text:
Can cysteine alone change pigmentation?
According to this graph (from here):

cysteine contributes to pheomelanogenesis, and having a high enough concentration of cysteine makes the shift towards pheomelanin instead of eumelanin. So my question is: theoretically, let's say I would feed my dog a cysteine supplement daily, would that change its coat color over time? If yes, how, and if no, then why not? What am I missing in this process?
Disclaimer: this is just an example, of course I do NOT intend to feed my dog anything at all, it's just a hypothesis. What I want to know is that raising cysteine/glutathione levels can really contribute to pheomelanin production? I know that theoretically, in lab tests a higher cysteine concentration means a higher pheomelanin production, but I am interested in actual living things. If this is possible, it can be a huge breakthrough. If you have the opinion that cysteine alone won't make the difference, than what will? According to the graph attached, that's the only thing making the difference.

Surprisingly, it is indeed possible! But, the fact is that the actual process is a bit more complex and might actually require more compounds along with cysteine to give such effects in living beings. First of all, see this image1:

As is clear from the diagram, GSH (glutathione) is also a factor for pheomelanin production, along with cysteine. Another factor on which one might not pay heed is Tyrosinase protein expression. High amount of L-cysteine is thought to decrease the expression of tyrosinase in cells2 (but since I found just one article, I'd suggest to not pay much attention on this point).
Apart from gene expression, cysteine affects tyrosinase itself too. High concentrations of cysteine and glutathione have been shown to inactivate tyrosinase in cells, and the cause has been suggested to be the thiol-group of GSH and cysteine, which somehow generates oxygen radicals and inactivates tyrosinase3. A concentration of 10mM cysteine is sufficient to inhibit tyrosinase activity in cells4. It is because of these kinds of effects that GSH and cysteine are now being used in cosmetics as skin whitening agents as they, in higher concentrations, inhibit tyrosinase activity and hence, melanin production in skin cells5.
Just to add, when it comes to gene regulation, then it seems that cysteine has some more effects too. As pointed out by @Chris, eumelanin production in skin is stimulated by a cascade which involves a receptor known as melanocortin-1 receptor (or MC1R). When activated by one of the variants of MSH, typically $\alpha$-MSH, MC1R initiates a complex signaling cascade that leads to the production of the brown or black pigment eumelanin6. Now, a research has concluded that 0.07 mg/ml concentration of L-cysteine greatly reduces expression of MC1R gene, thus literally leaving no way (not really) for eumelanin production7!
Thus, in short, it is not as simple as "Hey, you want a red skin tone? Here is some cysteine for you!" Cysteine, and other related compounds like GSH, have more complex effect on melanin production than just promoting production of pheomelanin over eumelanin. You can also have a look at this answer (by @Chris) for some more information.
EDIT: To tell where you're going wrong, I'll make two reaction flowcharts. First, this is (IMO) what you're expecting as an answer:

But this is what is actually happening:

The red line is what we're interested in. But as you can see, the diagram is already quite complicated (and expected to get more complicated as more factors are discovered). So, giving a simpler explanation than this would be, very much, impractical or impossible.
References:

Malathi M, Thappa DM. Systemic skin whitening/lightening agents: What is the evidence?. Indian J Dermatol Venereol Leprol 2013;79:842-6
The Inhibition Effect of L-cysteine on Melanogenesis in B16F10 Mouse Melanoma Cells; In-Sook An, Ji-Hye Kim, Hoe-sook Yoo, Rui Zhang, Sang-Mo Kang, Tae-Boo Choe, Tae-Jong Kwon, Sung-kwan An, Gi-Yeon Kim
The effect of catalase on the inactivation of tyrosinase by ascorbic acid and by cysteine or glutathione; Lindbladh C, Rorsman H, Rosengren E.
Inactivation of human tyrosinase by cysteine. Protection by dopa and tyrosine.
Jergil B, Lindbladh C, Rorsman H, Rosengren E.
Mechanisms Regulating Skin Pigmentation: The Rise and Fall of Complexion Coloration; Jody P. Ebanks, R. Randall Wickett, and Raymond E. Boissy
Melanocortin 1 receptor - Wikipedia
Substantial Effect of Melanin Influencing Factors on in vitro Melanogenesis in Muzzle Melanocytes of Differently Colored Hanwoo; Touseef Amna, Kyoung Mi Park, In-Kyung Cho, Tae Jeong Choi, Seung Soo Lee, Kang-Seok Seo, and Inho Hwang

Nice answer. There is also a genetic component which is important: The status of the MC1R gene. It is responsible for the shift between the eu- and pheomelanin production - how, is not really understood so far. If you have mutations in this gene, this will get less signal into the cell and people are prone for pheomelanin. And I doubt that this can be influenced by diet.

@Chris Wow I didn't know about this one! Thanks, I'll add it in as soon as I get some citations :)

Besides, this paper should be interesting for MC1R (and a ton of others, too ;-) ): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678743/

@another'Homosapien' thanks for your great answer! So it seems that my hypothesis isn't just a fairytale after all? To quote myself again: so if I would give cysteine to my dog/kangaroo/pigeon/myself/whatever(the accent is on actual living things, not plants or lab tests) then it could change pigmentation to some degree? This is actually a huge thing. Now I'm not sure how those numbers from those studies would translate to human consumption. In other words: in theory how much cysteine would a human need to reduce the expression of the MC1R and inhibit tyrosinase activity?

@Chris so you don't think that pheomelanin/eumelanin switch can be induced by diet/supplementation? Do you really think that we humans reached a point in research where we can say :that's it, we just don't know how to make the switch between eu and pheomelanin, we can't influence pigmentation? If you think that pigmentation, either darkening/tanning or lightening can be influenced in any other way and I am dead wrong than could you post some links? If cysteine is the building block for pheomelanin, than why cysteine supplementation won't make a difference? Legit question, I want to know really

@user30255 I don't think it's that easy. This is a heavily regulated process, that can be influenced by certain drugs. I am not sure (actually I doubt it at the moment) that this can be done by nutrition alone.

@Chris  What would those specific drugs be? Never heard of any, to be honest. On the flipside, I found Melanotan to increase eumelanin production(the stuff bodybuilders use to get 'tanned'), so I figured there must be something which does the exact opposite. This is scientific banter on my part, I do not recommend nor advocate the use of things like Melanotan or any other potentially dangerous drugs. I just want to investigate all the theoretical solutions to increase pheomelanin as well. So if my cysteine hypothesis might be wrong, care to mention those drugs/substances?

@user30255 your hypothesis is partly correct. It is partly wrong because this process is not as easy as you are supposing, there are many processes involved in it, and its difficult to get a simple answer for any situation

@another'Homosapien' could you tell me more about those processes? what am I exactly missing here? I don't mind if this gets complicated

@another'Homosapien' thanks! sure, take as much time as you need and make it perfect!

@user30255 does it make some sense now? :)

@another'Homosapien' yeah that's a good graph, but according to it cysteine is pretty much a super drug which influences everything in there, if it's in abundance. So my question stands: do you think that dietary/supplemental cysteine can influence pheomelanin/eumelanin balance? Not to a drastic measure, but still noticeably. Because right now, in 2017 cysteine seems to be the best bet which could do that, and it could be a breakthrough.

@user30255 of course it is! That graph was just to mention the complexity at molecular levels. Yeah, cysteine does influence pheomelanin/eumelanin balance quite noticeably. That graph involves only pigmentation factors, if I include other factors as well, its gonna be a long flowchart then ;)

@another'Homosapien' so you agree with me that dietary/supplemental cysteine excess can influence pheomelanin/eumelanin balance? I heard that l-cysteine, as a supplement is poorly absorbed, what do you think?

I can't be definitely sure about this point. The acetyl group makes cysteine more water-soluble, and functions to speed absorption and distribution on orally ingested cysteine yup thats why N-acetyl cysteine is ingested orally for better absorption.


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Lab experiment: Enumeration of Leukocytes
The images below were obtained in an experiment to enumerate leukocytes in a blood sample using Neubauer counting chamber.
The following solution was prepared and added to the Neubauer chamber and viewed under a compound microscope:
100 microlitres of acetic acid (acidic reagent to haemolyze RBCs) + 50 microlitre of Leishman's stain + 1-2 drops of blood.
Are these granular transparent circular objects in the images the leukocytes? If yes, do these include the smaller ones too? I am unable to decide which ones to take into account.
Moreover is this count normal (for instance, I counted around 250 (excluding the very small ones and applying the margin rule) in the top left box of the grid (Image 3))?

the amount of blood should be taken quantitatively ,not without measuring, so one or two drops of blood will not give correct calculations .

First I'd make sure all the RBC were gone just by visually inspecting. What should remain are your WBC and platelets at this point, and platelets are tiny so you can probably count anything between 5µm and 25µm. So for me that would include basically everything I can see minus background or debris.
So the problem now is with quantifying your count. You should know what the volume of your blood is, and here's why: What you're doing with a hemocytometer is counting #cells in a given volume, but you also diluted your whole blood with 150µL before you counted. So for example if a drop is ~60µL, and you diluted it with 150µL your dilution factor is 3.5, and it's important because your cell density equation is
For reference, you typically end up with 4-10 million leukocytes per mL of blood, however.

source: Stack Exchange

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

sort: votes


text:
Indian Snake Species Identification
Location: southern India
Time: noon
Approx. Size:
Length: around 2 feet;
Size: extremely small, like a straw.
Diameter: less than 1 cm.
Was very fast in climbing aisle of mud bed/uphill like 90 degree accent.

Ashok's Bronzeback (Dendrelaphis ashoki).

This is a relatively small snake (typically 70 cm in length) that feeds on lizards, frogs and small rodents.
More information can be found here or here.
It's range is Southwestern India:

You can differentiate this species from closely related D. girii based on it having a longer "postocular" black line than D. ashoki -- in D. ashoki it stops shortly caudal to the eye (e.g., see here).

+1 its like 100% close i would say, Only the bluish shiny thing makes me think, it might be very close family one.

@Umar I'm glad you added the third photo showing the blue shimmer of your specimen! That gives me even more confidence that this is your species. (the blue is only visible in certain positions -- again see here.

muahuhhaa i am seeing the blue stripes after you mentioned it (in the third photo)

Dumb question: When the differences are so minor (e.g. "longer "postocular" black line") what's the reason for designating them as two different species?

@curious_cat feel free to ask this in a new question. Comments aren't the best place for extended  discussion of additional questions.

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


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Has a beneficial mutation ever been documented?
I am trying to find a case/study where scientists documented a mutation in an animal or human that was to the benefit of the host.
The closest thing I have been able to find is sickle cell anemia (SCA) helping to fight malaria. However, the life expectancy for people with SCA is 40 – 60 years, and in 1973 it was only 14 years (source). I am looking for another case, preferably one that is not life-threatening.
Are there any other cases where a beneficial mutation — one where the good outweighs the bad — was documented?
By beneficial I simply mean that it helps or protects the host in some way, while not causing substantial harm. As in my example of SCA it can benefit the host if the host lives in an area with malaria. However, it is also life threatening and reduces the life expectancy of the host.
If — for example — SCA would only cause pain and not be life-threatening, then it would (in my opinion) be a beneficial mutation. While not purely beneficial, it would still increase the life expectancy of people living in an area with a high occurrence of malaria.

Macroevolution means that 2 groups of organisms diverged far enough that they cannot interbreed any longer and thus now form separate species. https://en.wikipedia.org/wiki/Macroevolution         I am not sure what you mean with "a purely beneficial mutation". A mutation/variation doesn't need to be "purely beneficial" (if something like that even exists). It just needs to be beneficial ENOUGH to prevail and spread in the population.

A beneficial mutation would be a seal born with functional legs, allowing it to hunt on land. A non beneficial mutation being a seal born with an extra flipper, the extra flipper does not benefit the seal and would only slow it down.

I also changed it to just beneficial instead of purely beneficial. So a mutation where the good outweighs the bad.

How is "disease resistant crops" not a beneficial mutation?  Note that that "macroevolution" is not a term much used by biologists; it's mainly used by creationists because it's essentially meaningless and fuzzy enough that they can always deny that anything meets their moving goalposts.  Your example of "a seal with functional legs" shows a profound lack of understanding of evolution, and you should probably learn some very basic information before continuing, e.g. Understanding Evolution (UC Berkeley)

A seal born with functional legs would be a detrimental mutations as legs would slow down a swimming speed.Making hunting in water more difficult and increases the likelihood of said seal pup being eaten by sharks it is first year of life.

Disease resistant crops (not GMO crops) are simply a variety of a crop that is more resistant to certain diseases. Much like dogs with long hair are more 'resistant' to the cold. My example was over-the-top to illustrate what I mean, not to be a functional example. I am also aware of the never ending macro v micro, evolutionists v creationists debate and that is NOT what I want this question to turn into.

Microevolution is not defined as variation within a kind but as evolution over short time scale (that is change in allele frequency over short time scale). Macroevolution are the same changes over long time scale. This is pretty much it. If your question is "do we have evidence for common descent", then the answer is yes.

I am voting to close as unclear. Please be clear about what evidence you are looking for. Try maybe to picture and elaborate on a specific process for which you would be looking for an evidence. One could also vote to close as opinion based as you seem to misunderstand the definition of microevolution.

Once you've managed to clarify your question for yourself, you might want to have a look at this skeptics.SE post which links to thousands of evidence for evolution that have been simplified for layman.

I am simply looking for a beneficial mutation. I had thought the micro and macro evolution example to be a good way of explaining what I am looking for. The post has been edited to remove all mention of evolution, micro and macro, and should be easier to understand.

I would appreciate knowing what is still unclear or too broad in my question?

In the current form, I think the question is fine. There is some ambiguity in how to judge whether a mutation is "beneficial", but I think there are answers where this becomes obvious. One example might be the deletion in the CCR5 gene that renders people resistant to HIV, https://academic.oup.com/femsle/article-lookup/doi/10.1016/j.femsle.2004.09.040   I am voting to reopen.

Milk tolerance in adult humans comes to mind: https://en.wikipedia.org/wiki/Lactase_persistence#Global_spread

Nylon eating bacteria would be a good example. They have an enzyme that does nothing but break down nylon, an artificial polymer invented in 1935. A similar mutation has even been induced in the lab, https://en.wikipedia.org/wiki/Nylon-eating_bacteria

The E. coli long-term experiment has several, even repeatable ones. http://myxo.css.msu.edu/ecoli/

You should have a look at this post if you're looking for examples from human evolution

Every common different cell type and enzyme that plays an important metabolic role in an animal is a positive mutation. photreceptors, heat sensors, opposable thumb, melanin, mucous glands, saliva glands, all other glands, hair color of snow rabbits and snow animals...

You can find a whole list here, http://www.talkorigins.org/indexcc/CB/CB101.html It includes things like nylonase, stronger bones, AIDS/plague resistance, and plant breeding for agriculture

Lactase persistence
This is a somewhat unusual example but has been well studied, and would seem to satisfy the criteria of the question. Let me start by quoting the Wikipedia entry for those unfamiliar with the phenomenon:

Lactase persistence is the continued activity of the enzyme lactase in adulthood. Since lactase’s only function is the digestion of lactose in milk, in most mammal species, the activity of the enzyme is dramatically reduced after weaning.[1] In some human populations, though, lactase persistence has recently evolved[2] as an adaptation to the consumption of nonhuman milk and dairy products beyond infancy.

Studies on the geographical distribution of lactase persistence (e.g. AJHG (2014) vol 94, pp. 496–510) show that lactase persistence is associated with cultures which practice pastoralism (specifically herding bovines), supporting the hypothesis that the trait evolved because of the benefit it conveyed to such populations in allowing them to use bovine (or caprine or ovine) milk to survive in adulthood.
There is no doubt that lactase persistence is a heritable — i.e. genetic — trait, as can be seen from consulting the OMIH (Online Mendelian Inheritance in Man) entry. This has extensive documentation, including description of the base changes associated with the trait:

Enattah et al. (2002) found a complete association between biochemically verified lactase nonpersistence in Finnish families and a C/T(-13910) polymorphism of the MCM6 gene (601806.0001) roughly 14 kb upstream from the lactase gene locus (LCT; 603202), located on 2q21. It was the C allele that associated with hypolactasia.

The molecular mechanism of lactase nonpersistence (the putative original human condition) — affected by mutation at this position — is still not completely clear. Recent work suggests:

Epigenetically controlled regulatory elements accounted for the differences in lactase mRNA levels among individuals, intestinal cell types and species.

Finally, I refer to the evidence for the Wikipedia statement that “lactase persistence has recently evolved[2]”. This is a paper by Bersaglieri et al. in The American Journal of Human Genetics (Am. J. Hum. Genet. 74:1111–1120, 2004). I am not a population geneticist, so I shall reproduce the relevant section of their summary unedited:

In northern European–derived populations, two alleles that are tightly associated with lactase persistence (Enattah et al. 2002) uniquely mark a common (∼77%) haplotype that extends largely undisrupted for 11 Mb. We provide two new lines of genetic evidence that this long, common haplotype arose rapidly due to recent selection: (1) by use of the traditional FST measure and a novel test based on pexcess, we demonstrate large frequency differences among populations for the persistence-associated markers and for flanking markers throughout the haplotype, and (2) we show that the haplotype is unusually long, given its high frequency—a hallmark of recent selection. We estimate that strong selection occurred within the past 5,000–10,000 years, consistent with an advantage to lactase persistence in the setting of dairy farming; the signals of selection we observe are among the strongest yet seen for any gene in the genome.

I have decided to mark this as the answer because it best fits with the question in its current state. Although the benefit from lactase persistence is small, it is beneficial and does not harm the host.

The answer depends on what you mean by "observed".
Bacteria acquire antibiotic resistance genes all the time, for example. This happens 'in the wild', but you can see in the lab that bacteria can become resistant overnight - I'd call that 'observed'.

There are many papers about the emergence of antibiotic resistance (not that I'm suggesting this is the only observable beneficial mutation).
In this paper, for example, several spontaneous mutations are induced in H. pylori in the lab in a short space of time:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC90364/
In this paper, estimation of mutation rates are attempted in the emergence of resistance:
http://aac.asm.org/content/44/7/1771.full
It should be pointed out however that the timeframes can vary wildly. If a bacteria acquires a resistance gene by horizontal transfer, for example, this could be considered virtually instantaneous. Spontaneous mutations may take longer to emerge, and might only do so in the presence of steadily increased selection pressure, by contrast.

Without additional explanation or resources/citations, this is not a proper answer. This is a comment. Please see How to Write a Good Answer. Thanks.

Well as a microbiologist it's based on personal experience. I believe that the acquisition of resistance genes by bacteria is such a widely accepted and cited example now that it didn't need an implicit source, much as I wouldn't cite Watson and Crick every time I mention DNA...

By observed I mean some scientist dude was all like; yo this bacteria's gone all resistant, I should write this down. So you got that right. Would be nice to have an example of a specific type of bacteria with a link to the study or report where it happened.

Though you're right, that doesn't change the need to provide necessary citations/sources. Clearly the OP likely doesn't know as much about this subject as you or they wouldn't be asking the question. Without substantiating our answers with  good sources, we'd be no different from Yahoo Answers or other error-ridden Q&A sites. By providing valid sources, we can better assure our visitors (as well as each other) that the information being shared is accurate.

I've edited my answer, but this really is too big of a question to just select a couple of examples. I would also point out that many of the 'observations' we make as scientists do go undocumented. For instance, every time I have an unsuccessful transformation (perhaps spontaneous mutants), I wouldn't go to great lengths to describe it, I would simply alter reaction variables and repeat.

@JoeHealey of course. But on this site, those undocumented experiences belong as comments or as anecdotal additions to otherwise cited answers. (This is the whole conept behind peer-reviewed science!). Thanks for updating your answer with examples :).

An example of a beneficial mutation we have probably all been on the receiving end of is the mutations of influenza. The whole reason we have to redevelop flu shots every year is because the influenza virus mutates so rapidly. Influenza loves changing its antigens to hamper our vaccine development and immune response. Normally you are immune to a pathogen after a single infection as our immune system recognizes the antigens on this pathogen in the future and reacts rapidly if it re-encounters them. This doesn't work with influenza as it mutates its antigens to the point that we can no longer recognize them from a previous flu infection, forcing our immune system to start all over again. This is what makes the flu so problematic for us; for influenza it is rather beneficial to put it mildly.
There are also specific human examples, some of which are mentioned in other answers. A mutation in low-density lipoprotein receptor-related protein 5 has been associated with improved bone density. This improvement in bone strength has fairly obvious advantages, like harder to break bones and improved resistance to age related skeletal weakness. Asides from (seemingly harmless) bony growth in their mouths no negative side effect of this mutation was discovered.
A particularly crazy human one is the potential of tetrachromacy (seeing 4 colors) in women. I'm not entirely sure about the genetics and test methods involved but apparently in this study they discovered that one mother of a color-blind male displayed genuine tetrachromacy.

Smith, D. J., Lapedes, A. S., de Jong, J. C., Bestebroer, T. M., Rimmelzwaan, G. F., Osterhaus, A. D., & Fouchier, R. A. (2004). Mapping the antigenic and genetic evolution of influenza virus. Science, 305(5682), 371-376.
Boyden, L. M., Mao, J., Belsky, J., Mitzner, L., Farhi, A., Mitnick, M. A., ... & Lifton, R. P. (2002). High bone density due to a mutation in LDL-receptor–related protein 5. N Engl J Med, 2002(346), 1513-1521.
Jordan, G., & Mollon, J. D. (1993). A study of women heterozygous for colour deficiencies. Vision Research, 33(11), 1495-1508.

Yes, many beneficial mutations have been documented, here are a few examples:
The Lenski experiment : https://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment
(the repeatable observation of the evolution of citrate metabolism in E.coli)
The Milano mutation : https://en.wikipedia.org/wiki/ApoA-1_Milano, http://blogs.sciencemag.org/pipeline/archives/2016/11/16/the-long-saga-of-apo-a1-milano
(a mutation in humans that gives resistance to heart disease; its first appearance wasn't observed per se but phylogenetic analysis allowed the identification of the first person with it, a guy called Giovanni Pomarelli in the 1700s)
The myostatin mutation in the German "super-baby" : http://www.nbcnews.com/id/5278028/ns/health-genetics/t/genetic-mutationturns-tot-superboy/#.WLkojjvyuUk
The nylonase mutations : https://en.wikipedia.org/wiki/Nylon-eating_bacteria
Antibiotic resistance in the bacteria Mycobacterium Smegmatis : https://www.sciencedaily.com/releases/2017/02/170221110808.htm
(this article looks at specific mutations) (FIRST EDIT: turns out that like the Lenski experiment it involves actually looking at the bacteria as they evolve the traits and looking at exactly what happens step-by-step. Awesome !!)
SECOND EDIT
Another example gotten from a Google Scholar search for "beneficial mutations":
http://atvb.ahajournals.org/content/25/10/2143.short
Quote from the abstract: "The naturally occurring human lipoprotein lipase S447X variant (LPLS447X) exemplifies a gain-of function mutation with significant benefits including decreased plasma triglycerides (TG), increased high-density lipoprotein (HDL) cholesterol, and reduced risk of coronary artery disease."
(note this isn't the same as the Milano mutation, see also this article about the discovery of this mutation and its development as a medical therapy :
http://online.liebertpub.com/doi/abs/10.1089/hum.2013.063 )
And another study of antibiotic resitance-related mutations, in the pathogen Pseudomonas aeruginosa:
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000406

Please do not only drop in links, write an answer that stands for itself and has the references for further reading.

@Chris the question was "Are there any cases where a beneficial mutation was documented" in the context of "I am trying to find a case/study where scientists documented a beneficial mutation in a human or animal", so I don't really see a better answer than "Yes there are, here are references to such studies/cases". I admittedly didn't have the "Yes" part, so I hope adding it was sufficient:


text:
Why are my assay absorbance values very low?
I am culturing SH-SY5Y cells in 96-well plates at a seeding density of $1.2 \times 10^5$ cells/mL. I differentiate the cells with retinoic acid for 6 days before giving them treatments. The cells look okay under microscope after the treatment. However, every time I read the plates, I get absorbance values of less than 0.2 (including my control).
I have tried increasing the volume of MTT reagent (5mg/mL), increasing the incubation time, but in vain.
Increasing the cell density indeed increase the absorbance, but the outcome seems illogical. A seeding density of $2 \times 10^6$ cells/mL gives absorbance values of 0.4+ (less than 0.5).
I am pipetting the mtt reagent and media out one-well-by-one-well using a micropipette. Assuming no pipetting errors and loss of cells, what are the possible causes of getting these low absorbance values?


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VCF files - examples for haploid organisms
I am trying to self-learn some aspects of bioinformatics (coming from a stats background), and i am trying to find / download some VCF files for haploid organisms as an input to some statistical analyses. I have seen a few sites where one can download example VCF files for human populations, but there are any sites where i can download some example haploid VCF files from e.g. bacteria as well? I have tried to look at http://bacteria.ensembl.org/info/website/ftp/index.html - but i was not successful yet. That said, as a newbie, i might very much be looking in the wrong location.


text:
Minor differences in morphology of a snake: Why designate it a different species?
I was motivated to ask based on an answer to another question that I read on SE-Biology:

You can differentiate this species [Ashok's Bronzeback (Dendrelaphis
  ashoki)] from closely related D. girii based on it having a longer
  "postocular" black line than D. ashoki -- in D. ashoki it stops
  shortly caudal to the eye...

When the differences are so minor (e.g. "longer "postocular" black line") what's the reason for designating them as two different species?
Is there a objective reason when to call them different species? Would those two not interbreed?
Note: I'm not just asking "If they interbreed why is it a different species?"
I'm more in the vein of asking: "If two species so similar are still different species why are they different? Is there an objective metric to draw the line at which point we differentiate as different species."
Edit:
I've asked a related question over here:
Can Eskimos be regarded a distinct species from Kalahari Bushmen based on morphological differences & geographic isolation?

While it is not obvious from the title of the other post, your question is possibly a duplicate of How could humans have interbred with Neanderthals if we're a different species?.

@Remi.b I disagree. That question asks specifically about how interbreeding could take place between 2 species. This question is focused differently and asks why differentiate two species that look so similar.Though your own answer from the other question could fill in the OP immensely about the concept of a species, I still think more specifics could be said about this instance.

@theforestecologist Fair enough! There are two questions though; 1) what's the reason for designating them as two different species? 2) I'm more in the vein of asking: "If two species so similar are still different species why are they different? Is there an objective metric to draw the line at which point we differentiate as different species.". IMO, the second question is a duplicate, the first question is not. If you agree, I let you edit the question to narrow it down to a single question.

Remi.b Yup, I agree. But I encourage @curious_cat to edit the question on their own in a way that narrows it down appropriately but still satisfies their original curiosity.

@Remi.b I feel like your answer to that question is comprehensive enough to apply to this question, but the questions themselves don't really seem to be duplicates - I'm not sure what the agreed SE meta is in that situation. I feel like the title of this question conveys a broader curiosity so it has some value beyond the value of the Neanderthal question.

Short explanation
According to the papers I could find, Dendrelaphis ashoki and D. girii aren't as closely related as you suggest: D. ashoki appears to be closely related to D. pictus, a Southeast Asian snake species, while D. girii appears to be closely related to D. bifrenalis, a Sri Lankan/South Indian snake species. They were distinguished from their sister species largely on the basis of morphological differences and geographical isolation.
How do we know D. ashoki is a distinct species?
The key to this answer is in Vogel and van Rooijen, 2011a, the scientific article in which Dendrelaphis ashoki was first described. Before their work, these snakes were thought to belong to the species Dendrelaphis pictus. To test whether this was in fact the case, they compared 9 individuals of D. ashoki with 34 individuals of D. pictus, and found statistically significant ($p < 0.05$) differences in five morphological characters: SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal diameter of the eye), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent). Here's the statistical analyses they ran:

The south Indian form that has previously been referred to as D. pictus (e.g., Wall, 1921; Smith, 1943; Whitaker and Captain, 2004) differs from Indochinese D. pictus in the characters SUBC ($F_{1,25} = 17.7, P = 0.0003$), TAIL ($F_{1,25} = 30.0, P = 0.00003$), EYED ($F_{1,35} = 22.5, P = 0.00003$), SUBL (Mann-Whitney U, $Z = −4.6, N=40, P < 0.00001$) and STRIPE1 ($\chi^2_1 = 42, P < 0.00001$).

They also compared the 9 individuals of D. ashoki with 48 individuals of D. proarchos, and found statistically significant ($p < 0.05$) differences in five morphological characters: VENT (number of ventrals), SUBC (number of subcaudals), TAIL (tail-length), EYED (horizontal eye diameter), SUBL (number of infralabials touched by the first sublabial, left and right added) and STRIPE1 (ventrolateral stripe bright/dull/absent).

[The south Indian form] differs from D. proarchos in VENT ($F_{1,49} = 24.1, P = 0.00001$), SUBC ($F_{1,28} = 13.7, P=0.001$), TAIL ($F_{1,28} = 40.1, P < 0.00001$), EYED ($F_{1,47} = 16.8, P=0.0001$), SUBL (Mann-Whitney U, $Z = −4.7, N=52, P < 0.00001$), and STRIPE1 ($\chi^2_1 = 53.0, P < 0.00001$).

The authors didn't rely just on morphological evidence: they note that D. ashoki, which is found in the Western Ghats, is also geographically isolated from other populations of D. pictus, which are found in Northeast India, Myanmar and South East Asia. Therefore, they concluded (emphasis mine):

The distinct morphology and coloration as well as strong geographic isolation of the population from the Western Ghats imply a unique evolutionary history that does not allow application of either the name D. pictus or the name D. proarchos. Consequently, we describe this form, previously referred to as D. pictus, as a new species, D. ashoki sp. nov., endemic to the Western Ghats.

How do we know that D. girii is a distinct species?
For this information, we need to look up another paper published that same year,  Vogel and van Rooijen, 2011b. Interestingly, the authors don't compare this snake with D. ashoki at all, but with Dendrelaphis bifrenalis:

Due to their double loreal shield, D. girii sp. nov. and D. bifrenalis occupy a unique position within the genus. A congeneric species with a double loreal shield has been described in the past, namely Dendrelaphis biloreatus (Wall, 1908). However, the presence of a double loreal in D. biloreatus appears to be based either on an anomalous specimen or on a misjudgement (Vogel & Van Rooijen, 2011b). Furthermore, D. biloreatus differs from D. girii sp. nov. and D. bifrenalis in its number of dorsal scale rows (13) and its number of ventral scales (190-199).
There are several differences between Dendrelaphis girii sp. nov and D. bifrenalis. The most obvious one is the light ventrolateral line, which is present in D. bifrenalis and missing or very faint in
  Dendrelaphis girii sp. nov. (see Fig. 3, 4).
The postocular stripe is much broader in D. bifrenalis. In D. bifrenalis there are black oblique bars in the neck region of some, but not all specimens (8 specimens out of 12 in our data) (see Fig. 3-5). This pattern is not sex related. It is absent in D. girii sp. nov. For Dendrelaphis girii sp. nov. we had only 1 male, so it is not possible to compare the sexual dimorphism in this character. The snout of Dendrelaphis girii sp. nov. is much broader than that of D. bifrenalis. Dendrelaphis girii sp. nov. has, on average, fewer subcaudals and more ventrals than D. bifrenalis, but the ranges broadly overlap.

Thanks Gaurav. But to play the devils advocate suppose I analyzed 9 individuals of the Eskimo tribe and another 34 belonging to the Kalahari bushmen I'm sure we could find a statistically significant morphological difference in at least five characteristics. e.g. Hair Color, Eye Color, Heights etc. Would that make the bushmen a distinct species from the Eskimos? Why not? Also, we wouldn't be relying on purely morphological evidence. The Eskimos are found in regions of the world geographically isolated from the parts where the Bushmen are found.

Even shorter, if perhaps overly cynical, explanation: if you've discovered a new species (or can 'split' an existing species), you can get a paper published.  Might even get grants if your new species are now rare enough to be considered endangered.

@jamesqf Actually, that's exactly the sort of explanation my reading is pointing to. But I just want to get other perspectives on things. Maybe I (and you) are overly cynical & we are missing something? I am no expert on this.

I've asked a related question here: http://biology.stackexchange.com/questions/56945/can-eskimos-be-regarded-a-distinct-species-from-kalahari-bushmen-based-on-morph?noredirect=1&lq=1

@curious_cat You could, but "Eskimos" (e.g. the Iñupiat) have only been separated from the Bushmen (San people) for around 15,000 years; D. bifrenalis and D. pictus are different enough that several species can be found in between, and are likely separated by millions of years of evolution -- so in some way these 5/6 snake characters are more revealing of evolutionary-scale patterns than human populations. IF that is your ultimate goal.

@Gaurav OK, that's useful to know. So if I interpret your argument correctly, mere morphological differences don't matter as much but the time period of separation on an evolutionary scale?

@Gaurav  Out of curiosity, if Eskimos vs Bushmen were separate for "only" 15,000 years; how many years have the Dendrelaphis ashoki vs D. girii been separated? Any idea? To get a relative comparison.

@curious_cat Yep, morphology is a way of getting at evolutionary relationships, which most (but not all) taxonomists agree is the best way to name taxa. But taxonomists often differ on where to draw the line (http://markscherz.tumblr.com/post/85470834478/a-not-so-brief-lesson-on-species-and-species has a nice diagram about that), and of course the line might move: other taxonomists might show that Vogel and van Rooijen about one or both of the species we discussed, in which case those species might be merged with others.

@curious_cat The closest I can find is http://www.sciencedirect.com/science/article/pii/S1055790315003127, which -- if I'm reading Supplementary Fig. S3 correctly, which I may not be -- suggests that Dendrelaphis bifrenalis and Dendrelaphis caudolineolatus shared a common ancestor 18.52 million years ago.


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Why are there still useless traits/mutations in our body
Why is it that through decades of evolution , some seemingly useless body traits such as earlobes and pubic/chest hair still remains while other traits are generally replaced through evolution?

Natural selection "selects" the trait that is less advantageous and removes/ reduces its frequency. It is like a filter paper. All solids are filtered out of mixture while clear liquid is collected. So if there is a difference in fitness of organisms by variations in traits, then only they are SELECTIVELY removed. Now, if a person without an earlobe would have had an increase in fitness, it would have had eliminated over time. And it might (I said might) be that there IS some pressure but it might be so slow that we can not realise it. But in case of earlobes, evolution will be evident in the case of elephants and Jackrabbits.


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How should the interval between serial dilutions be expressed?
The interval between simple dilutions is a constant value added to the preceding dilution to get the next. How should a factor for serial dilutions be mentioned? As there is no common difference between successive serial dilutions, rather a common ratio.

That depends strongly on your experimental needs. Sometimes 1:10 between two steps is necessary, sometimes 1:100 fits better.

I apologise, but I actually meant to ask how would you mention the interval. Like, interval for a simple dilution is 2% so how would the interval be stated for a serial dilution with concentration reduction by 1/10th every successive dilution?


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How can I get the coding region from gene sequences?
So, I have a file with 600+ sequences of a gene, each one from a different population. This file was obtained after blasting the chromosome sequences against the gene sequence. However, I need the coding regions as well. Should I do the same and blast the chromosomes against the exons, or should I blast the gene sequences against the exons?

Just to be clear, you want the coding region, not the mRNA transcript right?  if so swbarnes2 answer to use blastx should suffice

Not all the exonic sequence is coding. The ends have 3' and 5' UTRs.
Can you find gtfs for your organism?  Those would be easier to work with.
Or, I'd do blastx against the protein, that should pull out just the sequence that codes for protein.


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Different number of flaps in heart valves
Can anyone tell me why the different valves of heart have different number of flaps is it in any way related to evolution of homo sapiens.

This question has been asked before.. although still without an answer http://biology.stackexchange.com/questions/52276/evolutionary-explanation-of-the-bicuspid-on-the-left-and-tricuspid-on-the-right


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Can adenosine be cleared?
I've been thinking about this question for awhile, since reading this question: What causes adenosine build up in the brain when awake?
We know that a couple of things will block adenosine receptors: caffeine and hops. If you're overloaded with adenosine and it's early in the day, coffee (or other caffeine sources) make you feel alert by tricking your brain by blocking the adenosine receptors. The dubious downside is that when it finally quits blocking the receptors, you've got a much bigger load of adenosine. Which might not be a downside if it means you fall asleep more easily and deeply.
But what about just clearing the adenosine?

Adenosine breakdown / removal is usually handled by the enzyme Adenosine deaminase.

In order to do this you would need to find a compound that does all of the following:

Crosses the blood-brain barrier. Many pharmaceuticals are not able to do this.
Binds strongly to, or has some metabolic effect on adenosine. The resulting product must also cross the blood-brain barrier, and be excreted.
Not bind or react with other molecules that are similar to adenosine and cause side effects.
Not cause some sort of immune response - along with the blood-brain barrier issue, this rules out any sort of protein, and really limits the potential specificity for items (2) and (3): there simply isn't a lot of chemistry outside of biochemistry that is that specific.
Not cause systemic effects via depletion of adenosine and products of adenosine. There are several problems caused by a failure of the enzyme that metabolizes adenosine but it seems like most of the primary symptoms are due to an accumulation of adenosine rather than an absence of inosine, so I am not certain how much of a problem this would be.

And probably numerous other issues I haven't thought of yet. The point is, adenosine is a useful biological molecule, not just junk to get rid of, and developing something to "clear" just one specific compound is actually really complicated. If the main concern is the sleepiness caused by adenosine build-up, caffeine is widely available and relatively safe compared to some novel way of actually clearing adenosine.
In fact, I can't really think of many pharmaceuticals that work by actually "clearing" something, but feel free to leave any suggestions in the comments. Chelating agents come to mind, but those are only used in some very specific circumstances.

As @Bryan Krause pointed out before me, unless you can regulate adenosine signaling in a selective way any manipulation is probably going to cause important side-effects.
If your goal is to regulate adenosine signaling in a more specific way than caffeine, one way could be to selectively manipulate adenosine receptors of specific pathways. This approach was taken by Blundon et al. (2017) who used a compound that is able to cross the blood-brain barrier (FR194921) to selectively affect cortical map plasticity. It so happens that this compound selectively targets thalamocortical projections, so it could be a promising strategy. But even with such a selective approach side-effects cannot be excluded.

Full disclosure:
I have contributed a preview article for that study (Kehayas and Holtmaat 2017).

References
- Blundon, J. A., Roy, N. C., Teubner, B. J. W., Yu, J., Eom, T.-Y., Sample, K. J., … Zakharenko, S. S. (2017). Restoring auditory cortex plasticity in adult mice by restricting thalamic adenosine signaling. Science, 356(6345), 1352–1356. https://doi.org/10.1126/science.aaf4612
- Feldman, D. E., & Brecht, M. (2005). Map plasticity in somatosensory cortex. Science, 310(5749), 810–815. https://doi.org/10.1126/science.1115807
- Kehayas, V., & Holtmaat, A. (2017). Rejuvenating brain plasticity. Science, 356(6345), 1335–1336. https://doi.org/10.1126/science.aan8374


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Genetic Recombination and Mutation
Can genetic recombination yield mutation depending on the new DNA that is incorporated into the genome? I would say yes because when something foreign comes in, the genome is bound to not function properly.

Can you please try to clarify the question? My answer and @canadianer comment underneath shows that the question is a bit unclear.

When you say "new DNA that is incorporated into the genome", it suggests that you misunderstand what genetic recombination. You might to ensure you really understand this concept before going any further.
Mutation rate and recombination rate tend to covary throughout the genome (Lercher and Hurst 2002). So, yes processes leading to recombination events also tend to cause mutational events.

Recombination can be used to insert new DNA into a genome. For example: lambda phage or genetic engineering.

Sure, but that's not what most people think of when using the term genetic recombination and the OP did not comment on that.


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Oculus rift (or, what do other eye placements see?)
I could be WAY out of line in the placement of this question, but here goes:
Everyone I'm sure has heard of the Oculus Rift or any of the several other VR headsets making their way around.
It reminded me of a friend who, when in art school, said, "Dali's eyes were crooked [whatever the opposite of crossed is], and it may have helped him develop a different sense of perspective, and we have been taught to practice letting our eyes go relaxed to recreate similar effects."
I don't know if he did it, and I never saw a representation. But now I am interested...
If an Oculus used a model with eyes pointing different directions...or on the "sides of the head" with a wider field of view like many non-predatory animals...
What would we see?
(And maybe if it's an interesting answer... a VR Dali or VR cow simulator might be in order...)

Your question is not very clear. What exactly are you asking? Are you asking how our brains would process split imagery (i.e., VR with vision for one eye pointing one way and the image for the other eye pointing another way)??

I think the question is whether we can simulate for humans what we would see if our eyes were on the sides of our heads, as is found in many animals.

Yes to canadianer. A creature's sense of the world is certainly informed by the way it senses the world. Predators have eyes similar to ours, forward facing, focused, sharp. Many prey animals have eyes with wide fields of view, ostensibly for defensive purposes, sensing the most of what is around, if not in the tight focus of a predator. So, what might that look like for them, and us if simulated. It is one of those things that is hard to imagine because we have simply never experienced it. We focus tightly, not a wide field like a sentry. Like Dali, how would that affect perspective?

I might have to try this, since I have one and can program for it. Will report back if I get around to it.

It would probably be quite disorienting, maybe even make you sick.
There is a much more limited fun classroom demo that my institution uses with kids, where they wear goggles that shift their view a couple degrees to the left (this demo is quite common, you can find many examples on YouTube as well). They stand a couple meters from a wall and throw a ball at a target: inevitably, they miss wide right for the first few throws, but eventually they adapt and hit the target no problem; then when they remove the goggles, they miss again to the left.
So, your visual system can adapt to some shifts in visual field. However, if the view was very skewed, oriented for example like the eyes of cattle, on the sides of the head, it would be much more difficult to adapt to where it feels natural. I would expect the strategy people would use would be to attend to only one visual field or the other, since there is no longer any binocular area of vision, sort of like if you would look as far to the right as you possibly can you see a lot of visual space with only one eye.
An important element to immersive VR is that you feel like you are actually having the experience - in VR when you have some sort of joystick or controller to manipulate, for example, it is really helpful to orient people by allowing them to see the controller in virtual space. Providing the eyes with very unusual inputs is going to make it much harder to maintain the illusion.

Interesting... I wonder how this 'prism adaptation' (correct term?), would work if, instead of off a couple of degrees, each eye is straight ahead, instead of toward a focal point? That would approximate the 'Dali' example I mentioned. Or... if there was even a wider disparity so a view of, say, a cube, was rather cubist...like almost seeing the same face from two different perspectives?

@Mark The straight ahead situation you describe would be pretty hard to create, because the eyes themselves move. I suppose you could, with sufficiently responsive electronics, position the screen image such that the independent movements of the eyes are discarded. For the wider disparity, I am having a bit of trouble wrapping my head around that one but I suspect you would simply perceive things as being smaller and closer to you: disparity cues are one of the depth cues. There might be some confusion because other cues would be violated (like the expectations of particular object sizes).

@Mark For example consider the Wikipedia article on Binocular Disparity to think about what I said about disparity.

interesting. Thank you. Yeah, "having trouble wrapping [one's] head around" is exactly why I am curious. I wonder if, as a 'game' perhaps, one emulated a bovine perspective...if appropriate goals or feedback would increase immersion/minimize disorientation? Say, 'sensing'/detecting movement (of a predator), and responding or 'locating'? Or something similar that might function like holding a controller and having it on screen to orient oneself, something that pushes one to make 'functional' sense of the perspective...  Thanks!


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Can translation ever occur without transcription?
This question is aimed mainly towards viruses with ssRNA, is transcription required, for the +ve strand RNA? If so, why?

I thought I had commented on this, but apparently not. Please clarify what you mean by "is transcription required, for them?" What is "them"? The word "them" would seem to refer to viruses, but this alone makes no sense. Your title suggests you mean "the translation of their +ve-strand RNA". Please ammend, and I would suggest you delete the second part of your question because its premise would appear to be incorrect. "If so why?" would do.

I am assuming that the question is whether, in single-standed +ve RNA viruses, translation of plus-strand RNA can occur before transcription.
First, there are many different families of viruses, and there are bound to be counter-examples to whatever I say here. However, with that rider:

We generally refer to replication of RNA viruses by RNA-dependent RNA polymerase, rather than transcription. I am not aware of any RNA virus that has an RNA polymerase recognizing promotors and transcribing specific genes. These viruses tend to replicate in the cytoplasm and therefore do not have access to host RNA polymerase.
There has to be replication, and this tends to be conservative, rather than semi-conservative. By this I mean that when minus-strands are generated they act as templates for many plus-strands, which are needed for the virus particles.
In the case of picornaviruses, such as polio, translation can occur before replication. As is common with small RNA viruses, there is a single initiation site for translation — in the case of polio, a polyprotein is produced, which is subsequently cleaved into individual polypeptides. The diagram below is from the Wikipedia entry for poliovirus and is reproduced here under the Creative Commons license.

[Nidia H De Jesus (image and caption) - De Jesus NH (2007). "Epidemics to eradication: the modern history of poliomyelitis". Virol. J. 4: 70. DOI:10.1186/1743-422X-4-70. PMID 17623069.
The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent destabilization of the virus capsid (2). Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism (3). Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF) (5). Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI) (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation (7) or associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0 (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9).]


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Does Usnea (Old Mans Beard) have negative effects on the respiratory system?
Being a fungus does it have negative effects similar to that of mold, especially on the respiratory system?

According to the Institute for Traditional Medicine and the Gale Encyclopedia of Alternative Medicine:

Usnea (aka Songluo or "Old Man's Beard") is a fruiticose lichen (a type of symbiosis containing a fungus).

Used in traditional medicine worldwide, including historically in China, Europe and by native Americans, as well as globally today.

"Uses": topical antiseptic; therapuetic agent; medicinal herb; anti-cancer

It has traditionally been used in the treatment of bronchitis, in the treatment of tuberculosis, to ease coughing, to cleanse lungs and as an expectorant (i.e, to resolve phlegm).

Contains a secondary metabolite, usnic acid, which is claimed to be an effective inhibitor of gram positive bacteria-including tuberculosis, staphylococcus, streptococcus, and pneumococcus

So Usnea is often used for the lungs. In fact, today, supporters of traditional medicine still use it rather regularly as an expectorant. I could find no sources that claimed that this was unsafe or had any negative effects on the respiratory system. I would think that if you were to inhale any usnea, its effects would simply rid your body of any particulates during expectoration.

However, a number of sources (e.g., see Sanchez
et al., 2006, here , here and here) mention that usneic acid can cause liver damage (and failure).

Disclaimer: I did not find any reputable source acknowledging usnea to be effective at treating any of the aforementioned ailments. Use at your own risk.

Citations

Sanchez, W.T., Maple, T.J., Burgart, L.J. & Kamath, P.S. (2006). Usnic acidhepatotoxicity. Mayo Clinic Proceedings 81: 541-544

Yes you're right that a lichen is a symbiosis of fungi and algae (or other photosynthesizing organisms such as cyanobacteria). But simply calling a lichen a fungus is like calling salt water salt.

To my knowledge a lichen is a fungus and an alga living in a symbiotic relationship. The answer is A+, thanks a lot

First off I accidentally deleted my first comment. It is this relationship that made me wonder if it is harmful in the first place.

I think the fact whether it can be used therapeutically doesn't mean it won't do harm. Also, while a bit of drug X (say digitalis extract) may be beneficial, a lot of it may kill you. So from a toxicological vantage point things are never either good or bad.

@AliceD Right. And just because I did not find any sources discussing "dangers" of using usnea, does not mean that none could exist. In fact, it could be that the expectoration I mentioned is due to irritation from the usnea and that long-term use could cause damage. Again, I found no sources discussing this in detail. However, I would think that general or irregular use would probably not be too harmful since usnea has been used for so long without any acknowledged negative impacts on the respiratory system. But as I said: USE AT YOUR OWN RISK.

This is not my area of expertise but Usnea appears to be a fairly well-known phytomedicine (Prateeksha et al. 2016).
However, the US Food and Drug Administration (FDA) had received a number of reports of liver toxicity related to the ingestion of dietary supplements that contain usnic acid derived from Usnea (Lei Guo et al. 2008). Upon this, usnic acid and Usnea barbata lichen were analysed by the National Toxicology Program (NTP) for their toxicity.
The report issued as a nomination background does not mention any known negative impacts on the respiratory system.

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


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Database of time lapse stem cell differentiation
Currently I am working on a project about modelling the social behaviours of embryonic stem cells (or induced pluripotent stem cells). I need a series of time-lapse live cell images which recording the stem cells behaviours in cell culture, also with markers showing the differentiation state of each cell. I wonder is there public resources of this kind of data?


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How do migrating birds know where to migrate?
Migrating birds return to the same spot, year after year. These locations are often thousands of kilometers apart. How do the birds know where to fly to?
So far I have found that the birds tend to follow a leader. Like Canadian Geese flying after one bird in a V shape. It seems that this leader is the one who 'knows' where to fly, but how?

Some material in your mother language, I hope: https://de.wikipedia.org/wiki/Vogelzug#Orientierung

This may also help/interest you: https://www.ted.com/talks/jim_al_khalili_how_quantum_biology_might_explain_life_s_biggest_questions

Why do birds migrate?
The primary reasons for why birds migrate are food availability and nesting locations. There are many other factors that can also play a role in why a bird migrates; too name a few, it includes responses to weather patterns, geography, and day length.
Since you use Canadian Geese as an example, I’ll use North America as the example region. There are over 650 migratory birds in North America and many scientists are studying individual species and learning that different factors have a variety of importance when it comes to migration. Generally birds can be classified into residents (non-migratory), short-distances migrants and long-distance migrants.
Residents are able to find food year-round and there is no need to migrate. Short-distance migrants tend to respond to food and weather. Long-distance migrants are more complex, but it is thought that response to day length and hormonal changes are important influences in their decision to migrate.
Now how do birds know where to go?
The most important factor is genetic predisposition, which can be composed of many variables such as moult, reproduction, and physiology (Liedvogel et. al., 2011). Just because there is a leading Canada goose, doesn’t mean the others don’t know where they are going. They can all have the same genetic factors affecting their decisions. There also can be cases where a young Canada Goose, doesn’t know where he is going, but he joins the V-formation and learns where to go from others in which he can then pass this knowledge on to future generations (I’m just using Canada Goose as an example for birds in general).
Navigation cues can also play a role such as geography, suitable habitat, landmarks, sun position and earth’s magnetic field. Geography can play a role in migration by acting as a barrier or a funnel, in North America, migratory birds can be limited as to where they travel. For example, they will not cross the Rocky Mountains or Atlantic Ocean. Suitable habitat also plays a role, for example North America has a variety of habitats, but to classify them simply there are: deserts, plains/ prairies, deciduous forests, boreal forests and mixed forests. The bird in question will be looking for these locations to nest or spend its winter. Many birds exhibit a step-wise migration where they stop at sites along their route to feed and regain strength and these areas are frequented annually.
As you can see, there are many answers to why a bird migrates which can create even more questions and led to many different explanations. Here's a website with a nice summary and a good starting point to learning about migratory behaviour that could help you understand further.
Reference:
Liedvogel, M., Åkesson, S., & Bensch, S. (2011). The genetics of migration on the move. Trends in ecology & evolution, 26(11), 561-569.

This is a good answer as to why birds migrate but my question is how they know where to fly.

The answer does explain how they navigate, but not in a definitive way. There is no definitive answer; many factors can play a role in a bird’s decision on where to go, whether it is genetic or learned behaviour and this will vary depending on the bird studied. As explained in the answer, it could be geography (acting as a barrier, directing them), sun position (giving them cues of where they need to be at that time of year), earth’s magnetic field, areas of suitable habitat (during step-wise migration) and landmarks.

Perhaps there's something that can be added... when a bird (or flock, or whatever) decides to migrate... how do they know to go south for the winter? In flocks, I can see it being a learned behavior where the young follow the older birds... but in solitary birds, how do they know not to go north (or east or west) when food becomes scarce and the climate gets cold?

The question of how birds know where to migrate to as distinct from the navigational question of how they manage to find their way, is a puzzle that has fascinated me for forty years since Stephen Emlen's experiments with Indigo Buntings in the 1960s.
I recall reading at around that time ( but my memory is not good enough to wiote a source) that even buntings that had been raised in isolation still displayed the same migratory patterns indicating that this was not learned behaviour but instinctual.  This suggests that there is some genetic mechanism by which 'memory' of where to migrate to is passed down the generations.


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Why is insulin given in type 2 diabetes?

For this reason "insulin insensitivity", or a decrease in insulin receptor signaling, leads to diabetes mellitus type 2 – the cells are unable to take up glucose, and the result is hyperglycemia (an increase in circulating glucose), and all the sequelae that result from diabetes $^{(1)}$

Also

Type 2 diabetes is due to insufficient insulin production from beta cells in the setting of insulin resistance. $^{(2)}$

So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors? Isn't it illogical to give more of insulin for a deficit amount of receptors? So, what is the logic behind giving insulin?

Not all type-2 diabetics receive insulin. It depends on their HbA1C level in the beginning of treatment. See 2017 guidelines from the American Association of Clinical Endocrinologists and American College of Endocrinology.

Can you add reference for the two quotes in the question?

Isn't it illogical to give more of insulin for a deficit amount of receptors?
Seems like there is some confusion in the definition of type-2 DM itself. According to the American Diabetes Association:

If you have type 2 diabetes your body does not use insulin properly. This is called insulin resistance. At first, your pancreas makes extra insulin to make up for it. But, over time it isn't able to keep up and can't make enough insulin to keep your blood glucose at normal levels.

So the problem in type-1 DM and type-2 DM is quite same; both because of less insulin present than required, the difference being that in type-2 DM the cells need more insulin than normal. And that apparent deficiency of insulin is overcome by insulin injections. Also, the definition you cite doesn't say receptor deficiency anywhere, it just says decrease in receptor's response to insulin.
So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors?
This is not quite possible yet. Increasing the number of receptors means increasing the gene expression for that receptor, something that is called 'upregulation'. Now, just to add, the cause of type-2 DM has been regarded to be downregulation of insulin receptors on cell surface by high concentration of insulin. See this article:

The process of downregulation occurs when there are elevated levels of the hormone insulin in the blood. When insulin binds to its receptors on the surface of a cell, the hormone receptor complex undergoes endocytosis and is subsequently attacked by intracellular lysosomal enzymes. The internalization of the insulin molecules provides a pathway for degradation of the hormone as well as for regulation of the number of sites that are available for binding on the cell surface. At high plasma concentrations, the number of surface receptors for insulin is gradually reduced by the accelerated rate of receptor internalization and degradation brought about by increased hormonal binding. The rate of synthesis of new receptors within the endoplasmic reticulum and their insertion in the plasma membrane do not keep pace with their rate of destruction. Over time, this self-induced loss of target cell receptors for insulin reduces the target cell's sensitivity to the elevated hormone concentration.

Now, coming back to the main point, it is not yet possible to inject transcription factors in every cell of body so that more and more receptors can be produced. It is possible in vitro, but not in vivo yet. However, it is possible to inject something else instead of insulin which might have similar effects on the body, something known as insulin agonist. Researchers are already trying to create insulin agonists, but haven't achieved much success. See this paper for example, in which they talk about a peptide S961. The problem here is that most of the molecules synthesized act as both agonist and antagonist based on different concentrations. That is why this field has not seen much success.
EDIT: As mentioned by @Don_S in comments, some drugs reportedly do increase insulin sensitivity and number of receptors in cells. Though they have indirect mechanisms for this, unlike insulin itself, but this works too (at least in vitro). One of them, thiazolidinediones, activates a nuclear receptor PPAR $\gamma$, which in turn increases transcription of proteins involved in glucose and lipid metabolism and energy balance. Another drug, pioglitazone, works even in vivo and has been suggested to work by activating receptor kinases and thus increase insulin sensitivity.
Thus, in future, it is very likely that type-2 DM patients would get prescriptions of such drugs instead of insulin injections, but not until there are more such drugs available and at an affordable cost.
References:

Type 2 — American Diabetes Association
Downregulation and upregulation — Wikipedia
Knudsen L, Hansen BF, Jensen P, Pedersen TÅ, Vestergaard K, Schäffer L, et al. (2012) Agonism and Antagonism at the Insulin Receptor. PLoS ONE 7(12): e51972. doi:10.1371/journal.pone.0051972
Hauner H. The mode of action of thiazolidinediones. Diabetes Metab. Res. Rev. 2002;18(Suppl. 2):S10–S15. doi: 10.1002/dmrr.249.
Kobayashi, M, Iwanishi, M, Egawa, K et al, Pioglitazone increases insulin sensitivity by activating kinase of insulin receptors. Diabetes. 1992;41:476–483.

Somewhere I have read that insulin induces more receptor formation.

@JM97 if it did so, then how would insulin resistance develop? Upregulation would mean increased sensitivity of cells towards insulin, but this quite the opposite of what happens.

then why do insulin overdose occurs?

I mean to say why then in patients with type 2 diabetes hypoglycaemia takes place when there is insulin overdose.

Thats the point with type 2 DM. Though pancreas are producing more and more insulin, body cells are just not able to respond to it & thus take up glucose from blood, due to which most of the glucose remains in blood and hyperglycemia occurs.

yes , but excess injection of insulin (exogenous) will lead to hypoglycaemia( in extreme cases may lead to death immediately) , which should not happen if the receptors are in same quantity on membrane.

OP: "So why don't we give people a medicine which just increases the number of receptors or increases the sensitivity of receptors?"

"This is not quite possible yet." Actually, it is. There is a group of anti-diabetic drugs called Thiazolidinediones which is said to increase the sensitivity of body cells to insulin. This rather old study (from when these drugs were new...) indicates that these drugs activate insulin receptor kinase. This is not glucose receptors upregulation, but it is an increase in the response to insulin.

Sorry, ran out of space, here's the link to this rather old study.

@Don_S thanks a ton for the references, added them in the answer :)

@JM97: insulin overdose causes hypoglycaemia because insulin's main function is to regulate blood sugar levels. Even if a patient is insulin resistant / has reduced number of receptors, sufficiently high levels of insulin will cause blood glucose levels to fall. This will be a higher amount than in a non-diabetic patient but it is still possible.

Why the downvote? Did I miss something or say anything wrong? Please add a comment so that I can improve my answer.

@Artelius it is possible, but its amount required for insulin resistant patients is quite high, mostly more than the capacity of pancreas.

This is true for the beginning of the disease. As a reaction to the reduced sensitivity of the cells in the body to insulin (and thus less uptake of glucose from the blood and a resulting hyperglycemia) the body produces more and more insulin to cope with this problem.
At some point the insulin producing beta cells cannot increase the production anymore and due to the insulin resistance this amount is not enough anymore. At this point insulin needs to be supplied to the body to ensure normal function and to combat hyperglycemia. See this figure for a schematic overview (from here):

For more details see this paper:

Defining and Characterizing the Progression of Type 2 Diabetes

Insulin is a "last resort" treatment for people with Type 2 diabetes—partly due to the unpleasantness of injections, but partly due to the fact that high insulin levels can worsen insulin resistance.
People with Type 2 diabetes are generally started on Metformin and/or advised on diet and exercise, and progress to other oral medication, before insulin is considered. However, the oral drugs can have significant side-effects, and since Type 2 diabetes is progressive, insulin can eventually become necessary.
That said, injected insulin carries the risk of hypoglycaemia (low blood sugar), and starting insulin treatment early, before pancreatic insulin production has been severely impacted, can help reduce this risk, as the pancreas can play more of a role in keeping blood sugars stable.
So, the simple answer is: insulin treatment is used because it works; reducing insulin resistance is preferable, but current drugs can only do this to a limited extent.

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


text:
Do animals get "unhealthily" fat in the wild?
Looking at a picture of a seriously fat cat, apparently directly nurtured by humans, popping up in a language learning app, I started wondering:
do animals "in the wild" (this might be ambiguous, but you can discuss it in your answer) get obese? If so: which animals and how fat? Under what conditions do they get fat?
To be more specific (following the advice of user theforestecologist):
Do they become unhealthily obese (i.e. so fat that it negatively impacts their survival)?

Yes. Hibernating mammals store fat for the winter so that they don't have to feed all winter long. Other animals eat more fatty foods to build up their own insulating fat in order to survive colder weather.

Perhaps, though, you mean to ask "do animals become unhealthily obese?" (i.e., so fat that it negatively impacts their survival). ??

@theforestecologist I have followed your advice in the OP now, thanks.

http://sciencenordic.com/can-wild-animals-become-overweight


text:
What would happen if you "rewired" your eyes with your nose?
The nose sends sensory input through transduction of chemicals in the air via the olfactory nerves/tracts to the primary olfactory cortex.
The eyes send sensory input through transduction of light via the optic nerve/tract to the visual cortex of the occipital lobe of the brain.
Although both senses receive different stimuli, they (like all of our senses) convert external stimuli to a nerve signal. Given that, it seems possible that one could "rewire" the brain so that sensory organs sent sensory signals to different parts of the brain.

For example, it seems possible that we could splice olfactory tracts to the optic chiasm to send signals to the visual cortex.

My question: If we rewired the cranial nerves so that our nose was connected to our visual cortex, what would we see??

(or what would happen if we rewired any of our major senses with a different processing center of the brain?)

@ theforestecologist Not an olfactory route but this is sending signals via tongue.

"Rewiring" the brain isn't quite that simple: simply splicing a nerve to another doesn't necessarily mean the axons of that nerve will then grow into area. I am unaware of any studies that cross these specific pathways but as I am writing this answer I see you have already updated your question to ask about other modalities! So, with that in mind...
Crossing Auditory and Visual Pathways
Some related experiments have been done with other modalities: the ones I am aware of involve the auditory and visual systems. Both auditory and visual information traveling to cortex mostly comes through two nuclei in the thalamus: the medial geniculate nucleus, MGN, for auditory information, and the lateral geniculate nucleus, LGN, for visual information.
These thalamic nuclei are adjacent to each other. In Angelucci et al 1998 and Sharma et al 2000, lesions were made to cause retinal projections to innervate the part of thalamus that usually processes auditory information (medial geniculate nucleus, MGN). (note: there are also a bunch of older experiments in rodents and ferrets besides these, I'm not going to do a comprehensive review of the literature here but you can find many relevant citations within those other papers).
Briefly, the technique is to damage both the LGN and the pathways that normally project to MGN. The result is that the retinal axons, which normally synapse in the LGN, will instead path to the MGN. Note that it is important to do this very early in development, such experiments would not work in an adult brain.
The result, in the papers I cited earlier, is that the part of cortex that normally responds to auditory information begins to respond to visual information, and develops a hallmark of visual cortical response properties: selectivity to the orientation of presented stimuli. Therefore, it seems like if you give an auditory cortical area visual information, it doesn't "try to process it as sound" but rather processes it just like the visual cortex would.
Effects on perception
It is hard to ask the ferrets what their actual perceptions are, but the best guess is that perceptions are built by what we put into the system: there is no way for an area that receives anything but visual input to interpret that information as anything other than visual input. There is no context to interpret it any other way. Cortex develops and responds based on the information it is given. In the animals in these experiments, their auditory systems have been lesioned so there is really no way they could interpret the stimuli they "see" as "sounding like" something.
Similarly, if you send olfactory information to visual cortex, you will process smells in visual cortex. Olfactory processing is a bit different than the other modalities, so depending on where you took this information from things may not develop properly, but that gets into a lot of speculation that is beyond this .SE site.
Crossmodal plasticity in blind individuals
There are some experiments in humans that also look at this type of cortical plasticity. Probably the best ones are those in blind individuals. Again, I won't review the entire literature, but can give some examples: Cohen et al showed tactile representations in the visual cortex of blind individuals, such as when they are reading Braille. Bedny et al, 2015 show that, especially in children who are blind, the visual areas of the brain respond strongly to information from other modalities, especially spoken language. Again, these individuals are not "seeing" these stimuli, beyond the type of "seeing" that you can do when you reconstruct a scene with your eyes closed (if they were at one point sighted). Rather, part of their brain that would normally be used for vision is now being used for other tasks.
Effects on olfaction haven't been studied as often, but in Kupers et al, blind individuals were shown to have olfactory responses in brain areas that don't show olfactory responses in sighted individuals, including areas that usually process vision.

References:
Angelucci, A., Clascá, F., & Sur, M. (1998). Brainstem inputs to the ferret medial geniculate nucleus and the effect of early deafferentation on novel retinal projections to the auditory thalamus. The Journal of comparative neurology, 400(3), 417-439.
Bedny, M., Richardson, H., & Saxe, R. (2015). “Visual” cortex responds to spoken language in blind children. Journal of Neuroscience, 35(33), 11674-11681.
Cohen, L. G., Celnik, P., Pascual-Leone, A., Corwell, B., Faiz, L., Dambrosia, J., ... & Hallett, M. (1997). Functional relevance of cross-modal plasticity in blind humans. Nature, 389(6647), 180-183.
Kupers, R., Beaulieu-Lefebvre, M., Schneider, F. C., Kassuba, T., Paulson, O. B., Siebner, H. R., & Ptito, M. (2011). Neural correlates of olfactory processing in congenital blindness. Neuropsychologia, 49(7), 2037-2044.
Sharma, J., Angelucci, A., & Sur, M. (2000). Induction of visual orientation modules in auditory cortex. Nature, 404(6780), 841-847.


text:
Confused about the calculation of BLOSUM matrix
I am trying to understand how the BLOSUM matrix is calculated.
I found a very nice tutorial here: http://www.cs.columbia.edu/4761/assignments/assignment1/reference1.pdf
Also i read through the wikipedia article, and a book "Understanding bioinformatics" from Marketa Zvelebim and Jeremy O. Baum
After i thought i understand the method i tried myself with this "alignment" (i will refer to the variable as they are at the link i provided)
Q
Q
S

So it has only one column, and 2 type of amino acids.
The Count pair frequencies (C) for Q -> Q substitution is 1 (2*1/2) and for Q -> S it should be 2 (2*1).
To normalise it T = 3 as 3*2/2
The q values then seem to be q(Q->Q) = 1/3, q(Q->S) = 2/3
The p(Q) is then 1/3 + 2/3/2 = 4/6
p(S) is 2/3+1/3/2 = 2/6
The e(Q->Q) = (4/6)^2 = 4/9
e(Q->S) = 4/6*2/6*2 = 4/9
Thus
S(Q->Q) = round(log2((1/3)/(4/9)) = -1
S(Q->S) = round(log2((2/3)/(4/9)) = 1
So from this alignment it is more likely to substitute a Q to an S rather then Q to Q? This makes no sense for me.
What am i missing?

Ok I'll try to go through it myself and see what happens.
First, we get the pair counts: $$ c_{ij}=\begin{cases} \displaystyle\binom{n_i}{2} & i=j\\ n_i n_j & i\ne j \end{cases} \;\;\;\;\;\implies\;\;\;\;\; c_{11}=1, c_{12}=2, c_{22}=0 $$ Clearly, the normalizer is just $T=\sum_{i\geq j} c_{ij}=3$ and $c_{ij}\equiv c_{ij}^{(1)}$ since there's only one column. Then our pair distribution is: $$ q_{ij} = \frac{c_{ij}}{T} \;\;\;\;\;\implies\;\;\;\;\; q_{11}=\frac{1}{3},\;q_{12}=\frac{2}{3},\; q_{22}= 0  $$
Hence, the occurrence probability per residue: $$ p_i = q_{ii} + \sum_{i\ne j} \frac{q_{ij}}{2} \;\;\;\;\;\implies\;\;\;\;\; p_1 = \frac{2}{3},\;p_2=\frac{1}{3} $$
and the expected pair frequency:
$$ e_{ij} = \begin{cases} p_i^2 & i=j\\ 2p_ip_j & i\ne j \end{cases}\;\;\;\;\;\implies\;\;\;\;\; e_{11}=e_{12}=\frac{4}{9},\; e_{22}=\frac{1}{9} $$
Now we can finally compute the odds ratios:
$$ r_{ij} = \frac{q_{ij}}{e_{ij}} \;\;\;\;\;\implies\;\;\;\;\; r_{11}=\frac{3}{4},\; r_{12}=\frac{3}{2}, r_{22}=0 $$
Computing the log-odds $s_{ij} = \log_2( r_{ij} )$ gives the same values as you get.
So why is $r_{11} > r_{12}$? Well, notice they have the same normalizer, i.e. $e_{11}=e_{12}$. So the difference comes from the fact that $ q_{11} > q_{12} $, the empirical pair distribution. Essentially, because of the way we computed $q_{ij}$, we consider there to be only one pair QQ but two pairs of QS.
I would also note that sometimes results are a little unintuitive for very small samples (data sparsity throws off the statistics essentially).

Well I don't know whether this is right or wrong (I suspect right) but considering the irrelevant nonsense that gets up voted for other questions this surely deserves a +1.

This is what i thought, thabks for the confirmation!


text:
What's the difference between physical (direct) and functional (indirect) protein interaction?
I read that the Protein-Protein interactions one can consider are generally of two types, namely physical and functional, but I cannot get the difference between the two.
I was just thinking that if two proteins are linked in a Protein-Protein interaction network like the ones stored in STRING database, then they are experimentally observed or somehow predicted to physically interact through binding sites to explicitly perform a function, e.g. signal transduction. But as I am reading different sources making the separation between the two kinds of interactions I got a little bit puzzled.
Can you please help me?

What on earth is "I got the PPIs" supposed to  mean? And what is "a PPIN like STRING"? If you are going to post on this site you must take the trouble to define all acronyms (other than DNA etc) and express yourself clearly. Otherwise your question will be thown out as unclear.

PPIN: Protein-Protein Interaction Network,
STRING: one of the largest and more used database related to such networks. I'm sorry for the inconvenience, I thought the acronyms were known. Now the question should be more clear.

Thank you, but definitions belong in questions. Please edit your question.

Done, I hope now it's more understandable.

As I understand it, "physical" and "functional" are just two different ways of analyzing an interaction between proteins.
Proteins can and do interact physically, meaning they can bind in specific ways and sites, and this binding can produce changes in those same proteins (like conformational changes), which alter their properties. This is the purely physical analysis of the protein interaction. The functional analysis begins when we ask the questions "What is the role that this interaction performs in the cell/organism/living system?"; "What effects do these changes in the protein are going to create in the cell/organism/living system?". Often a conformational change in a protein induced by an interaction with another activates or inactivates it. In other words, an interaction can create a conformational change that enables (activation) or disables (inactivation) the protein to catalyze a given reaction, and so the referred interaction plays an important function in regulating the protein's activity. For instance, phagocytes (cells capable of phagocytosis) have in their membranes proteins capable of physically interacting with proteins present in pathogens membranes. They physically bind to them, changing their conformation in the process. This is the physical part of the interaction, it is what happens purely physically (and can be studied more deeply). This conformational change will enable the protein to catalyze a series of reactions inside the phagocytic cell that will ultimately lead to the phagocytosis and destruction of the pathogen. This is the functional analysis of the interaction, it is understanding what is functionally achieved by the interaction, in this case enabling phagocytosis (and can be studied more deeply).


text:
How to get the file of a published phylogeny of a taxon
If an article has a published phylogeny, is it common to get the newick file with branch lengths from the authors? In order to do further research with the tree.

Look at the R script related to this article. rotl: an R package to interact with the Open Tree of Life data
http://onlinelibrary.wiley.com/doi/10.1111/2041-210X.12593/full
install.packages("rotl")
library(rotl)
studies <- studies_find_studies(property = "ot:focalCladeOTTTaxonName",
                                    value = "Caesalpinieae", exact = TRUE)
tree <- get_study_tree(study_id = studies[["study_ids"]][1],
                           tree_id = strsplit(studies[["tree_ids"]],", ")[[1]][1])

# Example 2
cat_studies <- studies_find_studies(property = "ot:focalCladeOTTTaxonName",
value = "Felidae", exact = TRUE)
cat_tree <- get_study_tree(study_id = cat_studies[["study_ids"]][1],
tree_id = cat_studies[["tree_ids"]][1])
cat_tree
##
## Phylogenetic tree with 38 tips and 37 internal nodes.
##
## Tip labels:
## Neofelis_nebulosa, Panthera_tigris, Panthera_uncia, Panthera_pardus, ...
##
## Rooted; includes branch lengths.

It is standard practice for authors to publish their trees on TreeBase for other people to use. They'll usually list the link in the supplementary material of the paper. Some journals made this a requirement for authors.

@Ferroao I'm not sure what you mean, most of the trees on TreeBase have branch lengths

I haven't seen much with branch lengths, as the ones i needed


text:
What is the term for awareness of or inclusion of real sounds within a dream?
I fell asleep while listening to a podcast, and I am sure I was dreaming but I could also still hear the podcast.
The podcast played an important role in the dream, I was searching for the source of the voice, wondering if others in the dream could hear the same voice. I started to feel a bit panicky and woke up as the podcast also happened to end. I rewound the show and confirmed that it was all there, exactly as I had heard in my dream!
I would like to read more about this type of experience, but I am having trouble finding the right words to search. Is there a name for this phenomenon? Is there anything that contributes to experiences like these? I know it wasn't lucid dreaming, because I wasn't aware of being asleep.

People are voting to close based on personal medical advice... I think that might be overinterpreting that rule a bit, but you could try to rewrite your question to ask about the more general phenomenon rather than your personal experience, that would be better. Incorporation of external stimuli into dreaming is a bit controversial, but you mentioned you have a baby, and disruptions of or lack of sleep can mess with sleep cycles. You aren't directly describing "lucid dreaming" but searching on that topic might interest you.

OK, thanks @BryanKrause! I'm not looking for "personal medical advice" since there's nothing wrong with me. But I've edited the question now!

And also no, it wasn't lucid dreaming, I wasn't aware of being asleep.

Yes that's what I figured, which is why I asked you to edit rather than voting to close. I know you weren't describing lucid dreaming, but I feel like that term is sometimes overused. In the literature you will probably find people talking about it as "influences of external stimuli on the content of dreams" or something similar. However, there is some disagreement on whether people are really conscious of the external stimuli or whether they are actually just waking up a bit. The rest of what you describe just sounds like normal dreaming.

I made some fairly substantial edits to pare down the personal story to the most relevant details which will hopefully encourage people to not vote to close or revert their votes. I'm not sure if there is a name for the phenomenon beyond the suggestions I gave to look into awareness/influence of external stimuli during dreams but maybe someone else will come along with a good answer.

@ZeroOne I've retracted my close vote after you edited.
Thanks. Also, in my personal opinion, I think your baby has very likely trained you to sleep more lightly making you more aware of your surroundings while sleeping.

This phenomenon - of incorporating the sounds we hear into our dreams - is very well known, and has been studied. Of all the senses, the one least likely to reach a level of consciousness during sleep is smell. It seems our olfactory systems are very suppressed during sleep, though one can smell within a dream. For the life of me, though, I can't remember the neurological name for this phenomenon.

I think I found a good expression : "sensory incorporation in dreams"
https://www.psychologytoday.com/blog/dream-factory/201409/sensory-incorporation-in-dreams
It doesn't seem reflected in a Google Scholar search however, and I don't find a consistent terminology in the papers that do seem to be about the subject. That article can be a good starting point though.
EDIT: other good one: "influence of external stimuli on dreams".
https://journals.ub.uni-heidelberg.de/index.php/IJoDR/article/view/15754

Thanks, I'm going to accept this one, as I feel like this one answers my revised question the best. The latter article is actually a good one: from it I found a link to a web forum dedicated to everything about dreaming, so I should get further information from the people over there. :)

My answer is going to be verily based on my experience and thinking, so don't take it for absolute.
When we are dreaming, at the level of the brain, sensual (meaning from senses) experience is being created by projection in the sensitive cortices (visual, auditive, somatic...) from other zones of the brain. In this way the brain is creating a sensitive environment and experience to the self, which, usually unaware that it is a dream, lives through it, making decisions, solving problems, having experiences, remembering and even learning.
In your case, it seems that, while you were dreaming (creating a sensory experience from the "inside"), you were also being sensually stimulated (meaning form the "outside", through a real sensitive organ - the ear). The input from your audition, though not enough to wake you up, still originated the corresponding projections in your auditive cortex, creating the matching experience of hearing the podcast and overlapping it with the experience that was being generated in the dream. This way, the sound of the podcast was incorporated in the experience created in the dream, affecting it in the process.
I tried to explain this in the most biological (neurological) way I could!

Please add some references to your answer.

A classic of the genre of incorporation of sensation occurred in an 1865 dream of psychologist Louis Alfred Maury that S. Freud recounts at p. 21 of the 3rd. edition (1913) in translation, of his "The Interpretation of Dreams".

He {Maury) was sick, and remained in bed; his mother sat beside
  him. He then dreamed of the reign of terror at the time of
  the Revolution. He took part in terrible scenes of murder.
  and finally he himself was summoned before the Tribunal.
  There he saw Robespierre, Marat, Fouquier-Tinville, and a1l
  the sorry heroes of that cruel epoch; he had to give an account
  of himself, and, after all sort of incidents which did not fix
  themselves in his memory. he was sentenced to death. Accompanied
  by an enormous crowd, he was led to the place of
  execution. He mounted the scaffold, the executioner tied him
  to the board, it tipped, and the knife of. the guillotine fell. He
  felt his head severed from the trunk, and awakened in terrible
  anxiety, only to find that the top piece of the bed. had fallen
  down, and had actually struck his cervical vertebra in the
  same manner as the knife of a guillotine.

There is suspicion that the dream report was a backwards reconstruction from the awakening realization by Maury that he had been struck by the bed-board. From REM awakening studies, it is known that dreams take about as long to act out in real time as they appear to in the dream, so it could not be that the fall of the bed-board triggered the dream.
I think such hallucinoid dreams are not little stories, but pithy statements about the dreamers life at the time. If the dream images/scenes are viewed as letter-analogues, designed to elicit words or phrase in the dream report, to know what meaning to apply to those words one would need to know the true context -- what was on the dreamers mind at the time. The only clue we have is that he was sick in bed and his mother was with him!! My guess at the true context of the words in Maury's dream report, as understood by the cipher method, is:

"What a pain in the neck!"

Whether this refers to his illness, or his mother looking after him, or something else, we cannot know at this distance. The board falling on his neck brought the dream to a particular focus. There are many equivalent ways that such frustration can be vented, so if not that idiom, then another would have appeared in the words of the dream report.
Ken Arenson

For my blog on the cipher method in modern, post-REM dream science, see:

dreamstheciphermethod.wordpress.com

Welcome to Biology SE! Could you edit your answer to make the link with the question more explicit? It is not clear to me that it really contains an answer to the OP. Also, be sure to include some reputable references for your claims to avoid downvotes or deletion of your answer.

Sure. The roots are old: Aristotle's "De somno et vigilia" says sleep and wakefulness result from our ability to feel and comprehend the stimuli of our environment.The questioner added to his original q. "I would like to read more about this type of experience".  Maury's dream is considered a classic of the type. Cipher method is also ancient. e.g. see my Blog, 2nd post - Aristandros used cipher method on a dream of Alexander the Great in 322 BCE. See my Blog post 13, Ella Sharpe 1937 "Dream Analysis: A practical handbook for psychoanalysts", gives a modern version named "Poetic Diction".

rolled back edits because they introduced errors (in addition to fixing some things). Generally, please avoid editing quotes, especially when you change the meaning "(after all sorts of incidents)" vs. "after all, sorts of incidents".