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Is there an evolutionary purpose to armpit perspiration?
Given that most Americans seem to do fine using anti-perspirant, it got me wondering: is there an evolutionary purpose to underarm perspiration?  I can't imagine it acts to attract the opposite sex.
Or is it just likely an unfortunate side effect of whole-body evaporative cooling via sweat?

some hidden hints: http://biology.stackexchange.com/questions/5217/what-is-the-armpit-hair-for

There may be an evolutionary purpose to underarm perspiration, as alluded to in the "hidden hint" link of @DevashishDas, and also hinted at by the answer by @Chris. The apocrine sweat glands of our armpits produce steroids. One group of steroids secreted by the axillary apocrine glands are sex pheromones.  Although we may not consciously notice the chemical odors of sex pheromones, they do likely affect our behaviors.
For example, Wedekind et al. showed that females showed distinct preferences for certain male odors. Women tended to prefer the odors of males that were genetically different at the major histocompatibility complex (MHC) loci, a group of genes associated with our immune response system. Greater genetic variation of MHC genes generally translates to greater ability to combat disease.  Females that select males that are genetically different at the MHC would produce offspring with greater genetic variability at the complex, and therefore more likely to have greater resistance to disease or ability to fight disease.
These results suggest that the pheromones secreted in underarm perspiration is a sexually selected trait in humans. If so, underarm perspiration would have an evolutionary (fitness) advantage.

First: Not everything what happens in biology is necessarily directly selected for. Sweating is of course selected for, so our body can maintain its normal body temperature in hot climates.
There is a difference between sweat glands under our armpits and for example on the forearm. Under our armpits we have the so called "apocrine sweat glands" while most of the rest of our body is covered with "eccrine sweat glands". They are not only different in size, but produce different types of sweat. Eccrine sweat glands produce sweat, that is made mostly of water and salt, while the apocrine sweat glands sweat contains additionally lipids, proteins and also steroids. Decomposition of the sweat by bacteria which live on our skin produces the typical sweaty odor. The sweat glands also differ in their activation (see here for more details), so can the apocrine glands be triggered by stress.
According to this source ("A short history of sweat gland biology") is roughly comparable, although the total numbers vary quite a lot between the single studies. Assuming that the amount of sweat is comparable, than another factor comes into play: The different evaporation from our arms and from under our armpits. The last form a kind of cavity where the sweat can not easily evaporate and will then stay. It might also play a role, that they can be activated by stress, which will happen in situations which are uncomfortable for us and make the situation worse.
A paper which also looks very interesting in this context (to which I unfortunately have no access) is: "The evolution of sweat glands."

Armpit sweat does not have a strong intrinsic odor. What you smell is the waste of the microorganisms which colonize your armpits. It is a similar mechanism responsible for foot odor and bad breath. All external bodily surfaces have particular microbes which prefer different areas. This also includes the intestinal, oral and nasal regions.
If you charted these microbes on our body, their colonies would read like a map of microbial nations. Different lipids, sugars, proteins on individuals promote different types of microbes and different metabolic pathways giving individuals different scents.
Our ability to perceive a wide range of microbial odors might have an evolutionary pressure given the importance of detecting microbes in spoiled food, etc. I hypothesize our ability to detect body odor is inherited from detecting microorganisms in general.
Surely as our olfactory sense has diminished over evolution, these microbial odors are being taken out of some ancient context.


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Fasting gastric pH versus normal gastric pH
I want to know if someone is fasting (no food or drink for a whole day) will they have a higher or lower pH than a person who is eating regularly? If so what is an estimate of both of those pH's in the stomach?

Here's a website that talks about related topics (if answerers want to investigate it; I don't know if it's reliable or not): https://typeset.io/questions/what-happens-to-gastric-acid-production-when-fasting-29ngnon0s5?ysclid=lvvkyeuf6z455041284

The stomach linings generally secrete gastric acid (HCl, KCl and NaCl) and the native pH of the stomach is around 2. The longer you fast, gastric acid levels keep increasing until it reaches around 1-1.5. The food that you eat increases the pH levels of your stomach because the acid reacts with the food while digestion. Depending upon the type of food you eat, the pH levels of your stomach vary, but it is generally around 4-5 (again it varies depending upon the type and amount of food there is in the stomach).

Do you know what goes wrong in heartburn? Clearly eating sometimes generates an excess of H+, which is treated by inhibiting proton pumps.

"The longer you fast, gastric acid levels keep increasing until it reaches around 1-1.5." do you have any references to back this up? I could find http://www.ncbi.nlm.nih.gov/pubmed/2395805 and    http://www.ncbi.nlm.nih.gov/pubmed/2070698 but those don't mention the levels changing when fasting for longer

@YviDe  (http://ncbi.nlm.nih.gov/pubmed/2395805 ) mentioned the median pH levels come back to nearly 1.7 within 2 hrs after meal. Another interesting article, mentioning stomach pH levels of modern humans to reach 1.5(with some other interesting facts). As I mentioned before, it is not that the pH will keep decreasing with longer fasting period. The initial secretion is high, when food reaches stomach, but based on existing acid levels, the secretion rate stabilizes down. Will post if I find any other relevant article.

@Jory here is an article on what happens in heartburn, but interestingly I found another article which mentions that heartburn is not always a resultant of acid reflux

@Grb okay, I thought with "the longer you fast" , you meant something more like 8 hours and over. The OP is asking about fasting a whole day after all.

@YviDe yes, the longer you fast, it can be thought of that the longer the stomach lining is exposed to high gastric acid levels, which becomes harmful afterwards (ulcer?). But, the increase in levels is fast and happens within few hours at the initial phase, I think.

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ATP yield of fermentation: study to cite?
Everywhere I find the ATP yields of respiratory and fermentative metabolism of glycolysis. While that of oxidative phosphorilation I could find in Stryer to cite one study where this was addressed (Hinkle 1991 observed 30 ATP/glucose) I cannot find a study where the 2 ATP/glucose was observed and the textbooks I've searched do not provide a citation.
Can anyone please provide a link or citation to a paper where the ATP yield of fermentation (regardless of process) was quantified/estimated?
Thanks

See discussion of this paper.

For glycolysis this is really not so much of an issue, because the ATP yield is fixed by stoichiometry. The early biochemistry work by Embden, Meyerhof, Parnas and other that mapped out the reaction mechanisms of the glycolytic pathway shows that you always obtain exactly 2 ATP per glucose; this is simply the stoichiometry of those reactions. There are a number of primary papers documenting these reaction mechanisms, but it's a large undertaking to go through all of it; the glycolysis chapter of Stryer's Biochemistry is a good summary I think. A brief review of the historical development is described in: "A Fresh View of Glycolysis and Glucokinase Regulation: History and Current Status".
For respiration it's very different, since there is no fixed stoichiometry for chemiosmosis --- the ATP yield depends on the proton gradient across the inner mitochondrial membrane, which in turn depends on a number of factors. So in this case ATP yield will differ between cell types and conditions, and must be measured experimentally.

Interesting paper with the historical background, nice to read.

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Database of Multicellular and Unicellular organisms?
I'm trying to annotate a list of organisms taken from NCBI for cellularity (unicellular or multicellular). Does any of you ever found a database with association between an organisms' name or taxa and whether it is unicellular or multicellular? Desirably, I would like to get information both on species level and on higher taxonomic level (phyla, classes, etc.), but any information on this is welcomed.
In case it matters, I'm using Perl to do this annotation.
Thanks in advance

I think this might be useful if you are also looking for domain level classification.It has all domain classification.   ftp://ftp.ncbi.nlm.nih.gov/pub/taxonomy/taxcat_readme.txt  File:taxcat.zip. Link:ftp://ftp.ncbi.nlm.nih.gov/pub/taxonomy/  .Thanks.

though that may be useful for refining and curating the taxonomy itself, it does not help with the main issue here: finding an association between uni/multicellularity and specific taxonomic groups.

More like a comment:
It doesn't seem that such a database exists, but I think it's relatively easy to create a list of multicellular taxa and the rest should be considered unicellular. Since you use ncbi taxonomy, you can easily get higher-level parent for any species, so there is no need to define cellularity for individual species.
The challenging groups would be different algal and fungal taxa, but there are some good reference books. You also have to decide, whether to introduce a separate category for colonial/coenobial/filamentous organisms.

Yep, that's the whole thing: even though in some cases you can define multicellulars from higher level taxa (e.g. Metazoa), the problem lies on Fungi and Algae where it's more difficult. I ended up doing this by hand. For Fungi I sometimes had to go to the family level to be able to distinguish these taxa.
It surprises me that no one has ever done this.
However, I understand that in many cases, having this type of separation relying on taxonomic classification is not the best...

Recently i came across this text file which has Kingdom,Phylum etc.              https://app.box.com/s/hsmvie7vgjdj1z3g0iuf

That also exists in NCBI and a bunch of other databases. My problem is not having an association between the several clades - and thus your answer does not answer my question. Please read my question again and, specifically, where I wrote "Does any of you ever found a database with association between an organisms' name or taxa and whether it is unicellular or multicellular?"

I answered only for this "Desirably, I would like to get information both on species level and on higher taxonomic level (phyla, classes, etc.), but any information on this is welcomed."


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Glycocylation or glycosylation?
I came across a few sources that refer to glycocylation. Is this the same as glycosylation?
See for instance page 237, or the abstract in this paper.
"glycocylation" - 1210 search results on google
"glycosylation" - 5.98m search results on google

Ever heard of typographical errors or mistranslation from languages where the consonant C is pronounced like an English S? At 1 in 6000, that is the conclusion I would have drawn.

Yes, glycocylation is same as glycosylation. You can check out following links which explain glycocylaion same as post translational modification named glycosylation.
https://www.semanticscholar.org/author/Haudhiya/93411308
https://grantome.com/grant/NIH/R01-DA004166-05
https://quizlet.com/137217422/lecture-10-a-biochem-final-flash-cards/
https://books.google.com/books?id=3RbT3cpdCc0C&pg=PA508&lpg=PA508&dq=glycocylation&source=bl&ots=qIwbK6-ZdP&sig=ACfU3U18W_rG0D53R67_fzAywtMXGye5NA&hl=en&sa=X&ved=2ahUKEwjKrvfJp_foAhW3knIEHWLVB8gQ6AEwFnoECGQQQw#v=onepage&q=glycocylation&f=false

None of these references, except maybe obscurely the quizlet, do much of anything to support the equivalence of the two words.  The abstracts of the first two just mention one of the words, and the full papers are in Indonesian or unavailable, respectively.

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Soil microbiology reference
I am after some good reference on Soil Microbe Ecology and Biology. I am a biophysicist, and have read the very gentle approach of "Life in the Soil" (James Nardi). Another book I have been recommended is "Soil Microorganisms and Higher Plants: The Classic Text on Living Soils" by Krasil'nikov. This I found very hard going and I was wondering if there was anything more modern on the same subject.

Unfortunately, looking for books tends to be very opinion-based, and thus is typically not a good match for this site.

what would a good site/platform be for this?

Research Gate  might be a good place to post a question like this. It might also help if you provided a little more context about your specific interests re: soil microbiology. It's a broad, interdisciplinary field that has many overlapping themes with agricultural applications, biotechnology, conservation, bioremediation, environmental toxicology, epidemiology and public health, theoretical ecology and evolution, and even astrobiology. It's good to build a broad knowledge base when starting to learn a new subject, but it can still help to narrow your focus just a bit.


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Where do flies go?
Where are flies attracted most? Apart from food odours, of course. Why do they seem to be attracted by hot and humid places? Do they prefer shades or light? Why do they tend to get inside very easily?

As far as getting inside, they are small, and they can get in through openings you don't notice, or just sneak in when you open the door.

It's more of a comment.


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Are there any examples of predators that ambush scavengers?
I'm specifically asking about animals that use a hunting strategy revolving around hanging around cadavers to attack animals attracted to the cadaver, or even leaving part of their catches out to lure scavengers.

Saltwater crocodiles in Australia are reputed to do this; storing meat under water and later eating the fish and crustaceans that are attracted.
Having trouble finding a good source for this.
Article from national news service below.
https://www.abc.net.au/science/articles/2004/01/15/2045125.htm
Feel free to add references if you can find them.


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Is it possible to have sleep paralysis while sleepwalking?
At least from a conceptual level, these two disorders don't conflict. The effect of sleep paralysis is being conscious while having the inability to consciously direct motor functions. Sleepwalking is the unconscious direction of motor functions. So combining the two, the effect would be that you are consciously aware of yourself and your surroundings while you are also unconsciously moving about, outside of your conscious control.
Therefore the only way the two wouldn't be possible together is if their activation conditions were mutually exclusive.
From wikipedia

Sleepwalking occurs during slow-wave sleep (N3) of non-rapid eye movement sleep (NREM sleep) cycles. It typically occurs within the first third of the night when slow-wave sleep is most prominent. Usually, it will occur once in a night, if at all.

https://en.wikipedia.org/wiki/Sleepwalking#Causes

The first of these stems from the understanding that sleep paralysis is a parasomnia resulting from dysfunctional overlap of the REM and waking stages of sleep.

https://en.wikipedia.org/wiki/Sleep_paralysis#Pathophysiology
So from a small amount of searching it seems it is not possible, unless SWS, REM, and the waking stages of sleep can all be overlapped.

Dissociative states are not the same as sleep paralysis, which means paralysis upon waking from sleep, not sleepwalking or combining it with other movement. There are a number of sleep disorders. You can't be paralyzed while walking. You can be sleepwalking. It might be something else.

While it is hard to completely rule out this convergence ever happening (perhaps cases haven't been reported), it is highly unlikely due to the specific stages of the ultradian sleep cycle at which sleep walking and sleep paralysis occur [Ref. 1]. Sleep walking during non-REM sleep would have to continue through the REM stage in order to see intrusion of sleep paralysis that occurs at the exit of REM to wake [Ref. 2].
A key feature of REM sleep is deep muscle atonia that paralyzes the body and prevents among other things one from acting out dreams [Ref .3]. Thus, if a person sleep walking were able to enter REM before returning to bed, the sleep walking / other unconscious motion itself would cease.
I do question your reasoning that the combination of these two parasomnias would result in being:

consciously aware of yourself and
  your surroundings while you are also unconsciously moving about,
  outside of your conscious control.

because the intrusion of sleep paralysis would in fact lead to muscle atonia and prevent one moving about. This is not to say that terrible things have not occurred where muscle atonia has failed while the subject remains asleep/unconscious; this falls under the fascinating category of REM-behavior disorders (where people act our their dreams - including violently hurting themselves and their partners), which judging by your question I think you will find interesting! [Ref. 4].
References:
[Ref. 1]: sleep stages
[Ref. 2]: sleep paralysis
[Ref. 3]: muscle atonia
[Ref. 4]: rem-behavior disorder


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Reverse complement of reconstruction model for assembling reads
One way to assemble fragments produced by DNA sequencing (often called reads) is to seek for the shortest common superstring that contains all the reads of a given set of reads. One model for this problem is the reconstruction model, which calculates the minimal edit distance between a possible superstring (that contains all fragments) and each one of the fragments. What I don't understand yet is the fact that when calculating the edit distance for a given fragment, it's necessary to calculate the edit distance for the reverse complement of that fragment. An example of a fragment and its reverse complement could be:
 ACTGTCC fragment
 TGACAGG complement (the complementary strand as we know)
 GGACAGT reverse complement
According to the book I'm reading the ideia behind it is to find a superstring as short as possible that either the given fragment or its reverse complement must be an approximate substring of the superstring. I know that many mathematical/computational models don't have a biological sense for their way of soluting a biological problem, but this recontruction model I could think it's biologically reasonable to find a string that contains all the fragments of a certain region of a DNA sequence, and all the complement fragments, after all when assembling we can find both strand sequence. But a reverse complement is not something that exist for a given sequence, unless it has suffered some kind of break-recombination event, which is something not expected, mainly when talking about conserved regions. Do you any idea why this model takes into account the reverse complements ? Thanks in advance.

Isn't this just a case of keeping everything straight with respect to 5'>3' direction? If a read matched "TGACAGG" this would not correspond to either strand of your example, because writing it like that implies that it is 5'-TGACAGG-3' unless it is made explicitly clear that it is the bottom strand of a duplex.

So you're saying that in fact the model see every fragment in 5'->3' direction? It doesn't consider the real existence of a reverse complement, but simply uses it because the reverse complement is a way of seeing the complementary strand of a given fragment with 5'3'direction? I'm sorry about the slow reasoning.

Yes, if you have a read (which will be by convention 5'>3') then you can search for it directly on the top strand of the target (also 5'>3'). If you need to look for it on the other strand of the target you can't simply search on the complementary because this is 3'>5', so you derive the reverse complement. It's just the equivalent of turning the dsDNA sequence (on the page) through 180 degrees.

Nice! Thank you very much, Alan. You helped me a lot.

"But a reverse complement is not something that exist for a given sequence, unless it has suffered some kind of break-recombination event" I am not sure that I understand what that means. Why wouldn't a reverse complement exist? If your DNA is double-stranded then it must exist!


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To what extent is immature eggs in insects (beetles) a good approximation for maximum fecundity?
To what extent is the number of immature eggs from dissected, newly emerged individuals a reasonable approximation for maximum/potential fecundity in insects (more specifically beetles)? I know that many species must feed for the eggs to become mature and viable. However, can a comparison between species on immature eggs still be used to capture the range of maximum fecundity between species or to accurately rank species from low---high fecundity?

There are a number of things to clarify here; Fecundity is the number of offspring that is produced by an individual, and this can be separated into potential fecundity (maximum reproductive capacity) and realized fecundity (number of offspring actually produced). Realized fecundity is very similar to fertility, which is defined as the number of viable offspring that are produced.
Potential fecundity can sometimes be a good proxy for future fertility, and this is especially true for species where all eggs are present after metamorphosis of the adult insect (Awmack & Leather, 2002). However, in some species the formation of eggs is a continuous process in adult individuals, and this is relatively common in beetles. Therefore, the number of immature eggs might be a poor proxy of both potential and realized fecundity in these species (Awmack & Leather, 2002), and this is more likely in relatively long-lived species that feed extensively as adults. In beetle species that do not feed as adults (often lacking functional mouthparts), immature eggs is probably a better approximation of potential fecundity.
It should also be mentioned that the quality of host plants will often affect the maturation of eggs (Sterns & Smith, 1960; Hopkins & Ekbom, 1999), and will therefore also determine to what extent the number of immature eggs is a good indication of potential fecundity. When feeding on poor quality hosts eggs may e.g. be reabsorbed by females to use for other purposes (see references in Awmack & Leather, 2002 & Hopkins & Ekbom, 1999 for further information).
The review paper by Awmack & Leather, 2002 is very comprehensive, and contains a wealth of useful references on this topic.


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Why are scabies mites not found everywhere on the host?
The distribution of scabies lesions is not uniform. Sarcoptes Scabiei mites have an apparent preference for some places on human bodies.
They obviously prefer soft places, where they can burrow easily, but that's not the whole truth. For example, they generally avoid the face, even though there is plenty of soft skin to use. They burrow between fingers, but not on fingertips. They also completely ignore the scalp.
What factors are in play here? What makes mites so picky?


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Can color-blind people see the effect of combining red, green, and blue light beams?
When combined, red, green, and blue light beams result in white light. This effect is observed by most of us, but can color-blind people also see this effect?

There are many kinds of colour blindless, and most kinds aren't black/white.

Remember the comments on your previous version of this question? Please include your research when posting.


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Calvin cycle question
Why does the 6-carbon molecule produced when Rubisco attaches a Co2 onto RUBP split into 2, 3 carbon molecules? Is it because its unstable or is there another reason?

Welcome to SE Biology. It is important that new users learn how this site works. First, finish the [Tour]. We know you haven't because you don't have the badge, and it can appear discourteous when posters don't do so. Second read the Help on asking questions where you will see that you should do research before posting. This includes searching the site to see if the question has already been answered, which yours has.

Does this answer your question? Why the C6 intermediate molecule in the Calvin cycle is so unstable


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Can you use calcein to stain milk somatic cells and observe them through a fluorescent microscope?
I am currently working on an image cytometer that could automatically count somatic cells in milk samples. Can I use Calcein (i.e., C30H26N2O13) to stain the somatic cells? If not, what dye can I use for fluorescent imaging?


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drug-dna concentration
I want to understand how you calculate the final concentration of a Drug-DNA complex. I tried to mix equal concentration and volume of drug and DNA to form a complex and tried to see the absorbance spectra using UV-VIS but saw very little peak for drug. I think I am doing something wrong to calculate the concentration.
Here is what I did.
I mixed 500uL of 20uM of DNA to 500ul of 20uM of drug. I expect to see a large absorbance peak but I see very small peak at the wavelength of that drug. My aim is to have a drug-DNA complex of 20 uM. Could anybody please explain to me how to calculate the final concentration. Any reference articles so that I can understand are greatly appreciated. Also, I want to understand the job plot where we can find the binding of the drug to DNA.

Your ratios assume 1:1 DNA:drug stoichiometry. Is that correct? What is the drug, and how is it expected to interact with DNA? Is it an intercalating agent? Is the DNA a single sequence of a fixed length or is it a mix of sequences of different lengths?

Thank you for your comment. I want to check the number of base pair ligand is interacting with. DNA is double sequence and of fixed length. The ligand intercalates with DNA. I want to know what the feasible way is to do it.


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Linearising plasmids for CRISPR experiment
I am currently designing a mock CRISPR knock-out experiment, and I’m wanting to insert a plasmid for selection. Using a restriction enzyme at 2750bp for cutting, would the location of the cut site then be considered position 1?
I’m wanting to run PCR after insertion to confirm it has been successfully transfected, and I have been supplied PCR primers - would these primer locations have to be shifted to fit in with the new linearised plasmid from location 1 at cut site?
E.g primer at location 3320 would now become location 570 after the plasmid was cut at 2750?
I’m very new to this!

No. Plasmids should generally be considered as a circular DNA rather than linear. However, no matter where you cut it, the positions don't change.
The position of the cut site is still the position on the plasmid at which the RE cuts. The numbering on plasmids is based on the position of a common restriction site, which depends a bit on which plasmid you are using. For pBR322 based plasmids, it is in the middle of an EcoRI site. This is because when plasmids were first discovered and used, we didn't have sequencing so the sequences were determined by restriction fragment mapping. Thus the start site was determined based on the position of a cut site in one of the restriction enzymes.
The positions of your primers are relative to the sequence you are inserting  - if you are using something like SP6/T7 from the plasmid, those are sites on the plasmid and would be noted as such at the relevant sites when publishing the sequence. If you are sequencing off sites internal to your insert, then you would add on the bases of the plasmid when reporting these sites. You can also report the bases position on the insert; as an example:

We inserted gene ABC into plasmid pBR322 between HindIII and EcoRV and sequenced using primer specific to insert ABC, at position XX on the plasmid (YY on the insert).

However, if you take your linear (cut) sequence and put it into a sequence manipulation program (e.g. Snapgene, Lasergene, Genious, etc. (no affiliations or recommendations for any of those, just commonly used ones)), then it might annotate your plasmid as having position 1 at the cut site, but this is an artificial annotation based on what you have told the program. If you circularize the sequence, the program may well recognize the plasmid and annotate the sites of interest (e.g. resistance markers, MCS, Ori) correctly with their proper positions marked.
Edited to add: Some positions on the plasmid do change once you have put an insert into it. These are the positions after the insert. For example, let's say you have a (hypothetical) plasmid of 500 bp in length, which has a promoter at position 50 and a resistance marker starting at position 300. If you insert a 100 bp fragment at position 250. The plasmid is now 600 bp long, the position of the promoter is still 50, but the resistance marker now starts at 350.


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Are some immune cells contagious?
I was wondering if people can transfer immune cells through touch the same way we can transfer harmful bacteria. Is it possible for immune cells from one body to be transferred to another, and might some of those cells be able to survive in the biome of another individual? And is their a correlation between increases in allergies and auto immune diseases, and touch-conservative societies?

Similar to: Share immunity by kissing?.

Specifically from touch - No.
However, there is one natural mechanism for transfer of immune cells between individuals, breast feeding, particularly the early stages when the milk is known as colostrum.
In all mammals the milk contains immune cells as well as a range of antibodies, non-immune cells and various other components that aren't specifically milk1. These components are thought to provide immunity for the infant until its immune system develops enough to provide protection by itself2.
You should note that this doesn't mean that the cow's milk you drink in your coffee contains cow immune cells, because the processing of the milk destroys these. If you drink raw milk, then you will be consuming some cow cells with that, and your gut will destroy the active cells anyway.
There are more complicated medical treatments that can also transfer immune cells - one specifically for immune cell transfer is adoptive transfer, which involves taking cells from the patient or another person and then using these to transfer back to the patient, usually after modification of the immune cells to respond to a particular antigen (often a cancer cell type). You can also do this with non-immune cells, but the practice is used medically for cancer treatment with immune cells.
References:

Smith CW, Goldman AS. The cells of human colostrum. I. In vitro studies of morphology and functions. Pediatr Res. 1968 Mar;2(2):103-9. doi: 10.1203/00006450-196803000-00005. PMID: 4173318.

Hanson LA, Winberg J. Breast milk and defence against infection in the newborn. Arch Dis Child. 1972 Dec;47(256):845-8. doi: 10.1136/adc.47.256.845. PMID: 4567072; PMCID: PMC1648417.


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RNA Secondary Structure Prediction Algorithm
I am currently working on my Final Project for the Biomed Datamining class, where the main goal is to 'Predict RNA Secondary Structure'.
I am given a set of RNA sequences in FASTA format and am tasked with writing an algorithm to predict their secondary structures. However, I am restricted from using any external software (already available online) or machine learning libraries (like scikit-learn).
As I am not a Biomed major, I am kind stuck on this project rn. What are some of the simplest algorithms I could implement for this prediction task? Where can I find more information about these algorithms?
Thank you

This is an easy question but I am not sure this is the right site for it.

This question would be a better fit for SE Bionformatics. However it is not clear whether your task is to write (devise might be a better word) an algorithm or write a program. If it’s an algorithm, we can’t help you as it would be doing your homework for you.

In addition, the length of the sequence is very relevant. 10nt is easy, 1000 is not.


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Could a pond poisoned with chloride cause mutated mosquitoes
We've got an old, small concrete pond in our garden. There's no fish or plants in it, only green algae. Every summer, countless mosquito larvae teem in the water.
Normally we take out the water, but this time my wife just threw a bottle of chlorine into the water (toilet cleaner).
I'm concerned about the impact of this to the mosquitoes. I know chlorine is carcinogenic and thus can cause mutations in cells.
To my surprise, after a few days the mosquito lervae are still alive and their activity and number seems to be the same.
My question is: Can the polluted water damage the DNA and cause a hereditary change in the mosquitoes' family tree?
And are mosquitoes adapted so well to polluted water?

Use laborious fish (fish that eat mosquito larvae) they are far more ecologically friendly and has been used in mosquito control for many decades. A bottle of chlorine will wipe out everything, i.e. no mosquito larvae, microbiome, zero ecosystem - unless you've a massive pond that will sufficiently dilute the chlorine.  Laborious fish are tried and tested method globally.

There are a host of other "green" methods to stop the mosquito larvae, it's an area of sustained research since well before my time right up to the present. "Bottle of chlorine" was never amongst those methods. Based on mosquito resistance  studies to insecticides low concentration chlorine over a sustained period, could possibly produce "low concentration chlorine resistance" but it would have to be really low concentration, e.g. does this happen with chlorinated outdoor swimming pools(?? I don't think so).

@M__ comments are not for answers. If you believe your comments answer the question, please include them in an answer with proper citations supporting your claims.


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What is the simplest known metabolic pathway?
What chemical process that can be defined as "metabolic" is the simplest found in any organism, and are there even simpler theoretical metabolic pathways, that are simpler than any found in known organisms?

How would one objectively identify a metabolic pathway as "simple"? What are the criteria for simplicity?

We don’t do definitions much in biology. Certainly we define our terms in any discussion, but generally in our own terms, rather than by appeal to some authority. “Pathway” is a synthetic human concept — we, not Nature —define the first step and the last step, draw a ring round connected reactions of our choice, and call it a pathway.  Please go back and finish reading the [Tour] to find out what questions are acceptable here, then the Help on asking — particularly the need to provide context. What is the biological problem you are facing. And, as Bryan requested, define your terms.

Trivially: the protonation/deprotonation of water.
This is a process that happens spontaneously without any other inputs or outputs or catalysis under physiological conditions.
It feeds into basically every other biochemical process, and cannot be reduced into any of them.
I really agree with the commenters, so this answer goes to show that your definition is more about how you choose to draw the box around your focal point than it is about how biology works.

I appreciate this answer a lot. While I understand the problem with my intitial framing, I think you were able to see through the inexactitude of my framing and get to the real point of my question. Thank you all for the input on how I can better express and think about my questions, and thank you for trying to see the real question beneath my shortcomings in asking it clearly.

@blacktopshaman don't be too harsh on yourself. this stuff is hard.

This will not wash. The protonation of water is not a metabolic reaction, much less a metabolic pathway. First, metabolic reactions are generally regarded (any hit from a Google search or text book of biochemistry) as enzyme-catalysed reactions reacting on metabolites — chemical intermediates in energy generations, anabolism or elimination of waste products. Water participates in such reactions but is hardly regarded as a metabolite and its ionization does not require catalysis. Similarly, definitions of metabolic pathways refer to reactions in the plural, generally using the word "sequence".


text:
Lipid Bilayer composition
I am currently taking a course on introduction to biomolecules and the other day our professor showed us a photo describing the composition of lipid bilayers of various organelles in a eukaryotic cell. I just wanted to ask how would one go about to find these compositions? Me and my friends tried to think about it, one of them came up with an experiment in which you grow the eukaryotic cell in a medium where the only source of a particular lipid is "tagged". But the obvious mistake here is that the particular lipid you have tagged is present in all the organelle layers (how much so ever its percentage), so when you actually try to observe it, I would assume the cell will appear to be illuminated throughout. Any help would be appreciated.

The characterization of lipids in specific organelles would not be done in an intact cell, like you said, since the entire cell would light up with all the organelles spread around throughout the cytoplasm. They are separated, usually through subcellular and suborganellar fractionation so that each organelle can be characterized separately. Then, when the fractions containing each organelle or groups of organelles are separate, the lipids in each fraction can be further separated using a method like gas chromatography (essentially any good chemical separation technique will do) and then identified with mass spectrometry. One paper that describes this process in more detail is this one: https://www.jbc.org/article/S0021-9258(20)70077-3/fulltext


text:
Bottleneck in population that is already experiencing inbreeding depression
What would be the result when a population experiences a bottleneck, while already manifesting inbreeding depression?
I only found this article and it suggests that the inbreeding depression would decrease by a few points. I couldn't find anything else relevant, only about how a bottleneck increases inbreeding (obviously).
What are the relevant Mathematics?


text:
How are the "cartoon" images made and what is their "proper" name?
How are the "cartoon" images made and what is their "proper" name?

How do people create these cartoon-style images? One option I found is BioRender, but it seems expensive.

Is there any other -proper- name, besides "cartoon"?

Example image from https://sites.tufts.edu/opioidpeptides/pathways-and-receptors/general-opioid-signaling/

You can draw them in Illustrator or any other vector graphics program.

You can use BioRender for free with slightly limited utility. I would call this an illustration or schematic.

they are called illustrations or diagrams and traditionally they are drawn by hand.


text:
What is the difference between the books "Molecular Biology of the Gene" and "Molecular Biology of the Cell"?
I am a CS guy who is taking up studying biology in my free time. Both of these books have been recommended to me, but I am not sure of the differences. Can someone explain the differences, and perhaps offer a suggestion for me?
The books are:
Molecular Biology of the Cell - Bruce Alberts
Molecular Biology of the Gene - James D. Watson
Thanks!

Welcome to Biology StackExchange! You can find table of contents for both books online: Molecular Biology of the Cell and Molecular Biology of the Gene. Generally speaking, MB Gene focuses more on molecular genetics, while MB Cell covers a wider span of topics about cell biology. Since you say you are new to biology, I think MB Cell will be more useful as it will give you a broader overview.

This is a site for biologists about problems in biology. I think that your question is off topic for that reason. But in any case, it is badly framed. You do not say why you wish to read about biology in your spare time. Are you interested in the mating habits of the lesser spotted toad, for example? Neither of these books will fit. Or do you want to get into bioinformatics? In the latter case asking strangers who have a completely different background and in general have never been involved in teaching anyone, never mind CS students, is, in my opinion, an exercise in futility.

Full disclosure, I have not read both books. However, I think I can explain the difference between them just by looking at the table of contents.
Molecular Biology of the Cell has 5 parts: Introduction to the Cell, Basic Genetic Mechanisms, Methods, Internal Organization of the Cell, Cells in Their Social Context. Molecular Biology of the Gene is basically the second part expanded into an entire book.
Even if Molecular Biology of the Gene sounds more like what you are looking for, I would still recommend reading Part 2 of Molecular Biology of the Cell first. I think it would give a good overview of how the system works before looking at how particular parts function.

How do you know what the poster is looking for? And should you be answering questions about the content of books on a site dedicated to problems in biology? I think not.


text:
Can someone identify this insect?
I photographed this wasp like insect on a buttercup in my wildlife garden.  It can be no longer than 10-15mm.  The bands appear green rather than yellow but I suspect that might be due to the lighting.

Where are you located? Thanks.

Lincolnshire UK

I can't answer because I can't identify it positively, but I think it's a small paper wasp (there are 200 species worldwide.) Some of them are slender and very small with long wings like yours. A side view would be necessary for proper ID, by me at least!

Thanks for giving me a steer, I'll look at that group

Having looked through Steven Falk's amazing collection of photos, I'm now thinking its one of the Stem Boring Sawflies, most likely Cephus spinipes, a Grass Stem Borer, which Steven Falk calls the Timothy Stem Borer.
To quote his site "C. spinipes is one of our commonest cephids and is recorded widely as far north as Yorkshire in a variety of grassy habitats. The rather maggot-like, whitish larvae develop in the stems of grasses such as Timothy. Adults fly from May to July and can be numerous on buttercup flowers."
https://flic.kr/s/aHsmsWKR4q


text:
In what sense is Syringammina single-celled?
In what sense is Syringammina single-celled? For example, if it's true that all cells have membranes (is it?), then how do you identify its membrane? Or does unicellular simply mean that it has only one lipid bilayer (presuming --- since I don't know one way or the other --- that the crucial ingredient of any cell membrane is a lipid bilayer (is it?))
I'm not a biologist, so please excuse my possibly annoying question.


text:
How does $\ce{H2CO3}$ form in the blood with a ratio of 1:20 with $\ce{HCO3-}$ if there are not enough $\ce{H+}$ ions
I have recently been studying about the bicarbonate buffer in the blood and have a doubt regarding the concentration of carbonic acid in the blood plasma.
My understanding of the buffer system is that about 85% of the total carbon dioxide in the blood diffuses into the red blood cells. In the RBCs, $\ce{CO2}$ reacts with water(catalysed by Carbonic anhydrase) to  form carbonic acid($\ce{H2CO3}$), which dissociates into $\ce{HCO3-}$ and $\ce{H+}$. The $\ce{H+}$ binds with haemoglobin, and the $\ce{HCO3-}$ is released into the plasma by a chloride shift.
The doubt is how does $\ce{H2CO3}$ form in the blood from $\ce{HCO3-}$ to have an equilibrium with it and to form the buffer system.
I initially thought that some $\ce{HCO3-}$  would bind with the auto-ionised $\ce{H+}$(aq) ions to give $\ce{H2CO3}$, but the concentration of $\ce{H+}$(aq) is miniscule(about $4*10^{-8}$ molar) as compared to the concentration of $\ce{HCO3-}$(between 0.022-0.032 molar when in equilibrium with carbonic acid) and thus would not react adequately with $\ce{HCO3-}$ to give the concentration of $\ce{H2CO3}$(0.0011-0.0016 molar) required for the buffer to function.
Therefore my question is how can there be a 1:20 ratio between $\ce{H2CO3}$ and $\ce{HCO3-}$, if there is hardly any hydrogen ion concentration for $\ce{HCO3-}$ to form carbonic acid.
I have looked at multiple articles regarding the transport of $\ce{CO2}$ in the blood as well as the bicarbonate buffer system, but none of them explain how exactly does the carbonic acid form in the blood.
Some of the articles/videos that I have looked at before posting the question:
https://courses.lumenlearning.com/wm-biology2/chapter/transport-of-carbon-dioxide-in-the-blood/
https://www.ncbi.nlm.nih.gov/books/NBK532988/
https://www.khanacademy.org/test-prep/mcat/chemical-processes/acid-base-equilibria/a/chemistry-of-buffers-and-buffers-in-blood
https://youtu.be/QP8ImP6NCk8
https://chem.libretexts.org/Bookshelves/Physical_and_Theoretical_Chemistry_Textbook_Maps/Supplemental_Modules_(Physical_and_Theoretical_Chemistry)/Acids_and_Bases/Buffers/Blood_as_a_Buffer
https://youtu.be/gjKmQ501sAg
https://youtu.be/5_S5wZks9v8

Bicarbonate and its conjugate acid buffer the blood due to their intrinsic behavior (pKa/pKb) of donating $H^{+}$ if there is too few (high pH) or taking up $H^{+}$ if there is too much (low pH).
You will not run out of $H^{+}$ because of the intrinsic property of $H_{2}O$, that defines pH; $H^{+}$ is readily created by dissociation of $H_{2}O$ [source].
Taking up $H^{+}$ simply reduces reformation of $H_{2}O$ from $OH^{-}$ + $ H^{+}$  [source], but you will not run out of $H_{2}O$ as its in excess in the blood.
Temporarily, $H^{+}$ may come from other molecules (e.g. buffers), but can be imagined as being later "reimbursed" from (excessive) water.

It has to do with the buffering activity of Hb and $\ce{HCO3-}$ leakage.
$\ce{H2CO3}$ dissosiates inside the RBCs and the resulting protons, $\ce{H+},$ bind to Hb, decreasing proton pressure caused by the free $\ce{H+}.$ This shifts the reaction in the direction of forming more $\ce{H+},$ in turn forming more $\ce{HCO3-}.$
$$\ce{H2CO3}\rightleftharpoons\ce{HCO3-}+\downarrow\ce{H+}$$
At the same time, $\ce{HCO3-}$ formed inside the RBC is exported out in a chloride-shift similarly decreasing its concentration and pressure inside the RBC.
$$\ce{H2CO3}\rightleftharpoons\downarrow\ce{HCO3-}+\ce{H+}$$
That's the reason plasma concentrations of $\ce{H+}$ are low while of $\ce{HCO3-}$ are high relative to that of $\ce{H2CO3}.$ In short, the dissociating $\ce{H2CO3}$ overwhelms the $\ce{HCO3-}$ associating with the little free $\ce{H+}$ in plasma.


text:
is there an assumption of homology?
Recently, i watched evolution vs creationism especially in islam view of evolution. There is one particular guy called subboor ahmad (he is muslim apologist). he claimed that there is an assumption of homology and that assumptions are being disputed by homoplasy. so i want to know if the statement of of assumptions of homology is actually correct or not? if not then how we can determine homology or homoplasy in first place?

That's a pretty broad question. You'd have to start with a pretty good understanding of evolution to have a more specific question. Both have occurred in evolution.

i have very basic understanding on evolution. my apologies for asking very broad question due to lack brief understanding on evolution . Thanks for sharing the info. Its very helpful for me

there is no assumption of homology, homology is a conclusion of comparing billions of features across genera, Homology not existing would require a breathtaking amount of coincidence, to not have homology it would be much closer to the tornado assembling a working 747 the creationists are always on about.

@John - Both homology and homoplasy (aka convergent evolution) have occurred (and homoplasy not even rarely.) If you want to say homology is not assumed but an absolute, that's an erroneous statement. Continued expression of lactase arose at least three times in different populations, and sight multiple times as well. This is a valid question.

@anongoodnurse I was referring to to the fact that homology exists, the apologist the OP is referring too claims the existence of homology is an unfounded assumption

@John - From my understanding, the apologist is stating that we (non-creationists) hold homology to be a given, and arguing that the existence of convergent evolution discredits homology. The answer isn't a sweeping condemnation of the apologist's take; the answer is that both have and are occurring, and that the existence of homoplasy does not negate homology. Your comment is unclear on that.

@Piee3.14 - How to determine which characteristics are a result of homology and which are convergent evolution is not simple, but it's easier now that we can do genetic analyses on samples, even old ones. And as I commented, there are examples of homoplasy even recently, such as the development of continued lactase secretion, which allows for milk to be a source of nutrition beyond infancy. This has evolved on at least 3 separate occasions in different populations, meaning it's not necessarily homologous. The page I linked to has many short articles which should be helpful.

I can´t remember to have heard of an "assumption of homology"; i studied (evolutionary) biology in Germany for several years. If I understand correctly, you are wondering how to tell homology and homoplasy apart? For morphological traits there are for example Remane's criteria (a german zoologist, he developed this in 1952), that can help to determine if a given structure (a bone or smth. like that) is a homologous structure. There is the 1. positional criterion (a similar position in a comparable system of features points to homology, i.e. how the front limbs of land vertebrates are structured and placed). The second one is the 2. structural criterion and the third one is the 3. transitional criterion ("Stetigkeit" = continuity) where you try to identify transitions/intermediate forms of a trait in different organisms. It is definitely not just assumed that similar traits are homologous, even though there are lots of traits that remain "unsolved".


text:
What is a good expression vector for Salmonella enterica subsp. enterica serovar typhimurium
I am interested in expressing custom proteins in a Salmonella strain, however I am facing difficulties in finding the appropriate expression vector for it. It seems that most of the resources provide for E. coli expression. Does anyone have any recommendations?
Thanks in advance.

Is there a reason why you have to do this in Salmonella?

I assume that you want to e.g. express fluorescent proteins for doing some kind of experimental study of Salmonella, as opposed to industrial protein production.
I would suggest looking into prior work that uses Salmonella as a model. For example, I found this paper somewhat at random that uses several vectors in Salmonella to do experiments. Here is another. And here is another. Several of these appear to share authors, I don't know if that's Google SEO or a small research community.


text:
how can a ganglion be defined as cluster of neuron bodies when it has interneurons?
Let alone the presynaptic button existing there as well, how is a whole interneuron existing there not contradict the definition ?

Can you explain what you see as a contradiction? I don't understand.

1-ganglion: mass of neuron bodies. 2-an interneuron: a body+ an axon+ a terminal. 3-some ganglia do have interneurons, thus have body+axon+terminal.     Conclussion: contradiction. It's pretty straight forward.

Please don't tell people that ask for clarification that something is "pretty straightforward". Your question is badly presented. First there is no question in the body. The title of a question serves a different purpose and is quite distinct from the question itself (and should start with a capital letter). This renders your single sentence  ungrammatical — the first clause lacks an active verb. And your clarification should come in the question itself, not the comment. It would still lack sufficient context. You need to reference your definition, and explain where "there" is.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

In general ganglions are cluster of cell bodies . Presence of inter neuron in ganglion is a bit rare . Grossly they contains cell body.

Merriam Webster defines an "ocean" as:

the whole body of salt water that covers nearly three fourths of the surface of the earth

So, oceans are bodies of salt water. Yet, oceans also contain fish. They contain some mammals. They contain some human-produced trash. We might consider the ocean as "containing" things like islands that are mostly surrounded by ocean but are not themselves ocean. This does not create a problem for our definition of "ocean".
If someone defines a ganglion as "a cluster of neuronal cell bodies" they are telling you that you can expect to find a bunch of neuronal cell bodies there. They are not claiming you will find nothing else there. At minimum you will need to find some parts of axons and dendrites, because these are connected to cell bodies and there's no way to have a cluster of cell bodies without including at least parts of the things connected to them. They're also going to contain non-neuronal support cells (glia), and yes, can contain interneurons, synapses, etc. Interneurons, by the way, are neurons. That doesn't mean they're not clusters of neuronal cell bodies any more than the existence of fish means that the ocean is not a body of salty water.


text:
Why did the effects of the Pleistocene extinction not significantly impact African megafauna at the end of the Ice Age?"
It seems that megafauna extinctions did not have a significant impact on African megafauna at the end of the Ice Age. Humans also lived in Africa relatively commonly during the end of the Ice Age, just as they did on other continents.

we are currently at the end of the last ice age,can you please post some links to the research you have done so far as it will help you get better answers.

Most of the large mammals went extinct in North and South America, Europe, and most parts of Asia more than 10,000 years ago, but the number of large animal species extinct  was relatively low in continental Africa
https://www.sciencedirect.com/science/article/abs/pii/S001282521300175X
https://www.researchgate.net/publication/268077616_Late_Pleistocene_of_Africa


text:
Any idea what type of hawk this is?

Would like to know what this hawk is. Ground in So Cal

It is most likely a Red-tailed Hawk (Buteo jamaicensis). This is consistent with your location and the general markings on the bird:

The primary feathers are dark on the tips. There are "commas" (dark comma-shaped markings at the base of the primary feathers just under the alula). The patagial area is dark. There is a mottled/dark "belly band." You can sometimes use the "dark head, light crop, dark belly band" to identify Red-tailed Hawks when passing perched birds quickly and you have little other useful clues, such as the tail.
The bird's left leg looks somewhat unusual in this image, but I think this is due to having a bit of a strange posture in the moment. Buteos are not "booted", meaning the leg feathers end at the tarsus (analogous to your heel) which is the first joint above the toes. The right leg is sloping away from the camera position so it is not appearing to show the same length as the left leg.
There's a useful quick guide at Hawk Migration Association of North America that has this guide:

(Source PDF)
I can also highly recommend Hawkwatch International's Raptor ID page. I rely a lot on Jerry Liguori's books, which you can find at Hawkwatch's shop among other places.
Affiliation disclosure: I am an active volunteer of Hawkwatch International.


text:
Can contaminants in the DNA extract disturb the sequencing?
I'm having troubles with some DNA extractions. The yields are much lower than expected, and the Nanodrop spectrophotometer is showing quite a bit of contamination through the 260/230 ratios (see table below). The samples consist of mixed marine fine-mortarted fauna (environmental samples), of which I want to sequence a couple of marker genes to determine species composition (metabarcoding), using paired-end Illumina MiSeq. I could just go on with the PCR as I'm supposed to and see if that works, but my concerns are still:

As the DNA extracts contain an order of magnitude less DNA than expected, would you really consider them representations of their whole communities?
Assuming the PCRs work out and I get nice bands, is there still a risk that the contaminants could disturb the sequencing process? That is, given that I only input 2 out of 25 µl of DNA extract into the first PCR reaction, and just as little PCR product into the second (index/library prep) PCR. Can the Illumina flow cells be sensitive to these contaminants as well?

Sample ID
Nucleic Acid Conc.
Unit
A260
A280
260/280
260/230
Sample Type
Factor

1
7.6
ng/µl
0.152
0.086
1.76
0.71
DNA
50

2
24
ng/µl
0.479
0.249
1.93
1.16
DNA
50

3
21.9
ng/µl
0.439
0.238
1.84
1.15
DNA
50

4
18.6
ng/µl
0.371
0.190
1.95
1.29
DNA
50

5
18.5
ng/µl
0.371
0.200
1.85
1.44
DNA
50

6
6.9
ng/µl
0.138
0.069
2.00
0.70
DNA
50

7
7.9
ng/µl
0.157
0.092
1.72
0.78
DNA
50

8
35.2
ng/µl
0.703
0.363
1.94
1.67
DNA
50

9
9.6
ng/µl
0.192
0.099
1.94
0.85
DNA
50

extraction_blank
1.6
ng/µl
0.031
0.006
4.84
0.19
DNA
50

collection_blank
3.9
ng/µl
0.078
0.036
2.19
0.42
DNA
50

According to ThermoFisher "good" values are between 1.8-2.0 for the 260/280 ratio, and 2.0-2.2 for the 260/230 ratio. Less may indicate the presence of salts or EDTA for example. The concentrations are for 100 µl of DNA extract, that is, total DNA yield is given by multiplying the concentrations with 100. For the record, I have heard from people who get 200-300 ng/µl DNA concentrations from marine sediment extractions. My samples should in theory contain even more than that. Although I have earlier only gotten concentrations in the range of 30-100 ng/µl for the same type of samples with the same extraction kit.
What would you do in this situation? How do you go on with values like this from the spectrophotometer?

I have never performed environmental extractions, and I am not familiar with your specific protocol. I would defer to any other commenters with more experience with these methods. However, I would recommend redoing the extractions, if it is feasible. Any time a standard protocol gives results that are significantly unexpected, it's worth thinking hard about. In this case, where it is your initial step, it's even easier to suggest, since there's much less wasted time than if it were later in your protocol. The quality of your data depends on what goes in, so it's not worth risk it.
Nanodrop quantification is not particularly reliable for low concentrations like this. That makes the ratios even more questionable. I would not try to make too much of these particular metrics beyond "this was a poor extraction."
PCR could certainly give you plenty of DNA even from a minuscule sample - that's the whole point of exponential amplification! But if your extractions are poor enough that they are extremely biased, that would carry on through PCR.
I would worry less about contaminating the sequencing reaction at the end, but it's still worth trying to get pure DNA. What's your cleanup before dilution? Anyway, if you do have an inhibitor, I would expect it to give issues during PCR.  And you'll be diluting them 20? 100?-fold for loading onto the flow cell.

Hi. I forgot to add that I've redone the extraction four times already, following the kit manufacturer's troubleshooting guide for low DNA yields: heating up the elution buffer, letting it incubate for longer, running the elute through the spin column multiple times. I've even bought a new kit to try with. The values above are as good as it gets. Thought I was gonna do another thread about that... And I've double-checked the concentrations with Qubit, although not for this last specific extraction attempt. It doesn't differ that much.

The point of this thread was more to check which possible unforeseen problems I might encounter later, should I choose to continue with these DNA extracts. I perform post-PCR cleanup using magnetic AMPure XP beads. The final dilution of the DNA extract in the library will probably be closer to 1:100. But I take your answer then that I should not worry about contaminants as long as the PCR bands look nice – I should worry about bias from the low DNA yields?

With a bead clean and that dilution, I wouldn't worry about sequencing. I would still be a bit concerned  about bias. I don't know how quantitative you need this assay to be (do you want to measure frequency or just presence?), but I would be concerned by the extraction issues.

In metabarcoding studies, quantitative (read count) measurements are largely useless due to the large bias introduced by PCR. Presence/absence is the primary goal. I made another thread about the low yield issue: https://biology.stackexchange.com/questions/113837/why-are-my-dna-extractions-failing – Kudos to whoever can solve that mystery.

You might be able to get away with using these, then, but I would definitely qubit instead of nanodrop and be skeptical about any results you get.


text:
Why are my DNA extractions failing?
Alright, here's a tricky case. I am trying to extract DNA from mixed marine faunal samples, something that has been done in my group for a long time, and which I have done successfully before as well. Now it's just not working anymore for my last batch of samples, even though they should be very similar to my previous samples, and I'm using the exact same extraction kit (ZymoBiomics DNA Miniprep kit D4300). The yields are much lower than expected, and the Nanodrop spectrophotometer is showing quite a bit of contamination through the 260/230 ratios (see table below). My goal is to do metabarcoding of a couple of marker genes to determine species composition, so I need the DNA extracts to represent their whole communities. When yields are so low, I believe the chance of severe bias increases. I have heard of people getting 200-300 ng/µl from marine sediment, and my samples should in theory contain even more. Nevertheless, what I have gotten used to from earlier extractions are yields around 30-100 ng/µl (all values based on 100 µl). This is something different though. The table below shows the best results out of four extraction attempts. I have double-checked the concentrations with Qubit and they are approximately the same. I should also note that I ordered a totally fresh kit for this extraction, to rule out that something had gone bad in the previous one. But it's not much of a difference. I have also followed Zymo's advice to increase DNA yield: heat up the elution water, let it incubate for longer, run it through the spin column multiple times. It does not significantly affect the results. We preserve our samples in DESS (20% DMSO, 0.25M EDTA, NaCl saturated solution). Zymo suggested that the high salt content could disturb the extraction process. I'm not too sure, since it has worked earlier. But maybe that could be the reason why we are never seeing >200 ng/µl yields? What do you think?
What makes me believe that it's not the samples that have gone bad, is: a) That they would need to get really damn bad before yielding this little DNA, and b) That between every extraction attempt, there is usually one or two samples that spike and show quite ok DNA concentrations (30-60 ng/µl) – but rarely the same samples.

Sample ID
Nucleic Acid Conc.
Unit
A260
A280
260/280
260/230
Sample Type
Factor

1
7.6
ng/µl
0.152
0.086
1.76
0.71
DNA
50

2
24
ng/µl
0.479
0.249
1.93
1.16
DNA
50

3
21.9
ng/µl
0.439
0.238
1.84
1.15
DNA
50

4
18.6
ng/µl
0.371
0.190
1.95
1.29
DNA
50

5
18.5
ng/µl
0.371
0.200
1.85
1.44
DNA
50

6
6.9
ng/µl
0.138
0.069
2.00
0.70
DNA
50

7
7.9
ng/µl
0.157
0.092
1.72
0.78
DNA
50

8
35.2
ng/µl
0.703
0.363
1.94
1.67
DNA
50

9
9.6
ng/µl
0.192
0.099
1.94
0.85
DNA
50

extraction_blank
1.6
ng/µl
0.031
0.006
4.84
0.19
DNA
50

collection_blank
3.9
ng/µl
0.078
0.036
2.19
0.42
DNA
50

I don't see that this question is significantly different to your previous question, which is essentially the same the question as here. Either way, you will need a bit more detail on the samples - how are they stored, how much input, what is in the samples (tissue? soil?), what has changed between previous extractions and now, have you gone back to old (known working) samples and tried re-extracting?

Does this answer your question? Can contaminants in the DNA extract disturb the sequencing?

I'd suggest trying an alternate sample prep method that is a little easier to introspect than the kit and is optimized for difficult samples. For example this chapter describes a "difficult sample" extraction method that works on soil or fungi, which are notoriously hard to get DNA out of.

Bob: The samples are mixed marine faunal samples. That is, a mixture of anything larger than 40 µm that lives on a settlement plate in the sea, or swims near it at the time of retrieval. Directly upon retrieval, samples are mortarted thoroughly and preserved in DESS as described above, then stored in -20℃. What changed between the previous extractions and the last one is that I got a fresh ZymoBiomics DNA Miniprep kit for the last extraction. For the previous extractions I played around a bit with the tips that I got from Zymo, but the point is that it didn't make any significant difference.

Today I also tried with the Qiagen DNeasy PowerSoil Pro kit, but the results were practically the same, or possibly even slightly worse. So I will go back to the Zymo kit. Maybe redo some old samples that I know have been working before...


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Fridge vs freezer for short-term DNA storage – how long until freezer is better?
I know keeping DNA products in the freezer (-20°C) is preferred for long-term storage, but the downside is that freeze-thawing can cause shearing/breaking of the DNA. For short-term storage the fridge (+4°C) may therefore be better. But how short is "short-term"? I'm working with many samples of DNA products in several steps over the course of a few weeks (extractions, checking concentrations, PCR, cleanups, gels), and I can only do a few samples at a time. Questions is what I should do with the others in the meantime. If I keep them in the fridge to avoid freeze-thawing, the end-result may be that the samples spend these few weeks totally in +4°C (except for when I'm processing them at room temperature). On the other hand, I could save quite a few freeze-thaw cycles by having them in the fridge, because I'm doing something with each sample every few days. On the third hand... I'm working with amplicons (400-600 bp), so having long, intact DNA fragments is not really that important to me. I should also add that my DNA extracts are in water, not TE buffer.
So, at what point would you put these samples in the freezer instead? If we would generalize, how long until the "break-even point", when the degradation in the fridge can be comparable to the degradation from one freeze-thawing cycle?

The concern for freeze-thaw cycles is a bit overblown, I think, but it's hard to generalize. TE probably helps stabilize DNA, but any nucleases present will strongly contribute to degradation. If you're really concerned, I would check for myself by putting a dummy sample at 4 C and checking stability on a gel or bioanalyzer.

https://openbiotechnologyjournal.com/contents/volumes/V7/TOBIOTJ-7-10/TOBIOTJ-7-10.pdf


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How to balance PCR template amounts between high and low gene copy targets?
In eukaryotic DNA metabarcoding, whether you use a mitochondrial (e.g. COI, 12S, 16S) or a nuclear (e.g. 18S) marker gene will affect your yield for different reasons. Often it is recommended to use a multi-locus approach if possible – we use COI and 18S. But something struck me while I was PCR amplifying these libraries; We use the same amount of template DNA for COI and 18S, even though the number of gene copies in a given amount of DNA extract is hardly the same for them. Even with mitochondria only containing one gene copy each, per cell they still outnumber any nuclear gene, AFAIK. By how much is the question? What is a good target, if you want to have comparable amounts of template DNA for your PCR reactions? I've read that nuclear rDNA repeats can range from a handful to several hundred, and the number of mitochondria per cell can also vary a lot. Are there any guidelines out there?

How many cycles do you amplify for? Do you get amplification from each reaction? Think about the theoretical amplification of DNA in a PCR and how the number of cycles plays into amplification of rare targets.

What's the intended application? Are you trying to determine [a quantity of starting DNA] based on [a measure of sequences/DNA produced]? Or are you just trying to see if your target is present in the sample?

@Darlingtonia: Just standard procedure metabarcoding, trying to get a good representation of the overall community composition. We would just like to reduce bias introduced by varying template concentrations between marker genes. Ideally optimize the template concentration.

@bob1: We amplify 18S in 30 cycles, and COI in 31 cycles with a touchdown profile. Including an indexing PCR following that, that's quite a few cycles. So I basically always get a gel band from our PCRs based on 2 µl gDNA template, and it's always stronger for COI than for 18S, even with double the input amount for 18S.

@Joel In that case you might either have double the number of copies of COI than 18S in samples, or the efficiencies of the  two PCRs are different, or one is just a larger product, and therefore brighter as it incorporates more stain. You could put them on a qPCR machine and determine the efficiencies to see. PCR based approaches will always have some bias, you would need native barcoding to not I think.

@bob1: Native barcoding? Do you mean sequencing everything?

@Joel Yes - only works well if you are doing things like MinIon.


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Gene Mapping - Please explain in Lay terms
Taking an AP bio course, and for some reason I cannot comprehend the mechanism of how one determines the location of alleles on a chromosome. The math is simple and I can memorize it, but its bugging me that I don't understand a seemingly simple concept. Please explain to me like I am utterly inexperienced in biology (because for the most part, I am).

Stack Exchange isn't great for "explain this concept for me"-type questions; it's better if you can provide a specific explanation of what you understand and where you're stuck and ask a specific, directed question about that particular point. If you want a concept explained to you, better to use a textbook or Wikipedia. If you read that Wikipedia article or your textbook, can you identify where specifically you are stuck? What's the specific concept that you need to be further explained?

thanks, I'm still new to this, so I appreciate the advice. I will be sure to be more specific on my next post.

It's the 21st century.  You want to know where a gene is located in a species that's been studied?  You look it up.

Recombination happens every meiosis at some random location on every chromosome pair. If two loci are close on the chromosome, is unlikely that recombination happens between them, meaning they are "linked". If you look in a lot of meioses you can use the math to detect this linkage.
Gene mapping consists in considering every position in the genome, and measuring the linkage between that position and a phenotype (how frequently does recombination in meiosis separate the phenotype and the position).
Real world analogy: you measure how close two birds sitting on a telephone line are by measuring the rate at which some other bird lands between them. If they are right next to each other, then no other bird can land between them.


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RMSD / Tm metric for comparing local molecular structure similarity?
I would like to compare two molecular (protein) structures, but rather than comparing the total, global structures against themselves to yield an RMSD score (which would be straightforward with a structural alignment in PyMOL or similar), I instead am interested in a particular localised structural region in each protein.  Specifically, all atoms within a 20Å radius of a particular residue's alpha-carbon coordinates.
For example, I would have the local structure of L100 (in protein A) and L200 (from protein B), defined as the atoms that are within the radius threshold of those residues respectively.  To compare the "local structures" of L100 and L200, I know that they should be superimposed at the same site as they are the same residue (so I can "enforce" that the alpha-carbon coords of both residues should be in the same spot, i.e. the origin (0,0,0)).  Now, this becomes a "rotation optimisation" problem in order to get the minimal RMSD score.  I have so far found the Kabsch algorithm as one way to achieve this, as there is no need for working out the "translation" of the two separate structures (again, we know that we should enforce the centre residues to be in the same position).
However, the Kabsch algorithm can only work on the same number of points in structure A and structure B; but I may be comparing pairs of structures with an arbitrary number of atoms.  Additionally, due to differing amino acid compositions in the local structure, a different number of each element may be present between the two structures.
I am not sure if there is a solved way of getting the "distance" score between two local structures in this way; and I also am struggling to understand how other structure scores such as a global RMSD (between two different proteins of different length) or Tm (from Tm-align) work with two sets of points with different sizes.  Would appreciate any help!
TLDR;
How to find RMSD score / optimal rotation between two sets of atom coordinates (like Kabsch algorithm), when the two sets have differing numbers of points?

Don't have time to look into it too much right now but have you looked at methods like this https://bmcbioinformatics.biomedcentral.com/articles/10.1186/1471-2105-7-40


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Trying to find information about intraspecific allelic expression divergence in recombinant individuals due to changes in the cis regulatory regions
I am trying to find any research articles or resources that focus on differences in expression levels at the allelic level due to changes in cis regulatory regions in recombinant individuals. For example, when recombination occurs near a gene it can cause the promoter regions from the two parental alleles to swap places, which can then affect binding affinity so that one parental allele is preferred over the other and is thus over-expressed. I've seen work that deals with various hybrid crosses that show differences in parental allele expression. But I am curious if there is anything that shows how expression patterns can flip in a recombinant individual when compared to the expression patterns in the hybrid of the parental haplotypes. Further, I'm curious if this happens in a tissue specific manner, i.e. can the same gene have one allele that is overexpressed in Tissue 1 (the paternal allele can be preferred in this tissue), and then the same gene has the opposite expression where the maternal allele is overexpressed in Tissue 2. This is in a case where trans-acting factors are controlled for to ensure that differential expression is due to changes in the cis-regulatory regions. Hopefully my question is clear, if it isn't I can clarify. Thanks for any help!


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Why is phloem parenchyma absent in most monocots?
What evolutionary advantage did monocots get by losing this tissue that just seems to be storing food and metabolites?
I think this question has been asked before, but I didn't see an answer for that one


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Coefficient of fraternity between grandparent and grandchild from full-sib parents
I have the following pedigree and I would like to calculate the coefficient of fraternity between individual 1 and 5. R/AGHmatrix::Amatrix gives a coefficient of 0 for this pair. Shouldn't it be non-zero since there is still chance for individual 1 and 5 to have the same genotype? E.g. if the genotype in individual 1 is AB, there is still 1/8 chance to pass the alleles down to get AB in individual 5. Thanks.

ID
Parent 1
Parent 2

1
0
0

2
0
0

3
1
2

4
1
2

5
3
4

I think you're probably using the software wrong/there's a bug in your code.


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Why aren't all B cells memory B cells?
If we have a B cell for every possible type of antigen, why aren't all of them memory B cells? From my reading, I have deduced that memory B cells are effectively the better version of normal B cells, activating faster and being more effective, which is why pathogens that are exposed again are typically dealt with much quicker. But why go through the trouble of getting infected, only to have to gain "immunity" to easily defeat the threat the second time. If all B cells are memory cells, the thought of autoimmune diseases and allergies being extremely common may arise. However, our own B cells have mechanisms that prevent them to attack self and allergies. I know that this could just be a product of evolution, but I wonder if there is a clear reason of why this wouldn't work.
(please note that I have no other experience of the immune system besides reading books, watching videos, and google searches, so feel free to point out possible misconceptions I may have [also this is my first post so hopefully I am clear with my question!])

There are billions of different B cells which recognize different antigens.
B-cell activation occurs when one or a few of those bind to some pathogen. Activation involves proliferation. One B-cell becomes many many cells: some of them will fight the current infection, others go dormant and become "memory" B cells.
The main thing that makes memory B cells "better" and faster to respond to an infection is just that there are more of them. You already have billions of different B cells that each recognize different antigens. If you were to have thousands of each of those different types, you'd need to dedicate way more space to storing all of those cells and spend a lot of energy producing and maintaining them.
You also don't want the immune system primed and ready to take on any potential antigen with the same vigor: you want an immune system that responds strongly to things known to be threats, but it's just important to not respond to things that are not actually threats with a full-blown immune response.

When the naïve B-cell is produced, the body does not automatically "gain immunity" to a certain infection. There is only a certain amount of B-cells with a certain antibody for a specific antigen, and it is not enough to create an immune response on its own. When the antigen binds to the antibody and activates the B-cell, more of that B-cell is made, creating a secondary clonal selection process. This process is what kicks of the immune response. Some of the B-cells become plasma cells (the cell that produces large quantities of antibodies) and others become memory B-cells. The memory B-cells exist in greater quantities than the naïve B-cells, which means that the response will be better due to the greater number of cells present. The memory B-cells are also created to be more responsive than naïve B-cells when exposed to the antigen, which speeds up the process and leads to a better immune response the second time around.
In short, the reason why all B-cells aren't memory cells is because there are different types of B-cells that do something different:
naïve B-cells are the "parent" to all of the other types of B-cells which have to be activated to create other cell types, plasma cells produce antibodies, and the memory B-cells are cells that have improved upon the naïve B-cell to create a faster response. This is why the body needs to be infected once for the secondary immune response to be fast, the body needs to have that secondary B-cell selection that picks the right B-cell for the right antigen.
Source for Information: Prescott's Microbiology 12th Edition by Willey, Sandman, and Wood

Thanks for the response! However, why do naïve B cells have a slower response anyways? What's the point of created memory B cells that are faster when the naïve ones can be faster anyways? I mean evolution doesn't have a "point", but it would be a lot more efficient for naïve B cells to respond fast the in the first place.

I mentioned this in an answer for a different question (link), but evolution goes for survival of the fittest, not for efficiency. If it is good enough to survive, it doesn't need to evolve further. I hope that helps!


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Trying to identify a plant by its root
My kids were digging through a pile of dirt I had made for them to play with (my son wants to do bike jumps off it) and they brought in the attached root. I never got to see what kind of vegetation was growing from it, and the kids can't remember what it looked like.
This is from our backyard in central Texas.
The closest I have found was potato dandelion but there are very little picture references to this.


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Is there a way to isolate bacteria from a bacteria/phage plaque in order to PCR bacteria only?
I am writing a paper for a class that involves a mock grant proposal. I am looking at an experiment which requires sequencing of host DNA from a virus/host model, and am having a hard time finding a protocol which keeps bacteria as opposed to phage. From what I'm seeing, my two options for separating the phage and bacteria are either centrifuging or filtration, neither of which keeps the bacteria. Am I missing something?

What specifically are you trying to learn about this hypothetical system by conducting the experiment? You presumably already have the bacteria available in pure culture. That's what the plaques are forming on. If the phage are lytic then the infected bacteria are mostly lysed by the time plaques form.

make the PCR primer only bind to DNA found in the bacteria?

I think you may be confusing some of the terms.  On can only see, or visualize a phage plaque, if you have added an aliquot of infective phage to a growing bacterial culture, and then mixed that together with molten agar in the pour plate method.  As the bacterial lawn grows, the plaques are where the phage particles are either killing (lytic growth, like phage T4), or retarding (non-lytic growth like phage M13) bacterial growth.  If you are growing lytic phage and there are bacteria in the plaque, then those are bacteria that are resistant to that phage.

Some phage, like phage lambda, are capable of lysogenic growth, so they are integrated into the host chromosome like a hitch hiker and are basically dormant, until they are induced.  Depending on growth conditions, after induction they can grow lytically.  If you add lysogenic phage to a bacterial lawn, then the resulting plaques are said to be turbid, because there are some immune bacteria, growing in the middle of the plaques (i.e., lysogens).

Electrophoresis will separate DNA by size.


text:
Why doesn't the brain filter out tinnitus noise?
Human sense receptors quickly become insensitive to constant stimulation and even the human brain can effectively filter out and ignore constant stimuli. For example, people living by a busy road soon ignore the noise of traffic and even sirens are hardly noticed. I used to live close to a highway, but never noticed the noise, except for the occasional exceptionally noisy truck or motorbike, even though the actual traffic noise was constantly changing.  Why is it that people who suffer from tinnitus cannot do this?

Remember the need for showing your own research when posting a question. Perhaps look into the basis for tinnitus itself. The Wikipedia article seems to be a good starting place.

I think this question is the same as "what is the mechanism of tinnitus?" or similar; otherwise it's a bit tautological. Like any disease or disorder, tinnitus is what happens when the brain "creates noise" instead of filtering it out. There's no real sound in tinnitus, unlike the highway example.

"Why is it that people who suffer from tinnitus cannot do this?" Why do you think they can't? I've had tinnitus for about 50 years. While it was quite noticeable initially, I hardly ever notice it now. It's not that it's gone at times; it's always there. It just doesn't register most of the time.

@BryanKrause - That doesn't mean it never gets "tuned out". I know it's very distressing to some people (it must be worse than mine.) But I definitely tune it out; sometimes even if there's dead silence, it doesn't register unless I think about it.

@anongoodnurse Sure, but the symptom of tinnitus is specifically the experienced sound. If you're tuning it out and not hearing it, your tinnitus is by definition reduced or absent.

The link to the previous question does state that when the initial event is not traumatic people do experience spontaneous habituation. So this does answer my question.

@BryanKrause - I'm not sure I agree. The sound is always there. People can get used to a lot of things if they've had it for almost 50 years. I know the difference between fluctuating tinnitus (how it presented initially) and what I have now. It's not a case of now it's here, now it's not.

@BryanKrause - In one of the links in the previous answer, there is a mention of habituation, but it also stated that if someone has had tinnitus for more than 2 years, it's probably permanent. I wasn't able to tune it out initially for, I'd guess, a decade. I distinctly remember my surprise the first few times I realized i had tuned it out.


text:
How do retroviruses exit the cell
Do they just pass through the membrane? Is there some specific transporter or mechanism? Does it vary?
I've seen pictures if retroviruses outside the cell but no details

Retroviruses, like many other enveloped viruses, exit the cell by a process called budding. The virus uses the host machinery for producing transmembrane proteins to enrich areas of the host cell membrane in viral transmembrane proteins, and co-opts a host process for releasing vesicles.  You can see budding illustrated in the context of the life cycle of HIV in this figure from Murray Medical Microbiology.

The process has been studied in some detail in HIV and other retroviruses.

They would have to exit the bud as well and the bud would have to accept the virus which is unlikely.


text:
Is there no such thing as species?
If you recreated intermediate species between every species on the evolutionary tree, would every species be able to reproduce with each other through a series of intermediates? Would this blur the concept of "species"?

Without need to recreate any species, https://en.wikipedia.org/wiki/Ring_species offers a real life examples of the situation proposed by the OP. It challenges the concept of species somehow, but also sheds light on the process of speciation.


text:
Is the BMJ a reliable source for biology studies?
The BMJ published the Wakefield study, criticised it, and retracted it. They then argued that the Wakefield results they published were fradulent. Is BMJ reliable for biology studies or is it an anti vaccine conspiracy journal?

The Lancet published the study, the BMJ are the ones that exposed its fraudulence.

First: The infamous study by Wakefield et al., was published 1998 in Lancet, see here. Wakefield had indeed falsified his study, by selecting kids with certain preconditions, taking money from attorneys (and not disclosing it) and others. Here is a nice overview over it.
To your question: The British Journal of Medicine (BMJ) is indeed a reliable and credible source for scientific articles, as is the Lancet. Journals can check the content they get for publication to some extent, but if they have authors who deliberately falsify studies, then they can do little. The thing which can be criticized in the Wakefield case is the time that it took to withdraw this publication.

But there would be obvious inconsistencies if the results were fake.

If these are obvious, journals will most likely not accept the article. See pubpeer...

BUT they accepted wakefield

@Bobb so what's your point? I could write a paper with completely falsified data, add some collaborators who generated their own and described it truthfully enough, write a convincing but incorrect conclusion, and get it published in a mid to top tier journal. If someone is smart enough, they can get around the current checks in the system unless an incredibly thorough review is done and the results are essentially independently generated again, which almost never happens before publication. There is, and always will be some level of trust in the system, otherwise nothing would get published.

Hmm. Sounds like peer review is almost useless.

@Bobb Exactly as MattDMo says. There are pther cases, like the one of Olivier Voinnet who recently had to retract 7(!) papers and correct at least 15 (I lost track here) and return prestigious prices. This guy was once a star, but has now fallen. See ]here.

Peer review has it's drawbacks, and they are known. The problem is, there is no better system available. And still: Almost all papers are ok.

@Bobb tell me, are you a scientist? Do you actually understand what the peer review process is? Have you ever submitted a paper for publication to a halfway decent journal? If not, you very likely don't know what you're talking about. No one who actually knows what the process is and/or has been through it would say it's "almost useless." And if it is useless, what's your better alternative? I'm sure you've thought that through very carefully...

@Bobb if you're just here to troll, you will very quickly find yourself banned from the site, and potentially all Stack Exchange sites. If you want to engage in a thoughtful conversation about the pros and cons of the current system and how it can be fixed, fine. If you're just going to make asinine comments displaying your obvious ignorance about the subject, you may as well just leave now.

@Bobb peer review is good at identifying scientific quality but less so at detecting deliberate fraud. This is fairly well understood within the community (https://www.elsevier.com/reviewers-update/story/peer-review/as-peer-review-week-2016-begins,-our-infographic-highlights-what-researchers-really-think-about-the-current-process/) and is one motivation for the Reproducibility Initiative (see also http://academia.stackexchange.com/questions/74761/who-is-supposed-to-repeat-experiments).

+1 for the important point, that the problem was how long the study took to be pulled and the fact that the Lancets own investigation was so poor another journal had to show its fraudulence.


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Has anyone done a GCTA of leg length?
There is extensive genomic research on height, but nobody seems to have done a gcta of leg length.

What do you mean by "doing GCTA of leg length"?

Do you mean "do we know the QTL for leg length?"

I don't and only few people visited this post yet, so saying "nobody" sounds a bit extreme. I googled the thing a few times and found Genome-Wide Complex Trait Analysis. It seems to be a recent technic that has been only used a few times only and it seems to always be about height. There is therefore probably nothing on leg length. Seems not surprising if I (and others) don't know its meaning.

If a concept is likely to not be understood, please link to its definition (or even better, include a definition) and indicate what does the abbreviation stand for. I let you make the edit. Thanks.

I am a PhD candidate in population genetics and I find your comment (now deleted) offensive :) You should just add a link and definition to save everyone's time.

Voting to close as "homework" because it's extremely trivial: a Google scholar search is the service you need for this. You could also look at the articles citing the original methods paper. As far as I know there's nothing published specific to leg length (and I doubt it will happen soon - it's a fairly uninteresting thing to measure).

GCTA is not a well known term. I myself have worked a bit on genomics but I was not aware. Providing context and explanation is not only important for explaining your question but is also useful for users who refer to the post to learn some facts.

I am assuming you are referring to the use of the software GTCA (which stands for Genome-Wide Complex Trait Analysis). Original paper: Yang et al. (2011).
I looked to the papers who cited Yang et al. (2011) and quickly scanned through looking for "leg". I did not find anything on it. So my best guess is: No, nobody ever applied GTCA to leg length.


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Without plant breeding and domestication, would most of the foods consumed by humans evolve to become inedible?
Would this happen? Do species evolve to avoid being consumed, especially the animal species which have no need to leave seeds?

Plant defense against herbivory
Plenty of plant species evolved defense mechanisms. There is a large variety of defense mechanism. Have a look at the wikipedia article Plant defense against herbivory for more information. Such defense mechanism often comes at a cost and therefore the mechanism can be maintained only if herbivory is sufficiently common and costly. Note that herbivory might be beneficial to some animal species typically as it can help to disperse the seeds.
plant-herbivores Co-evolution
Herbivores co-evolve with plants and develop mechanism to deal with plant defense mechanism. Such coevolution often yield herbivores to specialize in feeding in a handful of plant species only.
Human consumption
Most of what human consume is artificially selection. We specifically allow the breeding of individuals that present trait that are pleasant to us. In such condition, a defense mechanism would be a highly deleterious trait.

Do species evolve to avoid being consumed, especially the animal species which have no need to leave seeds?

I don't understand this sentence. Do you mean "[..] especially plant species being consumed by animal species that don't help spreading the seeds"?
If this is what you meant, then yes. If herbivory comes at non benefit for the plant, the overall cost of herbivory will be more important for the plant. All else being equal, a mutant that present a defense mechanism would have a higher fitness if the herbivores do not offer any benefit to the plant being eaten.

It's a yes or no question

If you rephrased the question "without artificial selection" instead of "without breeding and domestication" (which sounds really alike but has the advantage to clarify your question), then the answer to the title question (there are actually more than one question in the post) is yes if we assume that our consumption comes at a cost (that outweigh potential benefit) to the plant and note that it may take quite a bit of time for it to evolve.