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What is the preferred way to abbreviate amino acids?
Amino acids are often denoted using either a 3-letter abbreviation or a 1-letter notation, e.g. Glutamine  is denoted via $\mathrm{Gln}$ or $\mathrm{Q}$.
When one notation should be preferred over the other and what are the reasons behind?
P. S. This is a follow-up to my question on Chemistry.SE Proper common notation for a ligand, where the problem of distinction between $\mathrm{L}$ notation for "ligand" and for "leucine" occured.

In my experience neither is preferred.
When simply presenting a protein sequence, e.g. in the context of a database of proteins encoded by a genome, then the one-letter code tends to be used.
When showing an alignment of a DNA sequence with the encoded protein sequence both can be used, although personally I prefer the one-letter code for this too because I don't like squished-together text like LysAlaTrpLeu.
In papers referring to an individual residue in a protein I would say that the three-letter code would be more likely to be used.
When referring to a mutation (or,  rather, an amino acid substitution) you might see Leu129Gln or L129Q.
And, by the way, I use L for ligand and have never found it to be confusing. If the reader of your text is sophisticated enough to know that L is leucine then I think they would be able to tell from the context that you were using L for ligand.


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Is it NAD+ or NAD- or neutral NAD ?
In glycolysis why NAD is positivly charged , why it's not neutral or negative ?

Why is this downvoted?

Question can include why is it NAD + and not NAD- or just NAD.

@AliceD I can't see any way to express my opinion about this other than to comment here. This is clearly a question about biochemistry as tagged. I disagree with your decision to put it on hold because you think that it is a better fit at Chemistry. It's really not about chemistry at all, it's about a convention in representing a biological coenzyme which appears to conflict with the underlying chemistry. A chemist would have nothing to say about this unless they were a biochemist. QED

@AlanBoyd perhaps you're right. But then, it shows no research effort whatsoever (homework) and the way it is framed makes it unclear exactly what the why in the question refers to (structural chemistry versus functional relevance of charge for enzymatic reactions), hence the question is unclear as well. I chose the Chemistry close-vote, but as is often the case when I mod-close stuff, it's lacking quality on various fronts. If you can clarify the question it might be re-opened. For what it's worth, I upvoted your answer, but w/o edits this question should be on hold imo.

You are correct in thinking that because of the presence of the diphosphate linkage between the two nucleotides in NAD⁺, both of which will carry a negative charge at physiological pH, together with the positive charge on the nicotinamide N, it would be more chemically correct to write NAD⁻. However I think the idea of using NAD⁺ is to emphasise the N atom in the nicotinamide moiety, which is the 'active site' of the coenzyme.
As it says at the NAD⁺ Wikipedia page:

Although NAD⁺ is written with a superscript plus sign because of the formal charge on a particular nitrogen atom, at physiological pH for the most part it is actually a singly charged anion (charge of minus 1), while NADH is a doubly charged anion.

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Uncompetitive inhibitors
In Uncompetitive inhibitors , the Km decrease .
With uncompetitive inhibitors , the affinity of the enzyme for the substrate (E+S) increases .
I've searched up on the net and it says that the substrate has now been taken up to form E-S and E-S-I , therefore consuming more substrate than the original inhibitor-free equilibrium .
E + S -> ES (equilibrium position shifts to the right)
I've read up on all these and more doubts form in me .
Why is substrate needed to form ESI ?
I understood what it meant by equilibrium position will shift to the right . It is harder to form E + P as more substrate will form ESI.
Thanks !

u should add the link where u read that the substrate is required for the intermediate complex formation otherwise the question is unclear.

An uncom-petitive inhibitor doesn't compete with the natural substrate of the enzyme for active site i.e. it binds at a site distinct
from the substrate active site and binds to the $ES$ complex.

$K_I$ is the equilibrium constant for inhibitor binding to $E$ and $K_I^{'}$ is the equilibrium con-
stant for inhibitor binding to $ES$. Uncompetetive inhibitor lowers the value of $V_{max}$ and $K_m$.

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Why are (most) right hand dominant people also right foot dominant? And the same for left handed/footed people
Just as the title states -- Why do people who are right hand dominant also tend to be right foot dominant? And, the same question for left handed/footed people.
Does the brain actually designate an entire side of the body to use by default, when only one hand/arm/leg/foot/eye/ear is needed, or available?

Is there actually such a thing as a dominant foot?  Certainly seems as though I use either foot equally, depending on the direction of whatever I'm doing.

@jamesqf Yes, I believe there is such a thing..if you were to kick a ball, which foot would you choose to use? Obviously not both.. in my question, I did mention, "..when only one hand/arm/leg/foot/..", so, tasks where one side of the body isn't favored, shouldn't be considered.

Actually I'd use whichever foot was closer to the ball - or if it's a soccer ball, both feet alternately.

@jamesqf "Over 90% of right-handers are also right-footers; right-footedness hence predominates in the general population." https://en.wikipedia.org/wiki/Footedness

Interesting.  Maybe I'm the oddball here, though it's perhaps not surprising, since I'm fairly ambidexterous (or perhaps ambi-clumsy would be closer to the truth).  I can do most things adequately well with either hand.  Though the right is better for most, some things, like baseball batting, I do better left-handed.


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Can you see the coloration of Sinosauropteryx with the naked eye?
In 2010 this beautiful fossil of Sinosauropteryx was put under microscopic examination in order to determine the colors of the preserved melanosomes. It was determined that the feathers were reddish brown with white stripes going down the tail and a white underbelly.
Is it just a coincidence that that's exactly what I would have guessed by looking at the color of feathers in the fossil? Am I falling prey to
hindsight bias? Or is it the case that the feathers are so well preserved that their color is visible to the naked eye?

By Sam / Olai Ose / Skjaervoy from Zhangjiagang, China - Dinosaurs!, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=4209411

Is it just a coincidence that that's exactly what I would have guessed by looking at the color of feathers in the fossil? Am I falling prey to hindsight bias?

Hmm.. TBH, I don't think anyone can tell you that! However, after taking a look at it, I myself may have suggested reddish feathers along the neck and back, with some kind of red/purple coloration going down the tail (though I have no significant expertise in this field).

Or is it the case that the feathers are so well preserved that their color is visible to the naked eye?

Melanosomes are actually fairly large; about 500 nm (source). Relatively speaking, this is somewhere between the size of the flu virus, and of mitochondria; see here for scale. According to this book, written by the Swiss Institute of Bioinformatics, it states:

... besides [zebrafish] being vertebrates like us - their epidermis and their eggs are transparent, and embryonic development can be overved and tinkered with at every stage. Likewise, even melanocytes and their melanosomes are visible to the naked eye.

So, it would seem that it's possible to observe melanosomes with the naked eye, given a high enough (melanosome) concentration. It should also be noted though that, although the fossil did preserve the melanosomes (here), I'm not necessarily sure that that means the color observed in the fossil is the same color that would have been observed in the living organism. If anyone can comment/add to this, that would be quite welcomed.

Here's an image that suggests what this dinosaur would look like, given the discovery and analysis of the Sinosauroterpyx's melanosomes, acquired from the fossil you provided a picture of.


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Are humans the only species who drink milk as adults?
I was drinking a glass of milk the other day and that got me thinking that no other animal to my knowledge drinks milk past their infant stages. One could argue that cats might but it isn't good for them to do.
Are humans the only animal that are able to drink milk as adults and not have it cause issues?
Of course, I know some people do have lactose intolerance too.

Comments are not for extended discussion; this conversation has been moved to chat.

I'm not going to give a full answer, but our pets get dairy from their owners all the time.

My cat seems OK.

Good observation!
Gene coding for the lactase
Gene LCT
Mammals have a gene (called LCT C/T-13910) coding for the lactase enzyme, a protein able to digest lactose. Lactose is a disaccharide sugar found in milk.
Expression of LCT
In mammals, the gene LCT is normally expressed (see gene expression) only early in development, when the baby feeds on his/her mother's milk. Some human lineages have evolved the ability to express LCT all life long, allowing them to drink milk and digest lactose at any age.
Today, the inability to digest lactose at all ages in humans is called lactose intolerance.
Evolution of lactose tolerance in human
Three independent mutations
Tishkoff et al. 2007 found that the ability to express LCT at an old age has evolved at least three times independently. Indeed, they found three different SNPs (stands for Single Nucleotide Polymorphism; it is a common type of mutation), two of them having high prevalence in Africa (and people of African descent) and one having high prevalence in Europe (and people of European descent). The three SNPs are G/C-14010, T/G-13915 and C/G-13907.
Pastoralist populations
Lactose tolerance is much more common in people descending from pastoralist populations than in people descending from non-pastoralist populations, suggesting a strong selection for lactose tolerance Durham 1991.
Selective sweep
On top of that, Tishkoff et al. 2007 focusing on the locus 14010 (one of the three SNP's mentioned above) showed that there is a clear selective sweep (which is a signature of past and present selection) around this locus.
They estimated the age of the allele allowing lactose tolerance at this locus (allele C is derived, the ancestral being G; see nucleotide) at around 3,000 to 7,000 years (with a 95% confidence interval ranging from 1,200 to 23,200 years) and a selection coefficient of 0.04 - 0.097 (with a 95% confidence interval ranging from 0.01 to 0.15).
I recommend reading Tishkoff et al. 2007. It is a classic, is short and is relatively easy to read, even for someone with only basic knowledge in evolutionary biology.
Are humans the only animal that is able to drink milk as adults?
I don't really know... but I would think so, yes!
Drink vs digest thoroughly
As @anongoodnurse rightly said in his/her answer

"Drink" and "digest thoroughly" are two different things

Pets
According to many dog health websites (such this one for example) claim that there is also variance among dogs where some dogs are lactose tolerant and others are lactose intolerant. I could not find any paper on the underlying genetics of lactose intolerance in dogs or other pets. It is not impossible our pets have also been under selection to be able to digest lactose as we humans could have given milk to them. It is also possible that pets do not actually produce any lactase at adult age but rather that some pets are just able to deal with having indigestible lactose in their guts! But then again, "Drink" and "digest thoroughly" are two different things.
Tits and robins in 20th century England
A funny and famous case is the case of blue tits and robins in the 20th century, in England. At that time, in England, the milkman was bringing the milk at home in the morning and would leave glass bottles with a simple aluminum cap in front of people's home. At some point, blue tits and robins learnt that by pecking through the aluminum they can get access to the milk. See this (non-peer-reviewed) article that tells the story.
Somewhat related
There are already a number of good posts on milk digestion in humans on Biology.SE. Consider having a look at:

What inactivates pepsin in infants? and Seriously, do humans produce rennin?
Are there any non-mammalian species known that lactate?
Can an adult without genetic lactase persistence still develop a tolerance for dairy foods?

My cats and dogs all drink milk when it's given to them. What about that?

Can confirm the anecdote about small birds pecking a hole in milk bottle tops (around the mid-90s for me). Happened to us every so often.

Milk is a limited access food, and I believe that's the only reason adult animals can't drink it in nature. Suckling well is not a skill adult animals retain. Given the opportunity, though, many adult animals drink milk. Even chickens love milk! (I sometimes fed excess goat's milk to my chickens. It seemed to be a holiday gift to them.) :)

@ZzZombo Exactly so. My friend's father's dog used to be given a cup of hot tea every day, with milk, and somehow they had figured out that he liked it with one sugar.

@Remi.b You're confused about who said what, and I don't know what 'typically' is doing in the sentence, but the dog concerned lived to a ripe old age. I could never figure out how they knew the dog liked tea, let alone milk and sugar in it. Just an amusing anecdote.

@EJP Oops indeed. I removed my comment.

I just read that fascinating article about the tits & robins.  The most interesting part to me was that milk used to be delivered with no cap at all, just open bottles.  Really???  Cats, flies, birds, dogs, raccoons, possums, beetles... ahhhh.  Yes animals will drink milk whenever they get the chance!  Yes my biggest problem with it is that I don't want to drink ANYTHING after ANY of them!

@BillK It is not so easy to reach the milk in a standing glass (let's assume the bottle would remain standing because of some sort of wooden box in which it stands). I don't think flies would be attracted to milk but I am not sure. Most insects can't climb on glass. There are no raccoons or possums in England (you North American fellow $\ddot \smile$). Squirrel sounds like a potential threat. I suppose that if they used to do so, it is because it worked!

@Remi.b: Just remembered another instance of animals learning to drink milk.  When I was a kid growing up in dairy farming country (small farms, not the massive ones of today), the barn cats would wait patiently while the farmer was milking, hoping he'd squirt a stream of milk into their mouths.

@BillK That took me aback too, and frankly I don't believe it. This page on the history of milk packaging in the U.K. says that originally cardboard caps were used.

As a non-native speaker of english that wasn't aware of the bird called "tit", the last section of this answer had a very weird albeit amusing meaning.

Can confirm - I witnessed my dog recently trying to consume poop. Milk seems a lot better than that :P

@T.Sar you may enjoy https://www.youtube.com/watch?v=ueuA-9pqRok then.

It was actually cream rather than milk that the tits would take. This was in the days of unhomogenised milk where cream would rise to the top.

"A strong selection for ... in pastoral population" most likely means that if you could not digest milk, you died.

@Thorbjørn Ravn Andersen: As far as I can tell, lactose intolerance is merely unpleasant, not fatal.  So if the choice is between eating dairy products or dying of starvation, I expect few people would choose the latter.

@jamesqf Lactose intolerance mean that you do not digest the milk sugar, which contains energy.   I do not know how much, but apparently enough to make it a strong selection factor.

There's quite an interesting contemporaneous discussion of this, and other tit behaviour, in John Barnes' Titmice of the British Isles which was published in 1975. As the image in the linked article shows, it wasn't just blue tits but also great tits.

@Thorbjørn Ravn Andersen: Sure, you don't digest the lactose, but that's far from being the only nutritious substance contained in milk.  Over time, it would create a selection pressure, but one far from a universal "digest this or die" elimination.

@jamesqf Perhaps.  What would you then suggest could cause said strong selection pressure?  If it is merely inconvenient and you don't die, you still reproduce.

@Thorbjørn Ravn Andersen: Just like any other selection pressure.  They're very seldom binary logic.  Just for instance, people might not want to mate with someone whose gut is rumbling all the time.

The problem with this question is 1) wording and 2) access.
"Drink" and "digest thoroughly" are two different things. The latter does not prohibit the former. It is only lactose that is not tolerated; Calcium and other minerals, proteins, fats, etc. are also present in milk and are beneficial to the consumers if the lactose intolerance is not incapacitating.

One could argue that cats might but it isn't good for them to do.

I don't know about this. My barn cats drank milk all the time without diarrhea or other untoward consequences; so did my dogs. Furthermore, feral cats steal milk, as do sea birds!

While censusing, satellite tagging adult males and rototag tagging weaned pups of northern elephant seals (Mirounga angustirostris) at Playa Norte, Isla de Guadalupe (14 - 19 February, 2003), we opportunistically observed the stealing of elephant seal’s milk by feral cats (Felis catus) and western gulls (Larus occidentalis). Western gulls have been previously  reported  stealing milk from female northern elephant seals in several elephant seal colonies... and this behavior has also been observed in other seabirds such as the Pale-faced sheathbill (Chionis alba),  feeding  on southern elephant seal (M. leonina) milk (Favero 1996). However, this is the first report that focuses on feral cats stealing milk from elephant seals.

Regarding access, how would most adults go about getting milk? If offered, though, many adult animals will drink milk preferentially over water if offered at the same time. When I had dairy goats, excess milk was fed to adult dogs, adult cats, and many adult birds (e.g. chickens, guinea hens, peacocks, etc.) The chickens acted like it they were children and the milk was free candy! (I never had pigs, but my uncle and grandfather did, and fed excess milk to the adult pigs.)
As noted above, wild birds will also steal milk when the opportunity arises. Cows will sometimes suck their own teats.
Humans only appear to be isolated in drinking milk as adults by their ability to obtain milk through farming.
http://www.scielo.org.mx/pdf/therya/v1n3/v1n3a5.pdf

That is an interesting point, one that a comment on the OP left me wondering how would other animals get milk since they lack the farming abilities that we have in general.  So really it seems that it isn't that they don't, but comes down to availability and if they can get it from a source.

I think access is the key.  Animals evolve to get nutrition from whatever source is available.  If there was "Milk" available some animal would have evolved to drink it.  This would be very bad for the milk providers so the access to milk is limited (General "Milk Providers" would die out quickly and be removed from the gene pool).  If we created a "Milk Lake" and kept it stocked I bet we'd evolve an entire new local milk-based ecosystem in no time.. this would actually make an awesome biology experiment.

Piglets apparently can reach cow udders... http://www.independent.co.uk/news/world/europe/pigs-drink-cows-milk-austrian-farm-a7198756.html Not to mention orphans of many species will nurse from a surrogate, if available. But one of the triggers for weening is the adult teeth coming in (painful for mom!), so even if a succession of lactating surrogates was available, that might stop them.

I don't know how true this is, but my understanding about cats, and how lactose intolerance works for most mammals is that the animal will become lactose intolerant after the phase where they're feeding from the mother, but  can remain lactose tolerant if they are still fed milk occasionally. If they go without milk from the time they're done weening to adult hood, they will be lactose intolerant, but will still attempt to drink milk when given the opportunity.

Just to point out an exception, adult cows sucking other cows' milk are not uncommon. At least, it's common enough to be a concern in dairy farms and for simple fixes to have been developed. The usual fix is just a piece of plastic pinned to the offending cow's nose that makes the suckled cow walk away.
I'm not sure of how much of this behaviour is feeding related, but concerns about direct impact on production make me suppose that inter-sucking cows are actually drinking a sizeable amount of milk - of course, there are also concerns about indirect impact on production by affecting the involved cows' health.

My uncle had a dairy farm. Self-suck(l)ing cows were... sold. A cow that drinks her most important asset wasn't anything but a large, feed consuming animal. (I don't believe that, but he did.)

Is this behavior found in nature too, or only when all the cows produce milk?

Here is a bit of a tangential example, because it isn't milk from cows. There are some varieties of ants (Primarily the Leaf-cutter ant, if memory serves) which will collect, breed, feed, protect and "milk" aphids for the honeydew they produce. It is generally classified as a mutually beneficial symbiotic relationship, though one could argue that it is closer to domestication. The adult ants will eat the honeydew secretion.
Source: https://en.wikipedia.org/wiki/Aphid#Ant_mutualism
The reason I bring this up is because one argument against raising cows in a "factory environment" is because humans are the only species that drinks milk after adolescence. While this was not hinted in the original question post, the wording made me think of this.

Lots of speciellt of ants do this  (not only leaf-cutter ants) - "herding" aphids to collect honey dew is very common in ants.

So humans are not the only domesticators!  :)

Pigs can. At least one milk, and milk derivates, producer around here used/uses their own pig farms to dispose of all byproducts of production, overdue products returned from stores, same day unused milk, etc. As they owned the pigs, that should not cause too many problems.
I also remember a photo of depression era USA where a farmer is giving milk to pigs. The caption said that the price was so low that they used it for animal feeding instead of selling for human comsumption. I can't find it now.
At some times and places, butter was the primary reason for dairies. After the cream was skimmed off, the remaining milk had a much lower sale value. In some cases, it wasn't worth the effort of trying to sell it, or no one wanted it, and so it was fed to the hogs.

Milk (or food prepared with milk) is used to feed various domesticated animals like pigs or cats, also when they are adult.

That is correct, but this doesn't happen naturally.

The question does not say must happen naturally.

The way the question is asked, I see this as implied.

@Chris Yes sorry I guess it seems I may need to note that.  Yes I am looking for NATURAL ability as in a normal part of their diet/food chain, though with today's food chain all messed up, who can say what is natural anymore for anyone.  But yes, you are correct.

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Which mushroom is this?
I found those mushrooms in my garden in Luxembourg and I was wondering what species they might be.

Where is your garden? Also, the picture is not very good for species determination (several pictures from top, bottom, showing the shape of the hat etc would be better), and I would be sceptical against most advice to eat/not eat based on that picture.

Mountains, Luxembourg area

@fatmau - Please don't ask strangers on the internet to give you advice with such potentially devastating consequences if they are wrong or want to troll. While death is probably uncommon, varying degrees of hepatitis is common, with hospitalization being a frequent event. Get a good guidebook to edible mushrooms and follow the instructions for identification carefully. There are only a handful of mushrooms that can be identified as perfectly safe with one look at a single view.

I added the location and removed the question for advice.

That mushroom is from the Boletus family with sponge gills. A Red Cracked Bolete.
Only one sponge gill toadstool neighbor of the boletus family mushrooms has ever been know to kill a single person, or require a liver transpant, because, if you get an amanite wrong, you can survive, but only with a liver transplant. It is said that: if you found an Amanite, and put a triangle of it in your mouth and spat it out, it may taste fairly scary, but it will not kill you or even make you vomit or Hospitalizeded, although you may experience some discomfort, as long as you spit it out entirely and not swallow it.
In temperate climantes, The only boletus that are quite noxious are the red and beige ones which sometimes smell ghastly are in the family of the devil's bolete. There are other boletes that can make you vomit or ill, i.e. some blue and yellow ones. some boletes are strange and interesting such as the pepper boletus which can be used to flavor a dish because it produces very hot pepper flavor same as capsiacin.
Your mushroom is clearly a Red-Cracked bolete, which make sludgy, insipid soup, they have no texture, gelatious, flavorless, are extremely common, have yellow gills changing to blueish grey, and small red cracks often appear in the top which has the habit of cracking when ripe, hence the name, red cracked bolete. it is harmless and quite a waste of time to cook. https://www.google.fr/search?q=red+cracked+boletus&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiWn7Ljg9fVAhXDJlAKHe-HADwQ_AUICigB&biw=895&bih=530
The only boletus: sponge-gill toadstool (tail and cap) mushroom ever implicated for someone's death (by artery malfunction in the gut) was a woody tough red one related to boletus satanicus: https://en.wikipedia.org/wiki/Rubroboletus_pulcherrimus
Anyone trained biologist who can identify species from books, has a good chance of never falling ill from Boletus species, as long as he makes very positive identifications of mushrooms that don't have potential deadly or noxious look alikes. many mushrooms like the death cap are particularly deadly because they can be mistaken for small farm agaricus in field edges. especially angel of death and Panther-Cap, which smell of humus, earth, and apples.
The main identifier on a red cracked bolete is the squishy texture, not fibrous, and the velvet. dryish, textured large sporing body which starts as pine colored and matures to olive or bark colored.


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How did sulfasalazine become a disease-modifying treatment for rheumatoid arthritis?
Sulfasalazine has been around for about fifty years, starting as an antibiotic. More recently it is used as a disease-modifying anti-rheumatic drug (DMARD, see also arthritis.org). While biologics (biopharmaceuticals) are becoming more widespread in early treatment of some types of RA, sulfasalazine has a known safety profile and is inexpensive. Sulfasalazine is on the World Health Organization's Model List of Essential Medicines. See section 17.3, Anti-inflammatory medicines.
Wikipedia says:

The mechanism of action is not clear, but it appears that sulfasalazine and its metabolites have immunosuppressive, antibacterial, and anti-inflammatory effects.[refs] It also appears to inhibit the cystine-glutamate antiporter.[ref]

Why was this "old antibiotic" tested as an anti-inflammatory medicine? Is the situation similar to Minoxidil where a "side-effect" turned out to have significant medical value? What is the evidence (if any) that sulfasalazine has a disease-modifying effect in the treatment of RA - that it actually slows down the progress of the disease rather than just temporarily reduce symptoms?

fyi I've just asked Considering its salicylate component, is Sulfasalazine contraindicated when aspirin is? Can it have similar therapeutic benefits? in Medical Sciences SE

Question 1:

Why was this "old antibiotic" tested as an anti-inflammatory medicine?

A 2016 publication by the Department of Medicine at both Imperial College Healthcare Trust, and Hammersmith Hospital (both in the UK), titled, "Rheumatoid Arthritis Treatments: A Historical Perspective", states:

"Sulfasalazine: After NSAIDs and Gold, Sulfasalazine (SSZ)
is the third oldest drug class that is still available to use as a
treatment of RA. In 1938, SSZ was the first drug to be synthesized
specifically for RA. The consensus at the time was that RA was
the result of infection and accordingly Svartz et al developed
the DMARD, SSZ (originally known as salicylazosulfapyridin)
by combining the anti-inflammatory, salicylic acid, with the
antibacterial sulfapyridine by an azo bond."

Also, according to a publication by the Department of Medicine at Princeton:

Sulfasalazine was synthesized almost 50 years ago specifically to treat rheumatoid arthritis. At that time bacterial infection was believed to be an important factor in pathogenesis. The linkage of sulfapyridine and salicylate with an azobond was viewed as a method of combining antibacterial and antiinflammatory actions while minimizing gastric irritation. Early therapeutic results were encouraging, but the drug was discarded as an antirheumatic agent for 30 years, until its serendipitous rediscovery. Subsequent controlled trials have confirmed its efficacy, which may be related to sulfasalazine itself or to the sulfapyridine moiety.

Question 2:

What is the evidence (if any) that sulfasalazine has a disease-modifying effect in the treatment of RA - that it actually slows down the progress of the disease rather than just temporarily reduce symptoms?

A 1995 publication conducted by Adis International affiliates states:

The efficacy of sulfasalazine in RA noted in many noncomparative studies has been confirmed in placebo-controlled trials and comparisons with other disease-modifying antirheumatic drugs (DMARDs). Sulfasalazine therapy produces significant improvements in many clinical and laboratory parameters associated with the disease, including erythrocyte sedimentation rate (ESR), Ritchie articular index (RAI) or number of swollen joints, grip strength and duration of early morning stiffness (EMS).

Wow! That's quite a story. It turns out to be effective for RA, but apparently at least, not for any of the reasons used in the original design of the molecule. I'll try to read Pinals 1988 tomorrow and see what more I can found out about the "serendipitous rediscovery" story. Thanks!

Sure! You can see I've accepted answers in the previous 16 of 19 questions I've asked here. One reason I don't right away is etiquette, others complain if one accepts too soon without giving anyone else a chance, and also you can get more points on your answer if I delay acceptance for a day or so. Consider it a "free bump" so more people are likely to see it. Finally, I will read the paper tomorrow, and if the "serendipitous rediscovery" story turns out to be really interesting I may ask you to include a line or two of it as part of the answer. I like serendipity.

@uhoh Ah, good to know! I'll be on the lookout for any follow up requests from you regarding this topic. All the best :)

I couldn't get access to the "serendipitous rediscovery" paper, so I've broken the issue out as a follow up question; How did the “serendipitous rediscovery” of Sulfasalazine as an antirheumatic agent after 30 years happen? This is a great job, thanks!

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Repeating sequences of genomes
How can we estimate what portion of a genome is repeating sequences without sequencing it?
Thank you

I'm pretty sure that's not possible. Without knowing the sequence of a genome (which means someone has to sequence it), you can't really know which parts are repeats.

@Nicolai This is one of my study questions, so there must be some way to estimate, although I am clueless to how this could be done.

This site has a policy for homework questions, so you should probably edit your answer to show your previous effort to answer this yourself. I can't think of any experimental way to this (but it might be possible), so the best estimate is probably by comparison with related genomes, that have been sequenced.

No, it isnt a homework question, its for study review

Yes, it is possible to estimate the amount of repetitive DNA in a genome without sequencing. This was an important technique in the 1960s, referred to as C₀t analysis and pioneered by Roy Britten.
The approach taken is to study the kinetics of renaturation of heat-denatured genomic DNA (in a fragmented form). As you can see in this idealised Figure taken from the Wikipedia article on the technique there are components which renature rapidly whilst other components renature more slowly:

The interpretation of this is that repeated sequences renature rapidly because they are at a higher concentration than are single-copy sequences.
As stated at the linked Wikipedia article:

...it was through C₀t analysis that the redundant (repetitive) nature of eukaryotic genomes was first discovered.

And finally here is a quotation from Britten and Kohne's 1968 paper in Science:

The rate of reassociation of the complementary strands of DNA of viral and bacterial origin is inversely proportional to the (haploid) DNA content per cell. However, a large fraction of the DNA of higher organisms reassociates much more rapidly than would be predicted from the DNA content of each cell. Another fraction appears to reassociate at the expected rate. It is concluded that certain segments of the DNA are repeated hundreds of thousands of times. A survey of a number of species indicates that repeated sequences occur widely and probably universally in the DNA of higher organisms.

In agreement with @Nicolai, I don't think you can!
Of course, if you assume having a priori knowledge about the fraction of repeated elements in related organisms, you could try to estimate it. Typically, if you consider a angiosperm, you know you're going to have much more repeated elements than if you consider a bacteria. Also, the size of cells and the size of the nucleus are correlated with the genome size (Gregory 2001) and the genome size is itself correlated with the number of repeating sequences (Flavell et al. 1974, Bennetzen et al. 2005). However, those correlations are pretty lose and it will not be possible to be accurate with these methods.


text:
Is it possible that nearly human mammals existed before the last mass extinction dinosaurs?
From time to time I am hearing people discussing about the possibility that men and dinosaurs meeting some time ago.
The oldest mammal remains seem to be about 35 million years old, quite some time after dinosaurs have perished.
Also, it is very implausible for a primitive man to manage to survive near the dinosaurs (I think they would be very hard to handle even using current technology).
Question: is it even remotely possible for advanced mammals (nearly humans) to have coexisted with dinosaurs?

Just a quick comment, the article that you linked exists on the ICR page, Institute for Creationist Research, which is more of a religious organisation than a scientific one. If anything, they're doing pseudoscience, so please, do take their claims with a (big) grain of salt.

Is it possible that nearly human mammals existed before the last mass extinction dinosaurs?

Short answer
No!
Longer answer
The ancestor of all mammals lived about ~180 millions years ago (see here), so much before the Cretaceous–Paleogene extinction event (~65 millions years ago). The ancestor of all primates lived ~65 millions years ago (see here), so pretty much at the same time as the C-P extinction.
But please, don't picture the ancestor of all primates as something that is too human like. It looked more like a lemur, a tarsier or a loris, than like a human!
The first great ape lived about 14 millions years ago (see here) and the most recent ancestor of chimpanzee, bonobos and humans lived about 6 millions years ago (see here). The discovery of how to control fire happened about 1.5 millions years ago (with a pretty wide confidence interval, see the wikipedia article). The first generally considered Homo sapiens lived about 200,000 years ago (see the wikipedia article). The wheel was first invented about 5'000 years ago (see the wikipedia article).
Related: Who are humans' closest relatives, after primates?

So, the answer is clearly to my question is No and such coexisting is pure fantasy. Thanks for the relevant references. Onezoom dynamic tree is particularly nice and useful for newbies.

Indeed it is no! I added this simple straight forward answer as a short answer. Yes OneZoom.org is pretty neat. You can find other good resources to represent the tree of life in the post The best free and most up to date phylogenetic tree on the internet?.


text:
Kidney transplant and adrenal glands
When a kidney is transplanted from a donor to a recepient does the surgery occur keeping the donor's adrenal gland intact over the kidney or is the kidney minus the adrenal gland over it transplanted to the recepient?

I called and spoke the University of Kentucky Kidney Transplant Center, and asked this question. They said that the de facto source for kidney transplant information & procedure is available at UNOS.org, and that any information that any transplant center is going to provide the patient would be from that site; though, some procedures and policies may vary from center to center. I also did another search online, and was able to find forums for patients, and there are people who claim of having received, and not received, the adrenal gland.


text:
What is the length of gene when calculating TPM (transcripts per million)
What is the length of gene when calculating TPM (transcripts per million)?
Assume I have a dataset matrix with k rows(each row is a gene) and n columns (each column is a sample), is there any way I could transfer the data set into TPM? Many thanks!

Trusted Platform Module? Total Productive Maintenance? Technology Park Malaysia? Come on, give us a clue!

@David I am sorry, TPM is transcripts per million

http://www.rna-seqblog.com/rpkm-fpkm-and-tpm-clearly-explained/

Nice walkthrough, thanks!
When I was using it for implementing it as a function, still I spotted a small error in the calculations. When normalizing for the gene counts, GeneB-rep3 should be 14 (not 35, which you get if you divide by the 2k).
F
(sorry, could not add as comment due to the newbie status ;) )

Assume we have
$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 10 & 15 & 30 \\ B\: (5kb) & 25 & 25 & 70 \\C\: (2kb) & 6 & 10 & 17 \\D\: (8kb) & 1 & 1 & 3 \end{bmatrix} \: \:$$

To transform this into TPM format, we need to normalize for gene length, and then normalize for gene depth, in that order.

Normalizing for gene length..

Step(s) To Perform: Divide each replicate count by the length of its respective gene.

For $Gene A$, it has a length of $2kb$ (kilobases), with replicate counts $10, 15,$ and $30$. Performing this operation on the entire table,
$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & \frac{10}{2} & \frac{15}{2} & \frac{30}{2} \\ B\: (5kb) & \frac{25}{5} & \frac{25}{5} & \frac{70}{5} \\C\: (2kb) & \frac{6}{2} & \frac{10}{2} & \frac{17}{2} \\D\: (8kb) & \frac{1}{8} & \frac{1}{8} & \frac{3}{8} \end{bmatrix} \: \:$$
yields
$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 5 & 7.5 & 15 \\ B\: (5kb) & 5 & 5 & 35 \\C\: (2kb) & 3 & 5 & 8.5 \\D\: (8kb) & .125 & .125 & .375 \end{bmatrix} \: \:$$

Normalizing for gene depth..

Step(s) To Perform: 1) Sum all counts within each replicate column; 2) Divide each column sum by the desired depth (this yields scaling factors); 3) Divide each replicate count within a column by its respective scaling factor.

$Rep1$

Sum: $5 + 5 + 3 + .125 = 13.125$
Scaling Factor:  $\frac{13.125}{1,000,000} = 1.325 \times 10^{-5}$

$Rep2$

Sum: $7.5 + 5 + 5 + .125 = 17.625$
Scaling Factor: $\frac{17.625}{1,000,000} = 1.7625 \times 10^{-5}$

$Rep3$

Sum: $15 + 35 + 8.5 + .375 = 58.875$
Scaling Factor: $\frac{13.125}{1,000,000} = 5.8875 \times 10^{-5}$

Applying these values to the table,
$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & \frac{5}{1.325 \times 10^{-5}} & \frac{7.5}{1.7625 \times 10^{-5}} & \frac{15}{5.8875 \times 10^{-5}} \\ B\: (5kb) & \frac{5}{1.325 \times 10^{-5}} & \frac{5}{1.7625 \times 10^{-5}} & \frac{35}{5.8875 \times 10^{-5}} \\C\: (2kb) & \frac{3}{1.325 \times 10^{-5}} & \frac{5}{1.7625 \times 10^{-5}} & \frac{8.5}{5.8875 \times 10^{-5}} \\ D\: (8kb) & \frac{.125}{1.325 \times 10^{-5}} & \frac{.125}{1.7625 \times 10^{-5}} & \frac{.375}{5.8875 \times 10^{-5}} \end{bmatrix} \: \: $$
yields
$$ \: \: \begin{bmatrix} Gene \: Name & Rep1 \: Count & Rep2 \: Count & Rep3 \: Count \\  A \: (2kb) & 377358.49 & 425531.91 & 254777.07 \\ B\: (5kb) & 377358.49 & 283687.94 & 594479.83 \\C\: (2kb) & 226415.09 & 283687.94 & 144373.67 \\ D\: (8kb) & 9433.96 & 7092.20 & 6369.43 \end{bmatrix} \: \:$$

The dataset is now TPM formatted, which offers an easier analysis of read proportions throughout the sample.

Sorry, I didn't make it clear. what I have is the single RNA count data from cells. Each row is a gene, and each column is a different sample (or I should say different cell?).

@user133140 It's okay, no worries. We're still talking about the same thing, and the steps provided in this answer still 100% apply. :)

@user133140 "The entire dataset represents one sample, and each replicate (column) represents an identical copy of that sample." -- What I mean by that is, although you may have a different cell for each column, each of those cells are from the same cell line (sample) and should be identical copies of each other (or as close to it as possible). This is true for your case, yes?

So, the gene length is not included in the data I got and I have to find the length of each gene somewhere else right?

And if one element of the matrix is 0, then after doing this transformation, it is still 0.

@user133140 Correct. In order to calculate RPKM, FPKM, or TPM, you need to already have the gene (transcript) lengths.

@user133140 "And if one element of the matrix is 0, then after doing this transformation, it is still 0." -- That's correct.

There is a mistake on the scaling factor of Rep1: it should be 1.3125 x 10e-5.

Also, the question is "What is the length of gene when calculating TPM...". The answer describes how to calculate TPM given gene lengths. But what do you use as gene lengths?


text:
May have killed a cutting. Can dead plant cells be revived?
Ok. So, I went to New York City for the first time! My parents picked a hotel, and we had a good trip.
And even cooler, that hotel wasn't very far from a cool cedrus Atlantic a tree.
I got a cutting, but accidentally left in in the car today, and my mom went to work. The new growth has died. The old hardened-off growth still exists, but may or may not be dead.
It's evergreen, and it's not easy to tell.
So, assuming it is dead, and since it will be a long time till my next family trip, how could I bring one of the cells back to life, so I can generate explants?
Obviously this is very hard to do with animal cells, but could it be different with plant cells?
Could I just collect a bunch of dead cells, and pour atp solution on them?
Could I perform a nuclear transfer?
How could this be done?
And most importantly, CAN this be done?

Are you asking how to clone an evergreen? Or do you want to revive dead plant cells? For the second, reading Frankenstein might be useful :P

#2. And frankenstein won't work.

Making viable cutting from trees can already be tricky and difficult, you need to cut the right part of the tree and at the right time of the year. Reviving dead cells is impossible. Only possible in movies (Jurassic Park, Frankenstein, night of the living dead, etc.)

Nuclear transfer?

Nuclear transfer is used with viable cells, and even then this is very difficult. You'll need a hi-tech lab with highly skilled personnel. To revive dead cells is really sci-fi.


text:
Insect identification - Oregon
Western Cascade forest, in a small clearing in the grasses. Possibly related to leafhoppers? Looks a little bit similar, and it was able to jump quite well. The last pair of legs are arranged the same exact way as leafhoppers. Assuming it's within Hemiptera. I've never seen one before.

Possibly related to leafhoppers? .. Assuming it's within Hemiptera.

Your assumptions are correct! This insect is related to leafhoppers, in that it's a planthopper, and, is of the order Hemiptera -- it belongs to the species Scolops sulcipes.
According to the College of Agriculture & Natural Resources at the University of Delaware, this is one of eight species in Oregon that belong to the Dictyopharidae family. (source)


text:
HELP hepes preparation
I need help: I would like to prepare an HEPES solution, without using the powder. It is possible? I remember that I did it once, but maybe I'm wrong...does someone know a protocol for HEPES preparation without using a powder? thanks!!
I need It for morpholino dilutions. 5mM, ph 7.6.

Why don't you want to use the powder? If not, you can only buy stock solutions from the usual providers of lab chemicals.

I'm voting to close this question as off-topic because this is not about biology but about preparing buffer solutions.

HEPES is a particular chemical, not a mixture of chemicals so unless you have the ability to synthesise your own chemicals you cannot produce it without having the dry chemical preparation.


text:
Why is there symmetry in animals?
If cut a cut down the middle, both halves are symmetrical.
Why is it that most animals are symmetrical?
Is there an energetic reason for this? (as in, it is energetically favorable to create the same thing twice instead of making something new)

I believe this question has already been answered: https://biology.stackexchange.com/questions/5588/why-is-most-life-symmetrical-externally-but-not-internally

Intuitively, symmetry is useful for balance. A weight-nonsymmetric animal would have to expend additional energy to keep itself balanced (and this would also increase neural complexity for maintaining balance).
Mirror-image pieces only have to be coded once in the genome as a rule-of-thumb, allowing reuse of (mostly) the same genetic pieces with a few orientation and growth-origin markers thrown in. If you put vastly different parts on each side, you have to encode them (making the genome larger with more opportunity for mistakes and harmful mutation)


text:
In a fitness landscape, is fitness relative or absolute?
I was asked if the fitness of a fitness landscape is absolute or relative.
Fitness landscapes are usually graphed with a fitness function that uses either phenotypes or genotypes in relation to fitness or one of its component.
More specifically, if the fitness measured is survival, and it's computed based on a quadratic model, does that means that every individual survival probability is an absolute measure of "fitness" (survival)?
Or since it's computed from a model, would it be better to find the relative contribution of a variable on the predictor in the model and say that the "fitness" is relative to a trait if it's computed with multiple traits?
How does the mean fitness of the population influence the model, which will determinate the fitness of all individuals? Is this "mean contribution of the population's fitness" a relative measure of fitness?
My specific questions are:

What type (relative vs absolute) of fitness is shown in a fitness landscape?
Does the type of fitness change if you change way to model it (For example, I want to know specifically for a quadratic model vs a spline)?
Does the type of fitness change if you change way to model it (For example, I want to know specifically for a quadratic model vs a spline)?
When using a mark recapture model (you use the survival of each individual to find a fitness function) is the survival estimated by the model relative or absolute? Does the mathematical formulation of the model changes something?

In the image below, I've graphed all the points (black line) and I've removed the 3 lowest values of y for the 3 largest x values (red line). If I was calculating the fitness of the individuals with or without the 3 smallest points for the 3 largest x values, then the fitness of all the other individuals would be affected (except at x~38 and y~38).

x = c(1:100,101,102,103)
y =  c(x[1:100]+rnorm(100, sd = 6), 50,60,30)

x = c(1:100,101,102,103)
y =  c(x+rnorm(103, sd = 6))

summary(lm(y~x))
plot(y~x)
abline(lm(y~x),col = "red")
points(38,38,col="blue")

Another example with crossbills:

Would you say it's relative or absolute fitness. Here the fitness measure is "performance" of eating certain types of seed.
In this article they are saying (Morrissey & Sakrejda 2013):

Regression analyses are central to characterization of the form and
  strength of natural selection in nature. Two common analyses that are
  currently used to characterize selection are (1) least squares–based
  approximation of the individual relative fitness surface for the
  purpose of obtaining quantitatively useful selection gradients, and
  (2) spline-based estimation of (absolute) fitness functions to obtain
  flexible inference of the shape of functions by which fitness and
  phenotype are related. These two sets of methodologies are often
  implemented in parallel to provide complementary inferences of the
  form of natural selection.

Are least squares-based approximation of the individual always computing relative fitness surfaces? For spline, is it always absolute values?

I put the 2 questions in bold. The rest is more of an explanation or avenue of research.

Could you provide labeling for your computed graph, or just mention what they are? Thanks.

This graph is just an example of a linear regression. Both lines are identical, but the red one, I removed the 3 "outliers" at the far right. That way you see how the line shifts and how it affects the expected value on the left and the right of the $(38,38)$ point

Let me ask you this: When considering the crossbills, do you think that, based on the nature of what the data represents, the datapoints are directly related to each other? i.e., is the performance of one type of crossbill immediately dependent upon the other profile types, in most cases? Which is the same as asking -- do you think that crossbills of significantly different bill profiles are directly competing with each other? Or, do you think it's that, since the crossbills beak profiles are different enough to then harvest different seeds, that they "stay out of each others way"?

From the website: [...]The potential benefits of specializing on a key conifer species, the diversity of key conifer cones, and the method that crossbills use to extract seeds from these cones, it is perhaps not surprising that crossbills have diversified into several forms, many of which appear to be more or less specialized for foraging on a single or a few key conifers. While the association between bill depth and cone size is pretty striking, there's more evidence inside each bill that some degree of specialization is occurring.

I was hoping that you would answer freely, lol. I was trying to get you to "connect the dots", In response to your voiced confusions. :)

By experience, most of the time, authors are talking about relative fitness. To
confirm my feeling, I looked at the three randomly chosen theory papers from the first page of results that Google Scholar returned when searching for fitness landscape and they all use fitness as a relative measure. The papers are Derrida and Peliti (1991), Merz and Freisleben (2000) and Woodcock and Higgs (1995).
However, I do not think this is in the definition of a fitness landscape. One could work with absolute fitness and still call his model a fitness landscape. I think that therefore the answer is specific to every model considered. Note that even the "landscape axes" for which a fitness value is assigned can be of different nature. Typically, one can associate phenotypic or genotypic and/or even environmental axes.

In the three articles, only one was talking about relative fitness. I don't understand what do you mean by 'they all use fitness as a relative measure'. Is it relevant to determine the type of fitness if it was estimated from a model?

I considered their definition of the letter $w$, not whether they commented much on it. But it is not impossible that I'd made mistakes. Do you think two of them use absolute fitness? If yes, please tell me which one(s) and I can have a second look at it.

What type (relative vs absolute) of fitness is shown in a fitness landscape?

A fitness landscape is just a graph with a regression line/curve. The reason why this graph is referred to as "fitness" is because it's specifically illustrating how well "fit" an individual is to survive & reproduce within its population; "landscape" however, has no special or unique meaning, and can freely be interchanged with "graph".
With this in mind, a fitness landscape can depict both types of models -- relative and absolute. I believe your confusion/uncertainty may stem from the fact that these two population measurements describe two different things, and, that the use of fitness landscapes isn't unique to just one of them.
(I would really like to address the differences between relative and absolute fitness models at this time, however, I feel that it would get to be off-topic, as that would require somewhat of a lengthy explanation/comparison. I strongly suggest posting a new question that asks this, and I will happily respond. That is, if you even want clarification between the two.)

Does the type of fitness change if you change way to model it (For example, I want to know specifically for a quadratic model vs a spline)?

Depending on the type of fitness model you're portraying (absolute vs. relative), the amount of variability in your data will (most likely) drastically differ; i.e., how sharp of a curve your data may produce within a given interval of your datapoints. That being said, different fitness models do require different regression models in order to most accurately characterize the data.
With absolute fitness, you'll be able to (much) more accurately describe your data using a non-linear equation that can handle a considerable amount of flexibility. This often in the form of a cubic equation (contains a term with $x^{3}$). Higher degree equations can also be used (contains a term with $x^{4}$, or $x^{5}$, ..), however, your regression model may become "too sensative" to variability, and as a result, will cause your (regression) model to be more inaccurate than it should be. Also, because of the sensativity & flexibility of these regression models, smoothening (spline) functions are applied to the model, so that the data isn't quite as chaotic; imagine the difference between a stock market graph (e.g., weierstrass function), with that of a more traditional, "smooth" graph (e.g., sigmoid or logarithmic function).
And then, with relative fitness, you'll want to use either a linear, or quadratic, regression model. Due to the nature of what relative fitness models describe, there isn't nearly as much of a change in your data, given an interval. Because of this, a simple linear (contains $x$ term, and no higher powered term) or quadratic (contains an $x^{2}$ term and nothing higher) regression model will sufficiently represent your datapoints.
(If you'd like more of an explanation as to the nature of absolute & relative fitness models, and why they may or may not bring with them a higher amount of variability in their data, that would be addressed when discussing the differences between the two models, or, you can also open a question that specifically addresses this.)

Are least squares-based approximation of the individual always computing relative fitness surfaces? For spline, is it always absolute values?

Yes. Given what was just discussed, a (near) linear regression model are (typically always) used for relative fitness models, and higher-ordered regression models are (typically always) used for absolute fitness models.

If there are any points where I am being unclear, or you'd like for me to be more elaborate in explaining, please let me know and I'll gladly make edits. I may make more edits later anyway, but have to leave work right now and get dinner :)

Looking at your graph, and given my explanation of which regression model should be used, that fitness landscape is most likely depicting a relative fitness model, and is using a linear regression equation to characterize the data. And to contrast, the crossbill graph is probably an absolute fitness model, and is using a higher powered regression model with smoothing.

Cool! Thanks, but I don't understand why you are able to say "it's relative vs absolute". Based on the definition of Absolute vs relative fitness, I feel that it doesn't make sense to call one or the other. The surface of a fitness landscape is actually the "expected fitness". You can estimate the fitness value of an individual by taking the actual parameters values of your model and plugging the phenotypes. In this case, the fitness is relative or absolute? How can you justify that it's one or the other?

@M.Beausoleil "Thanks, but I don't understand why you are able to say "it's relative vs absolute". Based on the definition of Absolute vs relative fitness, I feel that it doesn't make sense to call one or the other." -- There is a fine distinction between absolute vs relative fitness models. With abolute, assessments (of a genotype) are made within the context of frequency; it is not a proportion measurement, and therefore, is subject to drastic change over a short time interval. Relative fitness, however, is a proportion measurement, and so, is much less susceptible to drastic change.

@M.Beausoleil "The surface of a fitness landscape is actually the "expected fitness". You can estimate the fitness value of an individual by taking the actual parameters values of your model and plugging the phenotypes." -- Correct; the fact that you're using a regression model is what allows for you to do this. Regression models generalize datasets to where you can consider situations that the data doesn't already contain.

Evolutionary biologists are generally most concerned with relative fitness models, which describes the survival & reproduction success of an individual (genotype) with respect to the highest performing genotype. It is an immediately contextual measurement, and requires selection to have occurred. Absolute fitness, however, is neither of these things, and so, is not quite as relavent to the questions that most evolutionary biologists are concerned with (though [absolute fitness] is still important, as it can be used to calculate relative fitness).

I think we need to define relative vs absolute here. https://biology.stackexchange.com/questions/64925/what-is-the-difference-between-absolute-and-relative-fitness: "The absolute fitness (W) of a genotype is defined as the proportional change in the abundance of that genotype over one generation attributable to selection" and "relative fitness (w) determines changes in genotype frequency". Based on what you are saying "[...] relative fitness models, which describes the survival & reproduction success of an individual (genotype) with respect to the highest performing genotype"

This looks like an absolute measure of fitness (reproductive success would for example mean the number of offsprings, which for me sounds like an absolute measure. Especially in the context of the equation: $n(t+1)=Wn(t).$ where W could be the number of offsprings

@M.Beausoleil That wiki definition is quite misleading. Please see this SE post. And in that case, $W$ is a multiplier going from one generation to the next. For example a generation with $10$ members (of a given genotype), where $W = 1.2$, would yield a next generation count (for that genotype) of $12$.


text:
If an organism is supported only by cartilage, does it have an endoskeleton?
Lamprey and sharks lack bones, but does this mean they are not classified as having an endoskelton? Does an organism need bone to be considered as having an endoskeleton?

"Sharks have an internal skeleton made of cartilage .." - http://www.bbc.co.uk/schools/gcsebitesize/science/triple_ocr_gateway/the_living_body/skeletons/revision/1/

From wikipedia

An endoskeleton (From Greek ἔνδον, éndon = "within", "inner" + σκελετός, skeletos = "skeleton") is an internal support structure of an animal, composed of mineralized tissue.

Cartilage is a mineralized tissue so it counts as a skeleton from this definition. A bit further in the wikipedia article it says

The vertebrate endoskeleton is basically made up of two types of tissues (bone and cartilage)


text:
Which cell organelle is more important in giving colour to petals?
It was a question in our school test and given answer was vacuole. But I think it should be chromoplast as they are the organelles specialised to provide colour. But options were given, so which is more accurate? Is the question controversial (both are correct?)

From what I have seen, a chromoplast is the only correct answer. I cannot find any articles even mentioning a vacuole being used for the storage of pigments in plants. I cannot think of where the test creators would have gotten that information.

When I read your question (headline), my first thought was: "Vacuoles!"
After reading in more detail about your problem, I agree with you that there is some controversy with this question. The problem is in my opinion that the question is not well formulated. The term "more important" is not really scientific, because what decides importance? Do they mean with importance that it plays a role in more flower species? Or do they mean that the color palette is larger with vacuoles compared to chromoplasts?
I do agree with the answer though, the pigments in the vacuoles are responsible for more colors in petals, and probably also in more species. However, there might be some plants in which the petal colors are dominated by the chromoplast colors. So the question is not well phrased, "more important" is too vague for exact science.


text:
Do common terms for animals such as amphibian or reptile fall somewhere in taxonomy levels?
Where in the "ranks" of taxonomy (domain, kingdom, phylum etc.) do common words used to describe animals such as amphibian and reptile fall?

This is all a matter of how we define terms, and which definitions are scientifically useful.
Traditionally (since Linnaean times), organisms were classified based on their outward similarities (phenetic systematics). As such, the traditional definition of reptile, which is the same as any common usage that I've heard, includes organisms like snakes, lizards, turtles and crocodiles but does not include birds. This is the class Reptilia. As evolutionary understanding increased, however, it was found that some reptiles, like crocodiles, are actually more closely related to birds than to other reptiles. This makes the common use of reptile a paraphyletic classification.
In modern phylogenetic systematics, organisms are classified in monophyletic groups, or clades, that include an ancestor and all of its decedents (ie it is based on evolutionary relationships). Thus the class Reptilia, since it is paraphyletic, is essentially meaningless in this system. In order to have consistent nomenclature, you could either say that birds are reptiles (a new, cladistic meaning of the term, but which contradicts traditional/common usage) or come up with a new name that includes all traditional reptiles and birds. Taxonomists taking the latter approach use the term Sauropsida for this clade. Sauropsida does not have a taxonomic rank like class because such ranks are useless in cladistics (and actually quite arbitrary even in the traditional system).

So, to specifically address your question:
In phenetics, both Reptilia and Amphibia have the taxonomic rank of class.
In phylogenetics, what we commonly consider reptiles and birds are grouped in a single clade that can be called Sauropsida or Reptilia (re-defined to include the clade Aves) depending on who you ask or which paper you read. Amphibia form a clade.
Perhaps the most important take-away message is that taxonomy is largely un-standardized.

Actually phylogenetic nomenclature is extremely well codified: https://www.ohio.edu/phylocode/ (some would say too much so).

@kmm I'm not a taxonomist, but as far as I know PhyloCode has not been widely adopted. Even though standards do exist, taxonomy as a whole is not standardized (at least not well). That said, I can remove the last sentence if you think it is misleading.

Amphibians form a class in phylum Chordata.
Reptiles, when considered as a taxonomic group, are also usually seen as a class in phylum Chordata. However, some scientist don't see reptiles as a valid taxonomic group because they are not monophyletical and modern taxonomy tend to accept only monophyletical groups.
That is, according to the taxonomy I was taught at school some decades ago, fishes, amphibians, reptiles, birds and mammals where classes in phylum Chordata. Nowadays, it is known (and stressed) that some reptiles are evolutionary closer to birds than to some other reptiles: there were common ancestors of crocodiles and birds that weren't ancestors of turtles.
Since monophyletic groups are defined as all descendants of a common ancestor, reptiles defined in the usual sense aren't a monophyletic group because they don't include birds. Therefore, some taxonomist either expand reptiles to include birds (and then "birds" and "reptiles" can't be both classes, although remaining valid) or just discard reptiles as a valid taxonomic group.
In the other hand, extant amphibians seem to descend from a common ancestor, and therefore they aren't questioned as a valid class.
Interestingly, fishes, regarded as a class for long time, are also being questioned as a valid taxonomic group, since some fishes share a common ancestor with tetrapodes (terrestrial vertebrates) which is not an ancestor of some other fishes.

Evolutionary taxonomy is a ridiculous, nonsensical, complicated mess and we should go back to traditional morphological taxonomy (classification based on physiology, shape, and function). If it looks like a duck, quacks like a duck, and walks like a duck, common sense dictates that it probably isn't a reptile.

That's also a reason for some evolutionary to stop using reptiles as a taxonomic group instead of extending it: reptiles keep being useful as a word, just like "herptiles", "fishes" or "domestic animals", all of them useful although invalid in evolutionary taxonomy.

@user1258361 which works right up until you start dealing with extinct organisms in which modern notions grouping break down, where do you put pterosaurs, how about dinosaurs, how about feathered theropods. How do you deal with the fact crocodiles may be secondarily exothermic, or that turtles have lost their temporal fenestrae, hence the use of evolutionary taxonomy.

@John create new classes for those and group as normal instead of breaking existing terms that have been widely accepted for decades and remain well-defined according to their traditional definitions in common use. An article years back mentioned that dinosaurs ran on a spectrum between warm/cold blood, so you could well argue that they deserve their own set of separate classes.

so you have classes inside other classes inside yet another class inside yet another class, making the term "class" pointless. hence why ranks are being abandoned. Cladistics is still based on morphology just accurately compared morphology. Crocodiles share more features with birds than they do with snakes so why would you group them with the latter. PS there is no evidence for cold blooded dinosaurs.


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Autoimmunity - negative selection of T-cells - APC
Through negative selection of T-cell in the thymus T-cells lose the possibility to react to antigens which are "body own" -> self antigens.
Though there are more than just this negative selection for preventing T-cells recognizing own antigens some T-cell become self reacting.
This T-cell in our case cd4 T-cells can recognize antigens presented on MHC II complexes by APC cells.
And the question is:
Who presents the self-antigens to the wrong selected CD4 T-cell, which leads to autoimmunity? How does the APC cell get this self-antigen in the first place?

Welcome Croin!  Please add a little bit of detail to this question.  Tell us a few sentences explaining the facts you are presenting, then ask the question about those facts.  For example: In autoimmunity, a theory is that the wrong CD4 T cells...." etc and provide a reference so the person answering the question can look into your source of info for more insight.  That makes the question richer and you will get better answers!

Hi, thank you for taking time giving me a better insight. But the question is pretty straight forward there is no need for further details. Either a person knows the stuff or doesn't. The question is like "Hello world" for immunology - autoimmune diseases".

I get your point, but I'm advising you on SE guidelines for higher quality questions.  This isn't like every other Q&A site. Asking a question isn't just for you, it's contributing to building a body of knowledge.  Also without a little more info, your question sounds like a quiz or homework question otherwise.

Actually I am going to vote moving this to BiologySE.  There is a fine line between Health and Bio on physiology/pathophysiology topics, and I think there are more molecular/cellular science specialists on the Bio side, and more clinical-/pathology oriented specialists on this side.  I would love if we had more people straddling both sites, as I think more discussion of difficult concepts in physiology would really enrich this site!

I do think the underlying question about the mechanism is good.  I don't remember enough from immuno in school to answer off the top of my head.  I gave you that advice because looking at it, I know that there are thought to be multiple mechanisms of autoimmunity, and you state that like it's the only one.  Hence the recommendation to provide a better description in the question body. I upvoted your question because it is a quality topic that I'd like to see be discussed, but gave you advice how to improve the quality of the question itself.

Ok I will try, though there is not really more...

Since you already know that the repertoire of T cell receptors is developed in the thymus, the missing half of the story in the context of antigen-presenting cells is that MHC complexes do not discriminate between self, foreign and mutated self peptides. The take home point is that selection in the thymus is meant to produce a repertoire of T cells which can overcome this fact.
In all healthy tissues, nucleated cells express class I MHC molecules loaded with self-peptides. A T cell probably isn't going to respond to it, however, because trafficking of T cells into tissues requires signals such as cytokines and chemokines. The T cells circulate to and from the lymph node T cell zones.
In the context of inflammation and cellular injury, self proteins may be released into the extracellular space where they're regularly cleared by macrophages via endocytosis. The extrinsic antigen presentation pathway loads peptides onto class II MHC molecules. In this very context, T cells are trafficked into distressed tissues by activated endothelium, where they interact with tissue APCs. Autoreactive clones that escaped thymic selection have the opportunity, then, to react to self antigens, ignoring regulatory or suppressor cells (ref).
Not just self-peptides, however, but also potential self-antigen mimics that take well meaning T cells directed against bacterial peptides, which happen to closely resemble a self antigen, and pit them against your own tissues (example). Unlike autoimmune T cells that have escaped selection and attack your cells, this invites T cells that have gone through the proper channels to do so as well.
See Cellular and Molecular Immunology, 8th ed. for an even better overview of T cell-based autoimmunity.

So basically it goes like:
Injury -> self antigen in extracellular space -> Uptaken by Macrophages -> presented on MHC II -> so the presentation ONLY goes through Macrophages which endocytosed the antigen and presented it later on a MHC II receptor to cd4 T cells?


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Why do cats meow when they are adults?
Meowing for kittens is similar to a baby crying. As human adults grow, they stop crying, but as kittens grow up they continue to cry. Why is this?

I could not find a peer-reviewed paper, but there is a widespread popular belief that adult cats only meows to communicate with humans but never with other cats. Meowing allows a cat to obtain the attention of its human owner and eventually get what it wanted.
See this webpage from the american society for prevention of cruelty to animals for example or this quora post.


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What purpose do the opening(s) serve in diapsid and synapsid skulls?
Did synapsid skulls evolve from diapsid skulls or vice versa?
Aditionally, do birds have diapsid skulls? The research I have done has yielded some mixed results.

It is believed that originally the holes evolved to give the jaw muscles a place to expand into as they contract. They evolved as the the  otherwise larger jaw muscles are trapped between the bones and cannot contract properly. I say "believe" because the original function is still debated, and it is not something that can be easily tested.
Diapsids likely evolved from early synapsids, however the evidence is tentative at best and it is just as likely that they both evolved independently from anapsids.
Birds are diapsids. However many modern birds have lost the bony partition between the two holes, separating them by cartilage and soft tissue only. Just as some mammals have lost the bony partition between the jaw muscles and the orbit. Additionally in many mammals and birds the expansion of the braincase makes it harder to identify the holes for the laymen as they are pushed down and to the side.

thanks for the helpful answer! One more thing for clarification...so birds, dinosaurs, and most reptiles (except for turtles) are diapsids, but are amphibians, and fish diapsids as well?

turtle are sort a diapsids, they closed the holes after they had them you can see this is the early fossil turtles, they actually end up closer to crocodiles and dinosaurs than other lizards. euryapsids (extinct) did something similar . the ___apsids are all amniotes and are defined as such, so  amphibians and fish which do not have the holes and are not diapsids but are not anapsids either becasue they are not amniotes.


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Insect Identification - Ecuador
I took a picture of this bug while I was in Chucchilán Ecuador in June. I am wondering what type of insect this is?
It was about 1-inch long.
This was the only good photo I was able to take, sorry for the poor angle.

This is a phasmid (Order Phasmatodea) from the Genus Monticomorpha. Its common name in Spanish is (insecto) ututo.
Here is an image of it:

Source: http://www.projectnoah.org/spottings/1847685515
They are found in Colombia, Ecuador and Peru. You can see that the distribution matches your place:

Source: http://phasmida.speciesfile.org/Common/editTaxon/Distribution/ShowDistribution.aspx?TaxonNameID=1199515
Identifying the species may be a bit more complicated. The Phasmida Species File page I linked above lists 8 species of ututos (with pictures), 5 of them occurring in Ecuador.


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How did the "serendipitous rediscovery" of Sulfasalazine as an antirheumatic agent after 30 years happen?
This excellent answer describes the history of the ~50 year old drug Sulfasalazine, and it's worthwhile to take a moment and read through the answer now.
Roughly speaking the drug is an antibiotic molecule linked to a molecule of aspirin, developed at a time when rheumatoid arthritis inflammation was assumed to be caused by an infection. Ironically the drug is now widely used as a treatment for RA, but its mechanism of action does not seem to be related to the way that it was originally designed to work.
Sulfasalazine is on the World Health Organization's Model List of Essential Medicines. See section 17.3, Anti-inflammatory medicines.
Within one of the block quotes in that answer from a publication by the Department of Medicine at Princeton can be found:

[...] Early therapeutic results were encouraging, but the drug was discarded as an antirheumatic agent for 30 years, until its serendipitous rediscovery (emphasis added).

Pubmed shows this to be Pinals R.S., J Rheumatol Suppl. 1988 Sep;16:1-4., PMID: 2903922, but I can't find access to the Journal of Rheumatology Supplements that far back in time.
Can somebody track this down and relate the "serendipitous rediscovery" story here? Or perhaps find a link to another author's version of the story I can read? What was the serendipitous biological evidence that led to rediscovery of Sulfasalazine as a disease-modifying anti-rheumatic drug? (DMARD, see also arthritis.org)

Your question led me to:
Pinals, RS (1988) Sulfasalazine in the Rheumatic Disease. Seminars in Arthritis and Rheumatism 17:246-259. I reproduce the introduction to this paper below:

Most physicians are familiar with sulfasalazine (SSZ) as an agent commonly used to treat inflammatory bowel disease for more than 40 years. In 1978, McConkey et al reported preliminary studies suggesting that this sulfonamide might be effective in rheumatoid arthritis (RA).1 The use of SSZ arose from earlier open and controlled trials with a sulfone, dapsone, which had demonstrable efficacy in RA, but the benefits were accompanied by relatively frequent, often unacceptable adverse effects.2 Dapsone was effective in dermatitis herpetiformis, presumably because of immunosuppressive activity. Another therapeutic agent for this skin disorder was sulfapyridine (SP), a drug with a poor record of gastric tolerance. Therefore, McConkey et al elected to try SSZ, a compound that released sulfapyridine in the bowel after passage through the stomach. Ironically, McConkey was initially unaware that SSZ had been synthesized specifically to treat RA in the late 1930s. In 1980, McConkey et al reported their open experience with SSZ in 74 patients treated for up to 1 year.3 The improvement in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and clinical score (a global evaluation) was similar to that achieved with the disease-modifying antirheumatic drugs (DMARDs), and appeared somewhat sooner, often within 2 months. Moreover, although adverse effects were frequent, they were seldom of sufficient severity to discontinue treatment. This encouraging report led to several controlled trials in the United Kingdom and elsewhere, all confirming the efficacy of this interesting agent. The first study in the United States has been reported4 and, although SSZ has not been approved by the Food and Drug Administration for use in RA, many rheumatologists have used it as an alternative DMARD because of its availability and long record of safety and efficacy in inflammatory bowel disease.

What I have gleaned from this and a couple of papers cited there is that B McConkey, working at a hospital in Birmingham in the UK became interested in developing methods of clinical assessment of rheumatoid arthritis (RA) in the 1960s and this led eventually to the discovery that the drug dapsone is effective as a treatment but with an unacceptable level of adverse side effects. Then, to quote McConkey:

We had studied dapsone partly because of its effect in leprosy and dermatitis herpetiformis; its mode of action in those diseases may be through its immunosuppressant properties. Another drug used in dermatitis herpetiformis is sulphapyridine;it did not attract us as a contender but it is a constituent of salicyl-azo-sulphapyridine (sulphasalazine), a compound originally formulated for RA and latterly found to have immunosuppressant properties.
McConkey et al (1980) Sulphasalazine in rheumatoid arthritis. British Medical Journal 1: 442-444
(This is ref 3 in the Pinals introduction.)

So clearly there was a strand of chemical logic in the rediscovery of the drug; the only serendipitous aspect was that McConkey did not at first know that sulfasalazine was originally designed as a treatment for RA.

Wow, thank you for both taking the time to put together this material and for sorting things out re the serendipity angle. A quick glance as the structures of Sulfapyridine and its more symmetrical cousin Dapsone makes it even clearer.

fyi I've just asked Considering its salicylate component, is Sulfasalazine contraindicated when aspirin is? Can it have similar therapeutic benefits? in Medical Sciences SE


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Is the suicide of a moribund individual to be considered group selection?
When a moribund individual commits suicide (e.g., Refardt, Bergmiller & Kummerli, 2013; http://rspb.royalsocietypublishing.org/content/royprsb/280/1759/20123035.full.pdf), is this to be considered group selection?  It could be considered costly to the individual, since the individual commits suicide and, therefore, loses reproductive opportunity.  And it occurs to the benefit of the group, by saving resources for the group and sparing it susceptibility to infection.  Is this group selection or does group selection require an intentional formation of a group?  If not, what else is necessary for this to be an example of group selection?  (Thank you.)

this seems a subjective answer

@ina What answer are you talking about?

It depends on what form of group selection you are talking about.
Group selection carries a lot of baggage and can refer to two very distinct concepts.  Concepts of group selection comes in two forms type 1, selection occurring on the group level, and type 2 selection on the group level that produces adaptations in said group or organism. The latter is the traditional usage of "group selection" the first(type 1) is now commonly (and confusingly) referred to as multi-level selection. (type 1 and type 2 are my terms I am using them to keep the two concepts identifiable)
Type 2 aka multi-level selection
Group selection (type 2) is simply selective pressures that occur above the individual level, kin selection could be seen as a form of this or it could not. It is still producing advantages and disadvantages to the genes and genes are still acting as the basic unit of evolution. Selection is occurring between groups with the differences between the groups being a product of the genes of the individuals within those groups. The genes are still favored or unfavored there is just many levels on which that the genes products can manifest. This models of group selection are basically just another form of gene based selection and adaptation it just adds another layer in which selection can occur.
Now few argue this form of group selection could not occur just that it would be swamped by normal gene based selection in most instances. There are genes known that are horribly detrimental to the individual and population in return for greatly favoring their own spread, the famous R2D2 gene in mice is an example.
Bacteria can be problematic in this as relatedness may not be a good measure of whether they share the same genes, and kin selection only requires shared genes. Could the behavior in bacteria be group selection in this case, yes, of course it could also be kin selection, the relatedness (Hamilton's original description) description of kin selection is really only useful in animals. In organisms with more lateral gene transfer they only need to share the gene in question, they could be completely unrelated in any other way. Indeed the paper even proposes this low but non-zero relatedness.
Now the big problem type 1
Type 1 is the traditional and first usage of the term group selection, but also the one only rarely proposed today, making it a very confusing term.
the big difference between kin selection and group selection (type 1) is that kin selection (or any form of selection including type 2) is about the selective advantage to the gene, an already well established principle, while many forms of group selection (type 1) propose a new "thing" on which selection occurs. what this thing is is never well defined but then neither were genes when natural selection was discovered.
To prove this form group selection and not kin selection you would have to show no selective advantage (or disadvantage) to the gene, basically you have to eliminate kin selection and other phenotypical expressions as a possibility. Proposed forms of group selection (type 2) can be shown to be products of normal gene based selection so you have to show this is not occurring. (thanks to Remi for this source). Intentional group formation in intelligent organisms (humans) is so far the only proposed mechanism in which this could work, and this would fall under memetics, which means it is occurring when related genetic differences are minor or non-existent.
Your paper does not show this form of selection, it does not even attempt to.
for a further breakdown of the diffrent forms of group selection I recommend this paper, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850877/

Yes, group selection could have been selecting for suicidal behaviour.

[D]oes group selection require an intentional formation of a group?

There is clearly no need for intention or consciousness for group selection to occurs (e.g. Aviles 1986).
The majority of people working in social evolution agree that kin selection and group selection are the same thing (Lehmann et al. 2007; Abbot et al. 2013). However, people's intuition often fail when talking about group selection while it is not too bad when talking about kin selection (H. Kokko during a speech and L. Lehmann personal communication).

A comment when down voting would be welcome

By "intentional," I was not asking about consciousness.  I meant, does group selection require the selection of processes that would be oriented toward the formation of a group?  But I believe the answer is no because it doesn't even require the formation of a group.
In my understanding, kin selection and group selection are not the same thing, but they have the common property of selection of cooperative behavior (put broadly) via genetic similarity to the recipient.  But the attribution of this genetic similarity is different:  In kin selection, it occurs by descent.


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Correlation between morphology of neurons and neurotransmitters
Are there known significant (positive or negative) statistical correlations between the morphology type of neurons and the neurotransmitters that they use (presynaptic, i.e. transmitters that are released, and postsynaptic, i.e. transmitters that are received)?
This question assumes, that a definite set of morphology types has been defined. The answer depends on this definition, of course.

Yes, at least for the neurotransmitters that a given cell releases.
As far as the neurotransmitters a cell responds to, you are really better off thinking in terms of receptor expression. Most neurons will express receptors for many different neurotransmitters. It's far too broad to go into them all in an answer here.
As far as the transmitters that cells release, morphological types of neurons are very often associated with release of particular neurotransmitters. In the cortex, for example, pyramidal cells principally release glutamate while there are potentially dozens of morphological types (again, depending on how you define them) that release GABA; in the cerebellum, Purkinje neurons release GABA whereas granule cells release glutamate.
However, be careful: some terms like "granule cell" don't really refer to a special morphological type. They are really just describing "small cells in close proximity": these can be completely different types in different brain regions. It really makes no sense to ask these types of questions for the brain as a whole, you have to study individual brain regions, each of which is organized quite differently from the others.

Thanks a lot for this instructive answer, especially for the remark on granule cells and your last remark.


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What animal / insect carcass is this? (Victoria, Australia)

During a hike on a mountain in Victoria, Australia, I came across this unusual shedding in one of the small rainwater pools. The pool looks small, but was developed long enough to have several insect species thriving in it such as water fleas and others of which I'm unsure.
This was the only shedding found and no other large insects or animals were found in this pool.

This is a tadpole shrimp. The most common species here down under is Triops australiensis.
Here is an image of it:

Source: https://www.flickr.com/photos/euprepiosaur/23782620153
Here is some info from Western Australia Museum (I found nothing on Victoria Museum): http://museum.wa.gov.au/creature-feature-tadpole-shrimp
PS: This is not a duplicate of this question because the species here is clearly different.


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Can Fluoride be absorbed into the blood from within the mouth without swallowing?
I'm having a discussion with somebody regarding Fluoride usage. I told him that even if he doesn't like the idea of ingesting it, brushing and spitting it out will do you no harm. He then said this:

You have missed the point of ingestion massively! Brushing with fluoridated paste is NOT fine.
The mouth, with its gum entry and under tongue glands are the PERFECT entry point to the blood, without even swallowing? What do you think oil pulling is all about? Fluoride passes those barriers as easy as the shit that resides in your blood can!"

Now I call BS on this, but I'd just like an expert opinion with cited sources if possible. Can Fluoride be absorbed purely by the mouth without ingestion?

Absorption in the mouth doesn't happen, see this answer. But this will probably not persuade your friend.

@Chris definitely not a friend of mine, haha :)

@Chris whilst that links explains remineralization very well, it doesn't really talk about gums or the tongue or digestion in the mouth and why fluoride can't be absorbed that way. That's more of the kind of thing I'm looking for

If fluoride can't be absorbed through the mouth, then why do dentists recommend fluoride-containing dental rinses?

@jamesqf because it can be absorbed onto the teeth that way, but my question is can it enter the blood through the gums, tongue etc. I know it can be absorbed into the teeth through the mouth

@Charlie: If that's what you're actually asking, perhaps you should consider editing the question.  As of now, it says "absorbed into the body", and the teeth are part of the body.

@jamesqf ok will do

Oil pulling?  You know you are talking to someone who has bought quackery hook, line and sinker, right?

Sorry I'm a lil late at finding this but thought I'd share two studies I found proving 'absorption of fluoride through the oral mucosa of rats' https://doi.org/10.1016/0003-9969(68)90140-4 https://doi.org/10.1016/0003-9969(78)90219-4 *the second link is a study on radioactive fluoride.

Although I'm having a hard time finding a source that provides specific information on fluoride in toothpaste, this review explains that fluoride is most readily absorbed through intestinal epithelia and that fluoride absorption through other tissues, such as oral epithelia, depends strongly on other chemical properties of fluoride-containing compounds: their

"reactivity and structure, solubility, and ability to release fluoride
  ions."

This suggests that you would need additional information concerning the overall toothpaste formula.
This review shows the rates at which fluoride ions are released from various toothpaste formulations. Figures 2 and 3 show that the highest discharge rate is roughly 1.7ppm and the lowest was just under 0.5ppm, both occurring after a 24hr period. The authors note in the discussion that these measurements are likely higher than what would occur in the mouth, since they had to use deionized water for their experiments, in which fluoride is more soluble than in saliva.
Wikipedia lists fluoride toxicity levels as being between 0.5 and 1.0mg/L. Fluoride's molar mass is 18.9984 g/mol and this calculator shows that 0.5mg/L of fluoride translates to about 0.5ppm. While at first this makes the above results sound a dire, it's important to note that toothpaste remains on your teeth for far less than 24hrs and to remember that less fluoride is released into saliva than into deionized water.
Wish I could find better results on how much fluoride might be released during a typical toothbrushing session, but I'm inferring from the linked review that it would be small enough to not merit a health concern.
I emailed a dentist friend for more info and will update this post as I hear back from him.
As for the comment about glands, it's important to understand that the glands found in the mouth are secretory glands, which means that they are optimized for discharging fluids and not for accepting them.
--Update--
My dentist friend wrote back, confirming that no significant fluoride absorption occurs through the gums. From him:

the only significant absorption would be through swallowing fluoride.
  Any that was just in the mouth would not be well absorbed...
  that is why we do the high dose swish and spit treatments is to avoid
  fluorosis but deliver sufficient fluoride to the teeth.

In short, it looks like the answer to your question is: no, fluoride is not significantly absorbed into the blood from within the mouth without swallowing.

thanks for the info! I'll keep this open for now to allow time for you and others to find out more.