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.

I am looking at my notes from TPR, attempt 1 and am using Audio Osmosis for attempt 2 in addition to TPR class. TPR really only emphasized 3 types of mutations (i guess you could call them 2)...those being point mutations and insertion and deletion. AudioOsmosis mentions netural, transposition, back mutation, wildtype... What are the basics we need to know about mutations? Thank you.

Hi-

With regards to mutations, i would assume that the three (and i would call them three, they're all pretty distinct) TPR "classes" of mutations are going to be the most common fodder for questions asked. Point mutations are single base changes and can be neutral (do not change the amino acid being coded for), missense (the amino acid being coded for is changed to another amino acid due to the point mutation) or nonsense (the amino acid being coded for is changed to a "stop" due to the point mutation). Insertions and deletions are just like the name suggests.

I am not an authority on what will or will not be on the MCAT, but you should also have an idea of the other mutations you mentioned. wild-type is not a mutation, but the natural presentation of something. a back mutation usually involves an original mutation that is reverted back by a second mutation (so the sequence goes "back" to what it was). transposition usually involves mobile dna.

Hope this helps...

I am looking at my notes from TPR, attempt 1 and am using Audio Osmosis for attempt 2 in addition to TPR class. TPR really only emphasized 3 types of mutations (i guess you could call them 2)...those being point mutations and insertion and deletion. AudioOsmosis mentions netural, transposition, back mutation, wildtype... What are the basics we need to know about mutations? Thank you.

Hi!

Good information given above.

According to the AAMC MCAT student manual, the following is fair game for mutation material: "random, translation error, transcription error, base substitution, inversion, addition, deletion, translocation, mispairing."

Here are my quick thoughts (skipping insertion and deletion and point mutations since you said you had those):

Wild-type mutations: a base substitution that does not result in a change of amino acid, usually no effect on phenotype (apparently some really subtle things can occur but I wouldn’t worry about it for MCAT level questions). This one is confusing because here the "wild-type" refers only to the phenotype, not to both the phenotype and the genotype as I usually hear the term used.

Neutral mutations: have no effect on function.

Back mutations: When something was once A but is now B changes “back” to A again.

Inversion mutations: when a sequence of nucleotides is reversed (DNA level), or when a sequence of genes is reversed (chromosome level).

Transposition mutations: “jumping genes” (transposons) which can cause translocation, insertion, and deletion mutations.

Translocation mutations: genes from one of a pair of homologous chromosomes separate and attach to the other chromosome in the pair. Can occur during crossing over.

Obviously, errors can occur in translation (wrong AA) and transcription (wrong base) both.

Good illustrations available at:

http://www.biology-online.org/2/8_mutations.htm

http://www.people.virginia.edu/~rjh9u/chrominv.html

Nice, concise reference about transposition (but way more than necessary information):

http://wiki.cotch.net/index.php/Transposition

I hope that was helpful!

yes, thanks for the response!

What should I focus on for the nervous system and how it is organized(central, peripheral, motor, autonomy, etc...) in the area of action potential? How much detail should I know about the eyes, and ears?

What should I focus on for the nervous system and how it is organized(central, peripheral, motor, autonomy, etc...) in the area of action potential? How much detail should I know about the eyes, and ears?


Hmmm. I'm not quite sure what you're asking in the first question. You definitely need to know all the organizational levels of the nervous system (anatomical and functional). You should know the structure of neurons. I would try to be familiar with action potentials in as much detail as you can, but the really important features are that it's a threshhold (all or nothing) effect and that it's based on the sodium-potassium pump. I would also be very familiar with the major classes of neurotransmitters.

For the eyes and ears you don't need very detailed anatomy (I don't think they'd ever ask a question about naming the bones of the ear) but you should understand the basic mechanics of vision and hearing... which you get in physics!

Hope that helps and please let me know if you want some of that clarified... it's been a long day! :)

How much detail should I focus on the action potential? EK seems to gloss over it. In the bio course that I took, I had to learn how muscle contracts, what how it depolarizes on an already created action potential, resting potential, how it gets trasmitted thorugh a synapse (neurotransmitter).

I'm not familiar with the EK materials but my personal position would be to know all the things you mention from your bio class. I would absolutely memorize the shape of the time/voltage curve and the direction of movement of the ions, including calcium. I would definitely be familiar with saltatory propagation and the relevant anatomy. My personal theory based on my limited experience is that the test writers are in love with neurotransmitters so I would focus on that topic quite a bit.

I would encourage you to check out the MCAT Student Manual (the link is in the first post of this thread) which goes into a lot of detail about what material AAMC thinks you need to know for the test.

Hope that helps! Good luck! :luck:

I would encourage you to check out the MCAT Student Manual (the link is in the first post of this thread) which goes into a lot of detail about what material AAMC thinks you need to know for the test.
Caveat: the linked document shows what students are expected to know, not the relative importance of different items. Do your homework (including in this thread) to find out what's really necessary.

As to action potentials, what's really necessary here is exactly what DarkSide said.

Okay, I'm finding myself trying to get the overall idea of how certian systems like digestive, excretory and respiratory system work but I am unnerved by the fact that all the terminology in the EK book is what I gloss over. Should I memorize the terms in conjunction with getting the gist of the systems? :confused:

Okay, I'm finding myself trying to get the overall idea of how certian systems like digestive, excretory and respiratory system work but I am unnerved by the fact that all the terminology in the EK book is what I gloss over. Should I memorize the terms in conjunction with getting the gist of the systems? :confused:

I think it's important to know the terminology as wel as the overall functions of the system. I never used Examkrackers, so I'm not sure how they organize their material, but here's what helped me: when I was studying for the long-haul (sitting at the dinner table for 3-4 hours), I would make sure I got the gist of a system. For the details, I studied the hell out of flashcards -- I used Kaplan's which were pretty good, but I also made some of my own as I was studying. I would write down any significant facts or terms that I ran across when I was reading the material. I would do flashcards while I was eating, driving, on the toilet :o -- anywhere. After a while, the details sunk in.

One more question guys, this one about circulation and the MCAT. In tracing the blood around the heart and to the lungs I found Kaplan's explanation to be well...krappy. The left side I think pumps the deoxygenated blood, I know there's a systole and a diastole which are the lub/dub. Blood from the lower body is from the inferior vena cava, upper superior. But I'm just having trouble piecing it all. Can someone give me a good rundown for the MCAT?

Can anyone post how the digestive, excretory and reproductive systems work and what we need to know for the MCAT?

Can anyone post how the digestive, excretory and reproductive systems work and what we need to know for the MCAT?
wrong section..my bad..this should be in the biology section..sorry

Can anyone post how the digestive, excretory and reproductive systems work and what we need to know for the MCAT?

...I know there's a systole and a diastole which are the lub/dub.
The rest of this qestion's been addressed, but I thought someone better mention: The "lub" and "dub" are valve closures, not systole and disatole. Specifically, the "lub" is the closure of the two atrioventicular (AV) valves, the bicuspid and tricuspid, at the begining of systole; the "dub" is the closure of the semilunal valves, the ones between the ventricles and the arteries, at the end of systole.

Apologies if this answer has already been given, too; I missed it.

Not to be a thread Nazi, but perhaps issues of blood vessels would be more appropriate for the organismal biology thread...

I was wondering if Shrike's method for attacking PS passages applies to Bio-- is it a good to skim the passage at most and focus on the reactions, figures, graphs, equations, etc then dig into the questions? I could see where certain subjects (CAC, maybe certain physio passages) this would be great, but what about genetics passages? Any thoughts?

Aside to Shrike: I used your method for PS, and went from 9's and 10's to 12's on my practice exams. Thanks for making my toughest section my strongest!

There is no perfect answer to the question about how to attack a bio passage, but what I advise is very similar to my physics approach. Possible differences:


It may be acceptable to skim the entire passage, or skim until you get to obviously detailed information, because biology passages resemble verbal reasoning more than do physics passages.


Because tables of experimental values are likely to be of values you understand (in contrast to physics, where that's far from guaranteed), it may make sense to look briefly at tabular data and at graphs for general trends.


These things said, they're not what I advise (nor what I personally do) -- I advise the same approach as I do for physics passages (see link above). No reading the passage; just examine the figures, graphs, and tables. At most, skim the text. Total time prior to questions should be under 45 seconds. Then, on to the questions, on which you can now spend the needed time.

I always at least skim, but time has never been an issue for me and I honestly think you'd probably be fine doing it Shrike's way.

Thanks for the input, Mods-

As can be gathered form my previous post, I am a big fan of the technique, and would hope to see similar trends in Bio improvent using it. Just wanted to make sure that I wasnt missing anything by applying the method in Bio passages :thumbup:

I always get confused about this issue. Can someone please sum it up and help me see the light?

I always get confused about this issue. Can someone please sum it up and help me see the light?

Important things to know about acid/base balance in the human body FOR THE MCAT:
(i.e., this is not meant to be a complete discourse on the subject)

The buffer system you need to know: HCO3-/CO2 (think HCO3- = base and CO2 = acid)

Chemical equation: H+ + HCO3- = H2CO3 = CO2 + H2O (imagine the equilibria arrows)

The lungs independently control CO2 (fast response – minutes to hours) while the kidneys independently control HCO3- (slow response – hours to days).

Physiologic pH: 7.4

When the pH goes out of whack, the body has a few different ways to deal with it: buffering, compensation, and correction. Buffering is automatic and instantaneous – it’s a function of the chemistry shown above. When the challenge to the buffering system is too great and the pH becomes materially affected, chemoreceptors pick up this signal encourage the appropriate system to take action. The response depends on whether it is a metabolic problem (HCO3- too high or low) or a respiratory problem (CO2 too high or low). The kidneys adjust to compensate for respiratory problems (can do this by a variety of mechanisms but basically you just need to know that it affects HCO3- levels) while the lungs adjust the CO2 level by hyper- or hypoventilation to compensate for metabolic disorders. These compensatory mechanisms function best as a temporary stopgap (minutes to days) until the body can manage to correct the underlying reason for the acid/base imbalance. Of course, sometimes the problem is not correctable and people wind up living in a chronically compensated state.

Here’s a handy list of the four main problems and what happens with them:

Respiratory acidosis – caused by lung problems. Levels of CO2 are too high, causing pH to drop. The kidneys respond by increasing levels of HCO3-.

Respiratory alkalosis – caused by lung problems. Levels of CO2 are too low, causing pH to rise. The kidneys respond by decreasing levels of HCO3-.

Metabolic acidosis – not caused by lungs. Levels of HCO3- are too low, causing pH to drop. The lungs respond by decreasing levels of CO2 (hyperventilation).

Metabolic alkalosis – not caused by lungs. Levels of HCO3- are too high, causing pH to rise. The lungs respond by increasing levels of CO2 (hypoventilation).

Just for fun, some causes of each (not an exhaustive list):

Respiratory acidosis: pulmonary embolism, cardiac arrest, pneumonia, COPD, airway obstruction – you get the drift. Things that impair the lungs’ ability to move air or do gas exchange.

Respiratory alkalosis: pain, fever, things that cause respiratory rate and depth to increase.

Metabolic acidosis: diarrhea (loss of base via GI tract), ketoacidosis (from diabetes), lactic acid build-up, several drugs.

Metabolic alkalosis: vomiting (loss of acid via GI tract), occasionally gain of base (saw this once in a lady who drank multiple bottles of Maalox)

I hope that was helpful. As always, if I made an error or if someone has something to add, please feel free to comment. :)

Could someone please explain to me the female gametes from the time of her birth till ovulation. I was under the impression that at the time of birth the gametes are at Anaphase I but I recently read that it is at Meiosis I. So which one is it? Thanks

Could someone please explain to me the female gametes from the time of her birth till ovulation. I was under the impression that at the time of birth the gametes are at Anaphase I but I recently read that it is at Meiosis I. So which one is it? Thanks
The primary oocytes formed at birth (no more will be made, ever) start meiosis I and are arrested in Prophase I until puberty, during which time many of the primary oocytes regress. Once puberty starts, ONE primary oocyte, every month, will complete meiosis I, resulting in the formation of a secondary oocyte and a polar body. The secondary oocyte starts meiosis II and again stops, this time at Metaphase II.
During ovulation, the secondary oocyte, released into the fallopian tube, will complete meiosis II and form the mature egg (ovum) and another polar body, if and only if there is a sperm available. If there is no sperm available the secondary oocyte will be discharged during menstruation without underoging meiosis II.
The first polar body also divides resulting in 2 more polar bodies. Therefore, at the end of meiosis II, there should be at least 2 and maybe 3 polar bodies (if there is fertilization).
In short, the primary oocyte is at Prophase I until puberty.

Hope this helps.

The primary oocytes formed at birth (no more will be made, ever) start meiosis I and are arrested in Prophase I until puberty, during which time many of the primary oocytes regress. Once puberty starts, ONE primary oocyte, every month, will complete meiosis I, resulting in the formation of a secondary oocyte and a polar body. The secondary oocyte starts meiosis II and again stops, this time at Metaphase II.
During ovulation, the secondary oocyte, released into the fallopian tube, will complete meiosis II and form the mature egg (ovum) and another polar body, if and only if there is a sperm available. If there is no sperm available the secondary oocyte will be discharged during menstruation without underoging meiosis II.
The first polar body also divides resulting in 2 more polar bodies. Therefore, at the end of meiosis II, there should be at least 2 and maybe 3 polar bodies (if there is fertilization).
In short, the primary oocyte is at Prophase I until puberty.

Hope this helps.

Thank you so much it really helped.

im having trouble with the menstruation cycle. Im confused as to what everything comes from, ovary produces estrogen and progestrone, they thicken the endometrium together. But whats a follicle? and where does an ovum come from? The follicle or the ovary? Im just not getting the big picture, i think i got the hormones part down, LH and FSH surge because of estrogen and gnrh, progestrone+estrogen inhibits gnrh LH FSH.
oh and where does the corpus luteum fit into this picture?

im having trouble with the menstruation cycle. Im confused as to what everything comes from, ovary produces estrogen and progestrone, they thicken the endometrium together. But whats a follicle? and where does an ovum come from? The follicle or the ovary? Im just not getting the big picture, i think i got the hormones part down, LH and FSH surge because of estrogen and gnrh, progestrone+estrogen inhibits gnrh LH FSH.
oh and where does the corpus luteum fit into this picture?
The ova in the ovary are associated with the follicles; basically, the follicle is a subdivision of the ovary, with each follicle containing one ovum. The ova (plural of ovum) are all part of the ovary from early in life (at least, that is what I've originally been taught, but this has recently been found to not be the case in mice), with a finite number of ova that slowly mature one-by-one in the sexually mature female.

As the FSH stimulates the maturation of the follicles, eventually one will generally dominate, and it will release hormones that tell the pituitary gland that a cell is mature, and that inhibit the growth of other follicles, to make only a single mature egg cell at a time. When the follicle ruptures, the remaining scar tissue is referred to as the corpus luteum, and this will continue to release hormones (progesterone) to trigger the thickening of the endometrial lining in expectation of zygote implanting.

. . During ovulation, the secondary oocyte, released into the fallopian tube, will complete meiosis II and form the mature egg (ovum) and another polar body, if and only if there is a sperm available. If there is no sperm available the secondary oocyte will be discharged during menstruation without underoging meiosis II.
The first polar body also divides resulting in 2 more polar bodies. Therefore, at the end of meiosis II, there should be at least 2 and maybe 3 polar bodies (if there is fertilization).
In short, the primary oocyte is at Prophase I until puberty.
. . .
I'm pretty sure Travelbug is accurate.

I'm pretty sure Travelbug is accurate.
My bad. My bio teachers always referred to the primary oocyte as an ovum, regardless of stage of maturation.

Could anyone please describe fetal circulation in detail?

I finished studying all of EK and I have the basics down for the most part but there are a number of things mentioned in the AAMC MCAT Topic List that were not covered in EK materials and I did not go over them during my 2 semesters of bio this past year. Could you comment on what we need to know about some of these. Thanks.

Genetics:leakage, penetrance,expressivity
meiosis and genetic variability-sex linked characteristics:cytoplasmic inheritance
meiosis and genetic variability-mutation:advantageous vs deleterious mutations

could someone go over #ATP at different points of glycolysis & krebs that we need to know? thanks

The ATP count of glycolysis, Krebs cycle etc. is well covered in the biochem & cell Study Q & A thread.

I encounter things like Growth Factors, Intrinsic Factors and others in my readings, because they're not well explained. What are they? Proteins? Enzymes? How should I think of them?

Confused :(

Hey guys,

Where do B cells mature? I know that T cells mature in the thymus, but I can't find where B cells mature.

Thanks!

there was this dumb question in BR...


in the sliding filament model, which part has the least actin filament overlap?

so i thought "least," the ultimate least, would be "none." so of course the most non-overlap would be when it is at its longest length...

however, the answer is when it is at its second shortest length (before the optimal length), because they meant that "least" is "a little bit" overlap, not "none."

so if there is ever a question that asks "least"... should we never assume it means "none"?

in the passage, it said that "stibestrol is a crystalline NON-steroid hormone with estrogenic effects often superior to those of the strogen, estradiol"


and then have have questions about how it affects cells, etc.

since they said it was a non-steroid hormone, i thought that they meant it would act in a second messenger way. however, to my surprise, it locates to the nucleus like a regular steroid.. whattt?? why did they say it was non-steriod then? how are we suppose to know that it wont do the second messenger pathway?? :(

this is from 4921, bio passage number 3

...
The first polar body also divides resulting in 2 more polar bodies. Therefore, at the end of meiosis II, there should be at least 2 and maybe 3 polar bodies (if there is fertilization).
In short, the primary oocyte is at Prophase I until puberty.


I agree with everything else you said, however I believe the two polar bodies (one produced following meiosis I, and the 2nd following meiosis II) degenerate and do not divide. If you want to be picky, the 1st polar body degenerates, wherease the 2nd polar body (produced from the secondary oocyte, not the 1st polar body) is discarded.
According to Ross, Reith and Romrell's Histology (2nd ed.- the forerunner to Ross, Kaye and Pawlina) "in the human, the first polar body does not divide; therefore the fertilized egg can be recognized by the appearance of the second polar body. The polar bodies, which are not capable of further development, undergo degeneration".
Unfortunately, in the diagram on the subsequent page (pp. 656-657) it seems to suggest that the 1st polar body would divide.
My 3rd edition Moore ("The Developing Human") seems to bear this out.
I've usually taken to following text over figures in such cases, but to each his own. I haven't heard of any more recent research, and a medline search didn't reveal anything particularly exciting about 1st polar body division.

And I wouldn't give polar bodies a second thought in studying for the MCAT, except to know that the meiotic divisions are asymmetric in the female, but symmetric in the male. You won't be making calls on ovarian biopsies (unless they've come a long way in providing good images since I last saw an MCAT).

Cheers!

Kevin

Can someone please! go through the cell cycle and mark if it's N, 2N, or 4N at the respective stage? I am having a great deal of confusion and conflict, as my Kaplan book says one thing and my Bio-major friend says another which is in direct contradiction...and I believe him, but now my sister tells me that the Kaplan book is right! WTF!

Here, I'll start it for you so you can fill it in for me. Thanks in advance...

G1
S
G2
Prophase
Metaphase
Anaphase
Telophase

Same for meiosis too please (I know what's happening at each of the stages, just unclear of the genetic #s)

edit- Okay...now I think I'm just really trying to hurt myself...it's 1 cell @ 2N going into meiosis I and 2 cells @ N going into meiosis II producing 4 cells @ N?? I don't see how the genetic information is being conserved at all here....2 x N doesn't equal 4 x N?

Can someone please! go through the cell cycle and mark if it's N, 2N, or 4N at the respective stage? I am having a great deal of confusion and conflict, as my Kaplan book says one thing and my Bio-major friend says another which is in direct contradiction...and I believe him, but now my sister tells me that the Kaplan book is right! WTF!

Here, I'll start it for you so you can fill it in for me. Thanks in advance...


Same for meiosis too please (I know what's happening at each of the stages, just unclear of the genetic #s)

edit- Okay...now I think I'm just really trying to hurt myself...it's 1 cell @ 2N going into meiosis I and 2 cells @ N going into meiosis II producing 4 cells @ N?? I don't see how the genetic information is being conserved at all here....2 x N doesn't equal 4 x N?

Ploidy is the number of basic chromosomes in a cell (in humans one chromosome from father, one from mother = 2N.).

Mitosis (Ploidy never changes):

G1 2N
S 2N
G2 2N
Prophase 2N
Metaphase 2N
Anaphase 2N (sort of)
Telophase 2N (sort of)

Meiosis (Ploidy gets halved):

G1 2N
S 2N
G2 2N
Prophase I 2N
Metaphase I 2N
Anaphase I N (sort of)
Telophase I N (sort of)

Prophase II N
Metaphase II N
Anaphase II N (sort of)
Telophase II N (sort of)

I think the answer to the second part of your question is that Mitosis and Meiosis have different separation during Anaphase.

In Mitosis, you separate the chromosomes by moving sister chromatids in opposite directions.

In Meiosis, you separate homologous chrmosomes in opposite directions. The second division will separate the chromatids of one homologue.

X = chromosome 1, x = chromosome 1 homologue.
X' = chromosome 1's sister chromatid, x' = chromosome 1 homologue's sister chromatid.

Mitosis:

(Metaphase) XX'xx' ----->>>> (Anaphase) Xx | X'x'
(All genetic information is preserved during division, thus ploidy remains 2N)

Meiosis:

(Metaphase I) XX'xx' ------->>>> (Anaphase I) XX' | xx'
(Homologues have been divided, losing half the information in Anaphase I. Thus, the ploidy becomes N)

I hope this isn't too confusing.

I would argue that after S-phase, you have twice as many chromatids, which are only duplicated chromosomes (still the same chromosome number, only with two chromatids per chromosome).

So when the sister chromatids separate in anaphase, the resulting chromosome number (N) should be 4N, because you then have 92 chromosomes still bound together in one cell, until the cleavage furrow is complete.
My take would be:
G1 (2N)
S (2N, with twice the actual DNA complement)
G2 (2N)
M: Prophase (2N), Metaphase (2N), Anaphase (4N), Telophase (4N)

following cytokinesis, you have two cells, both 2N. Therefore the chromosome number in telophase has to be 4N.

Similarly in meiosis: (for accounting purposes much like 2 successive rounds of mitosis without the intervening S-phase)

G1 (2N)
S (2N with twice the DNA complement)
G2 (2N)
Meiosis I:
Prophase I (2N)
Metaphase I (2N)
Anaphase I (4N)
Telophase I (4N)
Cytokinesis : 2 x 2N. I'll write it as (2N) (2N) to indicate two cells.
Prophase II: (2N) (2N)
Metaphase II: (2N) (2N)
Anaphase II: (N+N) (N+N) maternal and paternal chromatids segregate independently to opposite poles of the cell
Telophase II: (N+N) (N+N)
Cytokinesis: (N) (N) (N) (N)

But it is little substitute for a book. Nevertheless, there must be a 4N complement following separation of duplicated chromosomes at anaphase for mitosis. Some authors describe a duplicated chromosome complement (following S-phase) as 4N. You should understand the difference. I'm not sure what is written in the Kaplan review, haven't read it myself.

Cheers

Kevin

in the passage, it said that "stibestrol is a crystalline NON-steroid hormone with estrogenic effects often superior to those of the strogen, estradiol"


and then have have questions about how it affects cells, etc.

since they said it was a non-steroid hormone, i thought that they meant it would act in a second messenger way. however, to my surprise, it locates to the nucleus like a regular steroid.. whattt?? why did they say it was non-steriod then? how are we suppose to know that it wont do the second messenger pathway?? :(

this is from 4921, bio passage number 3

This is a tricky question. Stibestrol is probably an amino acid derivative. This type of hormone can act both like peptide and steroid hormones. Since the passage states that its effects are superior to estradiol (a steroid hormone) you can infer that it must act in the same manner as steriod hormones by entering the nucleus. So I guess the key to answering this question is knowing that there are three classes of hormones - peptide, steroid and amino acid - and that amino acid hormones can activate target cells in the same manner as the other two.

A big bump for organismal bio.

bumping

Howdy.
The sympathetic NS uses norepinephrine to increase BP/HR + blood glucose, dialates pupils, opens up the lungs and shunts blood away from the GI. O.k., but why, oh why, would I want blood to go away from my brain and heart if I'm being chased by QofQuimica?

Caboose.

Howdy.
The sympathetic NS uses norepinephrine to increase BP/HR + blood glucose, dialates pupils, opens up the lungs and shunts blood away from the GI. O.k., but why, oh why, would I want blood to go away from my brain and heart if I'm being chased by QofQuimica?

Caboose.

I don't think the blood goes away from your brain and heart. It goes away from your GUT, which makes sense, because if you just sit around and digest, then I'm gonna getcha. :meanie:

I don't think the blood goes away from your brain and heart. It goes away from your GUT, which makes sense, because if you just sit around and digest, then I'm gonna getcha. :meanie:
:scared:

Caboose found an error. It's a good thing we realized it too because I would have been toast.
Caboose.

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.

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.

bump

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.

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?

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. :p

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.

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

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.

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

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?

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. ;)

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....

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.

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.

http://i29.photobucket.com/albums/c264/glimgirl/heartpic.png

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.

http://i29.photobucket.com/albums/c264/glimgirl/hemodynamics.gif

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. :)

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!? :eek: (notice that I actually had it backwards in my original question :laugh: )

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

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!? :eek: (notice that I actually had it backwards in my original question :laugh: )

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.

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?
----------

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 :confused:


Thanks!

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.

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)

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):
http://www.biotopics.co.uk/as/disaccharideformation2.gif

This one is cellobiose (beta link):
http://opbs.okstate.edu/~Blair/Bioch2344/Chapter10/CPT10FIGS/cellobiose.gif

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

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...

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.

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:

http://www.tgs-chemie.de/kohlen15.gif

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.

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!

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.

(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...

(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?

(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.

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.

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 :thumbup:

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 :thumbup:
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???

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...

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.

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'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.

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.

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.

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. :)

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. :cool:
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. :cool:
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.

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.

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.

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. :p

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. :p

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.

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. :p

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?

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?

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?

Are centrioles found only in animal cells?

and are vacuoles found on both plant and animal cells?

sympa vs parasympa, please help

which is vasocontriction and which is vasodilation, or is it all differently.

Are centrioles found only in animal cells?

and are vacuoles found on both plant and animal cells?

Yes and yes.

sympa vs parasympa, please help

which is vasocontriction and which is vasodilation, or is it all differently.

Sympathetic constricts circulation to the skin and the GI tract while increasing circulation to the lungs and the skeletal muscle. Parasympathetic is the opposite.

Easy and quick way to remember:

Parasympathetic = Restin & Digesting (aka increases circulation to the GI)...Think Homer Simpson sitting on the couch

Sympathetic = Flight or Fight mechanisms (bronchodilate, pupil dilation, increase circulation to skeletal m.)...Think here of Lance Armstrong on his bike

This may be beyond MCAT, but;

Sympathetic you can think of as "Running from a bear through the woods at night"
This gives you the bronchodilation, pupil dilation, increase circulation to skin and skeletal m. etc.

Hope this helps

yeah yeah this is where i am confused on, so when you increase your blood flow, do you constrict blood vessels or dialate them. and is it always the same?

Increasing blood flow necessitates an increase in diameter (aka dilation) or an increase in pressure (however the body likes to keep this as constant as possible).

so it depends then? ooh then how about a simpler question does epinepherine do anything to blood vessels, if not then which other sympathetic hormons does and how.

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.

Actually, HCG has been used successfully for treating infertility, in absence of FSH. There seems to be some debate on this very question within fertility medicine, by my readings. The usual protocol is a long (many months) course of HCG before adding in the HMG (FSH). Of course, it takes 80-90 days to get a swimmer (medical lingo) ready for his big trip.

Other studies show it is FSH operating in an environment of testosterone (via LH stimulation) which produces sperm.

Max

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.

Kevin,


The suppression is surely produced by the induced T. I am not aware that LH directly suppresses at the hypothalamus or pituitary. However, we are finding more and more sites where LH is bioactive, and this is also a good reason to use HCG throughout the steroid cycle in cases where LH production is reduced.

HCG is "to suppressive' only when itr is being administered while we are trying to recover the HPTA. Then it is, just as Androgel or 100mg pf test cyp per week would be. IOW, you cannot "hide" androgens from the HP.

DHT, Testosterone, Estrogen, Progestins, Prolactin, can all act on the HP negatively.

There are two potential feedback loops: a long loop and a short one. The long loop involves LH stimulating testosterone production, which along with estrogen suppress GnRH/LH production.

The short loop has LH or its synthetic analog hCG acting directly back on the hypothalamus to blunt GnRH, or acting on the pituitary to block LH production.


Max

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The simplified schematic of the ANS neurotransmitters generally has the Sympathetic branch's preganglionic neuron releasing Ach & the postganglionic neuron releasing epine. or norepine.
In the parasympathetic both pre & postganglionic releasing Ach.
The somatic system relases Ach at the neuromuscular junction.

There are than a host of questions in which altering the levels of Ach effect the Parasym & somatic ONLY while changes in norepine. effect the sympathetic?

As the sympathetic NS also has a Ach mediated synpase why isn't it's function also mediated by changes in Ach?

What exactly is the point of the loop of henle?

Thanks.

What exactly is the point of the loop of henle?

Thanks.
Please don't start new threads in the subforum. Just post your question in the appropriate question thread.

I don't really understand your question. The loop of henle is a part of the nephron and is involved with reabsorption of salts and water.

What is the difference between an absolute refractory period and a relative refractory period? At what points on the action potential graph do they occur? When are they over?

The refractory period allows the voltage sensitive ion channels to restore their original polarity. The absolute refractory period of approximately 1 millisec is when the Na+ channels are open. This is the left half of the sharp upward peak on the graph. No new action potentials can be generated during this period. The relative refractory period occurs largely when the membrane is hyperpolarized (-80 mV), when the K+ channels are open and the Na+ channels are recovering in a random order. The action potential is more difficult to generate during this period because a greater stimulus is required to reach the threshold as opposed to the resting potential (-70 mV). On the graph, this is the dip immediately following the large spike. Yet it can also happen on the right half of the spike as well, but the closer in time to the peak voltage, the greater the stimulus required. These refractory period are both over after approximately 5 milliseconds.

Nice answer Dr. D, would you like to take a whack at post 114.

How important is human physiology (i think the same thing as organismal biology) on the mcat?

How important is human physiology (i think the same thing as organismal biology) on the mcat?
This is a tough question to answer. Physiology is definitely not my strength either (yet, anyway!), so I spent quite a bit of time studying for it. I would say that it's advisable to make sure that you are comfortable with all of the AAMC topics in biology. If there are things on that list that you don't know, you should study them. That being said, you aren't in med school yet, and they don't expect you to know as much physiology as a med student does. So you don't have to have more than a basic understanding of each topic.

Lindy, I'm sorry, but I don't think any of us know the answer to your question. FWIW, it's definitely beyond the scope of the MCAT. ;)

I am having some trouble deciphering passages that deal with kidney topics like Renal Clearance, renal plasma flow, glomerular filtration rate and filtration fraction. I have come across two passage like this so far (one in EK and one in an AAMC test). I have a lot of trouble even reading these passages and understanding what these terms mean.
I have spent a lot of time learning about the nephron and its anatomy plus different hormones that act on the nephron but my review books (like EK) do not cover these filtration rate type topics.
Does anyone know any good websites or references that simply, and comprehensively cover these topics?
I am really scared I will get a filtration passage on my MCAT and get 90% of these questions wrong.

Thanks so much!

I am having some trouble deciphering passages that deal with kidney topics like Renal Clearance, renal plasma flow, glomerular filtration rate and filtration fraction. I have come across two passage like this so far (one in EK and one in an AAMC test). I have a lot of trouble even reading these passages and understanding what these terms mean.
I have spent a lot of time learning about the nephron and its anatomy plus different hormones that act on the nephron but my review books (like EK) do not cover these filtration rate type topics.
Does anyone know any good websites or references that simply, and comprehensively cover these topics?
I am really scared I will get a filtration passage on my MCAT and get 90% of these questions wrong.

Thanks so much!

Are you using the EK 1001 bio book? I think this had a lot of questions about this kind of stuff.

Are you using the EK 1001 bio book? I think this had a lot of questions about this kind of stuff.

I do not have the EK 1001 bio book. Any other suggestions?

Thanks.

Hi, quick question. Is aldosterone release stimulated by ACTH (which stimulates adrenal cortex to release hormones) or angiotensin II (the renin cascade)?? :confused:

Hi, quick question. Is aldosterone release stimulated by ACTH (which stimulates adrenal cortex to release hormones) or angiotensin II (the renin cascade)?? :confused:
both - however the major regulator of aldosterone secretion lies in the Renin-Angio system

both - however the major regulator of aldosterone secretion lies in the Renin-Angio system

great, thanks! :thumbup:

In the EK Bio book, they bolded and underlined a number of different dissacharides (sp?). I was just wondering, for the MCAT do we need to know which two monosacharides make up a particular dissacharide?

Thanks!

I can't be sure, but I think I remember having a passage about Lactose on my MCAT that required me to know the constituents. This was a few years ago, but I do not think that it would be the type of thing that is out of the testing realm.

On my tests, I've seen lactose, sucrose, and maltose show up. I would memorize those. I took the test last August and lactose was a free standing question.

I'm having trouble linking effect of blood pressure on glomerular filtration rate. When the blood pressure increases, the parasympathetic system should be activated to decrease the blood pressure, and this may cause an increase or decrease in the GFR? My logic is that increased blood pressure usually means high blood V, so to increase blood V, you increase GFR? How exactly does GFR do this?

And when body temp is low, the sympathetic system is activated right? Thanks!

In a pedigree chart, how do you figure out if it's a domnant or recessive inheritance? My notes says to check if it skips generations but I have no idea what that means.

Thank you!

For recessive inheritance, usually the parents don't have the disease phenotype, but the children have it, so it "skips" a generation. But for dominant dominant inheritance, both the parents and children will have the disease phenotype.

Thanks 4s4 for the quick reply!!! :)

I have two questions:

1. Do the parasympathetic and sympathetic divisions of the autonomic system have both sensory and motor divisions? Because it seems books only talk about the motor (efferent) parts.

2. What hormones does the hypothalamus synthesize? I know it makes the posterior pituitary hormones, ADH and oxytocin, but what about the anterior pituitary hormones?

Thanks!

I have two questions:

1. Do the parasympathetic and sympathetic divisions of the autonomic system have both sensory and motor divisions? Because it seems books only talk about the motor (efferent) parts.

2. What hormones does the hypothalamus synthesize? I know it makes the posterior pituitary hormones, ADH and oxytocin, but what about the anterior pituitary hormones?

Thanks!

1)as far as i know, motor only.

2)ADH, oxytocin, GnRH, and other releasing hormones.
anterior makes their own hormones.

I have two questions:

1. Do the parasympathetic and sympathetic divisions of the autonomic system have both sensory and motor divisions? Because it seems books only talk about the motor (efferent) parts.

2. What hormones does the hypothalamus synthesize? I know it makes the posterior pituitary hormones, ADH and oxytocin, but what about the anterior pituitary hormones?

Thanks!

1. Both sympathetic & parasympathetic nervous systems have an afferent (sensory) & an efferent (effector/motor) component.

2. First, you got the Post. Pituitary hormones correct (the post. pituitary is more or less a continuation of the hypothalamus caudally). The Ant. Pituitary is a gland in traditional sense. It secretes; GH (Growth Hormone), ACTH (Adrenocorticotropic Hormone), TSH (Thyroid Stimulating Hormone), Prolactin, & the Gonadotropins (LH & FSH).

I did not provide any detail to the first as your question did not see to need much.

Why is arterial blood pressure in legs greater than the arms?

In a pedigree chart, how do you figure out if it's a domnant or recessive inheritance? My notes says to check if it skips generations but I have no idea what that means.

Thank you!

From what i know, A recessive trait is carried genotypically through generations but wont appear phynotypically unless its homozygous..So when they say that the trait has skipped generations means tht its there in heterozygous form and hence not expressed phynotypically

I have a really difficult time understanding how to tell whether a response is the results of sympathetic or parasympathetic autonomic nervous system activity. I am a biochem major and I never took a physiology class. The Examcrackers books says that sympathetic is "fight or flight" and parasympathetic is "rest or digest," but this is not very helpful.

I have a really difficult time understanding how to tell whether a response is the results of sympathetic or parasympathetic autonomic nervous system activity. I am a biochem major and I never took a physiology class. The Examcrackers books says that sympathetic is "fight or flight" and parasympathetic is "rest or digest," but this is not very helpful.

well try to break it up into body parts:

Sympathetic Parasympathetic

blood flow to gut + kidneys decr incr
blood flow to skeletal muscles incr decr
iris dilate constrict
lung bronchioles dilate constrict
cardiac output incr decr
liver glycogen breakdown ----

hope these help

Here is a really good way to remember Parasymp. vs Sympathetic:

Sympathetic = RUNNING FROM A BEAR IN THE WOODS AT NIGHT...Meaning you are going to have eyes dilating to see trees (mydriasis) + all your fight or flight responses of increased HR, vasodilation to muscles, & glycogenolysis. Also negative GI effects

Parasympathetic = Resting & Digesting...Pupillary constriction (miosis) increased GI function, & your SLUDE effects (Salivation, Lacrimation, Urination, Defecation & Emesis). So again, Parasympathetic is rest & digest + SLUDE.

P.S.--SLUDE may be beyond the scope of the MCAT.

Kind of a dumb/basic question, but:

When bicarbonate (HCO3-) is present in tissues/blood in high amounts, is this considered alkalosis or acidosis? I would assume since it would act mostly as a base, that it would cause a pH increase? For some reason I keep mixing this up.

Look at the [H+] concentration only. if its increased then its acidosis, if its decreased its alkalosis.



I used to get confused about this a lot too. hope that helps

Hey, thanks for the replies above about parasympathetic vs. sympathetic. They really helped. =)

Another topic that I'm shaky on is action potentials. I know that the resting potential of a neuron is always negative on the outside and positive on the outside, and a depolarized neuron will be positive on the inside and negative on the outside. I just have trouble understanding the proton pumps and exactly why pumping out three Na "protons" per two Potassium "protons" is creating the resting negative potential inside the cell.
Thanks again guys

Hey, thanks for the replies above about parasympathetic vs. sympathetic. They really helped. =)

Another topic that I'm shaky on is action potentials. I know that the resting potential of a neuron is always negative on the outside and positive on the outside, and a depolarized neuron will be positive on the inside and negative on the outside. I just have trouble understanding the proton pumps and exactly why pumping out three Na "protons" per two Potassium "protons" is creating the resting negative potential inside the cell.
Thanks again guys


The "simple" answer is:

3 Na+ out = loss of "3"
2 K+ in = gain of "2"

Net loss of "1", which leads to an overall negative charge.

new question please help very appreciated.

Under what conditions would the flow the Na/K pump be reversed, and why or how

Also with refractory periods, does it raise or lower the threshold, and how.

new question please help very appreciated.

Under what conditions would the flow the Na/K pump be reversed, and why or how

Also with refractory periods, does it raise or lower the threshold, and how.
You mean to pump the ions in the opposite directions? I've never heard of that happening, but maybe one of the bio people can come up with an example. Refractory periods occur after an action potential, and they are a period when the neuron is not able to fire. Basically what is happening is that when the potassium leaves the cell through the potassium channels, the cell "overshoots" and becomes more negative on the inside with respect to the outside (hyperpolarized). So the threshold level itself does not move, but what does move is the place where you're starting from, which is now lower than the normal resting level. Take a look at this picture, and it should help you see what I mean. You will see that the refractory period level is in an energy "well," but the threshold is at the same level that it always was.

http://content.answers.com/main/content/wp/en/thumb/0/02/300px-Action-potential.png

Why is arterial blood pressure in legs greater than the arms?

probably due to gravity's (or the acceleration of gravity's) direct relation to force. Recall fluid dynamics: P=F/A

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probably due to gravity's (or the acceleration of gravity's) direct relation to force. Recall fluid dynamics: P=F/A

The way I look at it is just the P is related (in this sense) to h the height of fluid above it.

What are positive and negative Modulators

Acid= H+ increase=low ph
Alkaline/Base=H+ decrease=high ph
..is this correct?

thanks,
dxu

could somebody please answer this quickly?

i'd appreciate it

dxu

could somebody please answer this quickly?

i'd appreciate it

dxu
A few things:

1) Please do not start new threads in the MCAT subforum. You should post your question in the appropriate already existing thread.

2) I am a medical student, and thus, I am not on SDN 24-7 ready and waiting to answer questions the moment someone posts them in the subforum. I do log on every day, so your questions will generally be answered within 24 hours. But FYI, you should not expect to get a question answered right away unless you and I happen to be on at the same time. The same goes for all of the other subforum volunteers; this is a hobby, not our day job. We appreciate your patience and understanding on this issue.

3) Positive modulators are things that activate a receptor or enzyme. Negative ones then will do the opposite. Your analysis of acids versus bases and pH is correct.

A few things:

1) Please do not start new threads in the MCAT subforum. You should post your question in the appropriate already existing thread.

2) I am a medical student, and thus, I am not on SDN 24-7 ready and waiting to answer questions the moment someone posts them in the subforum. I do log on every day, so your questions will generally be answered within 24 hours. But FYI, you should not expect to get a question answered right away unless you and I happen to be on at the same time. The same goes for all of the other subforum volunteers; this is a hobby, not our day job. We appreciate your patience and understanding on this issue.

3) Positive modulators are things that activate a receptor or enzyme. Negative ones then will do the opposite. Your analysis of acids versus bases and pH is correct.

First off, I did not move this thread here, the mod did, so thank them. I posted it in the pre-osteopathic thread for the specific purpose of ppl are in there more than here and I didnt believe this to be the correct forum.

Secondly, I realize that you have other things and this is a hobby. I wasn't trying to pushy or impatient. I just had a test and was hoping someone that was looking at my post would answer it instead of just read it and not answer.

Lastly, thank you for the answer to my question. I appreciate it.

dxu

First off, I did not move this thread here, the mod did, so thank them. I posted it in the pre-osteopathic thread for the specific purpose of ppl are in there more than here and I didnt believe this to be the correct forum.

Secondly, I realize that you have other things and this is a hobby. I wasn't trying to pushy or impatient. I just had a test and was hoping someone that was looking at my post would answer it instead of just read it and not answer.

Lastly, thank you for the answer to my question. I appreciate it.

dxu
You're welcome on both accounts. I apologize if my previous post sounded testy; it's just been a rough week. :)

Hey guys,

Where do B cells mature? I know that T cells mature in the thymus, but I can't find where B cells mature.

Thanks!
I got the text books for the protocols for creating artificial white blood cells. If you would like to discuss artificial white blood cells let me know. Its all about Cloned Lymphocytes that are produced outside of the body. (Ex-vivo production)

http://khalidnatto.tripod.com

Where is a refractory period on action potential curve?
Is it on the repolarizaton or hyperpolarization?
Thanks

I got it.
Here is a link for people who are interested:
http://www.mfi.ku.dk/ppaulev/chapter1/Chapter%201.htm

Where is a refractory period on action potential curve?
Is it on the repolarizaton or hyperpolarization?
Thanks
Great link; thanks for posting it. For anyone who doesn't want to wade through an entire chapter, the short answer is that there are actually two refractory periods. One is during the action potential itself (absolute refractory period), and one is during the hyperpolarization phase (relative refractory period). During the absolute refractory period while the action potential is occurring, no further action potentials can be initiated. In other words, once the action potential begins, the cell cannot fire again until after that action potential is over. The relative refractory period occurs during hyperpolarization. During the relative refractory period, the cell can initiate a new action potential, but a greater than normal stimulus is required to do this. Both refractory periods are labeled in the figure below.

http://human.physiol.arizona.edu/SCHED/CV/Wright/ap-4.gif

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,

Hi
i have a Q about a reflex arch. In the kaplan review notes, it is noted "the sensory neuron synapses with motor neuron in the spinal cord" i take it means that they directly synapse with each other with one synapse in between them. and the pic in the book is drawn to confirm this. just one direct synapse.

But in one of their quizzes they mention that in a reflex arch a minimum of 3 neurons must participate (i assume the 3rd one is interneuron in the spinal cord), meaning that there is discrepancy between the book explanation and the quiz.
may be there is a difference between a simple reflex arch and some other arch. hmmm?

what is really going on there? am i missing something? please help.
thank you very much:)

Kaplan is over-simplifying the reflex arch.

The fact as I see it is: you have your monosynaptic and polysynaptic reflexes.

Monosynaptic:

sensory -> motor neuron (this corresponds to what you quoted the Kaplan Review as saying first)

Polysynaptic:

sensory -> motor neuron 1
and
sensory -> motor neuron 2

Sorry, I can't draw these out well, but in polysynaptic (this corresponds to what Kaplan says about a min. of 3 neurons) the sensory innervates 2 motor neurons. The end result is recruiting two muscles to perform the reflex. Think: antagonistic muscle pairs.

I don't _think_ that other interneurons are present in the reflex arch, mainly because they don't provide much benefit -- reflexes are very simple and an organism needs them to be fast.

.

but how do we know whether they mean poly or mono synaptic when they are asking about the arch? they just ask what is true about the arch--> minimum 3 neurons is their answer.?

Not my problem :p. MCAT questions will be more clear.

BTW, my diagram for the polysynaptic reflex arc is wrong. There's always at least one interneuron thrown in the mix for polysnaptic arcs.

repost. repost. repost. whoops

Some passages in the respiratory tract do not participate in gas exchange; these passages are known as physiological dead space. Compared to air in the alveoli, air in the physiological dead space will have:

A. a higher partial pressure of carbon dioxide and oxygen.
B. a higher partial pressure of carbon dioxide and a lower partial pressure of oxygen.
C. a lower partial pressure of carbon dioxide and a higher partial pressure of oxygen.
D. the same partial pressure of carbon dioxide and oxygen.

The answer is C. The explanation says that the physiological dead space is not involved in gas exchange. This means that the composition of air in the dead space is virtually identical to that of atmospheric air.

Why? I mean why wouldn't the answer be D since no gas exchange is happening. I don't exactly see why we can treat it like air outside the body.

Why? I mean why wouldn't the answer be D since no gas exchange is happening. I don't exactly see why we can treat it like air outside the body.

*scratches head* Well, it is air from outside the body, and because no gas exchange is occurring, it hasn't changed from "outside-air". That's the best explanation I can provide... unless you can explain in more detail why you think the answer should be D? First of all, you can eliminate D completely because you know that alveoli DOES participate in gas exchange (in contrast to dead space air). Therefore your above reasoning is wrong from the start.

Since all bacteria lack mitochondria, do all of them make 2 ATP per glucose via glycolysis? What about those aerobic bacteria? I mean since some have electron transport chains, and oxygen, which is very high in electron affinity, shouldn't they make more ATP than the amount from glycolysis?

This was confusing to me because I was doing one of the kaplan qbank problems and it stated that bacteria can only make 2 ATP per glucose

*scratches head* Well, it is air from outside the body, and because no gas exchange is occurring, it hasn't changed from "outside-air". That's the best explanation I can provide... unless you can explain in more detail why you think the answer should be D? First of all, you can eliminate D completely because you know that alveoli DOES participate in gas exchange (in contrast to dead space air). Therefore your above reasoning is wrong from the start.

hey trozman...thanks for the help. what you said totally made sense. my reasoning was just off. i was thinking since to exchange was happening that the partial pressure of oxygen and CO2 should be the same (i wasn't comparing it to the alveoli, but i see that even if i was thinking that my answer would still be wrong).

double post sorry

Can someone please explain me the concept behind this. I am totally confused about how hypotonicity and hypertopnicity relate to these

thanks

Glucose is a charged molecule so it can't pass through the cell membrane on its own. Normal cells have facilitated proteins to carry Glucose across their membrane. Intestinal and Kidney cells have Na+/Glucose symporters which concentrate glucose inside the cells, using the energy provided by cotransport of Na+ ions down their electrochemical gradient (meaning its energentically favorable for Na+ to leave the