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Why is GTP, not ATP, produced in Gluconeogenesis & TCA Cycle?
In both gluconeogenesis and the TCA cycle, there is a point in each that GTP is produced instead of the usual ATP. My question is why GTP and not ATP for these 2 specific steps?

I've added to your title to put the focus on GTP. It's a good question. I must say I've wondered about it myself and never seen or come up with answer, although I haven't put much effort into doing so.

Welcome to Biology.SE. This is a good question, maybe you are interested in this question about why ATP is the preferred energy carrier.

Nice question. Beginning with Krebs cycle, there is actually no specific answer as both GTP and ATP are produced. First, see this article for why GTP is the more frequent product:

It may be that at the beginning, both GTP and ATP were equally available for energy and that the succinyl CoA synthetase reaction happened to choose GTP and that reaction is still with us today, billions of years later, even though we run the TCA cycle clockwise (forward) instead of backwards.

So, actually both ATP and GTP can be produced. And indeed both are produced, depending upon the organism. See this article:

A step with significant variability is the conversion of succinyl-CoA to succinate. Most organisms utilize EC 6.2.1.5, succinate–CoA ligase (ADP-forming) (despite its name, the enzyme operates in the pathway in the direction of ATP formation). In mammals a GTP-forming enzyme, succinate–CoA ligase (GDP-forming) (EC 6.2.1.4) also operates. The level of utilization of each isoform is tissue dependent. In some acetate-producing bacteria, such as Acetobacter aceti, an entirely different enzyme catalyzes this conversion – EC 2.8.3.18, succinyl-CoA:acetate CoA-transferase. This specialized enzyme links the TCA cycle with acetate metabolism in these organisms. Some bacteria, such as Helicobacter pylori, employ yet another enzyme for this conversion – succinyl-CoA:acetoacetate CoA-transferase (EC 2.8.3.5).

So, there is no strict rule that only GTP will be produced instead of ATP at that step. And, afterall, it does not matter much as both of them carry equal energy.

Now coming to Gluconeogenesis, GTP is hydrolyzed by the enzyme Phosphoenolpyruvate Carboxykinase or PEPCK. This enzyme can also work with both ATP and GTP, depending on the sepcific type of enzyme. See this article (links added separately):

It is classified under EC number 4.1.1. There are three main types, distinguished by the source of the energy to drive the reaction:

4.1.1.32 - GTP (PCK1, PCK2)
4.1.1.38 - diphosphate
4.1.1.49 - ATP

Thus, there is no strict protocol for using specific energy carrier in the process, both ATP and GTP can be used in the reaction. Its just because GTP is more frequently used that it is mentioned instead of GTP/ATP in the reaction.

I would say it is not known if the GTP/ATP distinction is important -- maybe it really doesn't matter, since the two can be interconverted -- but maybe it does.The kinetics is probably different since the GTP concentration is typically an order of magnitude smaller than ATP. Maybe there is some compartmentalization effect that we don't understand, as with NAD/NADP.  It's curious that major anabolic processes use GTP (protein synthesis, gluconeogenesis), while other energy-demanding processes (pumps, motor proteins) use ATP ...

@roland this is a valid point, there is still a lot more that remains unknown. But on searching, I found that this distinction (GTP/ATP) is limited to just the different types of enzyme: different types of same enzyme use different molecules. So maybe it is that during evolution, enzymes either learnt that GTP is also useful or they tried to rely as much on ATP as possible. But I'll add more details when I find them :)


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What mushroom is this?
A lot of these popped up recently in our backyard (St. Louis, Missouri, United States).  They are all grouped into these clusters and there were probably 5 of these big clusters.
Anyone know what type of mushrooms they are?

Where do you live?

@Remi.b I live in St. Louis, Missouri, United States.

http://www.mycokey.com/newMycoKeySite/MycoKeyIdentQuick.html found a page might help.

Pick up one; and add a photograph of what are beneath the cap. especially if there is any annulus and volva around the stipe. add 1 photograph of close-up of gill-patterns.

source: Stack Exchange

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sort: votes


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Identification of brown butterfly with orange/black/white spots
These brown butterflies are very frequent at my place now. Two or three can be found quietly sitting with their wings folded everyday, at different locations. It's a transition period between Autumn and Winter here, West Bengal, India.
What species is this?
Why is it taking shelter inside a house? They don't seem to move much, even during the day I've found one sitting quietly by the window. It wasn't flying off even after being disturbed.

I think this is the "Dark Evening Brown" or Melanitis phedima possibly Melanitis phedima bela:

Some further information can be found here (image 1) and here (image 2). If you look close at the second image, you can see the spot on the wing.
Why they are coming into the houses is something I can only speculate about, but probably they are either attracted by light or by warmth.

As to your question why they come into the house: Some butterflies survive winter (hibernate) on a dry, cool but frost-free place such as parts of houses that are not heated. In autumn they actively search for such places. I often find them in a wood stack or on the attic. In Europe, examples are Gonepteryx rhamni, Polygonia c-album and Inachis io. I think the latter two belong to the same family as Melanitis phedima, so it might try to find a place to hibernate. For more info see https://www.britishbutterflies.co.uk/winter.asp

Slight wording issue; For these species (ones with a life history that includes hibernation as adults), it's not that they can survive winter as adults, it's how they survive winter. In most taxa of insects living in temperate regions species survive winter as either eggs, larvae, pupae or adults, or a mixture of hibernation stages.

@fileunderwater You are absolutely right. Improved that in my answer.

How long can these butterflies live?

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I just saw this bird outside my apartment. Anyone know what it is? (Texas, US)
Saw this bird outside my apartment in College Station, Texas  and have never seen anything like it before!
It is about the size of a hand.

The climber plant on the wall may be Ficus pumila

Nice camouflage and funny tail.

That species is so... special. Unique, beautiful and contrasting, all in one.

It's also worth noting that these birds are the subject of some wonderful youtube videos

It is American Woodcock, Scolopax minor.

Superbly camouflaged against the leaf litter, the brown-mottled American Woodcock walks slowly along the forest floor, probing the soil with its long bill in search of earthworms. Unlike its coastal relatives, this plump little shorebird lives in young forests and shrubby old fields across eastern North America. Its cryptic plumage and low-profile behavior make it hard to find except in the springtime at dawn or dusk, when the males show off for females by giving loud, nasal peent calls and performing dazzling aerial displays.

The newborns are even more camouflaged in downs.
References:

Audubon
All about birds

I've found whatbird.com to be pretty good for identifying American birds.  Asking it for grey and brown medium-sized birds that are commonly found in Texas gives 14 options, of which the best match is the American woodcock, as suggested by Sanjukta (which is conveniently early on the alphabetical list!)


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Is it possible for an organism that is polypoloid with an odd number of sets of chromosomes (e.g. 5 sets) to be fertile?
Is this possible, since there is five sets, there would be an unequal separation of homologous chromosomes during anaphase I of meiosis?

what do you think? have you thought through this question? have you looked somewhere for the answer? is this homework?

I think it is a good question +1

Yes, it is possible. There seems however to always come up with a cost in fertility eventually of the order of 2/3!
You should have a look at Ramsey and Schemske 1998. I don't remember it well enough to make a good summary (maybe someone else could do that?!) but it is a classical article. Here is a sentence from their abstract

In contrast to the common claim that triploids are sterile, our results indicate that the triploid bridge pathway can contribute significantly to autopolyploid formation regardless of the mating system, and to allopolyploid formation in outcrossing taxa.

The question was about odd numbers of sets, and talks about unequal separation, therefore I assume the question uses the word "odd" in the mathematical sense of having a remainder when divided by 2, rather than "unusual" - can you edit your answer?

@BryanKrause Ooops, I wrote 'tetra' instead of 'tri' by mistake (fixed now, thanks). I suppose this is what made you think I misunderstood the question. I understood the question correctly I think.

Indeed that was it; thanks for updating and for the additional quote from the article. Any other details you could add to your answer on how this mechanistically works out would improve your answer even more (e.g., the ploidy of the gametes and resulting offspring).

Triploid and pentaploid Rhododendron and deciduous azalea are sometimes fertile.
In our flow cytometry testing of seedlings from triploid Rhododendrons, the offspring can be diploid, triploid, tetraploid, pentaploid or aneuploids normally between triploid and tetraploid.  The seedlings of pentaploids tend to be aneuploids between tetraploid and pentaploid.
One can think of a fertile triploids as producing 1x to 2x gametes centered around 1.5x. Fertile pentaploid seem to produce gametes between 2x to 3x centered around 2.5x.
In general the question is not whether gametes are produced from odd ploidy but instead whether the gametes are successful in combining to create a viable seed.
We have many seedlings growing in our yard where the parents were triploid and pentaploid deciduous azaleas.
See the early work of C D Darlington on the meiosis of triploids.
Note: In our yard is a very fertile triploid deciduous azalea called 'Anna's Smile' bred by Ed Mezitt of Weston Nursery. This year we successfully crossed onto this azalea using pollen from diploids, triploids, tetraploids, hexaploids, and octaploids. 40 of the attempted 45 crosses produced seed. This triploid produces open pollinated seed. Another triploid deciduous azalea produced by Ed Mezitt called 'Deep Rose' also appears to be fertile.
Note: We crossed Rhododendron flammeum (diploid) X Rhododendron atlanticum (tetraploid) to produce triploid seedlings. One of triploid seedlings from this cross is semi-fertile. We have a dozen or so seedlings from this semi-fertile triploid.
Note: A pentaploid seedling from a fertile triploid seems to also be very fertile. We have 50 or so seedlings from this fertile pentaploid.
Note: The tetraploid Rhododendron cultivar 'Countess of Derby' is documented to have 2 triploid parents, namely 'Pink Pearl' and Cynthia'. The pentaploid Rhododendron 'White Ginger' is documented to have a triploid seed parent and a tetraploid pollen parent, namely 'Phyllis Korn' and 'Trude Webster' where 'Trude Webster' is documented to be 'Countess of Derby' selfed. So 'White Ginger' has triploids in the background of both parents.


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Estimation of tissue-partition coefficients and clearance for liposomic nanoparticles
I am working on developing a PBPK model for liposomic nanoparticles used to deliver drugs to fells in the bloodstream. However, I do not have any in vivo data or in vitro data. Given only chemical and physical properties like pKa or the octanol-water partition coefficient, how can a get a relatively accurate estimate of the tissue:blood partition coefficient, as well as the renal & metabolic clearance?

What is your overall goal or research question that you would like to answer?  We could collaborate on a research project.

@Polymania that would be great! How can I contact you? This has to do with modeling liposomic nanoparticles binding to cells that flow through the blooddtream. I want to estimate thr concentration of the cell-lipsosome complex in various compartments of the body, so I am trying to model the systems seperately for now. However, there is not much in vivo sata for both the cells and the nanoparticles, although I do have a little data on the cells. Hence, I need to estimate these parameters. I am new to PBPK modeling so i am not sure if this approach is suitable for my project.

@Polymania I have saved your email. I will send an email as soon as possible.

Regarding the tissue partition coefficient, Li et al. said:  "By using such a parameter, it is assumed that there is the same transfer kinetics of nanoparticles from blood into tissues as from tissues back into blood circulation, and an equilibrium of concentrations between blood and tissue exists. These assumptions may not be appropriate for nanoparticles."

Physiologically Based Pharmacokinetic Modeling of Nanoparticles
Mingguang Li, Khuloud T. Al-Jamal, Kostas Kostarelos, and Joshua Reineke
ACS Nano 2010 4 (11), 6303-6317
DOI: 10.1021/nn1018818

However if you are set on using a tissue:blood partition coefficient (Kp), Yun and Edginton have done a review of 6 in silico methods for determining Kp for small molecules.  You may be able to extrapolate to nanoparticles.

Yun, Y.E., Cotton, C.A. & Edginton, A.N. J Pharmacokinet Pharmacodyn (2014) 41: 1. doi:10.1007/s10928-013-9342-0

Finally, if you are looking for data to help determine a partition coefficient, there is an excellent review of liposomal doxorubicin pharmacokinetic data in animals and humans here.

Gabizon, A., Shmeeda, H. & Barenholz, Y. Clin Pharmacokinet (2003) 42: 419. doi:10.2165/00003088-200342050-00002

Do you work with PBPK models of liposomes?


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Aptamers for DNA
I know that aptamers have a high affinity for their target and are typically made of oligonucleotide s, but can I target DNA using aptamers? If not, what possible technologies can target DNA strands?

DNA can be targeted simply based on base complementarity. That's what antisense RNAs/oligonucleotides and CRISPR do.

@AlwaysConfused aptamer. It's actually a fairly common term in molecular biology. A single Google search would have answered your question.

@MattDMo Before writing that comment I've seen the wikipedia article; however i imagined the term is rare. I've deleted that suggestion-comment.


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The meaning of the $\alpha$ helix and $\beta$ sheets in proteins
I asked this question to my Biology teacher and he, in collaboration with a Chemistry teacher, couldn't find the answer. My question is the following: "What does the $\alpha$ and $\beta$ represent in the secondary structure of a protein? I do reference to the $\alpha$ helix and $\beta$ sheets in proteins." I had a similar question with the glucose and we concluded that it was related to the Chemistry, the $\alpha$ or $\beta$, was related with the functional groups bonded to the carbon.

use of term alpha and beta for protein-chain-folding is completely unrelated with alpha and beta forms of ring-form monosaccharide. A polypeptide chain can form a spring-shape that is called alpha-helix. A polypeptide can also fold into a flat sheet whose folding pattern is known as beta sheet.

Related http://biology.stackexchange.com/q/45735/3340

To add to the confusion, there is also "alpha sheet", which is rarer : https://en.wikipedia.org/wiki/Alpha_sheet and the "beta helix" fold https://en.wikipedia.org/wiki/Beta_helix

@gilleain Yes, that what I want, I would like to know why the $\alpha$-helix is not name "$\beta$-helix"? There must be a certain meaning of the $\alpha$ and $\beta$!

@Matt - Read WYSIWYG's link. It's really just an arbitrary label. The page for alpha-helix mentions William Astbury as calling the helix "the alpha-form" so presumably it's his fault!

@gilleain The problem with this answer is that it is a kind of an "easy" answer; ["They are sometimes used in science to enumerate or differentiate between a series of related things — proteins, small molecules etc."] the answer had never explained the difference, it just says that the use of the Greek letter is used to differentiate the thing, but why a specific helix can be $\alpha$ and the other one is $\beta$? Also, to admit the answer, do you have any reference?

@WYSIWYG, Would it be possible to get a reference of your answer?

The answer is very simple. As described in the accepted answer to the related question about alpha-subunits vs alpha-helices the alpha- and beta- are arbitrary names. It could easily have been 1 and 2 or A and B based on ordering of letters or numbers; indeed, there are "type I" and "type II" turns.
The history, from the wikipedia page on alpha-helices says:

In the early 1930s, ... William Astbury initially proposed a kinked-chain structure for the fibers. He later joined other researchers (notably the American chemist Maurice Huggins) in proposing that:

The unstretched protein molecules formed a helix (which he called the α-form)
The stretching caused the helix to uncoil, forming an extended state (which he called the β-form).

(Emphasis added). In other words, he named the "α-form" first, and considered the "β-form" to be an uncoiled form of the first one. These names later became "α-helix" and "β-sheet". It could easily have been the other way around.
Indeed there are other types of helix; the 310 helix and the π-helix. If either of these had been discovered first, perhaps they would be the alpha-helix. Of them all, the 310 helix has the most 'logical' name as:

the helix has three residues per turn, and ... has 10 atoms in the ring formed by making the hydrogen bond

so if we followed a similar naming scheme, the alpha helix would be a 3.613 helix. Admittedly this is a bit of a cumbersome name.
As well there are the alpha sheet - a sheet made of helical strands - and the beta helix - a helix made of strands. For both of these, the "alpha" and "beta" part of the name has been chosen because of the naming of the original structures they are related to.


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How do our muscles get tired?
I know one of the main reason why our muscles get tired is because there is too much lactic acid, but how does this lactic acid negatively affect the action of myosin on actin?


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Is the human ovum visible to the naked eye?
I'm a student in a field unrelated to biology or medicine, however I very much enjoy reading about it. I just read in Merck Manual that
Human cells vary in size, but all are quite small. Even the largest, a fertilized egg, is too small to be seen with the naked eye.
A very quick google search (caused by basic elementary school biology knowledge) results in Wikipedia article that says The egg cell is typically not capable of active movement, and it is much larger (visible to the naked eye)
Did I misinterpret something here, or I'm reading an unreliable source?
Merck Manual was reccommended for learning about these things since it's maintained by MDs so I was just wondering. Thanks!

bird and reptiles ovum visible to naked eye; including the hen eggs that you eat on breakfast. So please edit the question title  for human ovum or mammalian ovum that would help at a glance to figure out what you are trying to ask.

The line that you quote from the Wikipedia page is talking about ova in general, whereas your question relates specifically to human ova. The "Human and mammal ova" section of the same article states that

The ovum is one of the largest cells in the human body, typically
  visible to the naked eye without the aid of a microscope or other
  magnification device.

With the stated average size of 0.12 mm in diameter (same Wikipedia article), an ovum is very, very small, but presumably a person can still see it unaided.


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How do genes get passed from one hive to another?
In hive species, like honeybees, how do genes propagate from one hive to another?
If the queen only mates with drones from the same hive, and queens and drones are born to the hive they end up mating in, I'd expect that each hive would end up like its own little species, a tiny gene pool with no outside influence.  But since honeybees haven't broken into myriad local species, there must be some gap in my understanding here.

See https://en.wikipedia.org/wiki/Nuptial_flight


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What is "Peripheral Dogma"?
The book, Introduction to Bioinformatics, by Arthur M. Lesk, 3rd edition; Oxford; low-price-edition; in its chapter-1 (introduction), page-no. 6 ; provided a paragraph, entitled "Dogmas: Central and Peripheral".
As-if; there exist a contrasting term for central dogma.
But while thoroughly going through that paragraph (and other chapters linked(mentioned) in that-paragraph; I couldn't found the mention of the term "peripheral dogma" or such.
From the paragraph; it looks like the term "peripheral" has been used to indicate all information-flows other-than genetic codes, and including Junk-DNA and  protein-folding-variations. No mention of epigenetic codes found.
In Web too; I could found only 1 website  used the term "peripheral dogma" in context with biology. which, too, does-not mention the definition clearly.

So, What is peripheral dogma?

P.S. this is purely a terminology question; which is looking for authoritative reference about usage of a term.

@Kiritee (user:25705) you made an answer which probably has been deleted; because that was just like a comment and as well id did not cited any reference. But if you know something about that; then you could of-course write that as comment. Whatever is your source (from-where you came to know about that... a class-lecture? a seminar? a magazine? whatever); you could mention as comment. Btw plz dont take any criticism by this website from heart. Strong criticism is a nature of this website and it does not criticize you personally. It only criticizes your statements and ideas.

No issues man. I am also sincerely waiting for someone to put some reference for this term. :)

@Kiritee since you once wrote an answer; I think you have gone through the term at some-or-some source and not via magic. What was that source? a book? a cheap competitive success magazine? a class-lecture? what book or what magazine? any photograph or screenshot of that source? could you improve details please?

I was only able to see only one reference for this here other than the book you had mentioned in the question.

@Kiritee but this is same as my second-source.

Exactly and honestly I had thought someone was questioning what this second dogma was all about.

I think the author was just trying to make a point that while the "central dogma" is indeed key, there is more to it than that and that understanding of molecular biology has advanced beyond being simplified to that one tenet. Without having the passage in front of me, the ideas you gleaned from the paragraph make sense, though others such as epigenetics seem like they would fit as well.
As you've noticed, this term is difficult to find anywhere else, it isn't a standard term and therefore doesn't really have any meaning unless it is defined in the source. I wouldn't recommend using it yourself unless you plan to define it. The Wikipedia page for central dogma that you linked has a whole section on information transfer not included in the "central dogma" - I think you can safely assume the author was referring broadly to these items.
This all may be a bit of a joke, as well, given the definition of "dogma" and it's somewhat inappropriate use in the context of the central dogma of molecular biology - again, the Wikipedia article you linked talks about the problematic use of the word "dogma" in this scientific context.

Might be. But I suspect a bit; because one other source (and only one) quite boldly used that term ("peripheral dogma"). Seemingly, possibly I heard this term in seminars etc. (though very little part of these seminars I understand). May be all them doing the same mistake as me. I would wait, since 1 have 1 week bounty period; and on my experience at SE; drastically different answers may come from users. Thank you for response.

That second source seems to be using the term in a completely different way from the first you mentioned. In the first source, you referred to 'information flow' that is not contained in the genetic code. In the second source, they are talking only about protein folding and specifically mention that the folding is mostly due to the amino acid sequence: that fully fits under the "central dogma" because the information specifying amino acid sequence is the genetic code which is therefore also determining tertiary structure. Seems like evidence that the meaning of the term is not established.

(continued) In one source, "peripheral dogma" means other, secondary means of information flow that bypass "central dogma" - in the second source, "peripheral dogma" means the secondary consequences of the "central dogma."

the first source too; mentions about "protein folding" too many places on the same paragraph; so it seemed to me they've used it in similar or same sense. I've thought that already before asking the question.

Ok, but you also mentioned information flows that are not genetic codes - protein folding seems to be part of the genetic code (in most cases, at least; you can certainly have environmental influences on protein folding, or protein-protein interactions like prions). Without having the first source to consider, which is it?

couldn't understand what you're asking about. ("Without having the first source to consider, which is it?").

As well; I'm not 'claiming'; I'm just 'searching' and 'verifying' if there something called peripheral dogma. It is obviously possible there exist no-such terms; and both the users independently used that term  and in casual manner (not as any terminology).

Sorry for the lack of clarity - I meant to ask: Is the first source talking about information flow that occurs outside the genetic code, or is it talking about information flow that happens as a consequence of the information in the genetic code?

Let us continue this discussion in chat.

The first source (Book by Lesk, ed3) seemingly meant as if "information flow that happens as a consequence of the information in the genetic code". The author did not specified which one is central and which on is peripheral. (unlike the second, web-source). However on the book (Lesk) the section or paragraph could be divided into 2 parts. The first part describes about directly what we already know as central dogma. But the second portion deals mostly with protein folding, native-state, denaturation, encephalopathy etc. (the term prion was not found).

I'm sorry that my statement "the first source too; mentions about "protein folding" too many places on the same paragraph" is not factually accurate; it would be "on the same section the author dealt with different terms about protein folding". This error happened quite unknowingly; and when I wrote that comment; the book was not opened beside me.

May be it is an old and completely-obsolete term of the age when prions were in way to be discovered.


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Sitting in a closed room filled with regular air - for how long will the air last?
The question has implicitely a lot of variables attached to it:

volume of the room
activity
how closed the room is
size of the person (I'm 168cm long and 64 kg heavy)

That could probably be turned into some formula and I am interested in scientific insights.
But at the end of the day my question is actually of very practical nature. I have a small room - about 1m x 2m x 2.5m = 5m3 - and I would like to use it as super-quiet place for meditation, reading etc. - hence calm activities, no excessive moving around. To improve sound proofness I'll probably also increase the sealing of the door and there is no ventilation - no air exchange.
Now if I close the door - how long can I expect to stay there without the air quality deteriorating to a level where my mental processes start to be impaired by it?

Since you are considering to meditate in the room, without any excess of activity, you can consider the average resting O2 consumption, which is C = 3.5 mL/(min.kg) [1].
If we ignore the volume of your body, initially the room is filled with VO2(t0) = 0.21 * 5 = 1.05 m3 of O2.
With you breathing in the room, you can consider the volume of O2 in the room as a function of the time:
VO2(t) = VO2(t0) - C * M * t
where M is your weight in kg, and where C is converted to m3/(min.kg).
An oxygen defficient atmosphere is an atmosphere for which oxigen content is below 19.5 % of the volume [2]. An oxygen defficient atmosphere can be dangerous for your health. So in your case you need to find the value of t for which VO2(t) becomes inferior to the threshold Th = 0.195 * 5 = 0.975 m3.
So the maximum time you can spend in your room would be:
tmax = (VO2(t0) - Th)/(C * M) = 335 min = 5 h 36 min
Of course, this value is a bit surestimated, and you should leave the room before that time.

[1]  M. Kwan, J. Woo & T. Kwok (2004) The standard oxygen consumption
value equivalent to one metabolic equivalent (3.5 ml/min/kg) is not appropriate for elderly people, International Journal of Food Sciences and Nutrition, 55:3, 179-182, DOI:10.1080/09637480410001725201
[2] https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=STANDARDS&p_id=12716

There is another problem: The rising concentration of CO2. If the volume of it get over 10 Volume% in the air, this is dangerous.

@Chris During respiration 1 mol of CO2 is produced for 1 mol of O2 consumed. Both gas being at the same pressure, we can consider that C is also the average CO2 production.

Not because the volume is getting bigger - CO2 in large concentrations is a problem for breathing.

@Chris Sorry I involuntarly send the comment above before it was finished. So, CO2 production is also a function of the time: VCO2(t) = C * M * t (initial amount of CO2 can be ignored). So VCO2 gets above 10% of the volume for t'max = Th(CO2)/(C*M) = 37h12min. t'max being superior than tmax, the first limitation is O2 depletion.

@Flo Can you check your citations for dangerous CO2 and O2 concentrations? 19.5% might be OSHA's suggestion for a safe environment, but the more severe effects of O2 require much lower concentrations; CO2 on the other hand can cause mental confusion well before 10%. That said, the estimation in the original answer is still reasonable and should provide a decent safety margin given the assumptions made.

The average untrained healthy male will have a VO2 max of approximately 35–40 mL/(kg·min). [1]
So even if we take minimum value, your consumption in a minute is 35x64 = 2.24Liters.
   But NOT all O2 is consumed since about 16% is exhaled along with 5% CO2.
So, Oxygen will get 50% by around 4 hours and I highly doubt if even 50% Oxygen is enough to breathe properly, you will feel suffocation much earlier. [2]
[1] Guyton, A.; Hall, J.E. (2011). "Textbook of Medical Physiology, 12th Ed.". pp. 1035–1036.
[2] https://www.princeton.edu/%7Eoa/safety/altitude.html

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Doesn't meiosis form two pairs of similar cells and two pairs of opposite cells?
I am learning about meiosis in biology. I've learnt that the crossing-over in metaphase I only exchanges small portions of DNA at the tips of the chromosomes. Doesn't this mean that:

After meiosis I, there will be two cells that will be almost opposites (for each chromosome, if one cell has the mother's chromosome, then the other will have the father's chromosome), except for the parts where crossing-over happened
After meiosis II, each cell produced in meiosis I will produce two similar cells (the only differences will be where crossing over happened in one but not both of the chromatids)

This means that there would be a rare chance of two of the sperm cells produced by a single meiosis fertilizing two eggs, in which case we could have:

Almost-identical twins
Very different twins, which would have less than the normal 50% of DNA in common

Am I right about this?

Related: http://biology.stackexchange.com/questions/52409/genotypes-in-diploid-haploid-cells-under-mitotic-meotic-cell-divisions/52414#52414

Great question - I think there are two misconceptions in your question that are interfering with your understanding.
First, crossing-over occurring at just the "tips" is just for clarity in textbooks so you can easily follow the different pieces of chromosome.
Although crossover events tend to occur at particular sequences, these don't have to be at the tips. There can also be multiple crossovers on the same chromosome, or none at all. See this link for some estimates of recombination rates for different species.
Second, gamete diversity doesn't depend only on crossing-over during meiosis, it also depends on the incorporation of just a single chromosome from each pair. Humans, for example, have 23 pairs of chromosomes. There are therefore 2^23 = 8388608 different combinations of chromosomes - with NO crossing over! Therefore, even without recombination, the odds of two genetically identical sperm fertilizing two genetically identical eggs are incredibly small.

excellent answer. It is surprising that these particular misconceptions are so commonly and uniformly occurring.

But doesn't this random splitting of homologous chromosomes only happen in meiosis I? If there was no crossing over, then each meiosis II would produce two identical gametes.

Even with no crossing over, each pair of chromosomes splits randomly, not according to parentage. Imagine you have only 4 chromosome pairs, where each pair has one from the Mother (M) and one from the Father (F) - note, these will eventually be the 'grandparents' after fertilization - they could split MMMM, MMMF, MMFM, MMFF, MFMM, MFMF, MFFM, MFFF, FMMM, FMMF, etc etc etc - a total of 2^4 = 16 possibilities. If you have 23 chromosome pairs, like, humans, it's over 8 million. And that is still with NO crossing over within the individual chromosomes.

Then you add in crossing over and suddenly not only is the segregation of homologous pairs random, but now the individual chromosomes are random too, and you get an incredible potential for diversity.

Hmmm what seems to me from your statement;

"there will be two cells that will be almost opposites (for each chromosome, if one cell has the mother's chromosome, then the other will have the father's chromosome), except for the parts where crossing-over happened"

It seems to me; you're missing something.
It would happen if the haploid chromosome number n=1 and no crossingover is there.
But;
If the haploid chromosome number is more than 1; i.e 2n is more than 2 (such as in pea n=7, 2n =14 and human, n=23 and 2n=46);
then at segregation event in meiosis-1 ; any-1 of 2 homologous chromosomes will go to a doughter cell; in a probabilistic manner (and this assortment is  independent from other chromosome-pairs).
Take example. If all your somatic cells have a chromosome composition Aa Bb Cc (where with each letters I meant a chromosome and not gene);
then perhaps you are thinking it could be seggregated only into ABC + abc. But that is not the case.
In one cell at certain place at site of meiosis, it would be Abc + aBC; in some other cell  it would be AbC + aBc; and somewhere else it would ABc + abC, and that way.
In addition; irrespective of how many pieces of chromosome you have; crossing-over will take place in probabilistic way (so; that will make different-gene-exchange at different cells at the site of meiosis.)
So ultimately you get not 2 but many more types of gametes.

Here is 2 simple drawings.

Meiosis first division.

Meiosis second division.

The book, Concepts of Genetics by Klug, Cummings and Spencer, 8th edition (the ebook I have), chapter 2 (mitosis and meiosis); clearly mentions the random-assortment (physical shuffle) event with examples.
here is a picture from that book.

diagram from Klug et al.

Reference: Concepts of Genetics ; Klug, Cummings and Spencer; 8th edition

"In one cell at certain place at site of meiosis, it would be Abc + aBC; in some other cell it would be AbC + aBc; and somewhere else it would ABc + abC, and that way." <-- And that is exactly what I mean by "opposite cells"... If one cell inherited a particular chromosome from the mother, then we can say for sure that the other one was inherited from the father. That means that the percentage of DNA the two gametes have in common should be the same as the percentage of DNA that the parents had in common, which is less than the normal 50% between two gametes.

what is that "normal 50% in common"?

If you take two gametes at random (produced from different meiosises), then 50% of the DNA should be common. If you take the 4 gametes produced by meiosis, then two pairs of them will have a high percentage of common DNA and two pairs of them will be have a low percentage of common DNA.

hmm but that is correct only if we focus at 1 particular pair of chromosome. When we look for more than one pairs chromosome; the probability to co-occur the parental combination in a gamete; is lesser than 50%

so, the chances to get 1 gamete with exact parental set (if no cross-over theoretically)= 1/ (2^23) in human. Isn't? Think; 1/2 of all gametes contain chromosome-1 from particular parent. Now inside that group of gamete; only 1/2 of them contain chromosome-2 from that particular parent. (so this subset contains 1/4 th of total gametes). If thus we continue; at end we'll get 1/(2^23) th of total gamete that contains an accurate-half of 1 parent (only if no crossover that is unreal). Is there something wrong?

That's not what I'm saying. I agree that it would be extremely rare to get all of the DNA from one parent into one cell and all of the DNA in common into the other cell. What I'm saying is that during meiosis I, we will always get things such as "AbCdeFG, aBcDEfg", so the two cells will have no chromosome in common (there will never be an A in both cells or an a in both cells, it will always be A a). Since they have no common chromosomes, they ressemble each other no more than the gametes of two different people.

yes that is correct, in a gamete of an organism, chances to occur AbCdEf or ABCdef or ABcdeF etc (where any 50% chromosome came from any 1 of the organism's parents' haploid set); than extreme terminal cases like ABCDEF or abcdef (where 100% chromosome from 1 parent and 0% from another parent of that organism). However the statement "Meiosis-2...the only differences will be where crossing over happened in one but not both of the chromatids)" is not fully correct; because if on 2 chromatids; different-sorts of crossing-over could take place, that would cause difference.


text:
How do asexually reproductive organisms mutate?
In accordance to my limited knowledge of biology, asexual organisms exactly copy their DNA as there is no "contaminant", which in sexual reproduction is the other organism's DNA.

Your understanding is wrong; you have confused the mutation process with the process of genetic recombination.  The two are not related.

Mutation is mutation, a wrong nucleotide substituted (etc.) for the correct one. The mechanisms don't vary from organism to organism. It is, after death, the great equalizer.

It is not necessary that no mutation occurs in the system where no gene recombination or "contaminant" takes place. There are mutations (which are sudden abrupt inheritable changes)
There can be errors in genome which can cause mutations.
Take example of replication of DNA-:
There are many enzymes linked with it : DNA polymerases ( I, II,III) in prokaryotes where asexual reproduction occurs which add nucleotides to make replicas of DNA of parent ( you can check the complete process at wikipedia)
Come to the point : DNA polymerase III, after synthesising dna chains has ability of proof reading. It can correct the mismatches ( hope you know that adenine bonds with thymine and cytosine with guanine, they are nitrogen bases of dna)
DNA polymerase III can correct the mismatches but it is not error proof- it can't distinguish between thymine and uracil (another nitrogen base ; thymine is methylated uracil)
This is only one possible error, there can be many such hence asexual reproduction isn't error proof

@ collin is that right with you


text:
Why do some moles grow longer and darker hair than the rest of the skin?
In different parts of the body I have skin moles or in medical terms, nevus.
In some of them hair grow seemingly either darker/thicker (I'm not sure how much of the two) and notably longer. Here are pictures very similar to what happens. What is the reason behind this?

You could have easily find this answer on the internet (e.g. here: https://www.zocdoc.com/answers/3728/why-do-hairs-grow-on-some-moles

@RickBeeloo I ask this question here because I want this site to improve and to have many interesting biology questions. There was a discussion if easily google questions should be deleted or embraced, my position on that is that there are not stupid question and that this site should become the actual place where the answer is, the place that shows up when a google search is made. That's why I want the question to remain here. I thank you the link and not downvoting me, however!

Before answering the question (about the hairs) I will first go in some detail about what moles actually are:

Moles are growths on the skin that are usually brown or black.  They
  are formed by clusters of melanocytes, the pigmented cells responsible
  for your skin color.  Moles typically appear during the first 30 years
  of life, can be flat or raised, and can darken with sun exposure,
  puberty, or pregnancy.

There are no articles covering this topic in detail (most of them are about the skin cancer, if you are interested in this topic check out this article). However there are some medicial experts talking about the hair growth.

Joshua Zeichner, M.D., Director of Cosmetic & Clinical Research at the
  Mount Sinai Hospital in New York City. "If the mole also contains a
  hair follicle, the hyper-pigmentation can cause the hair that comes
  out of it to be coarser and darker."

Junji Takano, a Japanese health researcher said the following about this topic:

This is due to the fact that capillaries of a mole are growing rapidly
  and excessively, and this includes the hair follicles

Actually moles are benign tumors(wiki), the cells in the body in charge of normal skin color, are being produced at an extremely fast rate. Thus causing the melanocytes to form in clusters instead of spread out, causing abnormal skin pigmentation in some areas of the body(wiki). So based on the above quotes this "fast production" also affects the hairs which are present in this piece of skin. More interesting is that people hate these hairs (which make sense offcourse) but in most of the cases this is a sign that this mole isn't cancerous:

A mole that has a hair growing out of it usually means that is was
  present since birth or at a young age and is typically normal.

references: first quote, second quote, third quote, last quote


text:
How's idiotype different from paratope?
What I understand of these two terms is that:
Paratope is a portion of antibody that recognises and binds to specific antigen.
Idiotype is an antigenic determinant of antibody formed of CDRs that have specificity for a particular epitope. Some authors call the antibodies recognising a particular epitope an idiotype.
Well the CDRs, they actually form the paratope so is it right to say the CDR that acts as an paratope also forms the idiotypic determinant/ idiotype ?

I have read that the unique amino acid sequence of the VH and VL domains of a given antibody can function not only as an antigen-binding site but also as a set of antigenic determinants. the idiotypic determinants are generated by the confomation of the heavy- and light-chain variable region. Each individual antigenic determinant of the variable region is referred to as an idiotope. In some cases an idiotope may be the actual antigen-binding site (The paratope), and in some cases an idiotope may comprise variable region sequences OUTSIDE of the antigen-binding site. Therefore, each antibody will present multiple idiotopes, and the sum of the individual idiotopes is called the IDIOTYPE of the antibody.
I hope that had been helpful

Could you add your reference?

Kuby Immunology, 4th Edition, Chapter: Immunoglobulins: Structure and Function (83-113)

The following was a reply by an expert from assignmentexpert.com :

Paratope is only the part of Ab that binds to the epitope of an antigen. But this does not mean that every amino acid in the CDR should bind to epitope – it is possible that only 1-2 AAs per CDR bind directly to epitope.
  Therefore, paratope is the part of the idiotype that binds to the epitope.


text:
If the half life of Caffeine is ~6 hours, why do people consider it ineffective after its half-life?
Caffeine has a half-life of ~ 6 hours in the body.
So assuming you take 200mg of caffeine, after 6 hours there should still be 100mg of caffeine in your body.
Then why is it generally said that after 6 hours caffeines effect should wear off? Shouldn't it only be diminished since there is still 100mg of caffeine in your body?

You need to consider what concentration of caffeine within the body will have biological effects. That is, you could have 1 picogram of caffeine on your body but you may be well below the threshold needed to have a biologic effect.

@VanceLAlbaugh Yeah, but it's generally stated that after 6 hours regardless of dosage that caffeine "wears off", so technically my 200mg original dose becomes ineffective even though after its half life I'd still have 100mg (which is definitely enough to have biological effects?)

where are you reading that - what source?


text:
where can I find estimated costs of laboratory equipment?
Often when I am curious about purchasing new laboratory equipment I cannot find a ballpark figure for the price.  Companies that sell expensive lab equipment prefer if you contact their customer service or sales teams to inquire about prices.  I don't want to go through all of that hassle, as well as exposing myself to  potential marketing emails.  Is there any website that lists ballpark figures for lab equipment?  The type of equipment I am talking about are things like PCR thermal cyclers, Flow cytometers, nucleofection devices, centrifuges, etc.
Thanks in advance.

Yeah, it is annoying that nobody lists prices. Call them using a temporary forwarding e-mailadres.

Yeah, but calling them is what I'm trying to avoid..... I Just want ballpark figures, not exact price quotes based on all the details of my institution/grants etc.

I'm voting to close this question as off-topic because it's not about biology.

The best way (if you're buying new) is to contact the manufacturer/distributor. Sales people get inquiries like this all the time, and are generally more than happy to accommodate you (because they get commission on any sales they make). Most items have customized pricing depending on the customer, their order history, the number of items being ordered, add-ons like maintenance contracts, reagents, etc. Many complex instruments like flow cytometers have many customization options, including the number and type of lasers, different types of filter sets, tube vs. plate-based acquisition, type of computer, licenses for software, etc. Sales people know their company's product lines the best, and are willing to talk to you to figure out your needs and then recommend the product that works best for you, which may not necessarily be the one you were originally thinking of.
You can always ask to not be added to any email lists, and if you are added, commercial emails (in the United States, at least) are required to have an unsubscribe link in every email. Check out the CAN-SPAM Act of 2003 for details.

I specifically asked in the question how to get ballpark estimates for prices without contacting the company, so I cannot accept your answer.  I do agree with you based on my experience, that calling the company is the best method of getting this info, but I think that is ridiculous and annoying.  I don't want to spend that much effort/time when I am just brainstorming about potential possibilities.  It would be nice if the companies just had a price range listed for each machine, that would be a good starting point.

@Reilstein unfortunately, I don't know what else to say. Companies generally don't publish list prices for big-ticket items, although you may be able to find some info if they distribute through ThermoFisher or VWR or some place like that. There are sites that sell used equipment, so you could google them for ideas. But, if you're looking to buy new, contacting the company is the only way to go. Remember what I said, sales reps get these kinds of questions all the time, and if you clearly state you're just pricing options at the moment, they should be able to accommodate you. Good luck!

I Hear you, and thanks for your tips.  I will keep it in mind for when I get more serious about my equipment.  I was hoping for someone to have a website that users contributed their prices for equipment recently purchased, but apparently that does not yet exist. Thanks again.


text:
Why do eyes feel overwhelmed by light when we wake up?
Many people (I saw a 9gag post 3 days ago and couldn't find it, I'll edit later if I do find it)experience dry/hurting/overwhelmed eyes when they wake up because the light feels too bright. I happen to "suffer" the same. Why this occurs? Is it because the eyes are dry, or because the pupils are contracted, or why else?

When you are asleep, your eyelids are closed and your pupils dilate. When you wake up and open your eyes, you are not used to the light, and it takes some small amount of time for your pupils to contract and your eyes to "get used to" the light. Simple as that.

The reflex responsible for the phenomenon you described is called the Pupillary Light Reflex. According to the Textbook of Medical Physiology, Guyton & Hall, Elsevier, 11th edition, 2005, p. 649 (reworded by me in order to avoid direct copying):
When light reaches the retina of the eye, the optic nerves are stimulated. Most of the generated nerve impulses participate in the creation of an image in the brain etc., but a few reach an area in the brain called the pretectal nuclei. These nuclei then generate secondary impulses to another nucleus called Edinger-Westphal nucleus, which sends a signal through parasympathetic nerves to constrict the sphincter of the iris.
Conversely, in darkness, the reflex is inhibited, which results in dilation of the pupil.

To summarize, in darkness (either when you are in a dark room with your eyes open, or when you are anywhere with your eyes closed) the pupil will be dilated since stimulation by light does not occur. When stepping into the light or when opening your eyes, light immediately stimulates the optic nerve, which causes a signaling cascade that results in constriction of the pupil to a certain size, depending on the amount of light present (primarily to protect it from exposure to too much light).
Naturally, you can see this constriction happening every time you open your eyes in front of the mirror (focus on the pupil). It was also depicted rather accurately in the end of Disney's excellent rendition of the Hunchback of Notre Dame (skip to 1:22).


text:
Why does yeast react the way it does to water combined with sugar?
I almost wanted to ask this in Cooking SE, but thought it would be better fit here.
So I understand than when you mix yeast with sugar and warm water, you get CO2. When using baking powder, it's a standard redox reaction, but what is it with yeast? Is the yeast still present after whatever reaction happens there? I don't think so, because that would mean that the reaction would go on forever. But what evolutionary sense is there for yeast to evaporate into CO2 when confronted with sugar and warm water?

When you take in sugar and use it, you give off CO2; similar deal as with yeast.  Yeast, however, are tiny and fit better in a dough or batter than you do.

Yeasts are living organisms, they do not evaporate. However it is true that in most fermented food we eat, yeast are no longer there. So why is it so?
It is not the reaction with sugar and warm water that makes them disappear. Most of the time they get killed later in the food making process. For instance, if you consider yeasts in bread, like french baguette for instance, after the dough raised, it goes to the oven where yeasts cells get heat killed.
For other processes, like brewering, yeasts used to stay in the final product. But then you had to drink it before it got spoiled by yeasts that were consuming all the sugar. So nowadays, industrially produced beers are filtered or pasteurized, or both, in order to get rid of the yeasts. Only artisanal beers are still "alive", with living yeasts in it.

EDIT:
As for the question "why/how do yeasts react with sugar?", sugar is actually fuel for yeasts. Yeasts oxidize sugar into CO2 in order to gain energy for their metabolism.

A good start, but it doesn't really answer the question --- where does the CO2 come from? You might add that CO2 is derives from the sugar, and is a byproduct of cellular respiration to obtain energy.

@Roland thanks for the feedback. I edited my post and added a brief explanation


text:
Release of Nor-Epinephrine by presynaptic beta receptors
Presynaptic alpha-2 receptors on stimulation decrease the release of nor-epinephrine by certain mechanisms where as activation  of beta presynaptic receptors increase or facilitates the nor epinephrine an effect which is opposite to the alpha receptors
How does this facilitation of nor-epinephrine occur by the pre-synaptic beta receptors

This a very interesting question! I'm assuming the "presumptive" is a typo for presynaptic. I don't know what you mean by 'hetero tropic interaction' in this context (I thought that was for enzymes) but still, the alpha2 presynaptic acts by coupling with the Gi, thereby reducing Ca+2 and reducing vesicle release. How the beta presynaptic acts, I couldn't find out.. But increasing the calcium doesn't seem to be probable because beta receptrors couple with Gs and hence increase cAMP. Whether cAMP can induce vesicular fusion, that I don't know

@polisetty  I looked heterotrpoic interaction to find that the alpha-2 receptors located presynaptically for the cholinergic neuron but postsynaptically to the sympathetic neuron inhibit the release of acetylcholine by binding to the gi specifically in the intestine where there is close proximity of the sympathetic and cholinergic neurons. Though the term hetertropic interaction might just be an interaction and not a mechanism for inhibition of neurotransmitter release.


text:
Derivation for drug half life
The formula in textbooks for $t_{\frac{1}{2}}$ of a drug following first order elimination is generally given as $$t_{\frac{1}{2}}= \frac {\ln(2).V_d}{Cl}$$where $V_d$ is the volume of distribution and $Cl$ is the clearance.
Shown below is my attempt to derive the formula but I don't know where I'm going wrong.
Assuming first order kinetics of elimination, the rate of elimination ($R$) would be proportional to the plasma concentration ($Cp$)
$$ R = Cp . k$$
Where $k$ is the rate constant.
For calculation of $t_{\frac{1}{2}}$, since this is a first order elimination, $$ t_{\frac{1}{2}} = \ln(2)/k$$
Substituting,
$$ t_{\frac{1}{2}} = \frac{\ln(2).Cp}{R}$$
Since $ Cl = R/Cp$, substituting would give,
$$ t_{\frac{1}{2}} = \ln(2)/Cl$$
Since both the formulae don't match (this one doesn't have a $V_d$ term at all!), where have I gone wrong? Also then how is $Cl$ different from $k$?
According to the correct formula, $k=Cl/V_d$. How is that so?
EDIT
Volume of distribution is the apparent volume of blood the drug takes up and is given by $$V_d = \frac {Dose}{Pc}$$
Clearance is the volume of blood that has been cleared of the drug in unit time and is given by $ Cl = R/Cp$
Correct me if the basic definitions themselves are wrong.

Should this be asked in chemistry?

Can you define the terms, "distribution volume" and "clearance"? The problem certainly has to do with the way you have defined these terms.

$Cl = R/Cp$ seems incorrect. Cl unit is $volume \cdot time^{-1}$, R is $weight \cdot volume^{-1} \cdot time^{-1}$ , Cp is $weight \cdot volume^{-1}$. R/Cp is $time^{-1}$ which is imcompatible with Cl.

Well, $Cl = R/Cp$ is correct, but $R$ is not $Cp \cdot k$.
Given $X(t)$, the actual quantity (ie weight or moles) of drug in the system, $R$ should have the dimension of $\frac{dX(t)}{dt}$, that is $weight \cdot time^{-1}$ or $mole \cdot time^{-1}$ because the base definition of clearance is given by $$- \frac{dX(t)}{dt} = Cl \cdot C(t)$$.
The volume of distribution $Vd$ comes into play when converting from $X(t)$ to $C(t)$. Following the same steps as you did :
$$ R = \frac{dX(t)}{dt} = \frac{dC(t)}{dt} * Vd = C_p  \cdot k \cdot V_d$$
because (due to 1st order kinetics)
$$\frac{dC(t)}{dt} = Cp \cdot k$$

Substituting,
  $$ t_{\frac{1}{2}} = \frac{\ln(2)}{k}$$
  $$ t_{\frac{1}{2}} = \frac{\ln(2) \cdot C_p \cdot V_d}{R}$$
  Since $ Cl = \frac{R}{Cp}$, substituting would give,
  $$ t_{\frac{1}{2}} = \ln(2) \cdot \frac{1}{Cl}  \cdot V_d$$
  $$ Cl = \ln(2) \cdot \frac{1}{t_{\frac{1}{2}}}  \cdot V_d$$
  $$ Cl = k  \cdot V_d$$
  $$ k = \frac{Cl}{V_d}$$


text:
What is the difference between a species tree, a gene tree and a phylogenetic tree?
I have found websites and text books disagreeing over this. For example,

Phylogenies are also known as “species trees”...

http://biologos.org/blogs/dennis-venema-letters-to-the-duchess/evolution-basics-species-trees-gene-trees-and-incomplete-lineage-sorting/
and

It is well known that a phylogenetic tree (gene tree) constructed from DNA sequences for a genetic locus does not necessarily agree with the tree that represents the actual evolutionary pathway of the species involved (species tree)...

http://mbe.oxfordjournals.org/content/5/5/568.abstract
Although the second source, being from a journal, would seem to be more reliable, my original thought was that phylogenetic trees do show the evolutionary relationships between species and thus are species trees as opposed to gene trees.
Any clarification on the issue would be much appreciated.

They are all distance trees where the nodes represent different things and the distance measures are different as well.  You can make a dendrogram using (1-correlation) as distance, or using euclidean distance.  You could also do it using nt specific distance measures like kmer distance.  In networks you can make trees from something called a topological overlap distance.  Whatever distance measures you create that satisfies the rules of a distance measure can be used. Also, they may use different clustering techniques too.

Phylogenetic tree
A phylogenetic tree is a tree showing relationship between lineages. These lineages might be computed for genome-wide DNA or from only a single gene. As such the term phylogenetic tree is general.
gene tree vs species tree
If you compute a phylogenetic tree, from genome-wide DNA, then you are computing a species tree (although some sister lineages might not perfectly fit the definition of species). If the phylogenetic tree is computed from data coming from a single gene, then we are talking of gene tree.
Why would a gene tree not match a species tree?
But a gene tree is not just a species tree with fewer data. There are reasons for why a gene tree may not match a gene tree. Genes may duplicate within a given genome. The two duplicated genes are free to evolve independently since the split. All descendants lineages will then inherit these two genes but if you map the two different copies of the gene (red and green below) in two sister clade, they will be much more different then the two same copies (say the green copy) in two distantly related species. Here is a picture to show that

Also, copies of genes can be deleted later on and there might have horizontal gene transfer. For all these reasons the phylogenetic tree of a gene might well be very different than the phylogenetic tree of species.
Below is a gene tree and the associated species at the tips. Take time to make sense of what is going on on the picture.

What is a species tree exactly?
One could call a species tree as some kind of average tree among all gene trees.


text:
What is the difference between muscle tension and muscle tightness?
Is there any difference between muscle tension and muscle tightness?
I want to study the relation between forearm muscles tightness/tension and tendinopathy (specifically, medial and lateral epicondylopathy) in humans. In that context, I wanted to understand whether muscle tension and muscle tightness are synonymous, and if not what the difference is.

In what context do you mean? It's not clear what you are asking.

@kmm Thanks for the comment. I want to study the relation between forarm muscles tightness/tension and tendinopathy (specifically, medial and lateral epicondylopathy) in humans. In that context, I wanted to understand whether muscle tension and muscle tightness are synonymous, and if not what the difference is.


text:
Would this be called a complex?
When an intermediate is formed between a substrate and an enzyme, this is called an enzyme-substrate complex.
When a molecule is bound to its respective transfer protein, (the molecule being transported is unchanged when released from the protein at the destination) would this be called a complex? If not, what would this be called?

Yes, it's a complex. Anything bound to anything else in biochemistry is a complex, especially when you're talking about proteins. The bonds need not be covalent, either.

The same way we call "receptor-ligand complex"; "transcription preinitiation complex", "nuclear pore complex" et cetera. The word 'complex' used in more-than one sense in biology; not always necessarily as co-ordination complex.

Welcome to Biology SE. You could visit the tour-page for basic informations, the help-page for more detailed informations about what could be asked or could not be. For formatting tasks in command prompt, visit this help sub-page. Thanks


text:
What is so difficult about mushroom cultivation?
I am just wondering why it is so cheap and easy to cultivate this type of mushroom: Agaricus bisporus, however a typical forest mushroom such as Boletus edulis  has to be harvested. What makes one mushroom species much more difficult to cultivate compared to another?

Like many other strictly mycorrhizal fungi, B. edulis has to date eluded cultivation attempts.[107][117] The results of some studies suggest that unknown components of the soil microflora might be required for B. edulis to successfully establish a mycorrhizal relationship with the host plant.[118][119][120]

@HopefullyHelpful if you have supportive reference, could write it as an answer.

What makes some mushrooms easy to cultivate is that they grow profusely, they aren't tree symbionts, where as sponge gilled culinary musrhooms are symbionts. Cheap mushrooms can easily be controlled with temperature and or light to fruit year round with minimal labour, they have cheap and easily obtainable substrate, and that are very appreciated for cooking and transportable. Also Argaricus doesn't even need light as a signal to trigger fruiting bodies and can be grown in complete darkness, and the harvest can be with robots not even manual, https://youtu.be/iBENPHl4mBA?list=PLw1YvKXHZymsoJbFGRI_OFSWZ5Wwg_fVD, which makes them particularly cheap.
Mycorrhizal mushrooms like boletes and many forest associated mushrooms differ from Argaricus and
commonly commercially produced saprotrophic
types (such as shiitake and button mushrooms).
Saprotrophic mushrooms live and feed on dead
organic matter, whereas mycorrhizal mushrooms
grow in a close, symbiotic (mutually beneficial)
relationship with the living roots of a tree.
Field and dead wood mushrooms generally have simpler substrate that can be transported in boxes in the dark, and almost all cultivated mushrooms are of saprotrophic.
Saprotrophic nutrition /sæprəˈtrɒfɪk, -proʊ-/ or lysotrophic nutrition is a process of chemoheterotrophic extracellular digestion involved in the processing of dead or decayed organic matter. It occurs in saprotrophs or heterotrophs, and is most often associated with fungi (for example Mucor) and soil bacteria.
That's slightly different to Saprophytes are more generally plants which live on dead or decomposing matter and which can also be more accurately be called myco-heterotrophs because they actually parasitize fungi, rather than dead organic matter directly.
They say that Argaricus was first discovered in 1650 on melons! but as any theory, there were probably precedents. Any farmer that discovered sizeable populatons of fungi near horse and cow middens could have easily have experimented with placing some compost in a basement.
Morelles and truffles are such expensive mushrooms that the man who learns how to grow big truffles will be payign himself up to a 1000 dollars a kilo for his efforts, it illustrates the difficulty of micorrhizal cultivation.
If you are interested in fungi there is a fascinating ted talk about them from Paul Stamets.
and
https://en.wikipedia.org/wiki/Mycorrhiza


text:
Why are de novo genetic mutations usually NOT inherited?
I am told de novo genetic mutations (germ mutations in either parent's sperm or egg cell, or the newly fertilised egg) are not usually inherited, and do not contribute to heritability.
It would seem to me that, intuitively, a de novo mutation would be passed from the affected individual (assuming they survive and are fertile) onto offspring, just like any other inherited mutation. But apparently not.
Why is this?

A germ line mutation will be passed to the offspring only if (1) the individual reproduce (2) the individual reproduce after the mutation has occurred in the germline, (3) the spermatozoid that is transmitted is descendent from the individual cell who had the mutation, (4) the right of the two chromosome is being transmitted (last point applies only if the mutation occurred before the meiosis).

@Remi.b  That sounds like a pretty good argument, can you write up an answer based on it?

The statements at the beginning of your question seem to be separate issues; I think @Remi.b answered the first part but didn't address the second: "do not contribute to heritability" - this statement might refer to the fitness of the parent to reproduce, which is determined by that parent's phenotype, and not the genotype of the gametes, which is the only thing affected by a germ-line mutation (unless there is a corresponding phenotype effect in the gamete such as reduced sperm motility, or the mutation is lethal, which would clearly affect heritability).

A germ line mutation will be passed to the offspring only if

the individual reproduces
the individual reproduces after the mutation has occurred in the germline. Indeed if the mutation appears in the testes 5 years after the individual has reproduced then the offspring will never carry this mutation. Note that female mammals make a big storage of ovules early in life while mammal males do not. As a consequence the number of new mutations transmitted to offspring is age-dependent in males but age-independent in females. See this post for more info
the gamete that is transmitted is descendent from the individual cell who had the mutation. There is of course many lineages of gametes and their pattern ancestry will affect what fraction of gametes carry a given mutation.
the right of the two chromosome is being transmitted (last point applies only if the mutation occurred before the meiosis). Of course, there is always segregation who decreases the probability of a new mutation to be transmitted by half.

Of course, there are also all the mutations occurring outside the germ lineages (somatic lineages) which won't be transmitted but you specifically asked for germ line mutations.


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Why do bulls have a hump?
Camels have a hump as an adaptation to the heat. They store fat so that it minimizes the insulating effect the fat would have if distributed over the rest of their bodies.
Why do buffaloes/ oxen/ bulls have a hump then? The climates they are found in, I assume, are not as hot as that of the camels.

Bison humps are made of muscles, huge muscles. According to this and this pages bisons use their heads for snowplowing. This hump provides head support. It seems that also other animals have structures like that: giraffes, rhinoceroses, elasmotheriums,... this list can go on since this structure should be homologous of other animals'. From this page rhino humps made from muscles, nuchal ligament, fat, and dermis. And from the page, probably fat quantity depends on the nutritional state of animal.
I searched nuchal ligament, the remarkable structure of hump according to rhino page. This is a ligament spans from upperback vertebra to neck vertebra and to skull. Can be found on humans too. Also muscles of hump should be homologous to humans' notice that vertebras have spines not just for supporting ligaments they also for muscles. Human skeletons just don't have vertebra with long big muscle connection points and huge neck/back muscles connecting huge bones, this is why we don't have a hump or an obvious large hump. And I think even camels do have slighly bigger muscular humps but theirs are covered with big fat hump.
Bison skeleton and elongated spines supports huge muscles and ligaments.

Horse's nuchal ligament

Human nuchal ligament

Human nuchal ligament drawn with red lines and muscles (bison hump also consist of muscles).

Giraffes' this is an energy saving feature. Giraffes don't need to use muscles to hold their neck. They just use when flexing their necks down, when drinking water etc.

According to Wikipedia, for an alternative hypothesis Ouranosaurus have a hump. (Other hypothesis is display sail or termoregulation sail of course. Also spinosaurus have this kind of alternative hypotesis but this hypothesis not accepted much as sail. and spinosaurus' spine different from bisons. Bison spines concentrating at shoulder but spinosaurs' not at the shoulder. You can find spinosaurus info from this page.)

Thanks! But how does the hump help the bull?

bull hump provides all same of other animals'. and at the same time they are fighting for females. www.zoochat.com/community/media/the-skeleton-after-a-successful-bull.189073/full?d=1339424780 see from the picture if bull pushed their head to his opponent neck needs supported to pull head up. spines also connecting point of shoulder blade muscles. so maybe hump also gives extra strength on forelimbs too. i think ox humps are similar purpose but today ox hump provides pulling cart without slipping yoke from neck. i read, probably hump growth of bulls related to testosterone. @polisetty

but in some cases some cattles have fat hump at their backs this is from  selective breed or something like that. if last link doesnt work www.zoochat.com/community/media/the-skeleton-after-a-successful-bull.189073/

seems my answer/comments are needs to be improved a little. but because i think my answer and comments too much detailed for a desired answer anyways. so i can leave it unedited for not to spend extra time. if you confused ill leave a brief correction: correcting first comment: bull humps are for fighting for females and also provides support just like as in other animals. second comment: indian bulls etc.

http://9gag.com/gag/aAwKGgo i guess this is can be explained with hump. hes not got an very obvious hump but hes have one.


text:
Why is polyploidy much more common in plants than in animals?
There are very few animals with polyploidy like salamanders. Why is it that polyploidy is so uncommon in animals? On the other hand there are numerous examples of polyploid plants. If ut something to do with the gene dosage, how does it not affect plants?

I would suspect that the commonness of alternation of generation and haplondiplontie in plants to be related to change in ploidy level.

related:http://biology.stackexchange.com/questions/53055/why-is-aneuploidy-usually-lethal

plants often can support huge chromosomal variation and huge structural anomaly.

Polyploidy is common in plants than in animals because in animals sex determination mechanism involves number and type sex chromosomes. Polyploidy will interfere with this mechanism and hence it is seen rarely in animals. I believe its probably because an animal progeny with multiple sex chromosomes won't be able to reproduce more of its kind unless it can also reproduce asexually (which is seen in plants as mentioned below).
Plants, on the other hand do not have any such sex determination (based on number or type of chromosomes) and majority of them can also reproduce vegetatively. This vegetative propagation enables multiplication of polyploid plants. Sexual reproduction will result in loss of desired polyploidy as per the principle of segregation. However, if a polyploid plant can produce a viable progeny sexually, it might have a different ploidy than its polyploid parent which won't happen if the parent reproduces asexually. Hence, polyploid plants can be classified as sterile and fertile polyploids (the reference will give a detailed account on this mechanism).
Refer the section of Polyploidy (page 115, Chapter 6) of this book (Principles of Genetics, Snustad and Simons, 6th edition)
When it comes to gene dosage, animals do show gene compensation of X-linked genes by various methods. Example- formation of Barr Body in human females (Note that this has nothing to do with polyploidy, but happens since females have one X chromosome more than males). Whereas gene dosage in polyploid palnts has been exploited for improved agricultural yields as they have shown better productivity than their diploid couterparts.

Are there really more asexually reproducing plants than asexually reproducing animals? Can you back up the claim with a reference? Also, sex does not involve gender and gender does not involve sex chromosomes. Intuitively, I would think of the absence of gene dosage in plants (assuming this is true, reference would be needed) as preventing events of ploidy change, so your hypothesis is unclear to me.

Polyploid plants including rice and wheat can reproduce sexually.

@Remi.b I have tried explaining that why I think the sex determination mechanism has a role in this. I suggest to go through the reference once. It's really helpful and elaborate.

@AlwaysConfused Yes, you are right. These polyploids fall in the category of fertile polyploids. The reference gives an account on their propagation.

@ downvoters please explain why it is wrong/unclear/inadequate research-effort/doesn't contain reference or citation.


text:
Why calf thymus DNA is widely used instead any other body part?
Calf-thymus DNA is widely used as DNA sample. Such as testing anti-dsDNA antibody activity, nuclease activity etc, as well as certain books include calf-thymus-DNA in various examples (such as the book Molecular biology by Weaver (ed-5) mentions in a table on % (G+C), that %(G+C) of calf-thymus DNA is 40)
Now; my question is; why a peculiar organ like thymus is selected (and not liver or kidney etc); and not any organ from adult cows (which are more available at any meat shop)? whereas all the otherly-situations should contain the same DNA-sequence? Isn't it a bit weird?
Is it more easy to extract the DNA from a calves' thymus gland?
I've searched web, but nothing helpful I found.

The thymus gland is much larger in prepubescent calfs (and humans) than in adult cows, so more DNA can be extracted from it.

@user30455 but why not cow's  brain or heart or veins etc... such "common organs"  (though all of them should theoretically same DNA). That is the main point of this question. Your point is correct... to get the thymus-DNA, adult cow is not right source... but that is not the question here. Here the question is why thymus gland for DNA?

I have crawled through google and many, many journal articles. What I can make of it, is:
"It is generally agreed that from mammalian cells (as, for example, calf thymus..." are capable of yielding high molecular weight DNA from cells, with very little protein present to decrease purity. [From Welsh and Vyska]
Additionally:
"Calf thymus gland is a fairly good source of replicatiue deoxynucleotidyl
transferase (deoxyribonucleic acid polymerase)" [From Yoneda and Bollum]

So we have a good DNA coming from the calf thymus. Calf thymus is also something we have in great abundance (worldwide slaughter of cattle) and I don't know of any other demand for it (don't know of anyone eating it?). So it should be effective and not too expensive, relatively.
Perhaps there is a difference between the thymuses (thymi?) of calves and adults, given the immune role of the thymus, it's possible. But I can only speculate on that.

And yes. It does seem a bit weird. But it works and everybody does it, so we seem stuck with it.

My two sources:
Richard S. WELSH / Karel VYSKA, Relationship between the Purity and Molecular Weight of Calf Thymus DNA, Hoppe-Seyler's Z. Physiol. Chem.
Bd. 362, S. 969-981, Juli 1981
M. YONEDA AND F. J. BOLLUM, Deoxynucleotide-polymerizing Enzymes of Calf Thymus Gland, THE JOURNAL OF BIOLOGICAL CHEMISTRY, Vol. 240, No. 8, August 1965

Thymus gland tend to deteriorate with age, so I didn't asked "why not adult cow thymus DNA; rather I asked "why not adult cow organs' DNA". I meant adult-cows are more used for meat purpose so far I know... so people would look for any organ of adult cow- not of baby cow. And kidney etc are not ate so far I know... may be I don't know its details.

"we seem stuck with it" means its jut tradition? is that?

@AlwaysConfused and yes, "we seem stuck with it" basically means it's tradition. I more mean that it is accepted practice, in that it is the consensus of the scientific community  "this is how you do this".

So when it came time to identify a source of carrier DNA, calf thymus (obtained free from a slaughterhouse, as described above) was one convenient source.  Salmon sperm, was also popular, and salmon sperm DNA was eventually sold by Sigma-Aldrich. My postdoctoral mentor, Bill Wood, who was a graduate student at Stanford with Paul Berg (he started the year Kornberg was awarded the Nobel Prize) tells of dressing in a suit, and carrying an ice bucket to go collect calf thymus at an abattoir. The worker offered him some to take home for cooking (sweetbreads).

excluding chromosomal proteins; all cells of the organism should contain same-molecular weight DNA. Maybe certain organ contain more amount or copies of DNA; but since their sequence is same; no-one will be higher in molecular wt.

I am afraid if speculation based answers are tolerated here, but I assume DNA extraction from certain organs might were more easier than the other.
At a period when any kind of PCR or in-vitro replication methods were not available, people required to isolate bulk amount of DNA.
Now observe, 3 earliest natural sources from where DNA were isolated; have a difference from other cells.

Salmon sperm DNA : It did not contained histone. Instead it contained protamine. Also loose cells, lower extracellular debris.
Mischer's nuclein from pus cell: White blood corpuscles have enlarged nucleus and likely a high transcription and translation activity. A high transcriptional activity is likely create unwined portions of DNA that lack histones. The transcription and translation activity might be even higher when the WBCs are in fight with microbes because they will require to synthesize a lot of antibodies and lysosomal enzymes.  Also loose cells, not much extracellular debris.
Thymus gland : a site of cell division and maturation, i.e. high replication and transcriptioon activities. Also a spongelike tissue, not very adherent nor stiff extracellular matter.

It seems these factors were helpful to easily separate nucleic acids from random biomolecules such as proteins and polysachharides.


text:
Under what category should myosin come?
Are myosin microfilaments or intermediate filaments? Or are they simply motor proteins? Under which category should I put them? I am highly confused.

Myosin are motor proteins. Microfilaments (AKA actin filaments) are the tracks for Myosin. Filaments of different sizes are the structural components of cells, giving them their shape, rigidity, etc., as well as providing an intracellular network for transport. Myosin walk along these filaments.
In myocytes (muscle cells), myosin pulls actin filaments towards one another.

Picture from here: https://www.ncbi.nlm.nih.gov/books/NBK9961/

but in muscle cells?

@JM97 Please see edit.


text:
Determination of animal and vegetal pole
How do we determine which is an animal pole and which is a vegetal pole in a zygote?
My professor said that the zygote can be divided into two hemispheres, vegetal and animal poles. The hemisphere with yolk is the vegetal pole and the one without is the animal pole.
But I couldn't find an authentic book that I have access to saying anything about the polarity of the zygote. However I stumbled upon this paragraph from Objective Zoology and I'm not sure if it's right.

Zygote or egg of frog is spherical and measures about 1.6mm in diameter. The upper half of the zygote is black (pigmented) and contains nucleus and cytoplasm. The lower part of the zygote is white or light yellow in colour and contains the reserve food in the form of yolk. The upper pigmented part is called the animal pole and the lower part vegetal pole.

"Vegetal" and "animal" poles are archaic terms. As pointed out by Elaine, the polarity axis is defined by ectoderm and mesoderm. There are other kinds of polarity as well. You can read more about it, for different organisms, from Developmental Biology by Gilbert.

To resolve this question here's something I found in Developmental Biology by Gilbert $-$

The amount and distribution of yolk determines where cleavage can occur and the relative size of the blastomeres. When one pole of the egg is relatively yolk-free, the cellular divisions occur there at a faster rate than at the opposite pole. The yolk-rich pole is referred to as the vegetal pole; the yolk concentration in the animal pole is relatively low.

Do you have any reason to doubt this statement? The wikipedia article says pretty much the same thing. When reading the folllowing, don't forget that one can talk about such poles at different stages of development.

The animal pole consists of small cells that divide rapidly, in contrast with the vegetal pole below it. In some cases, the animal pole is thought to differentiate into the later embryo itself, forming the three primary germ layers and participating in gastrulation. [..] The vegetal pole contains large yolky cells that divide very slowly, in contrast with the animal pole above it. [..] The animal hemisphere is dark brown, and the vegetal hemisphere is only weakly pigmented.

and it comes with the following picture

You know, wiki article talks about polarity of an embryo and not a zygote. I haven't encountered any authentic book saying that they are the same, so is my question.

Molecular Biology of the Cell, 6th ed, p. 1156 http://i.imgur.com/ZNTT53Oh.jpg After sperm entry and rotation of symmetrization, the zygote has an animal and vegetal pole. It also says elsewhere that the name animal and vegetal are due to old beliefs, and roughly correspond to what will be inside (endoderm and mesoderm) and outside (ectoderm) respectively, after gastrulation. The v-a polarity is established by gradient of stocked mRNA and vitellin. Mecanisms vary extensively between phylum.


text:
Are there any examples of weighted edit distance genome alignments?
It has been said that weighted edit distance is a preferred way to compare/align genomes in practice, e.g., when identifying genetically similar patients. I wonder if there are some concrete examples when weighted edit distance is used this way and I am particularly interested to see some example weight tables. Some links to research papers showing such examples would be very useful.

Hi and welcome to bio.SE! I made some edits to your question including the title. Feel free to roll back, but I think this should help it get to the right people!

Where did you read  that "weighted edit distance is a preferred way to compare/align genomes in practice"?


text:
What is RNA Engineering
I've been hearing the term passed around, and my own research has led me to some very high-level papers which propose new tools for accomplishing RNA engineering.
From the abstract of one of the above linked papers:

These methods advance our ability to develop broadly applicable genetic tools and to elucidate the underlying sequence-structure-function relationships that empower rational design of complex biomolecules.

It seems as though we are edging close to designing fine-tuned lifeforms. It's easy to jump to exorbitant conclusions, so I'd like to make sure I understand what this is all about.
My questions are:

What exactly is RNA engineering and what can it accomplish (in plain english)
What are the implications of the advent of RNA engineering tools


text:
What physical evidence exists that shows motor proteins "walking" within a cell?
Various animations on the internet show the motor protein kinesin walking within a cell. Is this an approximation? How does this happen and (based upon what physical evidence) how do we know it "walks" like this?
https://www.youtube.com/watch?v=y-uuk4Pr2i8
https://i.stack.imgur.com/dXyJG.jpg
https://www.youtube.com/watch?v=tMKlPDBRJ1E

Closely related from Sceptics-SE: Is this what “happiness looks like”?.

It is known to be seen in-vitro (I've never yet seen practically). One technique includes using optical-tweezer (laser-trap); image example here and here

Since you chose kinesins as an example class of motor proteins, I will also stick to them. In general, the movement mechanisms of kinesins are well studied and the general structure of kinesin proteins, that is a dimer, is known by crystallography (see Kull et al. (1996) for the structure publication).
Even before that, the movement of single kinesin molecules in discrete steps of approx. 8 nm was shown by Svoboda et al. (1993). To resolve single molecules, they used optical trapping interferometry (see this practical guide to optical trapping by the Princeton University for more detailed information). Four years later, Schnitzer and Block (1997) were able to show that that for every step of approx. 8 nm lof a kinesin molecule, one ATP is hydrolysed. Visscher et al. (1999) used molecular force clamps to study ATP and load dependent characteristics of single kinesin molecules.
So far, it appears to be that kinesins move by a 'hand-over-hand' mechanism: Yildiz et al. (2004) labelled single heads of kinesin dimer molecules with a fluorophore and found that their data are congruent with a step of approx. 17 nm followed by a step of approx. 0 nm which indicates that the two dimer hands alternate in movement.
See also the review by Hirokawa et al. (2009) for a general overview of kinesin movement.


text:
How are nutrients absorbed by a pitcher plant?
I've read that pitcher plants thrive in nitrogen-poor soil, which is solved by dissolving insects and absorbing nitrogen that way.
I have a few plants, and when a pitcher start to rot, I cut it off and study the insects that've been trapped. I've never actually observed a dissolved insect. Both interior and exterior seems unharmed.
What digestive enzymes does the plant use?
What part of the insect gets dissolved?
What structures allows absorption and transport of nutrients into the plant? And how is it exploited?

You may upload a few small photographs of those insects which are not digested by the plant.

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Maybe they're just the ones that recently fell in. Older ones might have been digested. Just a guess!

No, they've not recently felled in. I usually feed them myself. Even insects placed there early in the season have not been visibly dissolved. Right now I only have one pitch left, as the plant is going into dormancy. I can post a pic of the content when the pitch start to rot.

Carnivorous plants use a variety of enzymes, including proteases which digest proteins to provide the plant with nitrogen. You might think that the hard exoskeleton would not be digested but pitcher plants (at least some types) produce chitinases which dissolve chitin (i.e. the exoskeleton), so there should be nothing left of the prey. The enzymes are secreted by tiny glands inside the pitcher.

The enzymes that have been detected in carnivorous plants include amylase, chitinase, esterase, lipase, peroxidase, phosphatase, protease, and ribonuclease.

From the Sarracenia faq.
Aside from the enzymes secreted by the plant, there are micro-organisms present in the pitcher which will dissolve organic matter.
In my experience of growing Nepenthes and Sarracenia it seems to take a long time for the prey to dissolve and there is always some material left. Which type of pitcher plant are you growing?
There's a good description of CP digestion from the ICPS.
A more technical explanation about chitinase.
I can't find any specific detail on how the plant absorbs the nutrients, though even non-carnivorous plants can absorb nutrients through the leaf surface.

Also see this SE topic on nutrient absorption via leaves


text:
Why is blood pressure different in different parts of our blood vessels?
Why does it change throughout our circulatory system ?

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Blood pressure changes throughout the circulatory system because the blood vessels (both veins and arteries) have different radius throughout the body. Also, the further you go from the heart, less pressure it will have. This is physics. Fluid Mechanics, specifically. Check out the Navier-Stokes for more insight on the subject. https://en.wikipedia.org/wiki/Fluid_mechanics#Fluid_dynamics https://www.boundless.com/biology/textbooks/boundless-biology-textbook/the-circulatory-system-40/blood-flow-and-blood-pressure-regulation-227/blood-pressure-855-12100/


text:
How do absorbance readings indicate diauxic growth of bacteria?
How is growth rate an indicator of carbohydrate use? How do absorbance readings from a spectrophotometer show growth of bacteria if the absorbance readings are taken several times over the course of a day [and plotted on a graph]? If the second absorbance reading of a sample with bacteria and particular substrate is lower than its initial absorbance reading is there less bacteria present or more? Do the presence of substrates affect the absorbance reading in other words do carbohydrates have any turbidity?
context if needed - experiment determines if a species tested in the presence of a carbohydrate and combination of carbohydrates is able to use each as its sole carbon& energy source and if any are used preferentially to others

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Converting my comments into an  answer.

How is growth rate an indicator of carbohydrate use?

Carbohydrates are the carbon and energy source available for the microbes, and their assimilation is correlated to biomass production. The relationship between microbial growth rates in an aqueous environment and the concentration of a limiting nutrient or carbon source is given by the Monod equation 1 :
$$
\mu = \mu_{max} \frac{[S]}{K_M + [S]}
$$
This relation is linear when the substrate concentration is lower than the constant $K_M$, this is when it is not saturating.
Now, when the culture is in the log phase of growth biomass ($X$) can be described with the simple growth equation:
$$
\frac{dX}{dt} = \mu X
$$
where $\mu$ is the growth rate of the culture, and it can be interpreted as the biomass production speed. So the fastest carbohydrate use is, the highest the growth rate will be.

How do absorbance readings from a spectrophotometer show growth of bacteria if the absorbance readings are taken several times over the course of a day [and plotted on a graph]?

This is explained by the Beer-Lambert law. Simply put: the absorbance ($A$) of an entity is proportional to its concentration ($c$) - all else being equal.
$$
A = \varepsilon \ell c
$$
where $\varepsilon$ is the molar attenuation coefficient or absorptivity of the attenuating species, $\ell$ is the optical path length in cm, and $c$ is the concentration of the attenuating species.
So, the changes in the concentration of your bacterial population (its growth) are reflected in an increase in its absorbance.
If you find a lower absorbance value at time $t+1$ in comparison to time $t$, yes it could mean that the bacterial cell number at time $t+1$ is lower than at time $t$. However, we know neither the protocol you have been following, nor the values you have been obtaining, so there could be other explanations, such as error of measurement.

Do the presence of substrates affect the absorbance reading in other words do carbohydrates have any turbidity?

Yes, molecules in the medium can impact your Optical Density (OD) values. However, that would only be true if these molecules absorb light at the wavelength you are using to measure the absorbance (eg $600$ nm). This is why you should always blank with some filtered medium (or at least with some fresh medium).

Turbidity (measured as absorbance) is direct indicator of numerical density of microbes in culture. The more microbe-cells: the more light is diffuse-reflected and scattered in the path of light; so the less amount light reach the photo-sensor given at colorimeter/ photometer.
Now; if with time the turbidity goes up; then it means with time the number of cell increasing.
Growth rate is an indicator of nutrient use. If certain nutrient is difficult to metabolize for that bacteria; the growth rate would decrease. So turbidity will not increase in that rate. Visit wikipedia that says

"The preferred sugar is consumed first, which leads to rapid growth, followed by a lag phase. During the lag phase the cellular machinery used to metabolize the second sugar is activated and subsequently the second sugar is metabolized."

(graphs from wikipedia)

Reference: Wikipedia.


text:
Does the dissociation of serotonin receptors and their ligands really take hours?
If I understand the principle of neurotransmission correctly, then after binding to a receptor on the postsynaptic side, neurotransmitter molecules must be dissociated from the receptor and removed quickly from the synaptic cleft (see this book).
This article states that the off-rate $k_{\text{off}}$ for the 5HT3 receptor and some ligand is approximately $43 * 10^{-6} s^{-1}$. If we ignore the binding process for now and denote by $C$ the complex formed by 5HT3 and the ligand, we can describe the dissociation process by the following simple differential equation:
$$
\frac{dC}{dt} = -k_{\text{off}} * C
$$
(see Wikipedia).
Using the $k_{\text{off}}$ from above, we get that the half time of this dissociation process is $\frac{\ln{2}}{k_{\text{off}}} \approx 16116s \approx 4,5h $. A similar $k_{\text{off}}$ rate for all other kinds of 5HT receptors binding serotonin can be derived from the dissociation constants found in the Ki Database.
But wouldn't that mean that, when serotonin is released from the presynaptic axon terminal and the 5HT3 receptor binds it, not even half of the neurotransmitter molecules are dissociated from the receptor after more than 4 hours? That seems to clearly contradict the statement from the beginning of this post - so is something wrong with my calculations or does it really take that long? Or have I understood something completely wrong about the principle of neurotransmission?

You're comparing5-hydroxytryptamine to 1,2,3,9-tetrahydro-3-[(5-methyl-1H-imidazol-4-yl)methyl]-9-(3-amino-(N-fluorescien-thiocarbamoyl)-propyl)-4H-carbazol-4-one (in other words, apples to oranges.)

That paper is describing the binding between the 5HT3 receptor and some high-affinity ligand, not serotonin.
Numbers of serotonin probably vary according to the precise receptor (species, subunits, etc), but for a ballpark figure this source says 1.7/s, giving half time of ~400 ms. That estimate is based on solution changes, so I'd say it's an upper bound.
Remember from the other questions you have asked and I have answered, serotonin is a slower-acting neurotransmitter, and clearance of serotonin is not as fast as for other, faster-acting neurotransmitters. However you are correct that your initial calculation of a ~4-hour dissociation time is unreasonable.