text:
Can someone identify this tree?
It appears to be a kind of fig tree (perhaps similar to the fiddle leaf fig tree but without the fiddle?), although the leaf shape doesn't match. It didn't seem very appealing to eat (!), it was oozing white sap from the stem and from the fruit itself when i broke it apart.
The fruit felt like a hard sponge.
I found the tree in Israel, although, in this location there are a number of non-indigenous trees.
Here are some pictures:

(NOTE: photo of full tree was taken in March, not at the same time as the first two photos)

Something similar to Ficus macrophylla that grows in Israel? https://en.wikipedia.org/wiki/Ficus_macrophylla

Fruit and sap are certainly reminiscent of a fig, but the leaves make me think Ericaceae. @skymningen's find of F. macrophylla, however, suggests to me that some figs do in fact have eliptic coriaceous leaves....I'll dive in to see what I find

Can you provide an image of the tree itself (demonstrating its overall growth form)? Additional images of the leaves would be helpful as would sizes of the leaves and plant overall. Thanks.

@theforestecologist I walked past the tree today, and took a photo. It should be noted that the first two photos were taken in August 2016, and the third photo was taken March 2019!


text:
Variation in deathstalker scorpion
I recently encountered a (probable) deathstalker scorpion in the Negev desert in Israel:

However, when trying to identify this species I found that in many/most photos of the yellow scorpion the final segment before the stinger was dark or even black (see the wiki link for examples) i.e., not yellow, as shown in the photo.
Is a black/dark pre-stinger segment an indication of some sort (perhaps venom?), or is it an indication of a separate species, or other? Clarification on this matter is most welcome.

Update - I contacted an Israeli PhD from Haifa University who wrote the following:
"...looks like Andrtoctonus amareuxi (also referred in the past as Andrtoctonus amareuxi hebraeus, Israeli fat-tailed scorpion (קטלן עברי)
the genus common name is fat-tailed scorpion... The color of the last segment of the abdomen before the stinger is not a very good sign alone for species identification, as it is variable in the population and also found in at least 2 other genera/species (in the genus Buthus and in some species of the genus Compsobuthus). Anyway for sure it is not the deathstalker which is easily identified by a marking on the prosoma, behind the central eyes, that looks like a lyre  and the ridges on the abdomen..."

The scorpion in question appears to be Buthacus leptochelys, and is not a Leiurus sp.

According to the Israeli Scorpions Field Guide, deathstalkers can have also pale metasomal segment V, so a black one isn't a sure identification sign although it is very common among deathstalkers. The characteristic of the Israeli deathstalker are 5 ridges along its back. The species of deathstalker in the Negev (and Israel) is Leiurus hebraeus.

I haven't found an official reference, just a mention that the metasomal segment V can be pale in some adults.
Perhaps after molting the colour is different?
Also, dont know if it is Leiurus quinquestriatus, L. hebraeus, or L. abdullahbayrami
I see picture with the same pale coloration at sciencedirect.com/topics/agricultural-and-biological-sciences/…

source: Stack Exchange

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sort: votes


text:
How to Determine the Most Conserved Sequence from BLAST Result?
I used BLAST to find the best aligned DNA sequence to my query sequence.  The BLAST result shows a number of sequences that it calculated to be the best aligned sequences to the query sequence that I give.  Each of those aligned sequences have an e-value score representing the best hit by chance.
My question is how can I determine if the query sequence is highly conserved with the aligned sequence, or not?  Can I determine that by saying the sequence with best hit e-value (lower e-value) is the one that is highly conserved? or are there other concepts that I need to consider in this case?
I appreciate your help!

Whats the identity score like?

The identity score is pretty consistent with the e-value score.  I mean the higher the e-value score the higher the identity.  I am curious what the "identity score" tells me about the aligned sequences. @RoverEye

The "best" is the one with the highest ID score, lowest e-value and greatest length. There is no magic bullet, all of these are important. You should always look for the most similar sequence that matches as much as your query as possible with the lowest e-value possible.
Furthermore, it will depend on what you are looking at. If, for example, you are blasting a protein with a specific domain and are looking to find its homolog in another species, it is often more important that the domain be conserved than that the whole sequence be very identical. If you find a sequence with high identity but where the domain is not conserved, that is probably not what you are looking for.

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Why are irises unique?
I heard that irises are different and unique for every person. According this link, probability of two irises having identical pattern is 1 in 10 to the 78th power. That's how iris scanners identify the identity of people. This technology is becoming very evident. So I ask, why are irises for each person different and unique?

What research have you done before asking this (interesting) question? Do you have evidence for, or have you "heard" that irises are unique (the latter, and lack of support for this statement can render this question off-topic). Can you support this statement? Do you think the same factors that control fingerprints can actually control the formation of the iris?

@anongoodnurse I edited it.. I added evidence and links... and you're right, the same factors that control fingerprints probably don't control the formation of the iris...Thanks 4 the help!

Iris is a thin, circular structure in the eye, responsible for
controlling the diameter and size of the pupil and thus the amount of
light reaching the retina. The color of the iris gives the eye its
color. In optical terms, the pupil is the eye's aperture and the iris
is the diaphragm that serves as the aperture stop.

Color and structure of iris is greatly depended upon genetic links, but the patterns are not. Iris is developed by the prenatal(before birth) growth through a process of tight forming and folding of the tissue membrane.

The human iris begins to form during the third month of gestation. The structures creating its distinctive pattern are complete by the eighth month of gestation, but pigmentation continues into the first years after birth. The layers of the iris have both ectodermal and mesodermal embryological origin, consisting of (from back to front): a darkly pigmented epithelium; pupillary dilator and sphincter muscles; heavily vascularized stroma (connective tissue of interlacing ligaments containing melanocytes); and an anterior layer of chromataphores and melanocytes with a genetically determined density of melanin pigment granules. The combined effect is a visible pattern displaying various distinctive features such as arching ligaments, crypts, furrows, ridges, and a zigzag collarette. Iris colour is determined mainly by the density of the stroma and its melanin content, with blue irises resulting from an absence of pigment: longer wavelengths differentially penetrate while shorter wavelengths are reflected and scattered, a phenomenon resembling that which makes the sky blue. The heritability and ethnographic diversity of iris colour have long been studied, but until the present research, little attention had been paid to the achromatic pattern complexity and textural variability of the iris among individuals.
Reference

Iris Recognition vs. Retina Scanning
Iris and retinal scanning are ocular based biometric identifiers. Iris recognition uses a camera to capture image of the iris. Iris is the only internal organ visible from outside the body. Iris scanners can acquire an image of the eye from a distance of 3 to 10 inches.
In retinal scanning, the device send a beam of light deep inside the eye to capture the image of retina, which is located on the back of the eye. retinal scanning is not widely used due to the intrusive methods used to capture the image.
Factors which enhance the iris scanning system,

reference

In the list titled "The Advantage of Iris Recognition", only the first two items are really biologically relevant.  The other points are just advertising the technical features of some particular iris recognition system.

@augurar:Uniqueness of iris is described above the title you mentioned. Your point is right but I deliberately put it there for sharing some knowledge about background working of an iris scanner

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Fab fragments of antibodies to fight viral infections
I was reading about Fab fragment and about using them to fight of viral infections. It seems that the Fab attaches to the viral receptors, which stops the viruses from attacking the cells. It seems that it has been done before. I was wondering, since Fab fragments can't activate immune response, what happens to the Fab-virus complex in the blood?

What virus or virus family? Could you also provide us with a link to the paper you're reading?

@Luigi hopefully as many possible viruses.. but the link I have talks about influenza virus

@Luigi here is the link: http://jvi.asm.org/content/77/15/8322.full.pdf

It won't trigger a full immune response since the Fc part of the antibody is needed for opsonization.

There are three pathways by which soluble antibodies (which is what the Fab fragments arise from) can inactivate viruses (from Janeway's Immunobiology):

What you describe with the Fab binding to the viral receptors is a type of neutralization. Janeway claims that the type of naturally occurring antibody primarily responsibly for neutralization, IgA, is mostly exported to mucous secretions, so presumably it gets digested/excreted along with the rest of the mucous proteins.

I want more info about the section your book doesn't talk about... I want to know what happens to that complex...so unfortunately, you have not answered the question.

For opsonization and complement activation the complete Ab is required (i.e. with the Fc fragment). But for neutralization I imagine the Fab is enough to prevent bacterial adherence. Maybe the poster can focus on this aspect.

yes.. I agree with @ddiez (BTW, which page is this on?)

oh.. I found the page.. (it's page 308)


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How to inhibit formation of specific antibodies (to antisera)?
Is there a way to inhibit an antibody response to a specific antigen using immunosupression? I am interested in reducing the anti-antibody formation to animal antibodies such as murine antibodies in antisera.
I have read that there are ways to decrease the immune response to antisera but haven't found a detailed paper on how they work.
Update 12/3/2014: Would this work? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374127/pdf/0100491.pdf
Although it is streptavidin, could a similar process be used for antibodies?

Related post

Are you asking about in vitro or in vivo?

in vivo... if possible...

As far as I know there is no way, except for suppressing the immune response at all. If it were possible, this would be a great help against autoimmune diseases.

If you are referring to reducing the titer in the immunized animal, you could give the animal a drug that has immunosuppressive properties. Velcade (PS-341) is a drug that effectively reduces plasma cell counts. There are many immunosuppressive drugs available.
If you  want to reduce the antibodies affinity, you are undertaking a much more delicate process. Affinity can be transiently affected by introducing a  unfavorable environment for the antibody. You can accomplish this by changing the temp, salt conditions, pH or introducing a denaturing agent like guanidine HCL.
Changing any of these conditions in just a little excess could also result in a permanent reduction in affinity.
If you are attempting to tailor the affinity constant of the Ab by changing the architecture of the antigen, you are correct this can be done using site directed mutagenesis. However I think it would be more effective to perform a random mutagenesis and then screen the mutants for the Ka value you want.
Lastly the antigen could also be post-translationally modified. After performing in vitro transcription and translation you could modify your antigen using different strategies such as ubiquination, phosphorylation, prenylation etc... All these could potentially affect Ka as well.
A Hybridoma system to produce a monoclonal antibody should also be explored. Here is a reputable company that produces monoclonal antibodies:
http://www.sdix.com/Products/Custom-Antibody-Services/Ab-Production-and-Services/mAb-Antibody-Development/Hybridoma-Development.aspx

Hello @rhill45 , I did read about reducing immune response to an antiserum so I would like more info on that.. but otherwise, thanks for the info... BTW, can site directed mutagenesis and ubiquination, phosphorylation, prenylation etc. be used to change the Fc region of an antibody? Can it  also be used to chimerize the antibody?

@TAbraham check this out http://m.peds.oxfordjournals.org/content/23/4/289

Chimerize the ab?? To the antigen? What are you trying to do?

I am trying to decrease the immune response to foreign antibodies (this is why i was talking about anti-sera) so the antigen would be the foreign antibody...

Also, would creating antibodies against the antibody-producing cells work?

If you are creating an antibody against another antibody what you are creating is called a secondary antibody. If you want to decrease antibody production in a host the way to do that is through immunocompromising  the host. That are many ways to do this with varying specificity: radiation, chemicals, viral infections, giving the host certain cancers; even an autoimmune disease could work I guess. Let me know what I'm missing in my answer to get it marked. Using Cyclosporine is going to be your easiest and most well studied method.

I am trying decrease the production of secondary antibodies...

@T ABraham Let me know what my answer is missing to get marked as correct.

are there any other studied ways to decrease the production of secondary antibodies? It seems cyclosporin won't work... I want the most specific way to do so if possible... BTW, Thnx for your answer...

Velcade is a proteosome inhibitor that is very specific for lowering plasma cell concentration (these are the cells producing the antibody).  Have you looked at a Hybridoma system to make a polyclonal secondary antibody?

What do you mean about polyclonal secondary antibody? i know about hybridoma systems for monoclonal antibodies but don't fit my needs... I am trying to stay away from chimeric and humanized antibodies as well...

Oops meant monoclonal (sorry iPhone)

also, I don't want to use hybridomas because it would take away the reason for the project I am using this info for...

Let us continue this discussion in chat.

Would you like to talk in chat?


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Why does DNA have its name?
Why is DNA called deoxyribonucleic acid and not something else? I get the nucleic acid part (because that's what DNA is made of) but what about the deoxyribo- part, especially the ribo- part. Maybe because DNA doesn't have oxygen, hence the "deoxy-"?
(Also, please tell me what is wrong with my question or whether there was a duplicate I didn't find so I can fix this question or delete it.)

Ribo- comes from ribose, which is a -ose(sugar). desoxy-ribose is a ribose with one oxygen missing. DNA uses desoxyribose while RNA uses ribose.

@Remi.b - perfect answer! Please convert to save the question from the closing frenzy. As never having received proper Latin training I sympathize with my fellow analphabetics :)

It is not "the" perfect name. Someone just named it that way. Friedrich Miescher called it nuclein. In earlier times DNA was actually called desoxyribonucleic acid. If your question was about why "deoxyribo-" then I guess it is mentioned in wikipedia. Hence I am voting for closure.

@WYSIWYG - I commented 'perfect answer' not 'perfect name'. I think it's a valid question with a valid answer, provided the comment is converted.

@ChrisStronks Oh I did not comment at your comment.. The "perfect" term is co-incidental

Deoxy because oxygen is missing at the second position

I'm voting to close this question as off-topic because it is a trivial question about chemical nomenclature that could be found easily.

The name is derived from the sugar which is bound to the base. For RNA it is Ribose (that why it is called ribonucleic acid) and for DNA it is Deoxyribose (hence the name deoxynucleic acid). The deoxyribose is missing an OH-group at positition 2 of the sugar ring, the name literally means "without oxygen". See the image below (from here) for further clarification:


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Is there any independent non-DNA based information system in the cell
The information in protein is not neccessarily independent of the genome as the information of amino-acid sequence comes directly from the  genome. The process of post-translational modification may be another candidate but the main players in this process are proteins so its not clear whether this process is totally determined by genome (total DNA-based information) or some portion of it comes from a different source.
Obviously the external world is a source of information but I am interested in internal sources.

What do you mean by "information system"? Information per se is defined only if there is a sender/receiver or rather a transmission process. In evolutionary terms, information is something that is heritable, e.g. is stably inherited from parent to offspring cell throughout an indefinite number of reproduction steps. Do you mean this latter interpretation?

yes, the latter.

According to the comments, the question is about inheritance systems of cells. The "mainstream" information storage and inheritance system is of course DNA (and RNA in some cases). However, there are additional and parallel inheritance systems even within a single cell (not to mention in multicellular organisms). These form a subset of epigenetic inheritance methods and - as expected - are less precise than the information copying mechanisms of polynucleotide replication (in eukaryotes) and certainly more limited in the amount of information that can stably maintained throughout generations. This was explored in detail by Eva Jablonka and Marion Lamb (among others) in a few books and many papers:

Jablonka, E. & Lamb, M. J. 1995. Epigenetic inheritance and evolution: The Lamarckian dimension. Oxford University Press, 346 pp.
Jablonka, E. & Lamb, M. J. 2006. Evolution in four dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life. MIT Press, 472 pp.
Jablonka, E. & Szathmáry, E. 1995 The evolution of information storage and heredity. Trends in Ecology and Evolution, 10, pp. 206-211.
Maynard Smith, J. 1990 Models of a dual inheritance system. Journal
of Theoretical Biology, 143, p. 41-53.

“An epigenetic ineritance system (EIS) is a system that enables a
  particular functional state or structural element to be transmitted
  from one cell generation to the next, even when the stimulus that
  originally induced it is no longer present. In other words, EISs are
  the systems that enable the transmission of various phenotypic
  expressions of the genetic information in an individual.” (Jablonka & Lamb 1995, p. 80.)

Epigenetic inheritance methods include the following systems that could in theory code for information that is potentially inherited from parent to daughter. The list is far from being exhaustive.

DNA methylation: a methyl group added to a gene's promoter represses its transcription. Methylation is heritable: when DNA replicates, methylation carries over. There are other chromatin-marking methods that are inherited.
Steady-state inheritance system: "the inheritance of functional states through self-sustaining metabolic networks, maintained by positive feedback." (Jablonka & Szathmáry 1995 TREE) The cytoplasm itself is also inherited by the daughter cells, but any information "stored" in the cytoplasm cannot effectively be "replicated" from cell to cell.
Structural inheritance system: 3D structures of the cell provide the template for similar structures to assemble, e.g. "transmission of cytoskeletal organization and of cortical organization" (Jablonka & Szathmáry 1995 TREE).
Symbionts and parasites (bacteria, viruses, plasmids, etc.) that can replicate within the cell (so that when the host divides, both daughter lineages receive the partner). Note, however, that if the parasite is too virulent then it is expected that horizontal transfer is more emphasized than vertical "inheritance".
Prion proteins. Prions are proteins that may exist in several distinct conformations, and at least one of these conformations is capable of replication by forcing its alternate conformation (and therefore alternate function) on the normal physiological form of the protein (both having the same amino-acid sequence). See Shorter, J. & Lindquist, S. 2005. Prions as adaptive conduits of memory and inheritance. Nature Reviews Genetics 6, p. 435–450.
...

How is DNA methylation "non-DNA based"?

@David Well, strictly speaking, it is. But a crucial difference compared to standard DNA-encoded genetic information is that heritable information is not encoded in the nucleotide order of the polynucleotide chain. On the other hand of course, (almost) everything is DNA-based when talking about biology (on Earth at least).

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How to get taxonomic specific ids for kingdom, phylum, class, order, family, genus and species from taxid?
I have a list of taxids that looks like this:
1204725
2162
1300163
420247

I am looking to get a file with taxonomic ids in order from the taxids above:
kingdom_id      phylum_id       class_id        order_id        family_id       genus_id        species_id

I am using the package "ete3". I use the tool ete-ncbiquery that tells you the lineage from the ids above. (I run it from my linux laptop with the command below)
ete3 ncbiquery --search 1204725 2162 13000163 420247 --info

The result looks like this:
# Taxid Sci.Name    Rank    Named Lineage   Taxid Lineage
2162    Methanobacterium formicicum species root,cellular organisms,Archaea,Euryarchaeota,Methanobacteria,Methanobacteriales,Methanobacteriaceae,Methanobacterium,Methanobacterium formicicum   1,131567,2157,28890,183925,2158,2159,2160,2162
1204725 Methanobacterium formicicum DSM 3637    no rank root,cellular organisms,Archaea,Euryarchaeota,Methanobacteria,Methanobacteriales,Methanobacteriaceae,Methanobacterium,Methanobacterium formicicum,Methanobacterium formicicum DSM 3637  1,131567,2157,28890,183925,2158,2159,2160,2162,1204725
420247  Methanobrevibacter smithii ATCC 35061   no rank root,cellular organisms,Archaea,Euryarchaeota,Methanobacteria,Methanobacteriales,Methanobacteriaceae,Methanobrevibacter,Methanobrevibacter smithii,Methanobrevibacter smithii ATCC 350611,131567,2157,28890,183925,2158,2159,2172,2173,420247

I have no idea which items (IDS) correspond to what I am looking for (if any)

The same question was answered here

I'll copy/paste my answer from StackOverflow here also.
The following code:
import csv
from ete3 import NCBITaxa

ncbi = NCBITaxa()

def get_desired_ranks(taxid, desired_ranks):
    lineage = ncbi.get_lineage(taxid)
    lineage2ranks = ncbi.get_rank(lineage)
    ranks2lineage = dict((rank, taxid) for (taxid, rank) in lineage2ranks.items())
    return {'{}_id'.format(rank): ranks2lineage.get(rank, '<not present>') for rank in desired_ranks}

def main(taxids, desired_ranks, path):
    with open(path, 'w') as csvfile:
        fieldnames = ['{}_id'.format(rank) for rank in desired_ranks]
        writer = csv.DictWriter(csvfile, delimiter='\t', fieldnames=fieldnames)
        writer.writeheader()
        for taxid in taxids:
            writer.writerow(get_desired_ranks(taxid, desired_ranks))

if __name__ == '__main__':
    taxids = [1204725, 2162,  1300163, 420247]
    desired_ranks = ['kingdom', 'phylum', 'class', 'order', 'family', 'genus', 'species']
    path = 'taxids.csv'
    main(taxids, desired_ranks, path)

Produces a file that looks like this:
kingdom_id  phylum_id   class_id    order_id    family_id   genus_id    species_id
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2160    2162
<not present>   28890   183925  2158    2159    2172    2173


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How valid are GO (Gene Ontology) terms?
I'm looking for papers quantifying the validity of ontologies such as GO.
I'm relatively new to using annotation terms, and I often hear things like "annotation is messy" and "GO is good but it's not perfect." So I'd like to find papers that give numbers for just how messy.
I'm looking for answers from any experts that have a sense of the "quality" of GO terms (however you want to quantify it). For example, what fraction of terms are just wrong? The more computational parts of me want to sum up GO (or other ontologies) with a few descriptive validation statistics. e.g. "GO terms have an 80% precision and an R^2 of 0.6."
I'd like to see a few more examples similar to this paper that shows that a good fraction of GO ontology can be rebuilt from the ground up from independent data. That seems like one way to validate GO quality. They include this line about lack of GO validation in general literature: "... problems [with consistency and bias] are difficult to assess due to the lack of any definitive gold standard for the rigorous validation of GO."

for what did you planned to use GO annotation? genes or proteins( maybe enzymes?)

@RickBeeloo Genes or proteins would be good. Although, really, any attempts to quantify bias or precision of annotation terms would be interesting.

There are quite a lot of articles(1,2, etc.) which have investigated this, I think this article did a great job to give a visual representation of the specificity, reliability and coverage:

also this article noticed the following:

Compared to electronic annotations, it is not surprising that curated
  annotations have a considerably lower average coverage (Fig. 8,
  vertical lines). Indeed, the main appeal of electronic annotations is
  precisely that they scale efficiently to large quantities of data. But
  in terms of reliability, and contrary to current beliefs, curated
  annotations that use evidence other than experiments from primary
  literature do not fare better than electronic annotations (Fig. 8,
  horizontal lines, Fig. S9 in Text S1). In fact, we observed a higher reliability for electronic annotations than for curated annotations (0.52 vs. 0.33). the figure blow is figure 8 from the article

I don't know if you are just curious in the reliabilty of GO or if you are searching for an other kind of hierarchical annotation method, but e.g. for enzymes there are also EC numbers.  I can continue citing the article but I would suggest to read the article from which I used the figures ( Quality of Computationally Inferred Gene Ontology Annotations). Secondly this article is more recent and  something similair was done here. Among other things they also compared the computional annotation from 2008 with manual annotation in 2010 for the same set of GO terms:

So I would also recommend to read The what, where, how and why of gene ontology—a primer for bioinformaticians. This article and the previous mentioned article will give you a good insight in GO terms.

No problem, I think the articles will make it clear for you


text:
How to quantify the "stability" of a protein complex?
From experiment we've identified a subset of known mammalian protein complexes as interesting (approximately 50 CORUM complexes). We'd like to do an enrichment-style analysis to know more about them. One question I have is whether these complexes are particularly stable, since stable complexes should be biased towards detection. However, I don't have a chemistry or molecular biology background, so I don't know how to approach finding the stability of a protein complex.
Given a list of proteins in a complex, are there any conventional, in silico ways to estimate the stability of that protein complex? If not, have people published numbers for the stability of well-known complexes?
Edit: I'm okay being vague about the definition of "stability" since I'll be satisfied with an answer that uses any definition of it.
Edit: This question is answered on biostars.

Is this a homework question? If so, you should add the homework tag. Also, in general I would avoid using the word stability, because it is a vague concept. If you are talking about free energy you are talking about the structure of lowest free energy. Binding of ligands may involve quite different thermodynamic properties like binding energies. It's not my field. But my point is you should define precisely what it is you want to measure.

@David Thanks. I edited the question to be more precise, although I'm not sure how to define "stability" in this case. Really I'm asking if there are conventional ways to estimate the theoretical tendency for protein complexes to "stick together", whatever that means exactly.


text:
Least painful way to die
There is a lot of talk about inhumane treatment of animals and how we don't kill them in the proper way. I wonder how much research is done on this subject. What is the overall least painful way for an animal to die?
I also wonder if this would be the same for a human. It is often said that its least painful to die in ones sleep and i wonder if this is true. I wonder what is the most humane way to execute a capital punishment (if that is at all possible)

Should we be worried?

hah, yea it does sound pretty grim. I think the actual answer is not something that is easily available to most people. I just wonder how much we actually know about it because people keep screaming for more ethical treatment and i just dont know if we even know what that would be. And if seemingly more ethical treatment (like sedating animals before) are actually more ethical. Chemical ways might seem easier on the eyes but they actually better.

Part of the problem is: how do you know when an animal is suffering or in pain? Maybe looking into pain management research that uses animal models would be informative.

The American Veterinary Medical Association (AVMA) has thought about humane methods of euthanasia quite a bit and has an extensive (102 p. PDF) set of guidelines for the euthanasia of animals. The guidelines are not the same for all animals. Some examples:
Companion animals (e.g., dogs and cats): injected barbiturates are recommended
Laboratory animals (e.g., mice and rats): injected barbiturates are acceptable as are inhaled agents (isoflurane, carbon dioxide).
As for humans, you might look into the physician assisted suicide literature. I think that these generally use a sequence of drugs. As far as natural deaths, kidney failure is supposed to not be very painful.

Good answer but... there is a big point to be made on lab animals. Certain drugs may or may not be appropriate if the animals are to be used for experiments, as the drug may inficiate the results (e.g. I would avoid barbiturates if the animal's brain is being used for doing electrophysiology afterwards)


text:
How to automate this custom gene expression microarray chip?
I have 16 gene sequences that I am interested in their detection in clinical samples. I already measured their RNA levels by using RT-qPCR technique and their benefit has already been proven to help in diagnosis of clinical cases. Now I want to take this gene expression profiling into another level of automation. The first thing came to my mind is the microrray chips. I don't have much experience in micrarrary, I want to have a custom chip containing these 16 genes in question. These are 13 target human genes and 3 reference genes (housekeeping genes) for normalization.
Question
- is it possible to have this custom chip?
- How can I get such a custom microarray chip?
- What is needed to automate this process at a production level?


text:
What is the suitable terminology to describe this study approach?
I need to know the correct term(s) which are usually used in the parlance of both biology and bioinformatics for this study approach:
About 11 transcripts were investigated using qPCR for a number of samples (about 200) and then  the gene expression data were subjected to data mining tools: principal component analysis (PCA), cluster analysis (CA) and the results were interpreted using other supportive data that were not included in PCA in order to reveal the nature of acquired clusters.
Clusters obtained were then predicted from the gene expression data using machine learning classifiers. In short, it is a blend of molecular biology, data mining tools, and machine learning classification (predictive modeling).
Please if you have ever done this kind of data analysis, what should be the appropriate term to describe this approach?
Likely candidates
Gene expression profiling study
Transcript profiling study
Transcript Wide Analysis Study or TWAS for short

I would bet the author is furthering a global screening approach (probably micro arrays). You don't really have enough info given , can you cite the paper? Right now There's a few different things going on here, like you deduced.

it isn't a microarray, it is a 96-well based gene expression analysis using real-time quantitative PCR (sample maximization approach, not gene-maximization). Unfortunately, I am not aware of any paper that did the same thing.

I didn't say IT was a microarray, I said the intial study could have been a microarray, and this experiment you describe is now "pin-pointing" genes from that microarray data, as is usually, but not always, the case. As of now I think all this experiment can be parlanced into would be gene expression and linking that to omics data.


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What kind of fish did I see in waters off a tropical island in the Philippines?
Found this while diving in the southern Philippines.

@AlwaysConfused you need not give an explanation for your votes (or for not voting).

This is a Blackspotted puffer, Arothron nigropunctatus a commonly found fish on coral reefs in the Philippines. Although this species has a large color variation, the photos provided show common coloration (white body with black spots, a large black area around the dorsal ray). The white strip above the mouth is also a commonly found characteristic of this species, along with a face and snout that resembles a dog.

CC- Attribution - Photo by John E. Randall


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What do firebugs do when they "connect" by their rear?
See this image for example.
What are they doing? What is the name of this process?

They mate!
These matings can be very long

When copulating, firebugs (Pyrrhocoris apterus) form tandems for prolonged periods. Half of the copulations of marked individuals in the field lasted longer than 12 h, and some lasted up to 7 days. (Schöfl and Taborsky (2002))

The likely reason for such a long mating is for males to guard the female to prevent future matings and therefore to prevent sperm competition

males prolong copulations as a form of ejaculate-guarding under high competition with other males. (Schöfl and Taborsky (2002))


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Is there any example of living beings destroying their environment?
I had an argument with someone about mankind being the only being destroying its own environment. I don't think this is true, yet, I cannot provide any example of significant importance.
Are there any examples of a living being destroying its own environment, making it uninhabitable to them? (Bonus point if this event led to an environmental catastrophe or to their extinction.)

You might want to explore the topics of "exceeding a carrying capacity" as well as "succession." Both represent examples where organisms are responsible for modifications to their surroundings -- sometimes (often times?) to their own detriment.

Species don't live in isolation
As simple as the question seems, it actually contains some issue in the conceptualization of a species in isolation that affect or does not affect its environment.
Species do not exist in isolation from others. Many species have very important impact on their environment. These transformations would yield the environment to be unsuitable for the survival of the species over time if there were no other species to interact with. But by the existence of other species creating a cycle of, say oxygen for example, the transformation that the species is bringing to their environment is not seen as destroying the environment. In fact, if they were to disappear that could be an important problem. Let's go through examples
Example 1: Cyanobacteria and the Great Oxygenation Event
In the history of our planet, about 2.45 billions years ago, some species started to produce oxygen. Before that the oxygen level on earth was very low. We refer to this rise in oxygen as the Great Oxygenation Event. At the time, there was very few species that were performing respiration (breaking up oxygen and producing carbonic gas). Oxygen is a very reactive molecule and the rise in oxygen level was actually a MASSIVE environmental impact (arguably the most important life-induced environmental that had ever happen on Earth). It lead to an event of mass extinction.
The main contributors to this rise in oxygen were cyanobacteria. Cyanobacteria were most definitely destroying their environment. However, today, while modern cyanobaceteria are still producing loads of oxygen, we don't consider they are threatening the environment. In fact, they are fixing quite a bit of carbonic gas, which we rather tend to see as beneficial.
Example 2: Ants
I will not develop this example too much... Ants are greatly affecting forests of the world. Without ants, forests would be pretty different (see this non-peer reviewed source of information).
Ants are typically considered indicator of a "healthy" forest (see Segat et al. 2017; Lawes et al. 2017 and the book Gorb and Gorb 2003). Howe ver ants can also be invasive species that cause massive "destruction" on their habitat (Tsutsui and Suarez 2003; Lach 2003; Ness and Bronstein 2004).
"Destruction" is context specific
So, wether a species is "destroying" it's environment depends upon what other species are around. It also depends upon what you are aiming for (species diversity vs stable communities vs ...) but I won't go into these details.
Instead of asking

What species destroy their environment

it would not be 'more wrong' to ask

What species are present in ecosystem that are not adapted to their presence

or even (although that is a little of a stretch and some may argue on it)

What species have recently been introduced in a new ecosystem? / What species have recently changed their environmental impacts?

Always keep in mind, that no species can live sustainably on its own alone.
Do humans destroy their environment?
What do we mean when we say that humans destroy the environment, then? Human activities have changed drastically very recently. This is caused for two main reasons 1) our technology and, consequently our needs and therefore consumption have changed drastically ever since the industrial era. 2) we went through a demographic explosion.

So, yes we are pumping lots of carbon dioxide in the atmosphere. We get this carbon from forests we cut down, from large carbon reserves that have accumulated over millions of years (petrol, gas, peat and others). This change in our environmental impact is often seen (and for rather good reasons) as destructive.
Other modern species that destroy their own environment
Pretty much any invasive species would qualify as an example of a species that destroys its environment in a way that is not sustainable for itself over the long term. Among the invasive species that have important environmental impact that are seen as highly destructive, I can think of

Emerald ash borer (North America)
European starling (North America)
Feral hogs (North America)
Brown tree snake (North America)
grey squirrel (North America)
Zebra mussel (Europe and North America)
Japanese knotweed (Europe)
Cane toad (Australia and Latin Amercia)
Northern Pacific seastar (Australia)
Common wasp (Australia)
Rabbits (Australia and New Zealand)
Crown-of-thorns starfish (Indo-pacific and Australia)
Water hyacinth (global)
black wattle (global)
Argentine ant (global)

Many of these examples are from western countries because 1) that's what we tend to have most data on 2) because that's what I know having only lived in Europe, North America (and a little bit in Indonesia) 3) There are many examples from Australia and New Zealand because they are the world champions in invasive species and in bad policies concerning these invasive species!
Some readers will probably complain (and some with good reasons) about the species listed as what we mean by "destroy" is very subjective and my list is not intended to show the species that are considered "most destructive". Also, the locations of where these species are invasive might be inaccurate and I welcome anyone to edit them.
You can also consider any predator (incl. herbivores) and parasitic species that is leading it's prey / host to extinction such as

The experimental case with lizards in the carribean (Schoener et al. 2001)
The atlantic salmons leading shrimps to extinction (with the help of human activities) in the baltic sea
The red foxes affecting (with the help of human activities) hares population in Europe.

Coming back to the question

Is there any example of living beings destroying their environment?

Yes... other species than humans are "destroying" their environment. Estimating how much they are destroying their environment is really hard to both define and measure. Without a good working definition and without looking at actual data, I would personally be happy to consider humans as being the species that "destroys" the most today.

Yellowstone National Park ecosystem will serve as a good example of this question.
Here is a link to an youtube video describing the situation pre and post introduction of grey wolves to Yellowstone (around 1940).
As you can infer from the video, when the wolves were hunted to the point they were non-existent in Yellowstone, the herbivores (majorly moose/elk) got free rein of vegetation. Since, they were left unchecked they went on to reduce river bank forest cover by a large margin. If the wolves were not introduced, the larger herbivores would have first driven smaller herbivores to zero by denying them nutrition and later find themselves suffering the same fate once they have completely consumed all vegetation.
However, it can still be argued that we are the only species to consciously destroy our 'habitat'. But the realization that we are doing so is quite recent and maybe, just maybe, if we had known what repercussions our activity would have on our 'habitat' we may not have done so.


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Can two proteins have equal primary structure but different secondary structure?
I've been reading lately about primary (which I understand completely) and secondary (which I do not understand that well since I'm not very good at chemistry) structure of proteins. My question is: Can two proteins have equal primary structure but different secondary structure?

By equal I assume you mean identical.
Yes, in fact several known proteins have different folding patterns for the same primary structure as part of their function. but most proteins can take on more than one folding pattern, in fact specialized proteins called chaperones exist to encourage (force) a particular folding pattern in some other proteins, especially ones that are essential or in which the other foldings can be dangerous.
The easy way to understand the difference is the primary structure is the amino acid sequence and the secondary is the first stage in how the protein folds (the other being the tertiary). the primary creates the secondary (and tertiary) but there is usually more than one stable folding.
this video contains a further breakdown of the different levels of structure.


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Dynamic of the number of cells over time as the embryo grows
I would like to investigate the dynamic of the number of cells over time as the embryo grows. I am interested in any multicellular animal species for which we can have some data. How does the number of cells change over time in an embryo?
I welcome any graphs, empirical data and/or mathematical expression for this dynamics.

Its a bit unclear what you are asking are you talking about how it has changed across many species or how it changes in a single species through a single organisms life cycle. in hte case of the former this may be a place to start, https://www.ncbi.nlm.nih.gov/pubmed/10225991

The question seems very unclear but I think this is because OP is using the term "evolution" where she/he should not. I don't think OP meant evolution as in the sense that a population evolve as to change the number of cells in the embryo (whatever that would mean as the stage is not specified) but rather the question is I would like to investigate the dynamic of the number of cells over time as the embryo grows. I am interested in any multicellular animal species for which we can have some data. How does the number of cells change over time in an embryo?. Is that right, @J.A?

@Remi.b it is indeed what I meant. Thx

your biggest limit is going to be how difficult it becomes to count the total number of cells, especially once you get past the blastula stage. In the beginning its fairly predictable often defined by the number of cells (2,4,8,16, ect) but once you reach blastula there just is not much incentive to try and count nor is it terribly consistent.  this may help https://www.researchgate.net/figure/Stages-and-molecular-events-associated-with-early-development-of-the-mouse-embryo-A_fig4_255951891

It also varies quite a lot by animal. nematodes for instance are famous for having exact cell counts (it can even be used to identify a species) which just does not occur in organisms with hox genes.

There are some interesting analyses in mice, zebrafish, and worms. These papers contain a lot of data at the single-cell resolution, so you'll need to read and find the exact numbers about cell counts over time. You might also want to take a look at this classic paper about cell counts in humans.

A starting point could be this very recent amazing movies and the corresponding research article published yesterday.
This is not my field of expertise, but I think you will find relevant information in the references cited by this article.


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why hens determine the sex of the chick?
So, I have an exercise where I have to correct the second part of the sentence. It goes like this:

In hens, the sex of the chicken is determined by hen, because the hen is the heterogametic organism

And I really can't find the mistake, please help.
 Also, I'd like to know why hens determine the sex of the chick.

Outside of small eventual semantic issues about the notion of "determination", there is no mistake in this sentence.

Do you know what the sex determination system is like in birds? Do you know how the XY and ZW sex determination system work?


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Original paper about the all or none law for neurons
I am looking for the original paper about the all or none law for neural activity.
I know that there is a very old article about the all or none law for mammalian heart muscle fibers, but I'm specifically interested in when this idea was first stated about neural activity.
In A logical calculus of the ideas immanent in nervous activity from 1943 this law is already mentioned like an established hypothesis, so it is probably quite old.

I would guess on the Hodgkin-Huxley paper.

Hodgkin-Huxley seems to be too new.

This probably goes back to Lucas (1909), Adrian (1912), and Bernstein (1912). But the idea might have started from Helmholtz (1850).

Lucas, K (1909). The ``all or none'' contraction of the amphibian skeletal muscle fibre. Journal of Physiology; 38: 113--133.
Adrian, ED (1912). On the conduction of subnormal disturbances in normal nerve. Journal of Physiology; 45: 389--412
Bernstein, J (1912). Electrobiologie. Braunschweig: Vieweg.

See also: Galvani's Spark: The Story of the Nerve Impulse and The great Era of English Electrophysiology:
from Francis Gotch to Hodgkin and Huxley


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Measuring genetic distance: $F_{ST}$ vs. Nei's distance
As far as I'm aware, Nei's genetic distance is quite old compared to $F_{ST}$. However, I have recently read more papers that utilized Nei's genetic distance alongside with $F_{ST}$. As I'm not very familiar with Nei, what are some advantages it has over $F_{ST}$?
Does Nei's genetic distance suffer from ascertainment bias?

What do you call Nei's genetic distance? Do you refer to $D_{XY}$ or maybe to $G_{ST}$ or something else?

A note about formating: $F_{ST}$ gives $F_{ST}$.  $D_{XY}$ gives $D_{XY}$.

Nei was born about the same time as $F_{ST}$ was first defined by Wright. So, Nei's genetic distance (whatever this is referring to) cannot be older than $F_{ST}$.

Apologies, but Nei's genetic distance in this case refers to $D_{XY}$. Thanks. Nei's $D_{XY}$ might be newer than $F_{ST}$, however there have been more extensive uses and research on $F_{ST}$ to address its shortcoming. To this date, I'm wondering how Nei's $D_{XY}$ compare to the current $F_{ST}$.

The question's interesting but it will be very hard to offer a general answer. They are two different measures of genetic distance. $F_{ST}$ is better known, more studied and is more closely related with the population genetic theory than $D_{XY}$. Depending on the question of interest you might want to use one or the other. Many authors now recommend computing both to get a better picture of the genetic distances. Note that there are many other related statistics such as $\pi_S$, $\pi_B$, $G_{ST}$, $G_{ST}'$, $G_{ST}''$, $\theta$ (I mean Weir and Cockerham estimator of $F_{ST}$) and $Jost'D$.


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Why is sex hurtful for some animals but pleasurable for others?
Sex seems to be pretty hurtful for feline for example. On the other hand sex is pleasurable for humans. Why is sex pleasurable for some and not for others? How do these things evolve?

what makes you think it is hurtful?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

There are various selection pressures that may lead to sex being more or less harmful. I don't think there is an easy way to summarize these selection pressures other than just going through load of examples. Here is an attempt to give you some notions of why can sex be pleasurable and/or painful. Note that I do not consider myself particularly knowledgeable in this field.
Why could it be pleasurable
We tend to seek for positive experiences. If we like sex, we have more sex. If we have more sex, we are more likely to have more offspring. Hence, the trait "liking having sex" is positively correlated with "fitness".
Why could it be harmful
Dick pics
In many species, the penis has spikes and stuff and is most definitely hurting the females. Here is a Drosophila penis

And here are penises of two dragonfly species

Here is a feline penis

By the way, according to wikipedia (could not find peer reviewed paper on the subject so take this with a grain of salt), some humans still have on remnants of those barbs you can still see on many feline penises left from our ancestor. They are called hirsuties coronae glandis. Here is a perfectly healthy (but I would tend to consider quite extreme) example of hirsuties coronae glandis

Some theory
There is a lot to say here and I only want to say a few words and hopefully you will go get more information by yourself.
So why do these species evolve these fancy and scary "armed" penises. In many species, it is a small investment for a male to make a baby (just mate and the job is done) but a big investment for the female (producing the egg, eventually even parental care, ...). Because the sex-ratio is always (assuming no group selection) pushed toward 0.5 (see this post and Fisher's principle), it happens that males end up with lots of free time looking for females (see Why are female not competitive for reproduction like males? and Bateman's principle). You might also want to read about sexual conflict.
Why would such penis evolve?
The reason vary among species. Here is a non-exclusive, non-exhaustive list of reasons:

In some species (e.g. nudibranch, damselflies)The goal is to remove the sperm from an eventual previous male so as to reduce sperm competition (Cordero-Riviera, 2016).

In some species, the goal is to damage the female reproductive track so that she will not subsequently mate with other males hence reducing sperm competition ().

In some species, the male can even leave toxic products in the female (Chapman et al., 1995).

In some species, females get severly harrassed by males for mating and rape is not unusual (e.g Drosophila). Some penile barbs and spikes can be used to get the female stuck in place. To avoid that the female can escape before the sperm has been delivered ()! That being said, in some circumstance such use of spiky penis might be beneficial to the female too. This non-peer reviewed article may bring some light.

In some species, the male can pierce through the female abdomen to deliver its sperm. This is called traumatic insemination.

In a classical experiment, Rice 1996 shows that there is an arm race between males and females. Race in which males increases their negative impact on female's reproductive organs and females protect themselves from it. The paper is free, is short, easy to read and has a pretty amazing experimental design. It is worth having a look at it.
Feeding the babies via the mother
I just want to point with other examples that sex does not have to be romantic in many species. In some species, the female eats the male after sex or even while having sex. To what I have heard (; please be cautious with this information), in some mantis prey, the male does not even release his sperm before the female has cut the male's head off. Why would the male do that?
A male that let himself get eaten by the females ensures that the female has lots of energy for taking care of her babies. Hence a male may increase his fitness by sacrificing himself to his partner.

Nice examples and good links! However, could you add some support for your first 2 bulleted points regarding reasons for armed penises (i.e., sperm removal and female injury). Thanks, @Remi.b!

Also note that your wiki link in support for a vestigial link to penile spines has no source/citation provided in the source text. Given my lack of knowledge of penile spines I can't be certain, but the remainder of your wiki link seems to suggest more of a glandular or sensory role which seems to deemphasize a spine origin. Could you dig a bit more to find more concrete support for this notion that HCG might have an evolutionary connection to spines. Thanks!

@theforestecologist Indeed, citations were lacking. It has been improved now (although some are still missing). I naively followed wikipedia's claim when talking about the evolution of hirsuties coronae glandis. I have now tried to find some peer-reviewed paper on that but could not find anything. I made sure to write "according to wikipedia (could not find peer reviewed paper on the subject)". Thanks


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What is that insect?
I was bitten by this insect (no big deal, but I cannot identify it). I took a picture of it (with my phone, so the picture is not great). I was sitting under some sort of vine tree (downtown though), and I think it fell from it. If that helps it happened in mid July 2016, in Montreal, Quebec, Canada.
I looked on several resources for biting insects in Montreal but I could not identify it. It was very small and yellow.
Also, the insect bit me, took some blood, and left me with a light burning sensation for about 10 mins. I am not a specialist at all in this, and I know nothing about insects, so I apologize for what I am going to write, but if I was to describe it, I'd say it was a weird mix between a very small yellow lizard (for the shape of the first half of the body) and a quite furry(for how it looked under). The head was shaped like a sharp triangle.
That's all the information I have, I hope that helps you identifying it!

Hmm, that's a difficult picture. How small would you say it was?

@picapica I would say it was around 1 cm long max, a few mm large max. This is actually the second one I saw. I killed the first one when I slapped my ankle (that's where I saw that it bled too much, and figured it took some from me)

I'm getting a leaf hopper feeling from the general shape of it. But I don't think those bite... Hope someone else can solve this mystery!

@picapica I checked leaf hopper, it looks a bit similar for under the body (I remember a few small "I don't know what" maybe small legs? hairs?), but the overall shape I am not sure. Thanks for the suggestion though. I met that bug twice at a coffee where I go on a regular basis, so next time I see it I'll do better pics! Meanwhile I'll keep looking on my own too!

The shape looks like a leafhopper for sure. There are several species that are known to bite humans though it is not very common. Without a better photo however it may difficult to say what species it is for sure.

Thanks for the feedback, I'll try to get a better picture when I see another one!

Looks to me like you were bitten by a yellow Katydid.

According to Wikipedia,

Large tettigoniids can inflict a painful bite or pinch if handled, but
  seldom break the skin.

Thank you, it looks similar but what is under the body does not match what I have seen. I should have taken a pic of the insect upside down, but it looked "furry" under. Thanks for the idea though, I'll try to look at more pics to have a better idea!

The leg configuration doesn't seem to match to me.

Very unlikely. By "biting if handled",  it literally means if you stick your finger in its mouth. Katydids wouldn't attack/bite a person under any normal circumstance.

Large katydids sometimes bite defensively if you try to pick them up.  E.g., true katydid Pterophylla camellifolia, predatory ones like Chlorobalius leucoviridis.

No, not a katydid.


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Why are children and adults so different?
In many animal species, juveniles aren't just smaller versions of adults. In mammals, the contrast is not as spectacular as in species that undergo metamorphosis, but still quite noticeable.
For example, puppies have shorter limbs and flatter faces than adult dogs. Fawns are coloured differently than adult deer, and males do not start growing antlers until they reach sexual maturity. There are behavioural differences as well: habituation is much stronger and faster in juveniles. In humans, children have different proportions than adults and lack secondary sexual characteristics. But why? Wouldn't it be simpler to form a small version of the adult and grow linearly?

Why delay sexual maturity in the first place?
Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
Why the different body proportions?
Why lose play behaviour and learning ability as adults?

I'm interested in mammals in general and humans in particular.

Narrowed down to mammals only.

Great question. Note that, while humans are often assumed to be born less developed than four-legged mammals, your question actually asks an even more profound (and general) question (with humans being perhaps the least interesting case).

From evolutionary standpoint (no time to look up resources) 1) delay before reproduction ensures weak DNA that leads to early death isn't passed on 2) there is a peak healthiness that provides stronger outcome for offspring, choosing partners based on age, in addition to other health factors often visible, gives an evolutionary advantage to one's DNA 3) nurturing and care is institutionally provided to the young looking offspring, which increases chances of reproduction, so those offspring that look young before reproduction have an advantage

if you've already lived a long life, then losing the desire to explore, be a dare devil, and learn new ways of doing things is an advantage - the patterns developed that brought you to old age will be better than trying new, untested patterns. So the evolutionary pressure would be to establish these patterns firmly and decrease the generation of new patterns of thought and behavior.

GREAT QUESTIONS!!!
Why delay sexual maturity in the first place?
-I believe it is also related to "the best-used" of resources. Firstly, it is unnecessary and impossible for children to have sex (biologically and evolutionarily), they don't have the physicality to sustain sexual intercourse or the ability to bear a children inside their body. Secondly, it is to focus resources on growth. Children uses lots of energy on growth. Human body does amazing jobs on allocating body resources or material so that we are in the best shape possible. If they don't do sex, they can focus more on growth.
Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
- This one is a hard one. I believe it is just how biologists categorize human growth. We can study how human bodies develop in each stage, which is I believe it's really important on morphology.
Why the different body proportions?
-Evolutionary advantages!!! It is believed that baby has a greater head portion than adult. That's why people say children learn better than adults. Human values their brains more than other organs of the body, developing intellectual capacity as early as possible allows them to win in natural selection.
Why lose play behaviour and learning ability as adults?
If I understand you correctly, you are asking why adults lose their play behaviour and learning ability as they grow up. For learning ability, I believe it is caused by degeneration, just like the other organs of the heart. We have a mortal body and so once the body hits its maximum growth capacity, it will start going downhill unfortunately. For play behaviour, I believe it is a human behavioural changes due to life experience, social expectation and peer interaction. We lose interest of 'games' as we grow up because they are considered to be childish, silly and not useful.

Can you provide references? What you believe isn't really broadly useful.


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Do swarm of the same species attack each other?
What happens when two swarms find each other?
For example: When a swarm of bats, of the same species, go through another bat swarm. Do the bats attack one another or they simply merge into a bigger swarm?

Welcome to BiologySE - thanks for your question... you are actually asking several questions that may all be difficult to answer in one posting. You may want to try and narrow the focus at bit.

Look for the keywords agonistic behavior, ethology, swarm, group, flock, herd... https://sciencebasedlife.wordpress.com/2011/09/26/what-do-you-call-a-group-of/ Not sure how accurate it is, but seems interesting.

@VanceLAlbaugh I don't think the OP is asking several questions. It's one interesting question with different answers depending on the taxon. That's the kind of question that makes biology so interesting.

I'm sorry if I was unclear. My question was about swarms in general and how they interact with their same species swarms. And if one single animal of its kind joins the swarm if he is accepted or not.

It will depend on the species and group you're talking about. If the species is territorial, one swarm will tend to chase the other away. If it's a locust, they'll merge until they get to trillions of tons...
A study on wasps (Vespidae) I've read years ago showed an interesting experience. One individual wasp was tied by the waist and put close to different nests. The violence demonstrated by the nest was greater in a different species, median in the same species with a greater genetic distance, and none to her own or related nests.
Some "solitary" bees are very interesting in this respect, because they show many different kinds of sociality in related or even the same species, like many Halictidae and Euglossina (Apidae).


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Why is this giant water bug out of the water?
I recently took a picture of a giant water bug actually out of the water.

Every instance that I have seen these of critters they have always been in the water (sometimes even feasting on frogs), but this one had climbed up onto a reed.
This could be totally normal behaviour, but it also occurred to me that there are pathogens such as Ophiocordyceps unilateralis that change insect behaviour, including climbing up blades of grass.
Is climbing up onto reeds a 'normal' or 'aberrant' behaviour for giant water bugs?

This observation was identified on iNaturalist to be an American giant water bug.

I couldn't find a definitive answer, just a suggestion that they fly to find other ponds and lakes: http://www.naturenorth.com/summer/bug/Giant_Water_Bug.html


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Is there an published method for removing the effect of isolation by distance from genetic distances?
Isolation by distance is the phenomena that (even partial) reproductive isolation due to geographical distance between reproductive populations will result in greater genetic distance between those populations. This phenomena is not the only thing that can affect genetic distances, including other forms of reproductive isolation.
Given that the example plot of genetic distance on wikipedia appears to be a linear-ish relationship, perhaps the effect that geographical distance has on genetic distances could be subtracted via a linear regression model. I'm not sure how common linear relationships are for this type of data, but you can find examples of non-linear relationships such as found in "Genetic and phenotypic divergence in an island bird:
isolation by distance, by colonization or by adaptation?". Other studies, such as "Direct and indirect measures of dispersal in the fairy shrimp Branchipodopsis wolfi indicate a small scale isolation-by-distance pattern", show pretty marginal linearity.
Is there a conventional procedure in the literature for removing the isolation by distance effect on the genetic distances?

I think that a first question might be why you would want to do such a thing. I am sure that you can come up with a statistical approach that "removes" isolation by distance effects, but isolation by (geographic) distance would be pretty convoluted with genetic distance in the first place, is my intuition.

You can kind of do this with Mantel tests and related methods. As always there are issues.
If we look at this publication, we for example find a similar motivation:

Another possibility for using the Mantel test is to compare the relationship between two matrices, but taking into account the effect of a third one (usually the geographical distances), as originally proposed by Smouse et al. (1986). When analyzing spatially distributed data, the main issue is to find out if the two matrices are “causally” related (i.e., in the sense that they indicate an ecological or evolutionary process), or if the observed relationship appears only because both variables are spatially structured by intrinsic effects (i.e., distance-structured dispersal causing more similarity between neighboring populations).

In this case, you would be correcting in some way for the effects of isolation-by-distance, probably using some measure of geographic distance as the third matrix in question. However, Mantel tests can't really be interpreted in terms of variance partitioning, which is what you seem to want.
There are more spatial regression methods available that may be able to do this, though they seem to be less popular (probably because Mantel is simple and relatively assumption-free). They treat the isolation by distance effect as a spatial autocorrelation, which makes a certain degree of sense. If you are interested in a variance-partitioning type analysis, these are probably a better bet than Mantel.
But there are issues because it is not clear how to interpret isolation by distance in the absence of the genetic distances; simple distance is probably not good enough, and there are multiple plausible formulations of the distancing mechanism that are not restricted to naive measures of distance. All this is to say, you can do this, but beware of the assumptions that you're making going in.


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What did Masatoshi Nei 1972 mean by "However, evolution does not occur so as to assure this property at least at the nucleotide level."?
In Nei 1972 he describes what is now called Nei's standard genetic distance. This math.SE post provides an exerpt to the definition of Nei's standard genetic distance. In this paper he states

In the present measure of genetic distance, the triangle inequality, which is often assumed in numerical taxonomy (see, e.g., Levandowsky and Winter 1971), does not hold. However, evolution does not occur so as to assure this property at least at the nucleotide level.

The triangle inequality can be nice to have, but it is fine that functions do not always have it. But I find his justification for not having it to be perplexing.
What did Nei mean that "evolution does not occur so as to assure this property at least at the nucleotide level"? And in what sense did use this criterion to decide that the other properties of his function were assured by evolution at a nucleotide level?

I don't have access to the paper so it's hard to place the quote in context. A little more surrounding text might help. But at a guess he might mean that the distance between individuals or populations does not satisfy it, because it may not be clear which mutational path is taken. For more on different metrics and the triangle inequality, see introduction here: https://dyerlab.github.io/applied_population_genetics/genetic-distances.html

@MaximilianPress The mutational path lengths may well have been what Nei 1972 was referring to. A metric computed on the nucleotide content alone would not necessarily be comonotonic with such pathlengths.

@MaximilianPress I wish I could send you the link directly. I can access it through my academic institution. Perhaps you can do the same.

No longer in academia unfortunately! And my alternative sources don't seem to be working right now.

I think this is just a way of saying that evolution is not sufficiently deterministic to expect it to follow simple mathematical relationships, and isn't meant to be any more profound than that. I'd think that saying "the purpose of evolution isn't to make neat mathematical results" or "biology doesn't obediently follow the assumptions necessary" would have the same meaning. Or "the triangle inequality doesn't hold here, and that's okay because you shouldn't expect it to". But I don't have access to the original document, either.

@BryanKrause Thank you for your perspective. The concerns about (1) degree of determinism, (2) purpose of evolution, and (3) necessary assumptions are not synonymous. Yet I can see any of them matching Nei's phrasing to an extent. I am sorry to hear that you are also unable to access the original document.

@DifferentialPleiometry Yes, I don't mean to say they are synonymous, just that I think they are all consistent with the intended meaning. I take it as a bit of a droll statement, in the spirit of https://en.wikipedia.org/wiki/All_models_are_wrong, and if so I am very sympathetic with the message it communicates.

@BryanKrause Thank you for reminding me that I want to read Science and Statistics by George Box.

@BryanKrause Having fresh eyes on the paper around the "All models are wrong" quote, I appreciate Box's point of view. I actually didn't know that the paper has a large focus on Fisher's career. I largely agree with Box that when it comes to Statistics, we should be wary of "mathematistry" rather than Math per se.


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I had an encounter with a cougar (mountain lion). What does the recurrence time look like?
I had an encounter with a cougar recently. I was walking down a muddy old forest service road when approximately 15-20 meters behind me a deer burst out of the brush with a cougar chasing it close behind. The cougar gave up the chase on the deer but watched it jump away (instead of turning around to see what I was doing). Meanwhile I am backing away around the corner to get out of the situation. I didn't see either the cougar or the deer again.
What I'm curious about that a biology perspective might be able to answer is how frequently cougars return to a hunting area. My qualitative understanding is that they have very large ranges, so under a quite few stochastic process models I would expect them to return to the same hectare relatively infrequently. But I don't have a quantitative understanding of this.
Has someone worked out some empirical distribution (conditional or marginal) on the return-time of cougars to a given hunting location?
Update
A cougar was spotted by someone else approximately 15 kilometres away within 2 weeks of my encounter.

This observation is a Casual observation on iNaturalist: ID 110726469

I'm guessing the variance on something like this is too great to be useful, beyond what you could roughly estimate by range. But perhaps someone will be able to answer anyways.

Yes, the variance could be very large. I also find that ecological models are not adequately validated, and rely too heavily on either linear preasymptotic AIC or asymptotic AIC to be realistic. But, I will take what I can get.

An obvious (at least to me) problem with doing such an analysis is that it assumes that all locations within the range are equally favorable.  But deer (a preferred prey of the cougar) have their preferred trails & feeding areas, so a successful cougar is likely to learn to hunt where the prey is, and not where it's not likely to be.

After a bit of googling: home range of a cougar is between 30 and 1000 km². If we assumed that it is a circle, the bigger number corresponds to a diamater of just above 60 kilometers, which is a two-three days walk for a human in a forest. So it is actually not that big.

@jamesqf In the case of a marginal distribution, yes. You can have conditional probability distributions that are conditioned on things like sources of water, trails, shelter, etc. Obtaining such detailed data is considerably more work.

@RogerVadim Thanks for looking that up, and for the back-of-the-envelope calculation. It raises interesting questions about the geometric properties of the home ranges of animals.

It did not answer my question, but this article on Fourier analysis of animal location is quite interesting.

this file gives the raw step-lengths and turning angles of a bunch of Florida panthers (from this paper). You could start there ...

@BenBolker Thanks! Considering another big cat is an interesting heuristic for representativeness.


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What precisely is the pairwise Fst calculated in GenAlEx 6.5?
A professor of population genetics informed me that there is not a unique notion of pairwise Fst scores in the literature. This information has made me more cautious about what may be implemented by a given software package.
I am considering the GenAlEx Excel plugin (Peakall & Smouse 2005, Peakall & Smouse 2012) for computing pairwise Fst scores. The documentation states

Pairwise Fst : Outputs the pairwise Fst values between populations.

Output Pairwise Matrix: Outputs pairwise population statistics as a triangular Matrix.
Output is to worksheet [NeiP] for Nei’s Genetic Distance, to [uNeiP] for Nei’s
Unbiased Genetic Distance and to [FstP] for Pairwise Fst. This is in GenAlEx format
for further analyses if required.
Output Labeled Pairwise Matrix: Outputs pairwise population statistics as a labeled
triangular Matrix. Output is to worksheet [NeiL] for Nei’s Genetic Distance, to [uNeiL]
for Nei’s Unbiased Genetic Distance and to [FstL] for Pairwise Fst.
Output Pairwise Matrix as Table: Outputs pairwise population statistics as a table.
Output is to worksheet [NeiT] for Nei’s Genetic Distance, to [uNeiT] for Nei’s
Unbiased Genetic Distance and to [FstT] for Pairwise Fst.

I gather from this that [NeiP] is for a function called Nei's genetic distance, but the Wikipedia page on genetic distance suggests that there are multiple distance functions named after Nei. This also confuses me because I thought that these functions named after Nei were distinct from fixation indices, and yet they are mentioned under this Pairwise Fst section in the documentation. I am similarly confused about the inclusion of [uNeiL] and [NeiT].
And then there is the mentioning of [FstP], [FstL], and [FstT]. Clearly the P, L, and T correspond to whether the function returns a matrix, labeled pairwise matrix, or the same but as a table.
I've probably misunderstood the documentation, but I didn't understand why Nei's distance was mentioned. But in any case, what is GenAlEx 6.5 actually calculating (i.e. formula/model) if I use any of [FstP], [FstL], and [FstT]?

I have emailed the authors of the GenAlEx6.5 package. I'll post an update if I get a response.

Nei's original genetic distance was described in 1972 (paywall). He described the unbiased calculation in 1978.


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Do moose usually browse woody foilage approximately perpendicular to the long axis of the branch?
I am trying to improve my understanding of moose browsing behavior. One basic question is whether browsing on woody vegetation can tell us anything about the orientation of the moose's head. The following are videos I have watched that feature moose browsing on woody vegetation.

moose eating trees
Moose Eating Tree
Moose Browsing in Winter
moosing eating tree
Alaskan moose cow and calf browse on budding tree branches
Moose fences to protect ... trees?
Bull Moose browsing tree branches in Maine
Albino moose getting drunk on apples and fighting the local lawnmower to the death! (just at the beginning)
Bull Moose browsing in meadow at 11,000 feet.
Moose Browsing in Platte River Wilderness
North Platte River Adventure (at t=39s)

From these videos I have made some inferences.

For really short trees and brush a moose is might feed on buds from above.
Depending on the height and thickness of the central stem of a bush or tree, a moose might bite on it sideways to bend/break it into a horizontal orientation.
For branches off the side of larger trees I see that often the moose's head comes from roughly perpendicular to the branch rather than straight-on.

Is it more generally known that moose tend to browse from the side (i.e. roughly perpendicular) to branches on (larger) woody plants rather than straight on?

Note that this other question is about teeth marks on bark, whereas this question is about how moose browse on branches.


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Can we infer the orientation of a moose's head from the teeth patterns on tree trunks?
Background
I am interested in studying the distribution and patterns of behaviour of moose (Alces alces).
Moose chew bark off of the trunks of trees, especially Populus tremuloides. See some of the following examples:
Older

iNat 114539552
iNat 114538310
iNat 114537859
iNat 114537795

Newer

iNat 114539470
iNat 114539399
iNat 114538848
iNat 114538783
iNat 114538569
iNat 114538481
iNat 114538387
iNat 114538247
iNat 114537633
iNat 115635455

Often the teeth marks are at a diagonal, which could be quantified with an inclinometer. In my imagination I see them applying most of the force downward with their top jaw teeth. I also suspect that for higher up parts of a trunk that are chewed that the inclinometer angle would be steeper due to the moose reaching up at a more acute angle with respect to the trunk. This could be confirmed quantitatively by measuring the height of the chewing from the ground and comparing to the chew angles at each recorded height.
The markings may depend on the type of tree. The examples given above are all on aspen trees and show lots of teeth marks, but this video Moose eating bark shows a moose both chewing and pulling in order to get bark off a maple tree. The iNaturalist observations from above are from a similar area, but this video Moose Eat Poplar Tree Bark is unlikely to be from the same area but also shows lots of teeth marks.
Question
Can we estimate the approximate orientation of the head of the moose relative to the tree trunk based on the chewing marks?

Note: This video How Humans Became (Mostly) Right-Handed claims that some information can be inferred from scrapes on surfaces. However, this considered scratches on teeth by (presumably) tools rather than scrapes on trees from teeth. This comparison is only analogical because the reasoning and methods could be quite different.

it might be possible from actual tooth marks but you don't have pictures of any of those. the a pic of the missing park probably can't tell you anything.

@John Suppose I can go back to this tree that clearly has teeth marks on it. Can you describe a method for taking those field measurements and from those estimating the head orientation?

Your best bet it to actually observe and record the feeding behavior then take detailed photographs of the tree, specifically close up shots that could actually show the marks left by teeth. then you can directly compare the two. tooth marks can often show the orientation of teeth by the marks left by the gaps between teeth. the fact moose only bite a very small portion of the bark they strip should work in your favor. keep in mind much of the stripped bark is imply pulled from the tree with only an initial bite to start it.


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How to biologically interpret path weight summation in weighted and directed gene regulation network?
I've considered asking this question on Bioinformatics SE, Mathematics SE, and Stats SE, however I've judged that my question belongs on Biology SE because I am interested in a biological (domain-specific) interpretation rather than a further development of the mathematics or software.
My question pertains to applying graph theory to biology, so first I will describe the graph in its mathematical properties and how they reflect biological properties.
The graph
Let's consider a weighted and directed graph whose nodes represent genes and whose edges represent the binary relation gene A regulates gene B. The directionality of the edges is imposed in order to reflect that gene A regulates gene B does not imply that gene B regulates gene A. The magnitudes of the weights are to represent some measure of how "strongly"  one gene is regulating another, and the signs of the weights are to represent whether the regulation is upregulation (positive) or downregulation (negative). For this graph, edges with a weight of zero are considered equivalent to 'no regulation' and should be excluded from the graph.
Path Analysis
Restricting ourselves to paths that do not visit the same node twice, what is the biological interpretation of the sum of the weights (of the edges) of a path between two nodes in the aforementioned graph?
I have conflicting intuitions. For example, why would these weights be additive? I'm not imposing that such weights have to be correlation coefficients, for example, but they are commonly used weights in networks that are not additive so it warrants some consideration in the more general case. If they're not additive, then their summation is not necessarily meaningful. Conditioned on being meaningful in the first place, my other inuition is that the meaning of such a summation would reflect the strength of 'indirect' regulation

There's quite a bit of use of graph theoretic approaches in gene regulation, so I'd suggest you start there and Stand on the Shoulders of Giants rather than reinventing gravity:
https://scholar.google.com/scholar?hl=en&q=graph+theoretic+gene+regulation
Although this isn't my area of expertise, I think the thing most obvious to me as a biologist and statistician is:
Sums are misleading in non-linear systems
Biology is very non-linear. You can probably get closer to linear in the graph you are describing if the weights reflect log-transformed ratios: this transformation makes a multiplicative system linear. But even after this transformation, you are making substantial assumptions. The only way to verify those assumptions would be with either a more complex model of the underlying system (since the graph you describe is quite abstracted) or the old-fashioned way: by experiment.

We have the same concern about the weights, as additivity is one of the conditions of linearity. Since posting the question I've been thinking about how to refine my question to be particular weight function, otherwise my question has multiple answers depending on what properties we can assume about these weights.

Yes, there are transformations that can linearize. A good point in general, although it doesn't answer my question. Partly my fault as I have not specified what operations are valid on these weights.

@Galen Overall, I think the question is a bit ill-posed. Rather than starting from graph theory and thinking about how graph theoretic measures should be interpreted biologically, I think you want to start from biology and figure out what biological question you want to answer. Then, the hard step that represents an intellectual contribution to science is deciding how to use the graph theoretic tools you have.

I think my question is ill-posed because it isn't specific enough. I think more would have to be said about the weights before an interpretation is possible.


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Evolutionary rationale behind migration proteins
Tumor cells are able to migrate due to specific migration proteins.
What is their evolutionary origin?
Or are they simply deregulated?

This would be a very long answer but just to give you some hints, the migrational mechanisms are already there and the cancerous cells makes use of them to metastasise. So in short its deregulation. What is under selection pressure tho are cancerous cells themselves to constantly change and evade cellular fail safes which kill (apoptosis) uncontrollably replicating cells. You can find out about this here (http://www.nature.com/onc/journal/v22/n42/abs/1206757a.html)


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How do beneficial features evolve in species without progressing through detrimental stages?
I'm thinking in particular of wings on birds that would - I'm guessing - have to progress through stages during which they confer no particular advantage. Or is it that all evolved features must have followed a path of incremental benefit therefore imposing a fundamental limit on what evolution through natural selection can "achieve"? (features that are not beneficial while gradually appearing cannot be evolved)

I thought i'd mention a thing about recombination, not as an answer since it's too short: two individuals may posses radically different sets of alleles if they have been part of lineages that have not had much contact (e.g. tribesmen of africa vs. urban dwellers) once they mate, alleles that have never met before may co-operate in a way that could lead to drastically novel features. Features that are due to the combination of alleles already existing but whose phenotypic output is entirely novel.

Features can evolve (or change already present features) which have no negative effect under the current conditions. You can very well have neutral changes which have no purpose. They can then prove positive later (or in a different environment). Changes are usually small and take place over very long time periods.
An example would be bacteria which mutated one of their enzymes for a energy pathway. Before the mutation the enzyme could only metabolize nutrient A, after it, it is a bit less specific for A, but can also metabolize B. As long as the living conditions are so, that only A is present, this will not change anything. If the conditions are so, that A and B are present and A gets limited, these cells will have a profound advantage over cells, which can only utilize A.

I see. So wings appeared through neutral changes in biped reptiles without going through detrimental stages? And more generally, the "path" of features never goes through detrimental stages - only neutral and beneficial?

There are some interesting hypotheses that wings initially evolved for display, not flight.  Then at some point, the winged dinosaurs also had a locomotive advantage, at which point the wings could further evolve with selection for even better locomotion and eventually full flight.
Here is an article about Darla Zelenitsky's work on this:  http://phenomena.nationalgeographic.com/2012/10/25/bird-mimic-dinosaur-hints-that-wings-evolved-for-show-not-flight/
There is also an article by Richard Prum in a recent Scientific American that mentions this.https://www.scientificamerican.com/article/dinosaur-feathers-came-before-birds-and-flight/


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Would our body adapt to changes that are not in our DNA?
If a person was to undergo a treatment or surgery at a very young age, that significantly reduced their final height, would the rest of their body adjust to the sudden change? If not; because our arms’ length is very similar to our height, would this give the person arms that weren’t proportional to the rest of their body?

It will be hard to discuss for the specific example you consider, mainly because it is unclear how would you treatment affect the person's height.
That being said, yes, our bodies can change in function of the environment. This is called phenotypic plasticity

Phenotypic plasticity refers to some of the changes in an organism's behavior, morphology and physiology in response to a unique environment.

Here the term environment does not only refer to outside temperature or other obvious environmental factor. For example, one can ask whether the size of a vein can react plastically to the blood flow. Here, blood flow is the environmental factor toward which, the plastic response is mediated.
Note that some plastic responses are adaptive and some are not. Note also that there are a lot of related terms (developmental flexibility, acclimation, polyphenism, developmental selection, ...) in the field of plasticity and different authors sometimes use these terms with slightly different definitions which can make everything a bit confusing.

+1 One note which might not be obvious to the OP. There are limits on the plasticity. A human somehow reduced to the size of a mouse would be very unlikely to survive, for example.