text:
What would be the shortest and optimal method of extracting human cells for PCR? Is there a colony PCR like protocol for human cells?
I am trying to devise a quick method to extract genomic DNA from human cells for a PCR.
I first collected cells by centrifuging  saline mouthwash (0.9% NaCl) and extracted genomic DNA using kit followed by a PCR protocol which works fine but is a rather lengthy process.
I tried to cut short the method and removed the DNA extraction steps by using pelleted spit samples as templates for PCR and increased the initial denaturing step from 3 minutes to 5 minutes. However this method was not reliable as some of my samples were amplified and some were not.
Can anyone suggest me a reliable protocol here?
Thanks!

Why do you need to shorten the protocol?

I am trying to make a protocol in which DNA extraction, PCR and gel electrophoresis could be done in a time frame of about 4-5 hrs and I am trying to compact everything.

@techtrix          I am curious, did you try the boiling method?

@RoSiv not yet. I may start my work next week. I will let you know how it turns out.

I am not confident in my reply, but the article linked below has methods for DNA extraction of various human sample types( blood, hair, urine, Cheek)
For what its worth, my professors always told me DNA extraction was more of an art than a science, and one has to tinker to get it just right.
Maybe for something really quick, you could try a protienase K "squishing buffer" and then boil it for like 10 mins in the buffer and then try running PCR.  I am just an undergraduate though so take my words with a heavy grain of salt.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792701/
Here is how they gathered the buccal samples:
buccal swabs:

five healthy adult volunteers were recruited (age range, 22–35 years),
  and demographic information, including age, health condition, sex,
  population ancestry, hair color, and hair treatments, was collected.
  The volunteers recruited were asked to rinse their mouth with tap
  water, 30 s before sampling of buccal swabs, to avoid the
  contamination as a result of food particles. For each individual, both
  sides of buccal mucosa were wiped with a cotton swab for 15 s, and a
  total of five samples was collected in 500 μl 10 M Tris-HCl, 10 mM
  EDTA, 2% SDS, containing 1.5-ml microcentrifuge tubes. Isolation of
  DNA from cotton swabs was performed.

Here is a copy paste, hyphens are mine.
DNA Extration:

Buccal swabs:
-samples were suspended in 500 μl lysis buffer [10 mM Tris (pH 8.0), 10 mM EDTA, and 2.0% SDS], and 50 μl 10% SDS, followed by 5–10 μl 20
  mg/ml proteinase K
-incubated 1–3 h at 56°C until the tissue was totally dissolved
-The DNA was then extracted from each sample with an equal volume of phenol:chloroform: isoamyl alcohol solution (25:24:1) and mixed gently
  by inverting the tubes for 3 min.
-samples were then centrifuged (Eppendorf 5415R; Hamburg, Germany) for 10 min with 10,000 g (4°C),
-upper aqueous layer was transferred to a fresh, sterilized microcentrifuge tube.
-RNase A (10 μl of 10 mg/ml; Fermentas, Thermo Scientific, Germany) was added, and the solution was incubated at 37°C for 30 min.
-Equal volumes of chloroform:isoamyl alcohol solution were added and centrifuged (Eppendorf 5415R), again with 10,000 g (4°C) for 10 min.
-The upper aqueous layer was transferred to a sterilized microcentrifuge tube, and double the volume of chilled isopropanol
  (Merck, Whitehouse Station, NJ, USA) was added, along with one-tenth
  volume of 3 M sodium acetate, and chilled at −20°C for 1 h for
  precipitation.
-After 1 h, the sample was centrifuged (Eppendorf 5415R) at 10,000 g (4°C) for 10 min.
-After decanting the supernatant, 250 μl 70% ethanol (Merck) was added, and the pellet was dissolved; the mixture was centrifuged at
  10,000 rpm for 10 min, and the supernatant was decanted gently.
-The pellet was air-dried under laminar air flow, and the dried pellet was resuspended in 50 μl nuclease-free water or 1× 10 mM Tris-HCl, 1
  mM EDTA, pH 7.6 (TE), buffer and frozen at −20°C or at −80°C for
  storage.

Thanks Ro Siv, but this process seems rather lengthy for me. I could try the protienase K "squishing buffer" method though.

I do a lot of gDNA and cfDNA extraction! What Ro Siv has explained is a pretty standard method of buccal swab extraction, however the pK incubation times do not need to be nearly that long. The gold standard in DNA extraction is QIAGEN kits. Specifically for your uses I would go with something like the QIAamp DNA Mini Kit (you can view their handbook protocols on their site - https://www.qiagen.com/us/resources/resourcedetail?id=67893a91-946f-49b5-8033-394fa5d752ea&lang=en) In practice, I have been able to do 4 samples without automation on their spin protocol in around 1.5 hours total.
PCR time will depend on your cycling conditions and how long it takes you to set up a reaction etc, and gels would depend on how precise you need your bands to be. I think the whole thing can easily be done in 4-5 hours. In my experience, blood samples take only slightly longer, but is obviously more invasive and less practical. I agree that buccal is the way to go. For reference, we use Puritan hydraflock swabs, but that's up to you.


text:
Textbook on molecular basis of memory
Looking at the rules in the meta, it seems book-recs are a little on the iffy side for on-topic so I hope this is okay.
I am looking for a (graduate-level) textbook that has a thorough treatment of the molecular basis of learning and memory. The issue I am having is that a lot of textbooks seem to cover bits and pieces or just focus on one area. Usually, they just have a few small sections on the molecular events and the rest of the textbook covers channel properties, pharmacology, systems neuro, and behavior.

Synapses - This one comes close but is now quite dated (2003)
The Neurobiology of Learning and Memory - A significant section on the molecular aspect but is not particularly detailed. Very basic idea.

Review articles tend to be difficult because they are more specialized for specific kinases (mTOR, CaMKII etc), events, or channels.
I am trying to get a sense of the broader picture of the just the molecular side of all of this. Specifically the molecular and cell biology that underlies:

Early-phase LTP (receptor trafficking, signaling pathways)
Proteins expressed from local translation in dendritic spines, signaling pathways that control this
Details on synaptic tagging hypothesis
Late-phase LTP events, pathways, proteins, and regulation
Downstream effects of activation of different channels, how they control pathways below, how they all intersect and how this differs by brain area and cell type
LTD events
Events at the post-synaptic density (receptors, ion-channels, protein composition, scaffolding, actin network)
Synaptogenesis, plasticity, maintenance during long-term memory
Kinases in learning and memory
Transcriptional control
Post-translational modifications and consequences for learning and memory
Scaffolding proteins and their contribution to signal stability
Pre-synaptic events
Contributions of glia/auxiliary neuronal cells
Bonus: Disease focus - what pathways and proteins underlie various well-studied genetic diseases?
etc.

I know this is a tall order but with 1000+ page textbooks out there on other neuroscience topics, surely someone has written something? Review article are great too, perhaps I just haven't found the right one yet.

From what I am aware of, most of the molecular basis of memory research is relatively new, and thus will likely only be in primary literature at this point, there is usually a 5 to 10 year lag for the most recent research to make it into the textbooks. There is the Cognitive Sciences Stack, where you might have a more focused audience for your question. @AliceD may have some advice on this topic though, or at least where to start looking for good reviews. The journal Neuron comes to mind, but I am not sure if there would be more specialized journals.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
height and bryophytes

Why does being taller provide advantages for Bryophyta but being
  shorter is better for Marchantiophyta? What disadvantages could being
  taller have?

I think that by being taller, you have better spore dispersal. However, the problem with being tall is that the temperature flucuates more. Am I correct? Is this the right answer? Am I on the right track?

The root of the question is going to be in the differences between Bryophyta and Marchantiophyta. What are some of those differences? Do they affect spore dispersal? Water use? Temperature?

@Resonating Bryophyta have a cuticle, stomata, and conductive tissue. But the question is guess is why does it need it? I can only think of water use.  Being tall provides advantages for spor diesperal as well.

So taller is better. Why isn't Marchantiophyta taller? Can they even be any taller than they are?

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text:
How thick is the residue from a fingerprint?
I am trying to work out the mass added to a small glass sphere when it is picked up with bare fingers.

Wouldn't that depend a lot on your skin type, how moist your skin is, what stuff you have touched before,... ?

Yes, but there must be an average. I am weighing stuff to an accuracy of a microgram

Figure in the range of a 25 micron cube of oil perhaps.

The average thickness of a latent fingerprint is .1 micron.
Or, <10 micrograms.
https://www.ojp.gov/pdffiles1/nij/225327.pdf

Presumably that would be for a full print from the first joint of the finger (i.e. the bit that they do the fingerprint ID from), and would decrease with less contact area and increase with more area covered. I wonder how big the "small glass spheres" OP is using are?

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text:
Energy of flight styles (birds)
What does take more energy (for a bird): to dive or gliding? My teacher thinks that gliding takes more energy, but I'm not sure about this: when a bird glides, it doesn't do anything (pretty much). But diving is stress, which takes much energy. Or am I wrong?
(edit: I don't mean the "going under the water" diving, but "nose dives")

How is diving stressful? The bird is just letting gravity do its thing.

Imagine: you're a bird flying towards the ground, getting faster and faster... not stressful? @MattDMo

No, not at all. Birds are not people. They have wings and are perfectly capable of controlling their descent.

But gliding souds much more like chilling, doesn't it?

For people like me ^^ ;-)

And you (as a bird) have to stop after that and fly up again... If you glide, you don't have to.

Google: (bird flight energy expenditure gliding) gives e.g. The Energetic cost of short flights in birds, Heart rate and estimated energy expenditure of flapping and gliding in black-browed albatrosses, Efficiency of Lift Production in Flapping and Gliding Flight of Swifts and ... [cnd->]

[...cnd:] Energy Expenditure and Metabolic Changes of Free-Flying Migrating Northern Bald Ibis. This might be a start.

@fileunderwater this articles are very detailed. But Strg+F gives no results for "dive", only for "glide", means that the article has nothing about diving. But it's a good beginning, thx.


text:
Does soap kill human cells?
I see many products, particularly hand soap and cleaning products, that claim to kill 99.9% or more of bacteria.
This makes me wonder, if the chemicals are potent enough to break down bacterial cell membranes, can they also break down human cells? If not, why not?

salamander is right about triclosan being the active ingredient in antibacterial soap, but the reason why it doesn't kill human cells doesn't have anything to do with the skin. From salamander's same source:

Once they are in microbes cells, triclosan poisons a specific enzyme (enzymes are proteins that have particular functions, think of them as cellular machinery) that is used in making microbes cell membranes. Humans dont have this enzyme, so triclosan doesnt poison us.

The enzyme in question is called Enoyl-acyl carrier protein reductase (ENR), and is used by bacteria as part of their fatty acid synthesis. Eukaryotes use a different set of enzymes for fatty acid synthesis, so we aren't effected by this activity of triclosan.
For some more specifics about the interaction of triclosan and ENR, we can turn a study about the antibacterial mechanism of triclosan that was done soon after triclosan was first crystalized in situ with its target enzyme.
From Heath, et al (1999):

Triclosan is a broad-spectrum antibacterial agent that inhibits bacterial fatty acid synthesis at the enoyl-acyl carrier protein reductase (FabI) step... The ubiquitous occurrence of type II fatty acid synthase systems in bacteria and the essential nature of the FabI reaction make this enzyme an attractive target for antibacterial drugs. Accordingly, triclosan is effective against a broad spectrum of bacteria, including multi-drug-resistant Staphylococcus aureus.

Your answer is correct. Thank you for clearing that up. +1

During the current coronavirus lockdown, there's much discussion that regular ole non-antibacterial soap will tear apart the lipid membrane of the virus. I'm fairly certain that human cells have a bi-lipid membrane, so it would seem that regular soap should also kill human cells like it does the virus. Any insight into this non-antibacterial case?

Yes, soap will absolutely kill human cells, under the right conditions. This is why if you wash your hands over and over again, they will become red, chapped, and damaged

The longer answer is that human skin is a complex, many-layered structure that is made up of both (highly specialized) cells and other non-cellular components. The barrier formed by the outer layers of your epidermis is what keep soap from doing you any real harm, so long as you don't overdo it. Some refs: Interactions Between Surfactants and the Skin... and Effect of Surfactant Mixtures on Skin...

Antibacterial soap commonly uses triclosan, which can pass through the phospholipid bilayer of bacteria and disrupt the production of essential enzymes, killing the bacteria (source). This triclosan
 would kill human body cells in the same way as it does bacteria, however we have a 1-1.5mm thick layer of dead skin cells(called the Stratum corneum) that exists to protect our epidermis from chemicals like antibacterial soap.
EDIT: I was absolutely wrong about triclosan killing human cells. In fact, it is impossible for triclosan to kill human cells, because the enzyme that is destroyed in bacteria by the triclosan does not exist in the human body.

Can you please add a specific citation for the stuff about the Stratum corneum blocking triclosan? I can't find it anywhere

Forgive my blatancy, but this is incorrect. Triclosan WOULDN'T kill human cells even if it did come into direct contact with them because it binds enoyl-acyl carrier protein reductase (ENR) used in fatty acid synthesis in bacteria. Human cells lack ENR and are thus unaffected.

@CDB No, I appreciate the frankness. According to the European Union's Scientific Committee on Consumer Safety's Opinion on triclosan  you are absolutely correct. I'll edit my post to reflect this.

Excellent! Your edit is perfect. +1 for a great answer.


text:
Why would villagers attack Orangutans?
I read today in the news that villagers in Borneo were attacking refugee Orangutans. Why would they do this?

In It’s Not Just Conflict That Motivates Killing of Orangutans by Davis et al. (2013), the authors identify number of conflict and non-conflict reasons reported in the study why orangutans were killed in a certain part of Indonesia:
Conflict reasons:

pest
fear/self-defence
paid or forced to kill
orangutans interrupted logging or forestry operations

Non-conflict reasons:

traditional medicine
food
to sell or keep young as pets
hobby/sport hunting
for other trade of animals or meat
killed accidentally or opportunistically while hunting other animals

The results from this survey are depicted in this graph:

Obviously in this case they were not attacked for food. The impression I got from the article makes me think it was probably motivated by people viewing them as pests or as a threat/danger. It is almost certainly more of a social reason than a biological reason. However, in the absence of specific evidence, it is probably not helpful to speculate why this occurred.


text:
What is this stick-like creature?
My wife noticed this on her trousers immediately after coming home - probably acquired after brushing past a bush. It's about one inch long, and does not move much - but when poked it will flex and appear to try to roll.
It looks for all the world like a stick - but I've googled "stick insect", and this doesn't seem to have enough (or the right kind of) legs.
We live in England, in a suburban setting. We both work in offices and don't have a lot of contact with nature.
Could it be a thorn moth larva?
Apologies for the quality of the photo; I can try to take a better one if it would help to get another angle.

Have just observed this same species here in Muskoka ,Ontario ,Canada .Never have come across this type of stick( almost slug like) creature with 4 lower stubby leg like appendages long body with two small eyes on top of the head. Almost giraffe like approximately 4 to 5 cms. Long brown with varigated markings gives appearance of bark.

This appears to be an inch-worm, the larval caterpillar stage of a moth (order Lepidoptera) in the  Geometridae family. According to Bugguide (my emphasis):

Larva - generally have only two pairs of prolegs (at the hind end) rather than the usual five pairs in most lepidoptera; the lack of prolegs in the middle of the body necessitates the peculiar method of locomotion, drawing the hind end up to the thoracic legs to form a loop, and then extending the body forward.

The systematics/taxonomy of this group is unclear, debated, and in flux. However, the majority of stick-like larval forms I could find seemed to be associated with the current Ennominae subfamily, which is also the largest of subfamilies in this family of moths.
Müller et al. (2019) just published the 6th volume of "The Geometrid Moths of Europe", which might be a good starting point for IDing this specimen more precisely. A book description from NHBS:

More than half of the European Ennominae, a total of 181 species, plus 21 new species for the European fauna are covered in two hardback parts (with text and plates in separate volumes), including difficult genera...

You could also keep an eye on or alternatively submit an ID request over at Wildlife Insight's Illustrated Guide to British Caterpillars.

Some stick-like examples: brown-variants of Odontopera bidentata, Biston betularia, Crocallis elinguaria, Colotois pennaria, etc. I do not know this group well enough nor is your picture good enough for me to go further than I already have. If you can provide more information or better pictures, I could try to delve in a bit deeper.


text:
Do mitochondria digest fats?
I am a student and I'm currently using the IB biology Oxford textbook. A few weeks ago I had a test on biochemistry. I studied on my textbook and it stated the following: "Mitochondrion: (…) fat is digested here if it is being used as an energy resource in the cell" (page 22) "The energy store from them (Triglycerides) can be released by aerobic cell respiration" (page 78). My teacher told me that I was wrong to write these statements in my test. Is there something wrong? Is the term 'fat' too generic? Do different kinds of fats undergo either aerobic or anaerobic respiration? I am currently confused as I do not know who is right and who is wrong… Can someone answer my questions?
Thank you

You are not far off the mark I would say. Strictly speaking it's not correct to say that mitochondria oxidize fat. By "fat" we usually mean triacylglycerides, and these must first be hydrolyzed into free fatty acids (by enzymes known as lipases) that can be oxidized in the mitochondria. But many researchers and textbook authors are not always careful with this distinction.
Most fatty acids are indeed oxidized ("digested" sounds strange to me) in the mitochondria into acetyl-CoA units, in a process known as beta-oxidation. The acetyl-CoA units produced are then further oxidized into CO$_2$ by the TCA cycle. These processes generate NADH and FADH$_2$ which is converted into ATP by the respiratory chain.
There are exceptions though. Very long-chain or branched fatty acids are instead oxidized in peroxisomes, which contain enzymes specialized for this purpose.
There is no such thing as "anaerobic respiration": in animals, respiration always uses oxygen as the terminal electron acceptor. Mitochondrial beta-oxidation is coupled to the respiratory chain, and therefore requires oxygen. Peroxisomal oxidation is not directly coupled to respiration, but the process still requires oxygen, which in this case is reduced directly by the fatty acid oxidases. So there is no truly anaerobic form of fatty acid oxidation.


text:
"synapses grow closer together in order to decrease the distance", is it true?
Is there a source?
That synapses get physically get close as their interaction increases.
I have also read that where neurons crosses each other they create new neuron, is that true?

What do you mean with interaction? Synaptic mechanisms? 2. No, as new neurons are born only in restricted areas of the nervous system.

I think you're talking about Hebbian theory? My neuro professor used to summarize this as "Cells that fire together, wire together" (although apparently he was in fact quoting Carla Shatz).

http://www.curiousapes.com/the-science-of-happiness-why-complaining-is-literally-killing-you/

" the synapses grow closer together in order to decrease the distance the electrical charge has to cross. "

The first red flag is that this sentence is incorrect, based on the explanation following it in the source you linked. It suggests that there would be a reduced distance from one synapse to the next, while the text really explains that there will be a reduction in the width of the synaptic cleft. I am not certain enough to give an answer, but the sloppy language alone makes me think the author does not know what he's talking about.


text:
Are antihistamines considered to be psychoactive substances?
I have heard many times that the widely used antihistamines are not considered to be psychoactive drugs. Yet their impact on ones cognitive functions can be substantial. According to some sources, sedatives are also attributed being psychoactive, but not antihistamines. What is the difference?
UPDATE
Some links for the "cognitive effects" that I am referring to include hallucinations as well as drowsiness, anxiousness and irritability.
Besides that, it is well known that antihistamines cause drowsiness and sleepiness which are artificially altered states of mind because they are 1) not naturally-occuring, 2) have different mechanics and flow than their natural counterparts.
from experience I know these effects can be very strong, up to the state when one sees dreams while being awake. I can't find any scientific papers on that, but I have found many reports on the web and among people I've talked to.

When you say "their impact on ones psyche functions", what effect(s) are you talking about?

@naught101 please see the update

Your links list kind of broke. format them like [link name](http://...). Can you actually mention the effect in the question  as well, so people know what you're talking about without going digging?

@naught101 that's strange, on my side the links are working. I don't know what else can I do with them. Also, please read the update, I have been more specific on the effect in there.

I fixed the two references, and removed the dictionary and yahoo answers link, because they didn't relate to antihistamines.

@naught101 Thank you for the improvement! Yes, I guess words would be better than numbers for the link names :) As for the link to yahoo and the dictionary - I can explain - I was referring to the definition of "psychoactive" because it plays a role here too.. However, the links seem to be intact, so it is ok.

Short answer
First-generation anti-histamines are psychoactive, second-generation equivalents may not be*.
Background
According to WHO, psychoactive substances are:

[...] substances that, when taken in or administered into one's system, affect mental processes, e.g. cognition or affect. This term and its equivalent, psychotropic drug, are the most neutral and descriptive term for the whole class of substances, licit and illicit, of interest to drug policy. ‘Psychoactive’ does not necessarily imply dependence-producing, and in common parlance, the term is often left unstated, as in ‘drug use’ or ‘substance abuse’.

Antihistamines are used to treat allergies. First-generation antihistamines readily cross the blood-brain-barrier and have been associated with performance deficits on tests of attention, working memory, vigilance, and speed. By contrast, second-generation antihistamines that do not readily reach the brain do not have these side-effects (Kay, 2000).
Since attention, working memory and vigilance are mental cognitive processes, first-generation antihistamines fall into the classification of WHO as being psychoactive.
Reference
- Kay, J Allergy Clin Immunol (2000); 105(6-2): S622–7
Note
*I am not an MD and data on 2nd generation drugs are based on a single study with a limited number of tests. Consult a medical professional for prescription of the appropriate treatment.

Yes, I follow the medical advice of doctors - having seasonal hay fever since I was a child. But they don't say anything except "take this". So, from the answer, at least, it is clear that AHs do fall under the category officially, although somehow nobody mentions it for some reason. Gen-I force people sleep and forget (too strong). Gen-II surely have psychoactive effects too and allow to stay sober enough to experience it. The prolonged use seems to change personality, giving access to moods and thoughts not availbale without them. It's just that I am so surprised there's so little research.

@noncom - my apologies for the note, but self-help questions are explicitly off-topic here. It's a miracle you question survived in the first place :)

Yes, I know, it looks like the question managed to be as impersonal as it could :) medical topics are very different in that from the technical ones... As for the matter - I see, really there's not much else to say, since nobody really went into researching this. Even MAPS does not pay any attention to it. But I believe AHs (and I mean gen-II too, azelastine, cetirizine) can influence people strongly, especially in long-term use, especially children and people with unusual mental conditions..  Well, maybe some time in the future someone will do more research..


text:
How fast is water transported from roots to leaves?
I understand basically how water transport from roots to leaves through the xylem works, but I have no idea of the timescales involved.
How long does it take for water to get from root tips to leaves? How does this speed change in different parts of the plant? How does it differ between different plant types? How is it affected by plant size?
Also, I guess it changes from relatively fast in the middle of the day to almost zero at night, but how does it change during a normal sunny day (e.g. sinusoidal? More like a square wave?)

Could someone please tag this "water" and "xylem" and then delete this comment?

You can retain this when you edit your question.

We usually use more general tags and not down to a very fine characterisation of the question. So plant-physiology is fine here.

If you assume the plant has a constant total supply of water, then uptake must equal output. If you could measure total water vapor escaping from a plant, you'd know the rate water must flow through the plant.

@user137: True. But I don't know where to get that data for a whole single plant (of any size)

related: http://biology.stackexchange.com/questions/1096/how-does-water-move-throughout-plants http://biology.stackexchange.com/questions/11044/how-do-trees-lift-water-higher-than-10-meters

@user137: Wrong. There is part of the water not evaporating but going down in phloem sap,  https://www.boundless.com/biology/textbooks/boundless-biology-textbook/plant-form-and-physiology-30/transport-of-water-and-solutes-in-plants-183/transportation-of-photosynthates-in-the-phloem-699-11924/images/fig-ch30_05_07/

@Joce It was a good first order approximation. Maybe if you had a potted plant and covered the dirt to prevent evaporation from anything except the plant, then put the whole thing on a sensitive scale. The change in weight might tell you the mass of water escaping the plant. That could give NET flow up the plant.

@user137: Do you have data showing that it is a good approximation? It seems to me that water efficiency would imply an evaporation much smaller than sap flux. This wouldn't contradict pore-pressure driven sap flow, although of course there is always some unavoidable evaporation for this process.

Yeah, net water evaporation is going to be much less than xylem flow rates. I'm interested in xylem flow rates. In particular, I'm interested in the (distribution of) time it takes for a parcel of water to get from the roots to the leaves. Approximations are fine though (e.g. for a Sequoia -  Minutes? Hours? Days?).

You can find some answers for your questions in this paper (it is only for Ricinus communis, but you may follow the cited by from google and find for other plants):
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-3040.2001.00704.x/full
velocity in the phloem (0·250 ± 0·004 mm s−1)
xylem in the light (0·401 ± 0·004 mm s−1), in the dark (0·255 ± 0·003 mm s−1)

Graphs on daily change are on the paper.

Great, thanks! That's about 1.5m/h in the light, and Castor plants get to a few meters, so I guess it might take a few hours to get from root tips to stomata.


text:
How fast do stomata respond to environmental changes?
How fast does stomatal resistance respond to environmental changes? Correct me if I'm wrong, but I assume that atmospheric humidity would be the fastest changing factor (e.g. rain storm on a dry day, or a warm change coming through). If the relative humidity changes from say 50% to 100%, how quickly will stomata open? And how fast in the opposite direction?

Stomatal speed varies depending on a lot of factors, especially anatomy even within species, but especially between species.

Evidence from several studies has also suggested that smaller stomata respond faster than larger stomata

The paper I just cited from (first link below) includes is a long review of the what is currently known and also original research into the process. It includes a really detailed, lengthy chapter on the stomatal speed, but which is mostly lacking in easily citable numbers except for closing times:

Stomatal aperture responds more slowly, typically with half-times of 10 to 20 min, reaching a new stable, (near) closed state after 45 to 60 min

A few more clear numbers come from the second paper I link to below, however this is in response to changes in light, not humidity.
It includes a table (table 1) on mean stomatal closing and opening time delays in four plant groups and plants adapted to two climate conditions. In most groups, closing happens slower, taking about 50 percent longer, with mean times varying between 6 and 18 minutes. Opening is faster in every group but one and takes between 4 and 30 minutes. In plants adapted to dry climate conditions stomata respond faster.
Sources:
Stomatal Size, Speed, and Responsiveness Impact on Photosynthesis and Water Use Efficiency
Effects of stomatal delays on the economics of leaf gas exchange under intermittent light regimes


text:
Do aquatic plants have stomata?
I am wondering if aquatic plants have stomata or not. I know that non-aquatic plants have stomata to release water(transpiration) and oxygen, and to take in carbon dioxide. Do aquatic plants also have stomata, and if so do they take in water through their stomata? If water is taken in through their stomata, wouldn't other substances such as dissolved salts get in the plants vascular system too? Does the aquatic plant use this salt or remove it, and how would they remove it?
Note: I am talking about fully submerged aquatic plants such as kelp.

No
First of all, stomata is of course important for gas exchange and also water conservation. Well, clearly, water conservation isn't needed! Also, gases can diffuse relatively easy in water so gas exchange using stomata isn't needed.
Technical notes
Second of all, technically organisms like kelp are thalloid plants. They are in separate kingdoms. Kelp is a brown algae, placed in kingdom algae in laminariales order of class phaeophyta. They does not contain any kind of vascular or conductive tissue as their plant body is thalloid.

@zack1544 you're welcome. If you have related questions, please ask me in the comments.

They're not in separate kingdoms. Algae and Land plants (embryophytes) are separate Divisions of the Kingdom Plantae.

@naught101 well, I didn't know that green algae were part of plants, as I learnt it as part of Protists. But other aquatic "plants" are not plants, like kelp is in brown algae which is in Protists.

Do you have references for your claims? To say that all aquatic plants lack stomata is quite a strong statement.

@fileunderwater: There are semi aquatic plants that ofter have their leaves above water. Those will have stomata. There are properly aquatic "plants", like kelp, but as Tanmath says, they're not embryophytes, so they don't have stomata.

@naught101 I was referring to fully submerged plants, since that is what the OP is mainly asking about. The answer needs references either way. I'm aware about semiaquatic plants etc (see my answer below).

According to the book Stomatal function (Zeiger et al, 1987), many aquatic angiosperm plants have stomata (since they have evolved from terrestial plants), while some have reduced or complete loss of stomata.
However, the book also states that:

...aquatic plants living underwater are devoid of stomata. Leaves that float in water, which are common in ponds, have stomata on their upper surfaces but lack them on the surfaces in contact with water.

It is true that plants that float on water (hydrophytes) have stomata on one sider, but I think the OP is referring to fully underwater plant-like organisms or plants.

@TanMath I was merely looking at a couple of sources I know of. As it seems, fully submerged plants indeed often/usually lack stomata.

Oops, I was mistaken when I said hydrophytes float on water. Many hydrophytes are submerged underwater.

Are there aquatic angiosperms that never have their leaves out of water? Or at least, where the leaves don't really work out of water?

@naught101 Angiosperms like Ceratophyllum submersum (Hornwort) lives fully submerged. I cannot say to what extent their leaves work out of water, but their supporting structures (branches, stems) aren't adapted do life out of water, and cannot support the weight of the plant.

@naught101 I can, from field expierence, tell you that most if not all submerged plant don't survive outside water (incl. Ceratophyllum). The leaves simply dry out. Sometimes they reach up to the water surface, but they rarely protrude more than a few mm. Many species, like potamogeton, myriophyllum, ranunculus do have flowers that grow a few cm above water level.


text:
Is the prostate problem unique to humans?
In human males the urethra goes through the prostate rather than around it, which tends to create problems for older men as the prostate enlarges. Is this only a human problem or do other animals, primates in particular, have the same problem?

Asking 'why' question in light of evolution is not a good idea !

The main question is 100% factual, and there may well be a sound scientific reason why the urethra goes through rather than round the prostate. Evolution is so central to biology that I totally disagree with Dexter's objection.

I think Dexter's objection is valid. Everyone who misunderstands evolution wants to know why we haven't evolved: wheels as lower limbs, wings to fly, bodies like fish, four legs, to not feel pain, etc., etc. (These are real examples.) Evolution is not directed by an intelligent process. "Why did...?" is a much better question than "Why didn't...?"

Dogs get benign prostatic hypertrophy, so, yes, other animals (in fact most old male dogs, so that would mean a whole lot of other animals) do get BPH.

The most common conditions affecting the canine prostate include benign prostatic hyperplasia, prostatitis, prostatic cysts, and prostatic neoplasia.

However, you're almost correct.

[T]here is no risk for prostate cancer in any other aging mammal except the dog.

Though this article addresses cancer, the same appears to be true for BPH.
The prostate and breast appeared at the same time with the origin of mammals (possibly as long as 195 million years ago). While all male mammals have a prostate, seminal vesicles only appear in  primarily herbivorous species with the exception of man. The human male has seminal vesicles and consumes meat. Thus, it has been postulated to be a dietary cause. Bonobos, on the other hand, exist primarily on a high fruit and vegetable diet. They don't get BPH.
It isn't known what dogs ate before domestication (were there 'dogs' before domestication?) But it's postulated that ~10-15,000 years ago, humans (and their newly domesticated partners, dogs) dramatically altered their diets, breeding animals for food.
Why haven't we evolved a solution? Well, on the one hand, if BPH is only 15K years old, that's only a fraction of a blink in the human evolutionary scale of things, so not enough time to "evolve" a way around it (maybe reroute the urethra?)
On the other hand, we have. We've evolved medications and surgery for treatment of prostatic hypertrophy.
Similarities of prostate and breast cancer: Evolution, diet, and estrogens
New concepts in tissue specificity for prostate cancer and benign prostatic hyperplasia

I love your two answers to the why question!

Why prostate surrounds urethra? The human prostate has different zones that form separately in the embryo from the urogenital sinus, but later fuse. The mouse "prostate" is actually several separate glands that remain distinct. Although there has be a temptation to associate specific humane zones with specific mouse types of prostate, the current feling is that this is not fully supportable. Why the human zones have fused remains unclear. See: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968575/
Regarding evolutionary pressures: In order for a trait to be selected against, it needs to be "active" or forceful during the period of reproductive activity. That's not the case for BPH. It occurs mainly after the time of typical procreation for humans in pair bonds. There are very few societies in which 60+ year-old men are a "reproductive" force. Furthermore BPH is not fatal, so even if we older men were actively engaged in siring more offspring, we could still be doing so into our 60's and 70's.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Can bacteria release free DNA into their environment?
Natural transformation AKA natural competence involves the uptake of DNA into a competent bacterium (for horizontal gene transfer or as a food source). My question is about where this extracellular DNA can come from. Typically this "free" DNA originates from lysed bacterial cells. Are there instances where DNA is released without lysis that other bacteria can uptake via natural transformation?
Note: I am not interested in bacterial conjugation because I'm specifically interested in extracellular DNA that can be internalised by competent bacteria.

Natural Transformation
The process of Natural Transformation (Lorenz and Wackernagel 1994) has a very huge importance in evolution of prokaryotes. Definition quoting from (Stewart and Carlson 1986)

Natural transformation is part of the normal physiology of the cell.
It is the only form of bacterial genetic exchange whose functions are
encoded on the chromosome, and competence is a heritable trait,
subject to selective pressure.

This is almost similar to our daily use artificial transformation. You need some chemical like $CaCl_2$ to cell permiabalized, some chelating agents like EDTA and DNA material. You can imagine naturally occurring cell encountering such conditions, like decrease in temperature in presence of certain chemicals and proteins.
This concept of one cell externalising, and another internalising DNA got stronger when researchers observed free DNA in culture media (Catlin 1959, Sinha and Iyer 1971).
The Creation of eDNA
The release of eDNA (extracellular  DNA) can occur via spontaneous excretion or autolytic action.
There are known mechanisms for the release eDNA like formation of blebs (Dorward and Garon 1990). This extracellular DNA production is affected by many physiochemical factors than biotic (Paul and David 1989). There are many in detailed reports which shows such DNA can be passed through cell wall without any cell damage (Hara and Ueda 1981). Half life of such eDNA in various environment is reported in following table from (Lorenz and Wackernagel 1994)

Now there are even more novel ways of production of extracellular DNA like in Neisseria gonorrhoeae secretion of chromosomal DNA occure via new type IV secretion system (Hamilton et al 2005). Not just experiments, mathematical models also shows novel role of such process in gene-level selection (Draghi and Turner 2006). I haven't touched upon uptake of these DNA, which itself has lot of literature and unique mechanisms like this.

This is exactly what I was looking for. Could I also add that in the 2004 Chen & Dubnau review, they discuss H.pylori having a mechanism related to the type IV secretion system for exporting macromolecules such as DNA.

Indeed. That (Lorenz and Wackernagel 1994) paper is very nice. You will get all sorts of references from that. Surprisingly, I hardly found any recent papers on this (after 2000). Is terminology changed or something ?

When I first "read" the Lorenz & Wackernagel paper (it's a chunky paper!) I thought it was mostly discussing the uptake machinery which is what I was interested in at the time. On a re-read it has an entire section on excretion! As for recent papers, there is the 2010 Burton & Dubnau review that rounds up a lot of the more recent studies. Particularly I noticed the FtsK/SpoIIIE proteins. These are pretty different systems to anything I'm studying though.

Good question, the only thing I can add is that in biofilms, although the DNA is released via lysis, the lysis is controlled using quorum sensing and effects specific subpopulations (Okshevsky & Meyer, 2013).

That is bizarre! Very interesting, but unfortunately doesn't help answer my question. There may be some information in the paper but unfortunately it's behind a paywall!

@GoodGravy You can find a copy of the paper here.


text:
Dendrodendritic synapse through axodendritic synapse at same dendrite?
Reading Wikipedia's article of dendrodendritic synapse, I find that:

Dendrodendritic synapses are activated in a similar fashion to axodendritic synapses in respects to using a chemical synapse. These chemical synapses receive a depolarizing signal from an incoming action potential which results in an influx of calcium ions that permit release of Neurotransmitters to propagate the signal the post synaptic cell. There is also evidence of bi-directionality in signaling at dendrodendritic synapses. Ordinarily, one of the dendrites will display inhibitory effects while the other will display excitatory effects.

Now I was wondering, does dendrodendritic synapse occur only when the neuron reaches the threshold action potential and "fires" or is it possible that dendrodendritic synapse occurs as a result of, for example, an axodendritic synapse at the same dendrite? (even though the neuron doesn't fire)
Edit

Clearly, we can see that the dendrite has multiple 'endings'. I was under the impression that a synapse can happen at any such 'ending'. Assuming that a synapse happens at one ending of the dendrite, is it viable that anything happens to a neighbouring neuron that is connected with a dendrodendritic synaptic connection to the other ending of the dendrite?

I'm not sure if you are asking if an axon that sends a signal to a dendrite would then be released from that dendrite to another dendrite?
I don't see how this is possible seeing as the dendrite is already paired with the axon and downstream of said dendrite there would be a neuron.
A dendrodenritic synapse is two dendrites of two different neurons in contact with each other. For there to be a signal an action potential must have been reached.
Synapse is a junction between two neurons where chemical signaling occurs, but it is not the definition of a signal occurring. If that makes sense.
It seems like you are confused on the location and anatomy of a synapse.
There wouldn't be an axodendritic synapse followed by a dendrodendritic synapse then the neuron. It would either be axodendritic or dendrodendritic. Now there can be multitudes of connections between neurons but I don't think that is what you were asking.
Edit: Seeing your edit makes your question much clearer.
If the signal from the axodendritic synapse excites the neuron enough to reach action potential then that signal would be sent out through its synapses, including the dendrodendritic ones. So I guess in this way it was a "consequence" of the axodendritic synapse.
Though I would rather you think about it in that the action potential of one neuron sent a signal through it's connections to the neighborhing neuron, thus causing that neuron to reach action potential and further send out the signal. It's not really a "consequence" of the synapse, the synapse is more a pathway for the signal to travel.
The stimulus for the action potential is what causes a signal to fire and travel through a synapse.
Hopefully that answers your question.

Yes, I might be confused. Thank you for your answer, I think you are right. See my edit for further explanation.

It does indeed answer my question. I already understood your answer, but I wanted to make absolutely sure that a dendrite cannot cause a synapse to another neuron if the initial neuron didn't fire.


text:
Acetylcholine and muscles- excitatory or inhibitory? (muscle atonia and myasthenia gravis)
I have heard that acetylcholine can be excitatory or inhibitory, but I am confused as to which it is when it comes to muscles. On the one hand, I believe that muscle atonia during REM sleep is associated with an abundance of acetylcholine in the brain stem, suggesting it has an inhibitory response on the motor neurons. On the other hand I know that the illness myasthenia gravis is caused by antibodies blocking acetylcholine receptors, which suggests to me that acetylcholine is excitatory. Could it be that with myasthenia gravis, the effect occurs at the neuromuscular junction where acetylcholine is excitatory, but it has an inhibitory effect on the motor neurons in the brain stem?
Thank you in advance.

I can write a full answer later if you wish, but quoting this source: https://www.ebi.ac.uk/interpro/potm/2005_11/Page1.htm -  "Acetylcholine release can be either excitatory (promoting a signal), or inhibitory depending upon the type of receptor on the adjoining cell." So yes, you are correct in that it depends on what type of neuron is receiving the signal and where it is located.


text:
Are human teeth only diphyodont or both diphyodont and monodont?
Many books say human teeth are only diphyodont .But premolars appear only once and one molar appears later which should be considered monophyodont.
 Dental Formulae :
CHILD -
 1. Incissor -2/2
 2. Canine -1/1
 3. Premolar-0/0
 4. Molar-2/2
ADULT-
 1. Incissor-2/2
2.Canine-1/1
3.Premolar-2/2
4.Molar 3/3 .
Here the 3rd molar and two premolar appear only once. Therefore human teeth should be both diphyodont and monophyodont

I wrote the dental formula for child and adult..

The definitions from the Oxford Dictionary of Dentistry:
Diphyodont

Describing the development of two successive dentitions, one primary
  and another secondary (permanent), as found in most mammals including
  humans.

Monophyodont

Possessing only one generation of teeth. It is a characteristic of
  some mammals, including the manatee, seal, and walrus.

As you can see, the term diphyodont is generally not used to refer to the individual teeth, but rather to the whole animal (i.e. the sets of teeth). A monophyodont is an animal that has only one set of teeth.


text:
Why do eggs lack an endoplasmic reticulum?
Trueman's Elementary Biology book I found says that the endoplasmic reticulum is absent in eggs, but no reason is given. Why is it absent?

I did not know there was no endoplasmic reticulum in the eggs. Can you please add a reference we could easily check up?

I just found in my book. It might had initially but i thing it is reduced later .But I will try to add a reference

I think there is some mistake, check [this] (http://www.sciencedirect.com/science/article/pii/S0012160699994459). It shows eggs (at least mammalian) have ER

In addition, these Calcium waves produces by ER stores are way to block another sperm entry into egg.

I THINK THE BOOK SAID ABOUT CHICKEN EGGS ..

I could find no indication that eggs are lacking an endoplasmic reticulum. On the contrary, I could find papers written on the ER in eggs of several species.
Mouse: The onset of activation responsiveness during maturation coincides with the formation of the cortical endoplasmic reticulum in oocytes of Xenopus laevis
Sea urchin: Structural changes of the endoplasmic reticulum of sea urchin eggs during fertilization
Human: The relationship between pregnancy outcome and smooth endoplasmic reticulum clusters in MII human oocytes
Frogs: The onset of activation responsiveness during maturation coincides with the formation of the cortical endoplasmic reticulum in oocytes of Xenopus laevis
However, as can be read in the sea urchin paper, the ER changes after fertilization:

We interpret these observations to indicate that in the first few minutes after fertilization, the egg's ER is fragmented

For other species, I could only find evidence that the ER reorganizes after fertilization because of changed calcium signaling needs


text:
Determine secondary structure (per residue pair) from a protein contact map
Given a protein map contact map (which for this particular case is a matrix of all Ca-Ca atoms in protein 1a3a that are less than 8 Angstroms):

Question: For each contact, is there an established heuristic to determine what kind (alpha, beta, or tertiary) of contact this is?
Observations: The contacts along the diagonal +4 clearly belong to alpha-helices, but I'm struggling to find a way to identify the parallel and anti-parallel beta-sheets and to differentiate these from a long range tertiary contact.


text:
Does the location of the double bond in chlorins yield a distinct biological function?
Chlorins differ by the number of double bonds and their location. Chlorin has 20 pi electrons, whereas bacteriochlorin and isobacterichlorin have 18 pi electrons, but at different locations.

Do chlorin, bacteriochlorin and isobacteriochlorin have distinct biological function due to this double-bond difference?

I only found a hint that this might be the case in this publication by Singh et al., stating

Porphyrins, chlorins, bacteriochlorins, and isobacteriochlorins each have unique photophysical properties that are exploited by nature and can be used for diverse applications (1, 2).

I don't have access to "The Porphyrin Handbook" (The first citation in the quote above), but I suspect it would be your best guess in finding more information.


text:
Why does size decrease across the sequence of human chromosomes?
The following graph shows a decrease in the number of base pairs per chromosome across the sequential set of human chromosomes:

Is this because chromosomes were originally numbered by their size on the karyotype?

You nailed it!
Nomenclature
Autosomal chromosomes
Chromosomes are numbered based on their size (in base pairs).
Sexual chromosomes
Sexual chromosomes (when they exist) are defined as the largest number regardless of their length. Note that the definition of a sex chromosome can sometimes be a little bit troublesome (see this book).
Exceptions
It sometimes happens that the first approximation of the length of a chromosome is inaccurate and that chromosomes are therefore numbered wrongly. In such case, when we realize the mistake, we just keep numbering the chromosomes the same way we did before even if it doesn't follow the standard nomenclature! This is, for example, the case of chromosomes 19 and 20 in Homo sapiens as you can see on your barplot. Chromosome 20 is actually a little bit longer (by about 4.5 Mb) than the chromosome 19. There are many other types of exceptions as well. Thanks to @Dexter  pointing out int he comments that in Drosophila melanogaster (model organism) the sex chromosome is numbered before the automosomes (autosome = non-sexual chromosome).

Sometimes people use sex chromosomes at starting and then autosomes (e.g: Drosophila melanogaster )


text:
What is the speed of neurotransmitter release and receptor binding in a neuronal synapse?
Obviously neural signals travel at extremely high speeds, but I'm wondering how much that speed is affected by the release and binding time of neurotransmitters.
If my sources are correct, a well myelinated axon generates an action potential with a speed of roughly 119.807 m/s. How much does the speed of neurotransmitter release by the presynaptic neuron and binding to the postsynaptic neuron's receptors impact that speed? In other words, I am wondering how much the total speed of a neural signal from one neuron to another is affected by the time it takes for the first neuron to release neurotransmitters and the second neuron to receive the neurotransmitters and propagate an action potential within its own cell.
I assume it takes at least some time, but exactly how much does it slow the signal down?
Thank you for your answers.

It seems to depend on the size of the neurotransmitter. The bigger the neurotransmitter is the longer the neuron has to be stimulated to actually release the neurotransmitter. But in the case of Acetylcholine it seems to need only about 2ms after a presynaptic stimulus to generate a postsynaptic membrane potential and after about 5ms all the Acetylcholine in the synaptic gap is cleaved allowing the postsynaptic cell to repolarize. The example get described here.

What do you mean by "cleaved"?


text:
Why is there a structural difference between the bicuspid and tricuspid valve?
There are three cusps in the tricuspid valve and only two in the bicuspid valve? Why is there such a structural difference? Does it have anything to do with that there is oxygenated blood on the left side and deoxygenated on the right?

Because that is how the heart evolved. You should really rephrase your question to "Is there a functional reason for the observed structural differences of the bicuspid and tricuspid valve (in humans/mammals)?"


text:
What is the significance of 9+2 arrangement in flagella?
Why eukaryotic flagella have 9+2 arrangement .? What is the significance?  a 9+0  flagella should have worked the same way .

What do you mean by 'normal flagella'?


text:
Are there any theories using thermodynamics/statistical mechanics or information theory principles to modelling in ecology?
So far, I've only known one: the MaxEnt theory. It uses the maximum information entropy developed by information theorist, which in turn inspired by the thermodynamics from physics, to predict the number of organism in an area. This theory is developed by John Harte.
You can read about this theory in Quanta Magazine.
I also know the book Towards the Thermodynamics Theory for Ecological Systems, written by Jørgensen and Svirezhev.
I find it hard to find another theory similar with the two theories above. Do you know any theories using the thermodynamics or information principles to modelling in ecology?
I have opened a reddit discussion about this.

I'm still not quite sure what you are looking for. Do you want to know about additional theories in ecology that are similar to Harte's MaxEnt? Or are you more broadly interested in the application of thermodynamic principles in other fields?

First question should be prioritize, but the second one is interesting to know too

You might wanna have a look at this paper: http://onlinelibrary.wiley.com/doi/10.1111/2041-210X.12152/abstract

@Hav0k thanks for the paper. I know what I'm looking for now: theories in ecology that use thermodynamic or information principles to modelling

John Harte's work on applying the mathematical theory of maximum entropy to ecology is certainly one of the better known examples of the application of this area of mathematics to science, in part because he literally wrote the textbook: Maximum Entropy and Ecology: A Theory of Abundance, Distribution, and Energetics (Oxford Series in Ecology and Evolution)
To be clear, maximum entropy (also known as MaxEnt in some of the literature, though most/all researchers use the longer form in publications) is a mathematical tool stemming from the fields of probability theory, statistics, and information theory.  Its use is classically most often seen in thermodynamics, statistical thermodynamics, physics, and information theory, primarily because these were the areas in which E.T. Jaynes was working when he posited the idea. Wikipedia has links to his two seminal papers.But because of it's mathematical form, it can be applied in a multitude of areas, typically where one can utilize probabilistic methods.
If you're looking for additional areas of application, simply google the phrase "applied maximum entropy" and you'll find a wealth of areas including: econometrics, natural language processing, nuclear medicine, queuing systems, mass spectrometry, image processing, machine learning, and many others.
For ecology related work, a cross search on maximum entropy and "genetics", "evolution", "species", and similar words will provide a wealth of papers like "A maximum entropy approach to species distribution modeling".
Given the generic nature of your question, I might suggest that you'll find E.T. Jaynes' paper "On the Rationale of Maximum-Entropy Methods" (IEEE, 1982) useful.
Those generally interested in the broader applications of information theoretic methods to biology will likely appreciate some of the work that came out of last year's NIMBioS Workshop on Information and Entropy in Biological Systems (which Harte both attended and presented at), the BIRS Workshop Biological and Bio-Inspired Information Theory, and the 2014 CECAM Entropy in Biomolecular Systems. The NIMBios Workshop was organized by John Baez, a physicist, who has worked with MaxEnt methods and explored them on his blog "Azimuth".
Those with a more sophisticated mathematical background (including measure theory, functional analysis, etc.) may appreciate Henryk Gzyl's text The Method of Maximum Entropy (World Scientific: Series on Advances in Mathematics for Applied Sciences, Vol 29, 1995).
-- Additional thoughts after the question was edited --
First for those who don't have the background, I highly recommend reading the two seminal papers on information theory and statistical mechanics by ET Jaynes and the standard text on information theory Elements of Information Theory by Thomas M. Cover and Joy A. Thomas.
In addition to the information theoretic related areas, you might want to take a look at the discipline of complexity theory, which has primarily grown out of the Santa Fe Institute over the past several decades and which includes information theory as part of its disciplines. If you're unfamiliar with the broader topic, Melanie Mitchell has an excellent overview with her book Complexity: A Guided Tour. Also related to complexity is the area of cellular automata which one could view as a very base model of more complex ecological systems. Here, perhaps Stephen Wolfram's A New Kind of Science or Cellular Automata and Complexity will be enlightening. The broader theories coming out of these primarily mathematical areas may be useful to you.
In particular, given the types of models in ecosystems, I might suggest taking a look at some of the mathematical modeling going on at the intersection of complexity and economics. For a relatively simple introduction to this area, one could look at the relatively introductory text Complexity and the Economy by W. Brian Arthur which is very interesting. The economy is essentially a very specific type of ecology dealing with human beings, assets, and the monetary system.
Another area which I've seen a lot of literature over the last few years is applicable to the ideas of resiliency and complexity in cities, for assisting in designing more robust city planning. This really isn't that far from the naturally evolving systems being looked at in ecology settings.
For those looking for researchers in the area of complexity, I have a list of many who are on twitter in a variety of sub-areas. In addition to individuals, it also includes a number of institutes and related organizations as well.
I'd also suggest, that for the broadest theoretical setting, one could actually start with the topic known as "Big History" which takes the broadest approach of looking at history and the evolution of the cosmos over 13.7 billion years since the big bang. This conceptualization includes ideas like evolution, complexity, and emergence on the biggest scales, a set of theories that could be similarly applied to ecologies both large and small. For this viewpoint, I would suggest two works by David Christian including Maps of Time: An Introduction to Big History and Big History: The Big Bang, Life on Earth, and the Rise of Humanity.
In essence, with many of these topics and viewpoints, one is treating individual animals or even entire species as elementary particles and then using the mathematical models of statistical thermodynamics to tease out specific types of data or trends. As layers of overlapping "particles" interact with each other, they cause emergent types properties, and then these resultant emergent properties combine to create further layers of emergent properties, none of which might have been necessarily deduced from the initial conditions. Within Big History, these types of emergence go from the big bang and basic particles in the early universe to the ultimate evolution of humankind by way of a variety of stages.

Chapter 10 in Harte's book discuss about the connections between his theory and other theories. Thanks for the link

I have rethought my question and slightly edited it. Glad if you come back and see.

Many of the papers and texts mentioned above will have a wealth of additional references listed in their bibliographies sections.
They're not necessarily ecology-specific, but I've been collecting literature at intersection of information theory & biology/molecular biology.  Textbooks that may be applicable: https://www.goodreads.com/review/list/3250760-chris-aldrich?order=a&shelf=itbio&sort=position. Similarly journal articles in a shared Mendeley group at: https://www.mendeley.com/groups/2545131/itbio-information-theory-microbiology-evolution-and-complexity/.

Thank you so much. I find the NIMBioS link is extremely useful

An alternative way to understand this issue has been ultimately named (in its more recent publications) as Organic Biophysics of Ecosystems. Some of their publications (several of them are available either on ResearchGate or on https://interdisciplinaryscience.es/publications) are (If you are interested, I would advise reading the articles in the exact reverse order of time to that shown below).
This approach uses equations whose mathematical structure is simpler than other models in this field, and which are equivalent in structure to those equations used by conventional physics.
Rodríguez, R.A., Riera, R., Herrera, A.M., Duncan, J.M., Vanni, M.J., Delgado, J.D., González, M.J. 2019. Degrees of freedom: Definitions and their minimum and most meaningful combination for the modelling of ecosystem dynamics with the help of physical principles. Ecological Modelling 392: 226−235.
Rodríguez, R.A., Duncan. J.M., Delgado, J.D., Vanni, M.J., Riera, R., González, M.J. 2018. Additional empirical evidence on the intrinsic trend to stationarity in the long run and the nested relationship between abiotic, biotic and anthropogenic factors starting from the organic biophysics of ecosystems (OBEC). Ecological Modelling 383: 23-30.
Riera, R., Rodríguez, R.A. Herrera, A.M., Delgado, J.D., Fath, B.D. 2018. Endorheic currents in ecology: an example of the effects from scientific specialization and interdisciplinary isolation. Interdisciplinary Science Reviews 43(2): 175-191.
Rodríguez, R.A., Riera, R., Delgado, J.D. 2017d. Ecology: Science or philately? An interdisciplinary analysis of sustainability by exploring if it is possible to get more and more information by reducing collateral environmental damages. Science of the Total Environment 596/597: 43−52.
Rodríguez, R.A., Duncan, J.M., Vanni , M.J., Melkikh , A.V., Delgado, J.D., Riera, R., Herrera, A.M., Camarena Luhrs , T., Quirós , A., Fernández Palacios, J.M., Miranda, J.V., Perdomo , M.E., Fernández Rodríguez, M.J., Jiménez Rodríguez , A., Otto, R., Escudero, C.G., Navarro Cerrillo , R.M., González , M.J. 2017c. Exploring the analytical consequences of ecological subjects unwittingly neglected by the mainstream of evolutionary thought. Ecological Modelling 355: 70-83.
Rodríguez, R.A., Duncan, J.M., Delgado, J.D., Vanni, M.J., Riera, R., Herrera, A.M., González, M.J. 2017b Assessment of ecosystem trophodynamic power: A model based on the power equation for an oscillating string. Ecological Modelling 362: 80-86.
Rodríguez, R.A., Duncan, J.M., Riera, R., Delgado, J.D., Quirós, A., Vanni, M.J., Camarena, T., Miranda, J.V., Perdomo, M.A., Herrera, A.M., González, M.J. 2017a. Thermostatistical distribution of a trophic energy proxy: Extension for modelling energy pyramids at the inter taxocene scale and under non stationary conditions. Ecological Modelling 361: 113−121.
Rodríguez, R.A., Herrera, A.M., Duncan, J.M., Riera, R., Quirós, A., Perdomo, M.E., Jiménez-Rodríguez, A., Fernández-Palacios, J.M., Vanni, M.J., Otto, R., Escudero, C.G., Camarena, T., Navarro-Cerrillo, R.M., Delgado, J.D., González, M.J. 2016c. Response to comments on “Uncertainty principle in niche assessment: A solution to the dilemma redundancy vs. competitive exclusion, and some analytical consequences”. Ecological Modelling 341: 1‒4.
Rodríguez, R.A., Herrera, A.M., Quirós, A., Fernández-Rodríguez, M.J., Delgado, J.D., Jiménez-Rodríguez, A., Fernández-Palacios, J.M., Otto, R., Escudero, C.G., Camarena Luhrs, T., Miranda, J.V., Navarro-Cerrillo, R.M., Perdomo, M.E., Riera, R. 2016b. Exploring the spontaneous contribution of Claude E. Shannon to eco-evolutionary theory. Ecological Modelling 327: 57–64.
Rodríguez, R.A., Herrera, A.M., Santander, J., Miranda, J.V., Perdomo, M.E., Quirós, A., Riera, R., Fath, B.D. 2016a. From a stationary to a non-stationary ecological state equation: adding a tool for ecological monitoring. Ecological Modelling 320: 44–51.
Rodríguez, R.A., Herrera, A.M., Riera, R., Escudero C.G., Delgado, J.D. 2015b. Empirical clues about the fulfillment of quantum principles in ecology: potential meaning and theoretical challenges. Ecological Modelling 301: 90–97.
Rodríguez, R.A., Herrera, A.M., Riera, R., Delgado, J.D., Quirós, A., Perdomo, M.E. Santander, J., Miranda, J.V., Fernández-Rodríguez, M.J., Jiménez-Rodríguez, A., Fernández-Palacios, J.M., Otto, R., Escudero, C.G., Navarro-Cerrillo, R.M. 2015a. Thermostatistical distribution of a trophic energy proxy with analytical consequences for evolutionary ecology, species coexistence and the maximum entropy formalism. Ecological Modelling 296: 24–35.
Rodríguez, R.A., Delgado, J.D., Herrera, A.M., Riera, R., Navarro, R.M., Melián, C., Dieguez, L., Quirós, A. 2013b. Effects of two traits of the ecological state equation on our current understanding of species coexistence and ecosystem services. Ecological Modelling 265: 1–13.
Rodríguez, R.A., Herrera, A.M., Delgado, J.D., Otto, R., Quirós, A., Santander, J., Miranda, J.V., Fernández, M., Jiménez-Rodríguez, A., Riera, R., Navarro, R.M., Perdomo, M.E., Fernández-Palacios, J.M., Escudero, C.G., Arévalo, J.R., Diéguez, L. 2013a. Biomass-dispersal trade-off and the functional meaning of species diversity. Ecological Modelling 261/262: 8–18.
Rodríguez, R.A., Herrera, A.M., Otto, R., Delgado, J.D., Fernández-Palacios, J.M., Arévalo, J.R. 2012. Ecological state equation. Ecological Modelling 224: 18–24.

it's a little weird to respond with just a long list of your own papers. Not that I discourage people with specific expertise from participating, but using expertise to break down a complex topic into a simple and direct answer is preferred.

"Some of their publications (...) are" -- Are what?

Hey Ricardo, thanks for the answer and for bringing your expertise to Bio.SE!  However, if you don't expand this answer to at least explicitly demonstrate/summarize how any of these papers answer or are are related to the OP's question, then this post will continue receiving negative votes and may even be marked as "spam" (only to promote your work). Please expand your answer so that the OP or future users actually receive an answer without having to leave this webpage. Your citations should remain as a source of additional details, but you need to expand your answer to avoid deletion. Thx!


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How do our smell receptors detect and tell apart exhaust or cigarette smoke, or other man-made chemicals?
Somehow we can tell apart exhaust gas and cig smoke, yet neither of those would have existed when we evolved. How is it that we can sense chemical compounds that we've only synthesized recently?

We can also detect the difference between the smell of swimming pools, paint, gasoline.. despite "not evolving with them" - I'm not sure that your question is on topic (it boils down to what are the chemical constituents that give cigarette and exhaust smoke their fragrance, which is a chemistry question). Also I would like to point the human species is continuing to evolve, we didn't evolve to the state modern humans are in and just stop...

This is definitely a chemistry problem, but remember that smoke from burning in itself is going to have many constituents! This would essentially boil down to what does cigarette smoke contain verses car exhaust. Here's an article on exhaust constituents and another on cigarette smoke. There's a lot to sift through, but generally the differences are in the pattern of chemicals that the olfactory receptors can detect.

@Kendall If OP made some small edits, I think this could asking about how our olfactory system can detect particulates that we haven't been exposed to over an evolutionary timescale. Currently I agree that asking which chemicals are similar to ones that we may have been exposed to us over evolutionary timescales is chemistry.

Yes, that's pretty much what I'm interested in - how is it we can sense something that we've only created recently. I'll edit the q. Is there a guide for newbies on how to make sure your q isn't too much on the edge of two disciplines?

It is all small molecule ligand receptor binding. The olfactory receptor has specificity for an epitope on the molecule and a signal is transduced through a G-Protein to create he action potential in the neuron. Different receptors will bind different epitopes on the molecule or molecules for complex odors and generate a signal into the brain that is perceived as a smell. Most compounds that release volatile compounds will have a chemical signature. As we develop, we learn to perceive and assign identity to those signatures as specific things.


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Front versus back in animal anatomy
Throughout various species, there seems to be a clear distinction between the front and the back. The musculature of the front, when engaged, closes or curls up the body, protecting it, while the musculature of the front straightens and stiffens. This feels intuitively to me like a pretty fundamental pattern.
Is this a "real" pattern at an embryological level, or just a common pattern of adaptation?
Is the innervation of the front and back musculature neurologically distinct in any way?
Which biological systems show a front to back separation?
How early in evolution does a front to back distinction occur?

I'm quite confused because the terms front and back are not very specific - it depends whether you're talking about front or back of humans vs quadripeds. For example, by front do you mean cranial (the head end) or dorsal (belly side)? https://en.wikipedia.org/wiki/Anatomical_terms_of_location

oops, that should read ventral (belly side)

@vervet I think the first paragraph ("musculature of the front closes or curls up the belly") makes it clear the question is about a ventral/dorsal distinction. I am not so sure about the clarity of the actual questions. What is a real pattern at an embryological level, what is a pattern of adaptation, and how do they differ? What is a "biological system", and how does one recognize a front to back separation in a "system" which is something else than one organism's body? The second and fourth points seem clear.


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Does music enhance neural activity/cognitive or cerebral function, or is it just mania?
I always find myself drew upon curiosity whilst studying, to whether certain types of music are or are not, effecting me in a sense of cognitive ability.
Take a fantastic piece such as, Mozart's, Symphony No. 40 in G minor, K. 550, for example. Whenever i'm listening to it, at the same time as studying, I feel more fluid... and somewhat enthusiastic. Is there a reason for this?
So to conclude, does music of specific  genre's (i.e. Classical) or, music in general, have any impact on cognitive performance? In particular, cognitive performance, in regards to Mathematics.

This sounds like it would be better received at cogsci.SE.


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Conserved acetylation sites in a given protein
I want to identify potential conserved Acetylation sites in protein X. As it is known, acetylation happens in Lysines (K), thereby I would like to identify conserved K residues for protein X during evolution. Eventually I would use different Acetylation site prediction tools to further filter the results, but initially I need the other data, does anyone know a user friendly but trust worthy bioinformatic tool to do so?

You can use the NCBI subpage HomoloGene
Halfway down page on left you can choose to show Multiple Alignment as seen in this screenshot.

I think you will then see what you are looking for as in this screenshot:


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What kind of spider is this and is it dangerous?
Found this spider on my couch the other day in Steubenville, Ohio. The spider is about 1 - 1.5'' (2.5 - 4 cm) long. The spider looks brownish in the image, but tends to a pale yellow color in reality.

It's not a brown recluse, the pattern on the head and the shape of the abdomen are wrong.

That looks like a good ol' wolf spider.  Call him spiderbro and leave him to hunt down obnoxious insects.

It looks like a member of the Thomasidae (crab spiders) To properly identify spiders to genus or species I would have to see the eye pattern. It is harmless, Dangerous spiders in Steubenville are unlikely

its face would have helped a lot

That's a nice female Nursery Web Spider, related to the Fishing Spiders.  They're rather pretty animals, and like almost all spiders, quite harmless to anything that's too big to eat.  The very rectangular cephalothorax ('head' end) pattern and the simple wavy line down the abdomen are the key clues for this one.  They also like to sit with the front legs arranged in pairs.
https://bugguide.net/node/view/2919/bgimage


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UACC-462 cell culture
UACC-462 is a pancreatic cell line established in the University of Arizona Cancer Center (UACC).
The cells are available from ATCC and there is the instruction for culturing UACC-462.
M-41 medium. The base medium for this cell line is ATCC-formulated Leibovitz's
L-15 Medium, Catalog No. 30-2008. To make the complete growth medium, add the following components to the base medium (final conc.):
fetal bovine serum to a final concentration of 5%
0.01 mg/ml transferrin
0.01 mg/ml insulin
5 µg/ml (55 U/ml) catalase
3.6 µg/ml (0.01 mM) hydrocortisone
10 ng/ml EGF
3 ng/ml Estradiol
70 µg/ml O-phosphorylethanilamine
0.0008 µg/ml L-thyroxine
extra 2mM L-glutamine
Atmosphere: air, 95%; carbon dioxide (CO2), 5%.
Temperature: 37°C
On the other hand, L-15 is designed to culture without CO2 and often used time-laps experiments under microscope.
My question is why L-15 based media can be used in CO2 incubator. Is the cell line acid-philic?

There are a number of cancer cell lines that are grown in various forms of L-15 in 5% $CO_2$ incubators. I don't know the exact biochemistry behind it, but it works, so that's what's used.

@MattDMo Regarding this cell line, an ATCC technician admitted the mistake. Do you have experiences culturing cancer cells with L-15 based media in 5% CO2? I would like to know which cells can be grown under the condition, for future reference.

unfortunately, I am no longer at the lab where they did this, so I can't check the database. So, ATCC said the line shouldn't be cultured with $CO_2$?

@MattDMo "It should read 100% atmospheric conditions." That's what they said.

@MattDMo May I post another question to ask cells that can be grown with L-15 based media in 5%CO2?

I suppose you could, but it seems like a fairly narrow question. I'd do some good googling for a while to learn the history of L-15 and see if you can find some lists on your own. A lot of labs post their protocols online, so you may find something there.


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What is the germ layer origin of human lung fibroblasts?
What is the germ layer origin of human lung-derived fibroblasts?

All normal fibroblasts are mesenchymal in origin, including lung fibroblasts. In certain situations, usually injury related, epithelial cells can undergo an epithelial to mesenchymal transition (EMT).

Even dermal fibroblasts?

Yes, all fibroblasts with the exception I listed in my answer.

The table at http://genome-mirror.duhs.duke.edu/ENCODE/cellTypes.html lists many commercially available cell lines. The four lung fibroblast lines, including adult and fetal, are listed as endodermal in origin.


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What is the aqueous solution for DNA immobilization?
This paper
Electric-field assisted immobilization and hybridization of DNA oligomers on thin-film microchips
Which is talking about how the electric field improve the DNA immobilization process.
Unfortunately, I have no biology background, I could only understand about 50%  contents.
In the section 2.3.1, its says "the chip was exposed to a aqueous solution of the DNA probe".
What is the aqueous solution of the DNA probe?
Is it DD water (DI water) + DNA? or it is some kind of buffer solution + DNA?

The methods mention a BSA buffer with reference 14 and a borate buffer with reference 30 for immobilizing on their 2 different types of chip. They also mention an SSC buffer, which is a saline sodium citrate buffer commonly used in DNA or RNA hybridization experiments.

But where they mention about BSA buffer if at DNA hybridization step. The solution is the same with DNA immobilization?

And in the 2nd type chip with E-assist experiment (section 2.4), They said "a solution of FITC-labelled ssDNA probes with a volume of 2 cm3 is added" which is different from "a 0.5 µM ssDNA probe solution in borate buffer" (section 2.3.2). The previous one did mention about in borate buffer but later one no. Should they be the same?

You're right to point out the BSA, the SiO2 crosslinking relies on either a thiol or amine reaction, and BSA could interfere with those reactions. They may have used the borate buffer for immobilization on both chips, or they may have just added water to their oligos directly from the manufacturer, in which case the buffer would be whatever salt the manufacturer provided. This seems unlikely, as most DNA storage solutions are typically a Tris buffered EDTA. I have only looked at the methods section, I don't have time to read the whole thing. Sorry.

Thank you very much for the detail explanation, it is very helpful.  :)


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Is it true that cats can drink sea (salted) water?
Found somewhere in the Net, that cats can drink sea (salted) water.
This fact seems to me as being urban legend, not true (because the purpose of water in body apparently implies it should be clear).
What is true and how to explain?

Can you add the link please?

This question would be better suited for Skeptick.SE if you can demonstrate that it is a notable claim.

I can drink sea water! Nothing extraordinary. You probably mean something like "be hydrated when drinking nothing but sea water"

Since cats are well adapted to dry environments, the question has some plausibility to it.
The book "Mineral Tolerance of Animals" suggests that cats may be able to tolerate slightly more salt in their diet than dogs (1.37 g salt/kg body weight for cats, vs. 0.64 for dogs).  However, these represent concentrations that were shown to be safe, not the maximum they could potentially tolerate. The reference in the book is Yu et al., 1997, and though the actual reference is not available in the Google Books version I believe it must be The minimum sodium requirement of growing kittens defined on the basis of plasma aldosterone concentration, so the goal was to identify minimum rather than maximum levels.
The ocean is about 3.5% salt.  The 1.37 value for cats came from kittens eating a diet that was about 2.5% salt, but another note in the book says that cats can safely eat a diet that is 3.8% salt, though they don't like it. I can't find the original reference ("Berger, 1979") for this claim, but I am pretty sure that this was with ad libitum water so they could flush out extra salt.  If so, cats would not be able to tolerate sea water unless they had another source of water as well.
It's often said that wild cats can get most of their water needs from their prey's blood.  It's also sometimes said (incorrectly) that the salt concentration of blood is like that of seawater; this is not true (blood is more like 1% or less NaCl) but it may be the source of the statement.

The Wikipedia article on cats makes this claim with references to https://www.ncbi.nlm.nih.gov/pubmed/13627238 and http://www.nap.edu/catalog.php?record_id=910


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Chemosynthesis in Bacteria
The light reactions, if seen as a whole, are basically the oxidation of water to provide energy (ATP) to fuel the Calvin Cycle. The photons provide the activation energy for the same.
How then can we say that during chemo-synthesis bacteria get ATP in the first step by oxidizing inorganic substances like $H_2S$ or $CH_4$ because ultimately, it is similar to the light reactions and will require some activation energy?
Where does this energy come from?

These chemo-synthetic bacteria gets energy from oxidation of inorganic compounds. Following table from Biology of Prokaryotes shows main reactions used by different species,

This oxidation happens only if electron acceptor is available. These all reactions have negative Gibbs Free Energy, hence they are favorable reactions and happens spontaneously. Generally oxygen is preferred electron acceptor but in case of lack of oxygen nitrate, sulfate, $HCO^{3-}$ etc are used.

Could you please list the Gibbs free energy for a normal photosynthetic light reaction?

Check this. It has all numbers and calculations you need.


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Is there a database providing information about optimum temperature and inactive temperature of enzymes?
I want to know optimum and inactive temperature of some enzyme, but I can't find these information in NCBI, wiki or UniProt. So I want to know if there are some database which provide these information?
Thanks for help.

UniProtKB has annotations for biophysical and chemical properties, such as maximal absorption, kinetic parameters, pH dependence, redox potentials and temperature dependence.
http://www.uniprot.org/help/biophysicochemical_properties
Such annotations are currently available for about 6800 reviewed entries: http://www.uniprot.org/uniprot/?query=annotation%3A%28type%3Abiophysicochemical_properties%29&sort=score
More specifically, temperature dependences is annotated in about 2000 entries: http://www.uniprot.org/uniprot/?query=annotation%3A%28type%3A%22temperature+dependence%22%29&sort=score

Yes, there is a database. It is called 'BRENDA' and can be found here. It doesn't have all the information you are looking for, but it always has the links to the relevant literature, so you can look it up.

您好, you can find more information about optimal temperatures on Uniprot. Look under section 5 and 我爱你.


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What happen if we inject restriction enzyme into the blood
Just a curious question, if we extract restriction enzyme and inject it to our body, what happen?

Does antibody recognize and block it?
Can restriction enzyme pass over cell membrane and destroy the DNA of a living cell ?

The appearance of any foreign antigens (e.g., proteins like restriction enzymes fall n this category) in the circulatory system should trigger an immune response.
There are actually two membrane barriers that the enzymes have to traverse to gain access to the nuclear genome: the cell membrane, and the nuclear membrane.  Proteins are typically too large and too charged to cross a lipid bilayer membrane--unless there is a pore (like on the nuclear membrane) or receptor for the protein on the cell surface.
When cells are engineered to express foreign restriction enzymes using transgenes, then yes, if the protein can enter the nucleus then the enzyme will start to digest all of its recognition sites.
Jasper Rine demonstrated this for the Baker's Yeast S. cerevisiae in 1986.


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Interpretation of F in inbreeding on the population level
The inbreeding coefficient for an individual gives the probability that the individual has two alleles at a locus that are IBD. What interpretation does the inbreeding coefficient have on the population level? Is it the average inbreeding value in the population?
It is possible to derive the genotype frequencies in the population when the population inbreeding coeeficient is given by F. These are given by:
$A_1A_1$: $p_{A_1}F+p_{A_1}^2(1-F)$
$A_1A_2$: $2p_{A_1}p(1-F)$
$A_2A_2$:  $p_{A_2}F+p_{A_2}^2(1-F)$
Is seems like F gives the probability that the two alleles in an individual in the population are IBD. Does this mean that F is the average inbreeding coefficient in the population?


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Do mammals and birds have a common warm-blooded ancestor?
Is it homogeneous or did they converge?  Did we both evolve from warm-blooded reptiles that are extinct maybe?

The previous answer is good. Here is a shorter one: no. Their common ancestor was most likely "cold blooded" and similar to a crocodile or some sort of crocodilian .

I think the OP meant "homologous" rather than "homogeneous" ...

Welcome to Biology.SE.
Did you say warm-blooded?
The term warm-blood is very unclear. The correct terms are endo-, exo-, poikilo- and homeo- therm. In short…
Source of heat

endo = inside
exo = outside

Variation in inside temperature

Poikilo = varies
homeo = does not vary

Any combination of these two axes exist. For example: If the temperature in the environment never varies you can be homeotherm without needing to be endotherm. A fun example also are the large dinosaurs that are thought to be homeotherms because their metabolism produce some heat and they are so large that they remain warm thanks to this heat source. However, they were probably not able to regulate actively their temperature. Therefore, I would tend to qualify dinosaurs as homeo-exo-therm but I wouldn't be surprised if someone prefers to call large dinosaur homeo-endo-therm individuals. Hope that makes sense to you.
By warm-blooded I will assume you meant endotherm.
MRCA of mammals and birds (and other things)
The Most Recent Common Ancestor (MRCA) lived 301.7 millions years ago (see on tolweb and on OneZoom). This MRCA was exotherm. In consequence, birds and mammals endothermy are an example of convergent evolution (even if they are not using exactly the same mechanisms).
References to go further into the evolution of endothermy in birds and mammals

Grigg et al. 2004
Hillenius and Ruben 2004
Ruben 1995

According to this, mammals and birds share common cold blooded ancestor. And also comment that reptiles are "Imperfectly warm blooded"

I added some info for the large dinosaurs. I wouldn't trust too much a paper that uses the terms "cold-blood" and "warm-blood". But anyway, we agree that the MRCA was exotherm I guess.

It does not appear borken to me. But I might have modified it right at the moment of yuor comment 2 days ago!


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Can radiation therapy cause cancer?
Radiation therapy is a very popular cancer treatment method. But can it have any risk for make a different cancer? Because i think that radiation exposure can make DNA mutation and thus increase the risk to cause cancer, so why we still use radiation to treat cancer? That's so contradictory.

Yup. Radiation induced secondary cancers exist and vary in their site of incidence and risk of incidence based on the site of treatment. In breast cancers treated with radiation, for example , there is upto a 3 fold increase in relative risk relative to the general population for leukaemias within five years and 1.5 times the relative risk for secondary lung cancers within 15 years.
The literature also reports 1 in 10 malignancies as being of a secondary nature, and radiotherapy amongst others is probably responsible for a fraction of those.
Despite this risk, radiotherapy is very often worth using because without it the risk of dying from the primary cancer is vastly greater than the risk of a secondary malignancy from therapy, and secondly, unlike systemic chemotherapy, the side effect profiles of radiation are more tolerable and localised.
It is also possible to "shape" fields of irradiation to maximise the dose delivered to the tumour and to minimise exposure to normal tissue; this is called intensity modulated radiotherapy (IMRT).
Also, a lot of the cancers radiotherapy is used for occur in older people, and the benefits of saving someone from their primary tumour again outweighs the risk of secondary malignancies later on. It is especially of concern in paediatric patients because that brings with it the risk of secondary malignancies in middle-age, but advances in intensity modulation I think has the potential to minimise that risk.


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In CRISPR bacteria, how does viral genomes get integrated into the spacers of CRISPR? Also, in its use, where does Cas9 cut the DNA?
I've been out of Biology for about a year polishing my programming skills. I know CRISPR/Cas9 allows targeted 'cutting' of DNA via RNA-guidance. Few questions regarding this.

Regarding to its natural phenomenon, when a virus infects a microbe with CRISPR capabilities, how does the genome get integrated into the 'spacers' of CRISPR region versus elsewhere of the prokaryote genome so that when transcribed, the Cas enzymes know that it's a foreign DNA element to be targeted? My understanding of virus infections is a little cloudy too; I'm thinking random transpositions.
I'm looking into it now, so I may figure this out before someone answers, but when the target DNA is located via the guiding RNA, where does the Cas9 enzyme decide to 'cut' -- rendering it useless -- the DNA, and how does it identify the location?

-EDIT- Ah. The target sequence must also include a 'PAM' sequence downstream (Protospacer Adjacent Motif), which allows binding of the riboprotein complex(guiding RNA + Cas9), and biochemistry magic cuts it ~3-4 bases upstream of the PAM). citation: https://www.addgene.org/CRISPR/guide/

Just thought of another question, if the DNA is cut at the seemingly specific spot, is the DNA repair that ensues downstream totally random? I feel like it would be in the organism's best interest (anthropomorphogenic, oops), and evolution generally says it usually does, to have a mechanism to repair it to its original state.

Right on, me too, this an amazing technique that i would like to know more about.

This paper should clear up a lot more than anyone on here truly can about the CRISPR system.
CRISPR/Cas9 is very unique, even compared to other proteins purified from bacteria like Taq Poly.

The reason is due to how complex it is actually induce this protein. Essentially you are transfecting a plasmid with the Cas9 protein and its guide RNA (gRNA) on the vector. Transfecting itself is not easy, not to mention you are essentially adding a mechanism to a cell trying to knockout genes and you've got a handful. In fact doing that for one cell line, and noting the effects of what you knocked out, would be enough to produce a paper in a pretty impactful journal. (Image from: https://www.systembio.com/)
Also some recent advancements in CRISPR include:

Light-induced CRIPSR/Cas9 (easier regulation of enzymatic activity)

Basically these researchers were trying to deduce a method allowing for more control of the CRISPR technique, since CRISPR has had issues with off-target effects. While it isn't a change in how CRISPR works, or even where, the change is how much you can control the reaction. Simply put they devised a way that allows you to turn CRISPR on/off using light allowing more precise control of its activity. Surely it will be helpful to reduce off target effects.
"This was accomplished by fusing the light-inducible heterodimerizing proteins CRY2 and CIB1 to a transactivation domain and the catalytically inactive dCas9, respectively." (Lauren R Polstein & Charles A Gersbach)

Cpf1 to replace Cas9 as cutting protein (more percise activity)

This one is a bit more interesting in that it is a direct change to the CRISPR system itself. Cas9 has been the standard cutting protein used for the CRISPR system although it has had controversy due to its somewhat imprecise cutting. Cpf1 has been shown to be more precise (so their data says) and it is now being implemented by some to see if this is truly the case. Combined with the above "light-induced" system this brings CRISPR down to safer levels when talking about off-target effects.
Here are some good online seminars to get you started:

CRISPR/Cas9 from start to finish
Improve CRISPR-Cas9 experiments with rationally designed guide RNAs

These seminars I can't really comment directly on because they explain everything so well on their own. Anything I say really will only detract from what they are teaching since I am by no means an expert with CRISPR but simply someone who is looking into possibly using it for my lab. Right now there is a lot of guide material on how to properly format your CRISPR experiments but my personal opinion is to give the technique maybe a year or two more when it is more standard for research.
That is unless you want to directly research the method and improve it in your own way.
Let me know if this answers your questions sufficiently.
Sorry that I cannot do much more in terms of explaining the links. The studies are not ones I can easily access unless I am at work since I usually access them through the university.
As far as the repair mechanism goes (your #3 question) I can't really answer that for sure but I have recently received a pamphlet that describes how to ensure the cells uses HJ rather than NHEJ.

This is a link-only answer, which are discouraged on StackExchange. Could you describe what is in these links and include relevant areas of the text?

I added some more of my own words. I'm afraid I was a bit hesitant to really say much more since I am not much of an expert.