Organismal Biology/Physiology Thread

[QofQuimica]

All users may post questions about MCAT, DAT, OAT, or PCAT organismal biology (anatomy, physiology, development, embryology, and evolution) here. Cellular bio, molecular bio, and biochemistry 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/studentmanual/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
-how best to approach to MCAT biology passages
-how best to study MCAT biology
-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 organismal 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 Organismal Biology Team:

Maddscientist (thread moderator): Maddscientist is a Ph.D. student in developmental biology.

TheDarkSide: TheDarkSide has several years of experience working as a nurse. She scored 12 on the BS portion of the MCAT, and 37 overall.

Occasional moderator: Shrike. Shrike is a full-time instructor for The Princeton Review. His primary expertise is in other subjects; he knows just enough biology to have scored 12 on the BS section without ever having studied organic chemistry.

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[frany584]

I had a question about the Bohr effect. In the case of decreasing pH or increasing [CO2], hemoglobin has a decreased affinity for O2; however, how is this related to cooperativity? Does a decrease in affinity mean there is an decrease in cooperativity? Or is cooperativity and affinity inversely related? Thanks.

 

[QofQuimica]

I had a question about the Bohr effect. In the case of decreasing pH or increasing [CO2], hemoglobin has a decreased affinity for O2; however, how is this related to cooperativity? Does a decrease in affinity mean there is an decrease in cooperativity? Or is cooperativity and affinity inversely related? Thanks.

Hmm, that's an interesting question. I'd guess that cooperativity and affinity are probably not related, because the curve is still sigmoidal during Bohr effect conditions. It's just shifted to the right, so that a higher pO2 is needed to saturate the Hb. If cooperativity were eliminated, you would expect to see the curve take a hyperbolic shape, like a myoglobin binding curve.

 

[QofQuimica]

bump

 

[travelbug73]

Hmm, that's an interesting question. I'd guess that cooperativity and affinity are probably not related, because the curve is still sigmoidal during Bohr effect conditions. It's just shifted to the right, so that a higher pO2 is needed to saturate the Hb. If cooperativity were eliminated, you would expect to see the curve take a hyperbolic shape, like a myoglobin binding curve.

Though this might be beyond the scope of MCAT, there is some research evidence that points to reduced cooperativity of Hb in low pH. This is the case when Hb is bound to allosteric inhibitors in the R state. It has always been believed that allosteric inhibitors bind only to the T state, but now research points to the binding of these inhibitors to the fully ligated R state that can result in reduced affinity and cooperativity. However, like you said, cooperativity is not affected in the T state.

 

[Lindyhopper]

I can not understand why the hyposecretion of parathyroid hormone (PTH) may lead to tetany. Tetany is prolonged near constant muscle stimulation. PTH increases blood serum levels of Ca++ by librating it from the bone matrix. It would seem that hyposecretion of PTH would lead to low blood Ca++. Low blood Ca++ would seem to make muscle contraction less likely because an influx of Ca++ into the axonal terminal of the motor neuron is required to release ACH at the neuromusclar junction.
Does lowering the blood Ca++, perhaps, lower the equilibrium resting potential, making deplorization easier?
Any thoughts?

 

[QofQuimica]

I can not understand why the hyposecretion of parathyroid hormone (PTH) may lead to tetany. Tetany is prolonged near constant muscle stimulation. PTH increases blood serum levels of Ca++ by librating it from the bone matrix. It would seem that hyposecretion of PTH would lead to low blood Ca++. Low blood Ca++ would seem to make muscle contraction less likely because an influx of Ca++ into the axonal terminal of the motor neuron is required to release ACH at the neuromusclar junction.
Does lowering the blood Ca++, perhaps, lower the equilibrium resting potential, making deplorization easier?
Any thoughts?

It sounds reasonable to me, but I don't know. Maybe travelbug does? But if it's any consolation, this is definitely beyond the scope of what you'd need to know for the MCAT.

 

[DrChandy]

I can not understand why the hyposecretion of parathyroid hormone (PTH) may lead to tetany. Tetany is prolonged near constant muscle stimulation. PTH increases blood serum levels of Ca++ by librating it from the bone matrix. It would seem that hyposecretion of PTH would lead to low blood Ca++. Low blood Ca++ would seem to make muscle contraction less likely because an influx of Ca++ into the axonal terminal of the motor neuron is required to release ACH at the neuromusclar junction.
Does lowering the blood Ca++, perhaps, lower the equilibrium resting potential, making deplorization easier?
Any thoughts?

Ca2+ efflux is associated with repolarization, so hypocalcemia will lead to hyperpolarization, making depolarization less likely.

It is possible that low [Ca2+] which leads to lessened presynaptic release of neurotransmitters affects (by not inducing as much as they normally would) postsynaptic inhibitory interneurons which normally function to prevent tetany/episthotonos.

 

[Laz]

On the AAMC MCAT student manual "fatigue" is listed under the synaptic activity heading...can anyone explain this for me. I couldnt find anything in my physiology books. Although it might be self explainable I just want to make sure I know. Thanks

 

[DrChandy]

On the AAMC MCAT student manual "fatigue" is listed under the synaptic activity heading...can anyone explain this for me. I couldnt find anything in my physiology books. Although it might be self explainable I just want to make sure I know. Thanks

Fatigue at the synaptic level is a result of continuous presynaptic action potentials which have a rate that is much higher than synaptic vesicle neurotransmitter release. This occurs because over time, the rate of the action potentials overcomes the homeostatic balance of vesicle formation, neurotransmitter release, and reuptake of neurotransmitters from the synapse by the presynaptic neuron. Thus, the presynaptic neuron cannot release enough neurotransmitter into the synapse as it could previously from the same amount of action potentials because either presynaptic neurotransmitter vesicles cannot be formed fast enough, or neurotransmitters cannot be reuptaken by the presynaptic neuron from the synapse fast enough, in order to meet the demand of the action potentials.

 

[Laz]

Fatigue at the synaptic level is a result of continuous presynaptic action potentials which have a rate that is much higher than synaptic vesicle neurotransmitter release. This occurs because over time, the rate of the action potentials overcomes the homeostatic balance of vesicle formation, neurotransmitter release, and reuptake of neurotransmitters from the synapse by the presynaptic neuron. Thus, the presynaptic neuron cannot release enough neurotransmitter into the synapse as it could previously from the same amount of action potentials because either presynaptic neurotransmitter vesicles cannot be formed fast enough, or neurotransmitters cannot be reuptaken by the presynaptic neuron from the synapse fast enough, in order to meet the demand of the action potentials.

Thanks...very helpful

 

[thadarknyte]

how extensively should we know all of the small intestine secretions during digestion? I was reading the kaplan book and it just seems like its way too much detail. i.e trypinogen, trypsin, enterokinase, chymotrypsinogen, carboxypeptidase, aminopeptidase- and where they are all secreted from? Do we really have to knwo all this?

 

[QofQuimica]

how extensively should we know all of the small intestine secretions during digestion? I was reading the kaplan book and it just seems like its way too much detail. i.e trypinogen, trypsin, enterokinase, chymotrypsinogen, carboxypeptidase, aminopeptidase- and where they are all secreted from? Do we really have to knwo all this?

I would be familiar with the enzymes and what they do, but no, I personally don't think that it's really necessary to memorize where they all come from. (In other words, I'd know that trypsin is the active form of trypsinogen, and trypsin digests proteins.) Most of the small intestine enzymes come from the pancreas anyway, so if you do have to guess, the pancreas are always a good choice.

 

[Lests55]

I have a question about blood pressure in the heart. I know bp decreases from arteries to caps to veins...but what about in the heart intself? I think I remember reading that bp is actually the lowest anywhere in the heart (I think from AAMC 7), but this seems counterintuitive (at least according to my logic). Thanks for the help....

 

[QofQuimica]

I have a question about blood pressure in the heart. I know bp decreases from arteries to caps to veins...but what about in the heart intself? I think I remember reading that bp is actually the lowest anywhere in the heart (I think from AAMC 7), but this seems counterintuitive (at least according to my logic). Thanks for the help....

Hmm, I'm sorry, but I don't know the answer to that. But you definitely don't need to know physiology in this much detail for the MCAT; we'll be learning more than we ever wanted to know about it once we're in med school.

I'll see if MollyMalone can answer your question; she used to be a nurse, so she might know.

 

[MollyMalone]

I have a question about blood pressure in the heart. I know bp decreases from arteries to caps to veins...but what about in the heart intself? I think I remember reading that bp is actually the lowest anywhere in the heart (I think from AAMC 7), but this seems counterintuitive (at least according to my logic). Thanks for the help....

The pressure in the right atrium/ventricle during diastole is pretty close to 0, and you can't get much lower than that.

The trick here is to remember that the heart is separated into 2 sides of 2 chambers each, and the pressure within each of those chambers is not the same. The intricacies of this are beyond what you need to know for sure. That said, I think it's fascinating. Let's look at a diagram of the heart. Remember that systole is contraction, and diastole is relaxation.

The blood from the superior and inferior vena cava flows into the right atrium (RA) during diastole. (If the pressure in the right atrium were higher than the vena cava pressure, this wouldn't happen - at this point, the pressure is almost 0.) The blood flows through the RA, through the tricuspid valve, into the right ventricle (RV). As atrial systole begins, the RA contracts, ejecting the blood it contains into the RV (this is when the pressure rises). The tricuspid valve closes when the pressure in the RV exceeds that in the RA, which prevents backflow. As ventricular systole occurs, the RV contracts, and when the pressure in the RV exceeds the pressure in the pulmonary artery (PA), the pulmonic valve opens. As the RV pressure falls, the pulmonic valve closes. The blood flows through the pulmonary capillaries to the pulmonary venous system, emptying into the left atrium. On the left side of the heart, the same sequence of systolic and diastolic events occur (except that the valves are different, of course!). The pressure in the RV is much lower than in the LV, because the pressure in the pulmonary arteries and capillaries is much lower that the systemic pressure -- the resistance in the pulmonary system is much, much lower.

In clinical practice, we can measure some of these pressures directly, and calculate others, using a pulmonary artery catheter, aka a Swan-Ganz catheter.

You can see in the tracings how the pressure changes in the RA, RV, and PA (note that these tracings aren't synchronous, they're just examples). The "wedge" pressure is obtained by inflating a balloon near the tip of the catheter to occlude one of the branches of the pulmonary artery. The pressure is then measured on the left heart side of the balloon and should be about equivalent to the pulmonary vein pressure, which is equivalent to the LA pressure. The LV systolic pressure will equal normal systolic arterial pressure, which of course can be measured with a blood pressure cuff.


Remember that this is vastly, vastly more information than is necessary for the MCAT, but I hope it was helpful in answering your question.

 

[Lests55]

WHOAH! Thanks for all the help. I went back to AAMC 7 and noticed that one question essentially asked "which of the following has the lowest pressure"

heart
caps
artery
something else irrelevant

the answer was caps, and that is what i chose...anyone else find it odd that this is blatantly incorrect on an official MCAT!? (notice that I actually had it backwards in my original question )

i think picking veins having the lowest pressure followed by caps would be the safe choice because it seems more simple and more along the lines of the basic stuff covered by an mcat....still shocking to me

 

[MollyMalone]

WHOAH! Thanks for all the help. I went back to AAMC 7 and noticed that one question essentially asked "which of the following has the lowest pressure"

heart
caps
artery
something else irrelevant

the answer was caps, and that is what i chose...anyone else find it odd that this is blatantly incorrect on an official MCAT!? (notice that I actually had it backwards in my original question )

i think picking veins having the lowest pressure followed by caps would be the safe choice because it seems more simple and more along the lines of the basic stuff covered by an mcat....still shocking to me

In my opinion, the answer would be only be wrong if the choice listed was "right atrium" instead of "heart." I think if you look at the heart and the circulatory system holistically, it's pretty clear that pressure *somewhere* in the heart at some point would have to exceed capillary pressure in order for circulation to continue.

I agree that it's not the world's best question.

 

[j-med]

Given the structure of these disaccharides:

Maltose: Glc(alpha-1,4)Glc
Sucrose: Glc(alpha-1,2-Fruc
Trehalose: Glc(alpha-1-1-alpha)Glc

---------
What is the difference between maltose and trehalose? (*edited* i said sucrose before but I meant trehalose*)

Why can't trehalose be metabolized?
----------

 

[j-med]

Is it because trehalose, even if it's alpha linked, is flipped over ?
And that makes it looks like a beta-1,4, which is something we cannot metabolize (like that in cellulose)?

Or is it because trehalose has no reducing ends, whereas maltose has at least a reducing end?
But if that's the case sucrose has no reducing ends too, and we hae sucrase to metabolize it.

WHYYYY


Thanks!

 

[QofQuimica]

Given the structure of these disaccharides:

Maltose: Glc(alpha-1,4)Glc
Sucrose: Glc(alpha-1,2-Fruc
Trehalose: Glc(alpha-1-1-alpha)Glc

---------
What is the difference between maltose and sucrose?

Why can't trehalose be metabolized?
----------

1) Maltose and sucrose are two different disaccharides. They actually contain different sugars in them: maltose has two glucoses, while sucrose has one glucose and one fructose. Maybe you meant to ask about the difference between maltose versus trehalose. In that case, they are different because of how they are connected. The numbers in parentheses tell you which atoms are connected to one another.

2) Evidently we don't have the enzyme needed to metabolize trehalose. It would be because of that 1,1-alpha link. I've never seen this particular example, but one common example is to compare cellulose (1,4-beta linked glucose polymer) with starch (1,4-alpha linked glucose polymer). We can metabolize the latter but not the former b/c we aren't able to break 1,4-beta linkages between glucose molecules. Termites contain microorganisms that have the proper enzymes, so they *are* able to do it.

 

[j-med]

Thanks, QofQuimica!

Yes I meant to ask trehalose not sucrose in the first question. (i just edited it, thx)

So you mean it's because of the alpha-1,4-alpha link?
But cellulose we cannot break it because it's beta 1,4 link. So the beta1,4 is analgous to alpha1-4-alpha?
Is it because the fact that the adjacent rings are flipped in relation to each other?

Also, it has nothing to do with the reducing end then?
(e.g. maltose has a reducing end vs. sucrose which does not)

 

[QofQuimica]

Thanks, QofQuimica!

Yes I meant to ask trehalose not sucrose in the first question. (i just edited it, thx)

So you mean it's because of the alpha-1,4-alpha link?
But cellulose we cannot break it because it's beta 1,4 link. So the beta1,4 is analgous to alpha1-4-alpha?
Is it because the fact that the adjacent rings are flipped in relation to each other?

Also, it has nothing to do with the reducing end then?
(e.g. maltose has a reducing end vs. sucrose which does not)

Yeah, the enzymes are very specific. The only difference between maltose and cellobiose is that maltose has an alpha-1,4-glucose link, and cellobiose has a beta-1,4-glucose link. But that one little difference in stereochemistry (and that's all it is; these two compounds are almost identical) has huge repercussions, because the enzyme can break down the maltose and not the cellobiose. I'll try to post the images.

This one is maltose (alpha link):

This one is cellobiose (beta link):

Notice that they are almost exactly the same except for the stereochemistry at the linked atoms.

 

[j-med]

Thanks, QofQuimica! It's nice to have some good pictures to help visualize things.

But okay, so perhaps I'm not phrasing my question well enough, since yours was a very good illustration... but I don't think my problem is all answered yet. (see my previous post). Is cellobiose indigestible? but still this doesn't answer my question on trehalose.. Anyways, please allow me to try again:

1. What is the difference between maltose (or even cellobiose) versus trehalose that make trehalose indigestible?
Note that:
- Maltose has Glc(alpha-1,4)Glc link
- Trehalose has: Glc(alpha-1,4-alpha)Glc link
Is it because:
a) that trehalose does not have an reducing end? or does reducing end does not matter?
b) that trehalose's alpha-1,4-alpha link is similar to beta-1,4 in that: alpha-1,4-alpha adjacent ring structure is flipped relative to one another
c) it's not because of H-bonds is it? that doesn't matter since unlike cellulose (beta1,4), trehalose is dissacharides and doesn't form H bonds?
it is simply beacuse of the alpha-1,4-alpha link that is ANALOGOUS to the indigestible beta-1,4?
(see here for structures: http://cem.msu.edu/~reusch/VirtualText/carbhyd.htm, search text for trehalose)

2. Normally, is it because of the LINKS that make a sugar indigestible,or is it because of the REDUCING END?
(NON-reducing endmeans substituted anomeric carbons cannot ebcoverted tothealdehyde configurationand thus cannot participatein the Redox reactions of reducing sugars)
Or does ENDS that not matter? since cellubiose has reducing ends and still indigestible...

 

[j-med]

MMm~!!

Maybe it's just because of the LINKS not ENDS?
And it depends on ENZYMES we have?

Since lactose has beta-1,4, it's only because most humans have lactase for it and it's the lactase, as I remember from somewhere, is the only beta-1,4 specific ENZYME that we have.

In any case, please still read through my last post and let me because the similarity of trehalose and how it comes into play. (especially question 1(b) of the post right before this one.) (i.e. whether mostly because beta-1,4 and alpha-1,4-alpha are flipped/ turned over)

Thank you so much.

 

[QofQuimica]

MMm~!!

Maybe it's just because of the LINKS not ENDS?
And it depends on ENZYMES we have?

Since lactose has beta-1,4, it's only because most humans have lactase for it and it's the lactase, as I remember from somewhere, is the only beta-1,4 specific ENZYME that we have.

In any case, please still read through my last post and let me because the similarity of trehalose and how it comes into play. (especially question 1(b) of the post right before this one.) (i.e. whether mostly because beta-1,4 and alpha-1,4-alpha are flipped/ turned over)

Thank you so much.

I think part of the problem is that you have written down the wrong linkage for trehalose. Here is the structure:

It's an alpha-1,1 connection, not a 1,4 connection! If that's what you meant by "flipping" the second molecule, then yes, the second sugar ring has been turned around and is connected from the 1-carbon instead of the 4-carbon like it is in maltose or cellobiose. Compare this structure to the maltose one above, and you'll see that they are connected to different atoms, albeit both with an alpha connection.

 

[j-med]

I think part of the problem is that you have written down the wrong linkage for trehalose. It's an alpha-1,1 connection, not a 1,4 connection! If that's what you meant by "flipping" the second molecule, then yes, the second sugar ring has been turned around and is connected from the 1-carbon instead of the 4-carbon like it is in maltose or cellobiose.

Ahh!... sorry I keep making these mistakes when I type online, I forgot to refer carefully back to my notes! Yes I actually knew it's alpha 1,1. But back to my question.. what determines whether something is digestible or not (see my earlier posts)?

Thanks again!

 

[QofQuimica]

Ahh!... sorry I keep making these mistakes when I type online, I forgot to refer carefully back to my notes! Yes I actually knew it's alpha 1,1. But back to my question.. what determines whether something is digestible or not (see my earlier posts)?

Thanks again!

The links. The enzymes can only break certain linkages and not others.

 

[Lests55]

(Not really sure if this belongs here or the cell bio post, but...) I have a pretty good feel for the B lymphocytes and T lymphocyte system, but where exactly does this take place? Are they floating in the blood, the lymph, interstitial fluid? I know antibodies are in the blood plasm, but I don't have a feel for the rest...

 

[QofQuimica]

(Not really sure if this belongs here or the cell bio post, but...) I have a pretty good feel for the B lymphocytes and T lymphocyte system, but where exactly does this take place? Are they floating in the blood, the lymph, interstitial fluid? I know antibodies are in the blood plasm, but I don't have a feel for the rest...

As far as I know, T cells and B cells also are present in the blood. (B cells are the ones that make the antibodies.) I would guess they're in lymph fluid too. I don't think they're in interstitial spaces, though. Any biology people want to comment about this?

 

[travelbug73]

(Not really sure if this belongs here or the cell bio post, but...) I have a pretty good feel for the B lymphocytes and T lymphocyte system, but where exactly does this take place? Are they floating in the blood, the lymph, interstitial fluid? I know antibodies are in the blood plasm, but I don't have a feel for the rest...

Check out Post09 in the cell bio sticky. The immune system was sort of explained. If you are still confused/unsure, please post or PM me.

 

[kevin86]

is this the right thread? Ok I have a question about testesterone. Since it inhibits FSH secretion, wouldnt it inhibit spermatogenesis? Like those body builders who took too much testesterone. But why does the TPR book and another book say it also facilitates spermatogenesis. Is there something I'm missing here?

Also the same goes for estrogen right, that it inhibits FSH, which inhibits ovary. Is that what happens in a birth control pill?

Just a bit confused.

 

[Lests55]

I think I feel pretty good about the immune system...thanks. But I do have a few more questions....

(1) I know veins contain valves, is it true that arteries and capillaries do not ?

(2) Can you differentiate pleural and peritoneal cavities for me?

Gracias

 

[QofQuimica]

I think I feel pretty good about the immune system...thanks. But I do have a few more questions....

(1) I know veins contain valves, is it true that arteries and capillaries do not ?

(2) Can you differentiate pleural and peritoneal cavities for me?

Gracias

1) Yes. No valves in arteries and capillaries.

2) I think pleural is the lungs and peritoneal is the abdomen? Is this stuff actually part of your MCAT review???

 

[Lests55]

Is this stuff actually part of your MCAT review???

Yeah, that was my thought, but on AAMC Test 7 there was a question about it. It asked if some organ was ruptured what cavity would be invaded...I was a little taken back as I was not expecting such a question...

 

[QofQuimica]

I could be wrong on #2, but it sort of makes sense if you look at the back ass-wards way the body regulates itself.

Yes, you are wrong; progesterone does the opposite of what you said. That is, it actually causes the uterine lining to be prepared for implantation and maintained. Menstruation occurs due to the atrophy of the corpus luteum (that's what the follicle surrounding the egg turns into after ovulation), because the corpus luteum is what stimulates progesterone and estrogen production. With lower levels of progesterone and estrogen, the uterine lining sloughs off.

There are two kinds of BCP. One kind contains both estrogen and progesterone, and this negatively influences the hypothalamus, inhibiting the production of gonadotropin releasing hormone. Since GnRH stimulates the anterior pituitary to produce FSH and LH, a drop in GnRH means that FSH and LH levels also drop, and ovulation does not occur at all. The progesterone-only pill, or mini-pill, works differently. It basically makes the cervix impassable for sperm by thickening the mucus.

 

[kevin86]

I'm still a little confused. So is testosterone or I guess estrogen the actual hormone that cause either spermatogenesis or ogenesis? Does LH merely turn it on? Then what is the process in which people taking steroids like testosterone become sterile. I mean I know LH and FSH in them gets turn off through negative feedback, so a little help here. Do you need both testosterone or estrogen along with FSH present to have either spermatogensis or ogenesis going?

 

[QofQuimica]

I'm still a little confused. So is testosterone or I guess estrogen the actual hormone that cause either spermatogenesis or ogenesis? Does LH merely turn it on? Then what is the process in which people taking steroids like testosterone become sterile. I mean I know LH and FSH in them gets turn off through negative feedback, so a little help here. Do you need both testosterone or estrogen along with FSH present to have either spermatogensis or ogenesis going?

I think that the main reason too much testosterone causes sterility is because it gets metabolized to estrogens. This is not my area, but I think you are right that testosterone is needed for spermatogenesis, along with FSH and LH. As far as the specifics of how it all works, we need to ask one of the biologists. I'll ask MollyMalone to help us out.

 

[Krazykritter]

Q is right about the cavities. The pleural cavity does pertain to the area w/in the thorax that is not the pericardial area. The peritoneal cavity is the area below the diaphragm containing the abdominal organs. However, some of the organs are non-peritonealized or retro-peritoneal, but this is beyond the scope of the MCAT.

 

[Krazykritter]

I think that the main reason too much testosterone causes sterility is because it gets metabolized to estrogens. This is not my area, but I think you are right that testosterone is needed for spermatogenesis, along with FSH and LH. As far as the specifics of how it all works, we need to ask one of the biologists. I'll ask MollyMalone to help us out.

Testosterone is thought to have small role in stimulation of spermatogenesis by stimulating maturation of germ cells (this may be what the TPR book was referring to). FSH is, however, the major hormone that stimulates spermatogenesis. When FSH stimulates the Sertoli cells to both increase spermatogenesis and also increase the release of Testosterone and inhibin. The testosterone directly inhibits the Hypothalamus which releases the tropic hormone GnRH. GnRH is the hormone that causes the release of FSH & LH from the Ant. Pituitary. W/out FSH, you cannot produce sperm and thus become sterile.

 

[MollyMalone]

Testosterone is thought to have small role in stimulation of spermatogenesis by stimulating maturation of germ cells (this may be what the TPR book was referring to). FSH is, however, the major hormone that stimulates spermatogenesis. When FSH stimulates the Sertoli cells to both increase spermatogenesis and also increase the release of Testosterone and inhibin. The testosterone directly inhibits the Hypothalamus which releases the tropic hormone GnRH. GnRH is the hormone that causes the release of FSH & LH from the Ant. Pituitary. W/out FSH, you cannot produce sperm and thus become sterile.

There you go.

 

[Caboose]

Howdy! I was just listening to Audio Osmosis and they said that without BPG the hemoglobin binding curve wouldn't be sigmoidal. As previously discussed on this thread and to the best of my knowledge, the cooperatively of the subunits is what gives it that shape, (as opposed to the simplicity of myoglobin). What's the role of BPG and cooperatively? Is BPG the reason there is cooperatively between subunits?

You guys are so cool - I hope I don't wear out my welcome here.
Caboose.

 

[QofQuimica]

Howdy! I was just listening to Audio Osmosis and they said that without BPG the hemoglobin binding curve wouldn't be sigmoidal. As previously discussed on this thread and to the best of my knowledge, the cooperatively of the subunits is what gives it that shape, (as opposed to the simplicity of myoglobin). What's the role of BPG and cooperatively? Is BPG the reason there is cooperatively between subunits?

You guys are so cool - I hope I don't wear out my welcome here.
Caboose.

Ok, this is definitely beyond the scope of the MCAT, but it is an allosteric effect. The role of 2,3-BPG has to do with the fact that Hb has two forms: a T conformation with a lower affinity for oxygen, and an R conformation with a higher affinity for oxygen. 2,3-BPG binds to the T conformation (the deoxy one) and stabilizes it. This leads to the T conformation being the dominant one. (The T and R conformations are in equilibrium with one another.) Since the binding of the ligand (oxygen) increases the proportion of R conformation, you get a scenario where each ligand binding will make it easier for the next one to bind because the R conformation has a higher oxygen affinity. Thus, cooperativity is positive and the curve will be sigmoidal.

 

[Caboose]

BLAST! I always have beyond the scope questions. Perhaps this is why things are a bit slow going.
Thanks Q, you're the peachy.
Caboose.

 

[BlackBantie]

Is there an easy way to remember which body systems and organs that are derived from each embryonic tissue layer? Ectoderm is pretty easy, but I always get mesoderm and endoderm confused.

 

[QofQuimica]

Is there an easy way to remember which body systems and organs that are derived from each embryonic tissue layer? Ectoderm is pretty easy, but I always get mesoderm and endoderm confused.

What I did was just memorize the ectoderm and mesoderm. Most other things (internal organs) come from endoderm. Five important things arise from mesoderm: circulatory system, gonads, kidneys, muscles, and bones. I don't know, maybe we can come up with a good mnemonic for these if this is hard for you to remember, but it's 3:30 AM, and I am too tired right now.

 

[Lests55]

What I did was just memorize the ectoderm and mesoderm. Most other things (internal organs) come from endoderm. Five important things arise from mesoderm: circulatory system, gonads, kidneys, muscles, and bones. I don't know, maybe we can come up with a good mnemonic for these if this is hard for you to remember, but it's 3:30 AM, and I am too tired right now.

My 0.02....

Ectoderm: Nervous & Sense organs (weird...easy to remember); skin (obvious)
Endoderm: Gi Tract & associations (liver, pancreas); Lungs
Mesoderm: Everything else! muscles, bone, heart, etc.

 

[QofQuimica]

My 0.02....

Ectoderm: Nervous & Sense organs (weird...easy to remember); skin (obvious)
Endoderm: Gi Tract & associations (liver, pancreas); Lungs
Mesoderm: Everything else! muscles, bone, heart, etc.

Yeah, that works too. Same basic principle: Pick any two germ layers, memorize them, and whatever else is left comes from the third layer.

 

[StreetGenius]

What muscle has more mitochondria? Skeletal muscle or Cardiac muscle. Can someone explain and elaborate with respect to mitochondria. In my old notes, I have that cardiac mito are larger and more numerous, but then again I have in my notes that skeletal muscle cells have the greatest number of mito.


Anyone?

 

[QofQuimica]

What muscle has more mitochondria? Skeletal muscle or Cardiac muscle. Can someone explain and elaborate with respect to mitochondria. In my old notes, I have that cardiac mito are larger and more numerous, but then again I have in my notes that skeletal muscle cells have the greatest number of mito.


Anyone?

I think cardiac has more than skeletal. But slow-twitch fibers have more mitochondria than fast-twitch in skeletal muscle; maybe that's what you wrote about in your notes?

 

[kevin86]

would the slow twich and fast twitch something we need to know?

Can you explain how the dct concentrations becomes more hypertonic compare to near by capillaries in the presence of ADH. This was the answer in the book. Since ADH increase water permeability, wouldnt the water stop flowing after it becomes isotonic. And does the recta vasa play into it. Does it continously carry the water away to insure that the flow of water doesnt stop even at isotonic?