Na is smaller than K, right? not really, if you were to meet Na+ in person.

Na+ is stuck to 6 water molecules in real life

the hole in the K+ transporter protein is just big enough to admit K+, which is completely dehydrated to be admitted through the channel.

but Na+ (H2O)6 is too big

so Na+ does not get through.


I just noticed your reply about my previous question right now, thank you:)

:luck:
 
this is the reason why NaK pumps are selective

this is taught in inorganic chemistry :) so MCAT probably won't need you to know it.

Na is smaller than K, right? not really, if you were to meet Na+ in person.

Na+ is stuck to 6 water molecules in real life

the hole in the K+ transporter protein is just big enough to admit K+, which is completely dehydrated to be admitted through the channel.

but Na+ (H2O)6 is too big

so Na+ does not get through.

By the way, I was looking at your signature:

N'aie pas de regret
Fais moi confiance, et pense
A tous les no way
L'indifférence des sens
N'aie pas des regret
Fais la promesse,tu sais que
L'hiver et l'automne n'ont pu s'aimer

and I copied and pasted it in freetranslation.com, and I got this:

Have not any regret Does me confidence, and thinks HAS all the no way THE INDIFFERENCE of the direction HAVE not regrets Does the promesse,tu knows that THE WINTER and the fall were not able to like themselves

lol, those online translators suck I guess. Wold you be able to tell me what it means? Thanks!:love:
 
Hi there, there's something renal confusing me I was hoping you could help me with. Thanks in advance

Amino Acids are absorbed in the proximal tubule by a secondary active transport mechanism down the concentration gradient of sodium. A high protein diet would most likely lead to…
Answer: An increase in glomerular filtration rate and renal blood flow.

It's question 131 on page 219 in the EK bio book. Although it's passage-based, I would really like to know the reasoning behind it.

To increase the glomerular filtration rate, we'd have to increase the systemic pressure. How would an elevated level of proteins in our diet induce the elevation in systemic pressure (or the oncotic pressure for that matter)?

Another question I had was more of a general one. When we're talking about secondary transport of something like, let's say amino acids hitching a ride on sodium who's going down its concentration gradient; now if we didn't have any amino acids, the sodium is still going to be going to the other side. In this case, whether we increase or decrease the rate of amino acids, it's not going to affect the rate of sodium transfer, right? So for example, sodium can be transferred alone to the other side, OR if amino acids are present, they can bind to it, and hitch a ride to the other side. If my reasoning valid?

Again, many thanks in advance for your time.

1. to increase the glomerular filtration rate (up to a certain extent), you increase the pressure of the fluid before the glomerulus. Pressure P = MRT, and M = a concentration. So, if you have more amino acids, you have more concentration, and domino domino domino voila you get an increase in gfr.

2. sodium can be transferred alone yes. but not by the same protein that does coupled transport.

Don't have any regrets
Have confidence in me, and think
To all, the impossibilities
The indifference of the senses
Don't have any regrets
Make the promise, you know that
The winter and the autumn weren't able to love each other


you can see the music video it comes from here. It's the chorus of the song.
http://www.youtube.com/watch?v=RYzArhzCR54
 
1. to increase the glomerular filtration rate (up to a certain extent), you increase the pressure of the fluid before the glomerulus. Pressure P = MRT, and M = a concentration. So, if you have more amino acids, you have more concentration, and domino domino domino voila you get an increase in gfr.

2. sodium can be transferred alone yes. but not by the same protein that does coupled transport.

Don't have any regrets
Have confidence in me, and think
To all, the impossibilities
The indifference of the senses
Don't have any regrets
Make the promise, you know that
The winter and the autumn weren't able to love each other


you can see the music video it comes from here. It's the chorus of the song.
http://www.youtube.com/watch?v=RYzArhzCR54


I see what you mean... But I guess I'm sort of confused by something. What do you mean by "not the same protein" in coupled transport? So basically if there's no amino acids, sodium will use another protein to go towards the part where it's less concentrated? Here's another thing that's sort of throwing me off here, wikipedia says:

Co-transport also uses the flow of one solute species from high to low concentration to move another molecule against its preferred direction of flow. An example is the glucose symporter, which co-transports two sodium ions for every molecule of glucose it imports into the cell. It contains water and also has no ATP.

I'm confused because I thought ATP was used here, although it's used indirectly. However, if the sodium is simply diffusing, then no ATP s supposed to be used. Where exactly is the ATP being used then?

Thank you so much...and I love the song, I just put the link on my favorites.:)
 
there is a kind of protein who transports sodium down its concentration gradient in order to transport something else up its concentration gradients. These proteins do symport, never require ATP, but require both substrates (sodium + something) to work. The energy comes from the potential energy of the sodium gradient. They don't do anything if you just give them one of the substrates. There are other proteins that are called sodium channels, that transport sodium into the cell only without transporting other substances, from low to high concentration, expending some ATP in the process.

and yes like you mentioned there is another sort of protein that just lets sodium flow in passively without any energy expenditure. a sieve for sodium.
 
there is a kind of protein who transports sodium down its concentration gradient in order to transport something else up its concentration gradients. These proteins do symport, never require ATP, but require both substrates (sodium + something) to work. The energy comes from the potential energy of the sodium gradient. They don't do anything if you just give them one of the substrates. There are other proteins that are called sodium channels, that transport sodium into the cell only without transporting other substances, from low to high concentration, expending some ATP in the process.

and yes like you mentioned there is another sort of protein that just lets sodium flow in passively without any energy expenditure. a sieve for sodium.

thank you:)
 
EKs & TPR teach a clear straight forward distinction between the mechanism of action peptide & steroid hormones. The peptide hormones bind surface receptors. Their signal is said to be transduced intracellularly by some secondary messanger. Their rapid cellular response is some enzymatic modification of an existing molecule. Steroid hormones on the other hand bind their recptors in the cytoplasm & activate transcription. (Amino acid derivatitives are another story.)
My concern is about growth hormone & peptide growth factors signaling by the JAK-STAT pathway, the MAP kinase pathway, or other pathways leading to transcription. I believe growth hormone induces mitosis by the increased synthesis of cyclins by way of the JAK-STAT pathway.
Does anyone know the signaling pathway(s) of growth hormone? Is the EKs TPR model valid or overly simple? What's a reasonable framework to conceptualize the understanding needed for the MCAT?
 
EKs & TPR teach a clear straight forward distinction between the mechanism of action peptide & steroid hormones. The peptide hormones bind surface receptors. Their signal is said to be transduced intracellularly by some secondary messanger. Their rapid cellular response is some enzymatic modification of an existing molecule. Steroid hormones on the other hand bind their recptors in the cytoplasm & activate transcription. (Amino acid derivatitives are another story.)
My concern is about growth hormone & peptide growth factors signaling by the JAK-STAT pathway, the MAP kinase pathway, or other pathways leading to transcription. I believe growth hormone induces mitosis by the increased synthesis of cyclins by way of the JAK-STAT pathway.
Does anyone know the signaling pathway(s) of growth hormone? Is the EKs TPR model valid or overly simple? What's a reasonable framework to conceptualize the understanding needed for the MCAT?

I have never heard of the pathways you mentioned; I’m hoping we don’t have to know them for the real thing. I can tell you what I do know though:
It’s AKA somatotrophin, and it has two types of effects, direct and indirect.
The direct effect is when it binds to receptors on the outside, just like the rest of the peptide hormones. Eg. When it binds to receptors of adipocytes.
The indirect effect is when it has the liver secrete IGF-I – this happens in most cases when we’re talking about hgh. Other than that, I have no idea. I hope this helps:)
 
I see what you mean... But I guess I'm sort of confused by something. What do you mean by "not the same protein" in coupled transport? So basically if there's no amino acids, sodium will use another protein to go towards the part where it's less concentrated? Here's another thing that's sort of throwing me off here, wikipedia says:

Co-transport also uses the flow of one solute species from high to low concentration to move another molecule against its preferred direction of flow. An example is the glucose symporter, which co-transports two sodium ions for every molecule of glucose it imports into the cell. It contains water and also has no ATP.

I'm confused because I thought ATP was used here, although it's used indirectly. However, if the sodium is simply diffusing, then no ATP s supposed to be used. Where exactly is the ATP being used then?

Thank you so much...and I love the song, I just put the link on my favorites.:)

ATP might be used to maintain the concentration gradient, thus being indirectly used.
 
I have never heard of the pathways you mentioned; I’m hoping we don’t have to know them for the real thing. . . . .
I did not mean to imply one needs to know the JAK Stat or MAP kinase pathway. (& I'm sorry if I gave that impression.)
I currently teach the MCAT for TPR. Our review book states, ". . .Because peptide hormones modify the activity of existing enzymes in the cytoplasm, their effects are exerted rapidly . . . ". It suddenly stuck me that this seems to be an overly broad statement. Clearly, growth hormone and erythropoietin are peptide hormones that upregulate transcription.
I'll write to our research gurus & report anything of interest.
 
Two quick questions:)

You know how the vagus nerve decreases the heart rate, since the SA node is making the heart beat faster, etc. Is it valid to assume that when the sympathetic nervous system wants to stimulate the heart, i.e. make it beat faster, all it has to do is inhibit the vagus nerve?

My second question is in regards to respiration. If we hold our breath, what exactly happens? I know by holding my own breath, my heart is all of a sudden beating slower. Obviously, it’s still beating, so is the heart just pumping the blood into circulation pointlessly? In other words, the blood is going through the pulmonary circulation, and coming back to the heart with no change in it at all?

Many thanks in advance.:luck:
 
My second question is in regards to respiration. If we hold our breath, what exactly happens? I know by holding my own breath, my heart is all of a sudden beating slower. Obviously, it’s still beating, so is the heart just pumping the blood into circulation pointlessly? In other words, the blood is going through the pulmonary circulation, and coming back to the heart with no change in it at all?

Many thanks in advance.:luck:

Cellular respiration does not stop just because you hold your breath. Think about it, you are recirculating the CO2 that is in your blood stream so you are increasing the concentration of carbonic acid in your blood stream and throwing off your pH. The circulatory system is separate from your pulmonary system, which is why you can hold your breath and your heart wont stop beating. Your heart will just keep on pumping your blood through the system, your blood chemistry will be a little off though.
 
Cellular respiration does not stop just because you hold your breath. Think about it, you are recirculating the CO2 that is in your blood stream so you are increasing the concentration of carbonic acid in your blood stream and throwing off your pH. The circulatory system is separate from your pulmonary system, which is why you can hold your breath and your heart wont stop beating. Your heart will just keep on pumping your blood through the system, your blood chemistry will be a little off though.

thank you for the reply...:)

so, are you saying that the pulmonary venous blood will just pass the alveoli, with no changes, and simply return to the left side of the heart?
 
Hello,

I am having trouble with a practice question.."How many high energy phosphate bonds or equivalents are consumed to make cytoplasmic glucose from two molecules of DHAP (assume normal gluconeogensis)?

By looking at diagrams of gluconeogenesis it seems to me the answer would be 0. The last 3 steps to yield glucose from DHAP involve H20 in and inorganic phosphate out..I do not see where anything is consumed..

Thanks for the help
 
I think you are correct. There are 2 phosphates yielded from DHAP to glucose, but none consumed. Does your answer source say different?



Hello,

I am having trouble with a practice question.."How many high energy phosphate bonds or equivalents are consumed to make cytoplasmic glucose from two molecules of DHAP (assume normal gluconeogensis)?

By looking at diagrams of gluconeogenesis it seems to me the answer would be 0. The last 3 steps to yield glucose from DHAP involve H20 in and inorganic phosphate out..I do not see where anything is consumed..

Thanks for the help
 
thank you for the reply...:)

so, are you saying that the pulmonary venous blood will just pass the alveoli, with no changes, and simply return to the left side of the heart?

possibly, but I think more likely there will be gas exchange even while the breath is held - tidal volume is generally less than 10% of lung capacity, so there is probably more oxygen around at least for a while.

can someone knowledgeable pls confirm or add?
 
For all of the pre-health tests (MCAT, PCAT, DAT, and OAT), you should be able to follow the generation of ATP in each step, and also the energy carrier reduction (NAD and FAD) in each stage. You do NOT need to memorize any enzymes or pathway intermediates; they will make you do that in your professional school biochem class. You should also know that oxygen is the final electron acceptor of the electron transport chain, and that anaerobic respiration is insufficient to sustain human life. In addition, fermentation produces lactic acid as a byproduct in humans, and ethanol in yeast. Finally, you should know where in the cell each stage of respiration occurs. Here is a list of the energy conversions for each stage and where in the cell they take place:

Glycolysis: (anaerobic, occurs in the cytoplasm)
  • 2 net ATP (4 total made, but 2 needed to complete this stage)
  • 2 NADH produced (making 4 ATP in ETC for eukaryotes and 6 ATP for prokaryotes)
Fermentation: (anaerobic, occurs in the cytoplasm)
  • 0 ATP; its main purpose is to reoxidize the NADH produced in glycolysis
Pyruvate Decarboxylation: (aerobic, occurs in the cytoplasm for prokaryotes, mitochondrial matrix for eukaryotes)
  • 0 ATP produced
  • 2 NADH produced (making 6 ATP in ETC)
TCA Cycle: (aerobic, occurs in the cytoplasm for prokaryotes, mitochondrial matrix for eukaryotes)
  • 2 ATP produced
  • 6 NADH produced (making 18 ATP in ETC)
  • 2 FADH2 produced (making 4 ATP in ETC)
Electron Transport Chain (ETC): aerobic, occurs across the inner cell membrane for prokaryotes, inner mitochondrial membrane for eukaryotes
  • NADH oxidation back to NAD and FADH2 oxidation back to FAD occur along with ATP production, allowing the earlier stages to continue
Summary: 36 net ATP produced in eukaryotes, 38 net ATP produced in prokaryotes (because the electrons from the NADH produced from pyruvate decarboxylation do not have to be transported across the mitochondrial membrane in prokaryotes; doing this causes a net loss of two ATP in eukaryotes)



So you're saying we don't need to know the detailed steps involved in each of these processes? For instance, in Glycolysis, Glucoses goes to Glucoses 6-phosphate, then Fructose 6-phosphate, etc.....? All we need to know is what carrier coenzymes are involved, how much of each, and how much ATP is produced in the end?
 
So you're saying we don't need to know the detailed steps involved in each of these processes? For instance, in Glycolysis, Glucoses goes to Glucoses 6-phosphate, then Fructose 6-phosphate, etc.....? All we need to know is what carrier coenzymes are involved, how much of each, and how much ATP is produced in the end?

Yep!
 
Hello
I have seen this topic come up numerous times: Oncotic and hydrostatic pressure. Can someone please explain these terms and what it means when the solute concentration becomes too high in the capillaries, etc and the concept of edema please. Its quite confusing. Thank you.
 
Here's a quick & dirty explanation of edema w/ those forces:

Hydrostatic pressure: A high hydrostatic pressure is a force favoring filtration. This generally occurs the greatest at the arteriolar side of the capillary (a much higher pressure system that the venous side). Hydrostatic pressure is therefore pushing fluid out of the capillaries.

Osmotic pressure: This is the gradient created by solutes dissolved in the solvent. In blood, the main determinant of this is albumin & other plasma proteins. Osmotic pressure is generally high on the venous side of the capillary. High concentration of solutes then "wants" to draw fluid back in so that there does not exist such a disparity in concentration (just as simple as osmosis).

Edema: There are a large number of things that that cause edema, but basically it occurs b/c of a mismatch btwn the filtration/reabsorption forces. For example, let's say that the arteriole side has high hydrostatic pressure. This force favors fluid moving out of the capillary early in the arteriole side. Now, b/c of years of long standing Htn & atherosclerosis, your capillaries have been damaged & you lose albumin along w/ the fluid.

Once you reach the venous capillary side you have a much lower oncotic pressure & therefore you reabsorb a lot less of the fluid that you originally filtered.

Fluid is left over in the tissues & AB-RA-CA-DA-BRA you have Edema.

Hope this helps,
Kritter
 
HI all I am new. And need a help on a question.

It's the last question on 7R(216).

The cells were exposed to radioactive labeled thymidine. Then there is a peak on percentage of cells dividing that has radio active label. WHy is the answer to what process is happening------ DNA synthesis, not Mitosis?:confused:

I understand that this stuff (radio active thymidine) is being incorporated to make new DNAs. But aren't the these new DNA containing neclei ( at the peak) dividing here instead of synthesizing?

I am throroughly puzzled. I mean when I looked at the solution passively or brushed by it, I might have thought I understood. But I don't and I am not sure if I saw a similar question, I would have arrived at the right answer.


Help! please!
 
Can someone explain to me independent and non-independent assortment?

Independent basically just means that each side of the dividing cell has an equal chance of receiving either allele being separated.

I picture it like this: When the chromosomes line up during metaphase, picture them as spinning around each other as they're being pulled to the center. Once in the center, they stop spinning. If you had allele A and allele a, it's completely random which one ends up pointing towards the bottom half or top half of the cell.

It's kind of a weird explanation - but basically just know that it means that either side of the dividing cell can get either allele with equal probability.

Non-independent assortment occurs when genes are linked. If you're still following my previous example, picture the two genes in question right next to each other on the same chromosome. You can spin it all you want, but they're going to end up in the same spot because they're physically connected.
 
possibly, but I think more likely there will be gas exchange even while the breath is held - tidal volume is generally less than 10% of lung capacity, so there is probably more oxygen around at least for a while.

can someone knowledgeable pls confirm or add?

If you hold your breath, you are basically just keeping in worthless air. Remember that the gas exchange happens as a passive process - your lungs equalize the partial pressure of O2 with the partial pressure of O2 in the blood. Once you equalize, the O2 in your blood would have to drop to allow more diffusion - but you only get halfway each time so it doesn't help much - and you need oxygen levels high to live so 50% doesn't do too much good.

But basically, when you hold your breath everything stays the same as usual until your blood starts becoming acidic due to high levels of bicarbonate being created (respiratory acidosis). Then your body gets PISSED. :)
 
HI all I am new. And need a help on a question.

It's the last question on 7R(216).

The cells were exposed to radioactive labeled thymidine. Then there is a peak on percentage of cells dividing that has radio active label. WHy is the answer to what process is happening------ DNA synthesis, not Mitosis?:confused:

I understand that this stuff (radio active thymidine) is being incorporated to make new DNAs. But aren't the these new DNA containing neclei ( at the peak) dividing here instead of synthesizing?

I am throroughly puzzled. I mean when I looked at the solution passively or brushed by it, I might have thought I understood. But I don't and I am not sure if I saw a similar question, I would have arrived at the right answer.


Help! please!

Well from what I understand of your question, what you're looking at is a pulse chase experiment. The only way thymidine can be incorporated is by DNA synthesis, so now here's perhaps where you're getting confused. The cell cycle consists of G1->S->G2->Mitosis. Now if a cell is continually undergoing mitosis, it must first undergo DNA synthesis (and remember this is the only point where DNA is being synthesized), therefore when mitosis occurs, it is merely a growth in size of the cell followed by division, which causes allocation of the DNA into the two new cells. Therefore, the cap size on how fast thymidine is incorporated into the cell is controlled by DNA synthesis and not mitosis.

Hope that helps.
 
Well from what I understand of your question, what you're looking at is a pulse chase experiment. The only way thymidine can be incorporated is by DNA synthesis, so now here's perhaps where you're getting confused. The cell cycle consists of G1->S->G2->Mitosis. Now if a cell is continually undergoing mitosis, it must first undergo DNA synthesis (and remember this is the only point where DNA is being synthesized), therefore when mitosis occurs, it is merely a growth in size of the cell followed by division, which causes allocation of the DNA into the two new cells. Therefore, the cap size on how fast thymidine is incorporated into the cell is controlled by DNA synthesis and not mitosis.

Hope that helps.
yes it makes sense now. thank you!.
 
Independent basically just means that each side of the dividing cell has an equal chance of receiving either allele being separated.

I picture it like this: When the chromosomes line up during metaphase, picture them as spinning around each other as they're being pulled to the center. Once in the center, they stop spinning. If you had allele A and allele a, it's completely random which one ends up pointing towards the bottom half or top half of the cell.

It's kind of a weird explanation - but basically just know that it means that either side of the dividing cell can get either allele with equal probability.

Non-independent assortment occurs when genes are linked. If you're still following my previous example, picture the two genes in question right next to each other on the same chromosome. You can spin it all you want, but they're going to end up in the same spot because they're physically connected.

ooo. That helps a lot. Kaplan's stuff didn't help whatsoever.
So what determines whether it's independent or non-independent? Is one just ideal and the other non-ideal?
 
Well from what I understand of your question, what you're looking at is a pulse chase experiment. The only way thymidine can be incorporated is by DNA synthesis, so now here's perhaps where you're getting confused. The cell cycle consists of G1->S->G2->Mitosis. Now if a cell is continually undergoing mitosis, it must first undergo DNA synthesis (and remember this is the only point where DNA is being synthesized), therefore when mitosis occurs, it is merely a growth in size of the cell followed by division, which causes allocation of the DNA into the two new cells. Therefore, the cap size on how fast thymidine is incorporated into the cell is controlled by DNA synthesis and not mitosis.

Hope that helps.

This is not directly related to this question, but DNA can also be synthesized by reverse transcribing RNA.
 
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