text:
Which concentration of BSA is recommended for dynamic light scattering experiments?
What is the recommended concentration of BSA to be mixed with water so as to prepare a very dilute solution in order to clearly study the intensity-intensity correlation with single scattering ?
I want to plot the intensity vs time correlation curve/graph, and eventually calculate the hydrodynamic radius in each case. I've seen different journals and texts provide varied concentrations ranging from 0.001 g/L to 3 g/L.

Needs more context. What is your goal? What have you tried? What references have you consulted?

I've edited the question a bit, it would help a lot if you could add more detail. It would help if you added more detail about the method (I guess it's DLS?) and equipment you're using, I'm don't know much about this area, so I can't say if the information here is sufficient to answer your question.

Yes i'm using DLS. The objective is to find the hydrodynamic radius of the corresponding protein. I'm doing a project on it and require to know the range of concentration to prepare a dilute solution of the protein with water to visualize single light scattering. Hope that might help.

You can easly calculate the absorbance from Beer's Law
A = εlc
Here you can get the values for Extinction coefficient by sequence at http://web.expasy.org/cgi-bin/protparam/protparam1?P02769@25-607@
So for your example 0.001 g/L  3 g/L with this R code, you can get the absorbance values for each concentration.
> PM <- 66432.9 #g/mol
> c <- seq(0.001,3,0.05) #get values from 0.001 to 3, by 0.05 increment
> V <- 1 #liters
> M = c((c/PM)/V)
> #Lambert Beer Law
> e <- 42925
> l <- 1
> A <- c(e*l*M)
> plot(A ~ c, ylab="A (280nm)", xlab="g/l")
> data.frame("conc"=c, M=M, A=A)
    conc            M            A
1  0.001 1.505278e-08 0.0006461407
2  0.051 7.676919e-07 0.0329531753
3  0.101 1.520331e-06 0.0652602099
4  0.151 2.272970e-06 0.0975672445
5  0.201 3.025609e-06 0.1298742792
6  0.251 3.778248e-06 0.1621813138
7  0.301 4.530888e-06 0.1944883484
8  0.351 5.283527e-06 0.2267953830
9  0.401 6.036166e-06 0.2591024176
10 0.451 6.788805e-06 0.2914094522
11 0.501 7.541444e-06 0.3237164869
12 0.551 8.294083e-06 0.3560235215
13 0.601 9.046722e-06 0.3883305561
14 0.651 9.799361e-06 0.4206375907
15 0.701 1.055200e-05 0.4529446253
16 0.751 1.130464e-05 0.4852516599
17 0.801 1.205728e-05 0.5175586946
18 0.851 1.280992e-05 0.5498657292
19 0.901 1.356256e-05 0.5821727638
20 0.951 1.431520e-05 0.6144797984
21 1.001 1.506784e-05 0.6467868330
22 1.051 1.582047e-05 0.6790938676
23 1.101 1.657311e-05 0.7114009023
24 1.151 1.732575e-05 0.7437079369
25 1.201 1.807839e-05 0.7760149715
26 1.251 1.883103e-05 0.8083220061
27 1.301 1.958367e-05 0.8406290407
28 1.351 2.033631e-05 0.8729360753
29 1.401 2.108895e-05 0.9052431100
30 1.451 2.184159e-05 0.9375501446
31 1.501 2.259423e-05 0.9698571792
32 1.551 2.334687e-05 1.0021642138
33 1.601 2.409950e-05 1.0344712484
34 1.651 2.485214e-05 1.0667782830
35 1.701 2.560478e-05 1.0990853177
36 1.751 2.635742e-05 1.1313923523
37 1.801 2.711006e-05 1.1636993869
38 1.851 2.786270e-05 1.1960064215
39 1.901 2.861534e-05 1.2283134561
40 1.951 2.936798e-05 1.2606204908
41 2.001 3.012062e-05 1.2929275254
42 2.051 3.087326e-05 1.3252345600
43 2.101 3.162590e-05 1.3575415946
44 2.151 3.237854e-05 1.3898486292
45 2.201 3.313117e-05 1.4221556638
46 2.251 3.388381e-05 1.4544626985
47 2.301 3.463645e-05 1.4867697331
48 2.351 3.538909e-05 1.5190767677
49 2.401 3.614173e-05 1.5513838023
50 2.451 3.689437e-05 1.5836908369
51 2.501 3.764701e-05 1.6159978715
52 2.551 3.839965e-05 1.6483049062
53 2.601 3.915229e-05 1.6806119408
54 2.651 3.990493e-05 1.7129189754
55 2.701 4.065757e-05 1.7452260100
56 2.751 4.141020e-05 1.7775330446
57 2.801 4.216284e-05 1.8098400792
58 2.851 4.291548e-05 1.8421471139
59 2.901 4.366812e-05 1.8744541485
60 2.951 4.442076e-05 1.9067611831

And you can get this plot from 0.001 to 3 g/l for albumine

Now you can choose the desired concentration for the absorbance you wanna work with


text:
How should I ship plasmids?
I shipped 10 µL of my vector miniprep to a collaborator in a 1.5 mL eppendorf parafilmed shut and stuffed into a 50 mL conical with some paper-towel padding.  However, something happened on the way and there was nothing (no liquid) in the tube when it arrived.  They didn't make any comments about the microcentrifuge tube popping open or broken parafilm, so nothing crazy happened but something did.
What's the most reliable way to ship plasmids?

Summary

the 10 uL of plasmid miniprep may have been splattered in the cap of the tube (AnnaF)
the eppendorf tube may have depressurized during air shipment and allowed the 10 uL to escape and evaporate
solution: try air-drying or blotting (Jonas) your minipreps prior to air shipment

Details
As AnnaF wrote, the 10 uL of your plasmid could have been hidden in the cap or dispersed around the tube, making appear empty.  You should check with your collaborators to be sure they centrifuged it.
According to a fedex document on shipping perishables (pdf) and a paper measuring the temp and pressure of air shipments (pdf), fedex and ups air shipments may experience low pressure environments around 0.56 - 0.74 atmospheres (atm).  At these relatively low pressures, perhaps an eppendorf tube sealed at 1 atm might breach.  The papers also note that ground shipments that pass over the rockies (i.e. in Colorado) may experience ~ 0.64 atm.
So perhaps your 1.5 ml eppendorf tube depressurized during the shipment?
It would be interesting to do some tests on the pressure-worthiness of eppendorf tubes.
Regarding the original question, in 2007 I prepared and shipped (fedex) a library of thousands of minipreps to hundreds of users.  1uL of miniprep was dispensed into wells of 384-well plates and airdried, then sealed with aluminum, then mailed.  Users rehydrate a well with 10 uL of water.  Generally it works.

A quite safe way of shipping plasmids is to put them on filter paper (see protocol and send a letter. Much cheaper.

+1 Fast, easy and very stable even for overseas shipments.

Plus, customs are much less fussy about a piece of paper than they are about anything liquid.

Did they try to centrifuge the tube when it got there to push all the liquid to the bottom? I know that especially when working with such little amounts that even shaking it up a little can disperse the contents all over the tube.
We have received plasmids from other labs before. Generally speaking the plasmids are sent in Screw-cap microcentrifuge tubes inside of some sort of canister. This is then packaged in a little foam cooler with dry ice to keep everything cold.

Since tubes can be crushed in the mail, the safest way to ship plasmids is to drip a few uL into a filter paper, and then wrap it up to seal it with parafilm, and fill out a detailed form about its content.
Good luck.

We have gotten into similar situations when other labs have sent us plasmids (or when we have taken out ancient tubes out from storage boxes at -20), and have since adopted the filter paper method. Another point to note is that you can just add, say, 10 μL of water to the "empty" tube (Mac) and use 1 μL for a transformation. It has always worked for us. DNA is seemingly invisible!

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text:
How do I prepare a PDB for submission to the Protein Data Bank?
I have a couple structures that are nearly ready to be deposited in the PDB.  Out of curiosity, I ran them through the ADIT's precheck tool and they failed with one error after another, as I lacked all sorts of additional records (TER, SEQRES, HETNAM, etc.) that my refinement and modelling tools don't seem to care about.
From what I understand/guess, the online submission tool will help fill in all the metadata (REMARKs, etc.), but how do I turn my coordinates into something acceptable?

Question has been reasked at http://www.biostars.org/post/show/42502/how-do-i-prepare-a-pdb-for-submission-to-the-protein-data-bank/

If you don't mind I'll borrow this question to add it to the crystallography.se proposal as an example

These two links go through the specifications required for the PDB format:
Link1: http://deposit.rcsb.org/adit/docs/pdb_atom_format.html
Link1 primarily goes through the specs. required if you say have a NMR file you would therefore require the MODEL statement. It also goes through other statements such as when to use TER and how each ATOM line should look etc...
Link2: http://www.wwpdb.org/documentation/format33/v3.3.html
Link2 goes through the other statements such as HEADER, REMARKS and TITLE

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


text:
Can I image Coomassie and GFP in gels at the same time with a fluorescence scanner?
I'm working with a GFP-tagged protein and am routinely using a fluorescence imager (GE Typhoon) and a standard optical scanner to capture fluorescent and absorption images, respectively, of my SDS-PAGE gels.  The Typhoon supports multiple channels, so is there some way that I can scan for the two on the same device (GFP + total protein)?  I assume I can't do absorption on a fluorescence scanner..
I could manually register the two images, but it would be laborious as they are at different resolutions, slightly different rotations, and the gel can stretch ever-so-slightly when placing it on the platens.

@leonardo the standard running/gel/loading buffers do not seem to be so aggressive as to destroy (all) the GFP; it may be denatured in the loading dye, but when washed out into the gel buffer it seems to recover.  On the other hand, putting the gel into destain or fixing solution is very effective at obliterating the fluorescence.

Coomassie blue fluoresces in infrared when bound to protein, so if your reader has the appropriate filter set, it should be possible.


text:
How many times did endosymbiosis occur?
According to the endosymbiont theory, mitochondria and chloroplasts originated as bacteria which were engulfed by larger cells. How many times is it estimated that this occurred in the past? Are there any examples of this process being observed directly?

What do you mean "how many"? Do you mean how many time it should have happened before mitochondria became our endosymbionts? This question doesn't make any sense for me...

I think this is a good question. Was it a unique or rare event, or an inevitable consequence of bacterial colonies cooperating? This is a fundamental issue in the development of multicellular life.

I think @mbq has covered the frequency question better than I can.
There is at least one modern example of this kind of new organelle formation.  Aphids have a deep, intracellular endosymbiont Buchnera involving some genome transfer that has developed in the last 200 million years.
There are many articles about this topic (eg: Nature from 2000), and it was a little controversial 15 years ago.  Now, it's largely accepted that this is a modern development of endosymbiosis, and a confirmation of the theory.

@Thomas Ingalis, with the example of Buchnera, why does a intracellular endosymbiont involve genome transfer? What is that referring to exactly?

@Vass, to be correct, I should say functional redundancy. Nikoh et al published an analysis in 2010 screening a complete aphid genome for transfered genes.  From the abstract: "Our results excluded the hypothesis that genome reduction in Buchnera has been accompanied by gene transfer to the host nuclear genome, but suggest that aphids utilize a set of duplicated genes acquired from other bacteria in the context of the Buchnera–aphid mutualism."  This redundancy can be construed as a step to organelle formation.

It depends of what you call endosymbiosis. In the sense of mutualistic interaction between host cell and intracellular organism, it also include Rhizobium bacteria and Fabaceae plants, some Cnidaria and algea in their cells, and even some micorrhizal fungi that invade into plants cells. But parasitic interactions are also sometimes call symbiosis, as symbiosis means just “living together” and the balance between profits and costs for each partner are sometimes difficult to measure and even changes in time. So in this wider meaning even Trichinella worm that live in mammal cell is an endosymbiont and endosymbiosis is very common.

There are evidences of secondary endosymbiosis i.e. organelle within an organelle. This is quite evident in Chromaveolates. Many unicellular Chromaveolates which had been classically referred to as unicellular Algae, have chloroplasts derived from other algae. This organelle in turn has a membrane bound suborganelle. For a quick reference you may see this article. Euglena and diatoms are some famous examples of this phenomenon.


text:
Spatial resolutions in optical microscopy
I have read that different optical imaging techniques such as  such as wide-field microscopy, confocal microscopy or STED microscopy can theoretically achieve a different spatial resolution.
However, I was only able to find information about the STED microscopy's spatial resolution (5.8 nm) on Wikipedia.
Does anybody know of any references or recommended reading (preferably free) where I can learn more about different optical microscopy methods and how the cope with the diffraction limit?

The theoretical resolution for an optical microscope depends on the wavelength used, but is close to 0.22 um (220 nm). Confocal microscopy does not greatly improve axial resolution; it dramatically improves the in-plane resolution (x and y directions, by excluding extraneous light). Theres not a lot to do to "cope" with that using those techniques. If you need more resolution, you can use the super-resolution techniques you mention, or the good old TEM.
There is some more information on the Nikon website: http://www.microscopyu.com/articles/formulas/formulasresolution.html
and on Olympus website: http://www.olympusconfocal.com/theory/resolutionintro.html

You could also have a look at Leica Microsystems' Science Lab. You will find lots of articles and tutorials on the different microscopy methods, ranging from basic microscopy knowledge to specific know-how, including latest information on STED: www.leica-microsystems.com/science-lab
For example:
gCW-STED Microscopy: When the Arrival Time of a Photon Matters
http://www.leica-microsystems.com/science-lab/gcw-sted-microscopy-when-the-arrival-time-of-a-photon-matters/
From Molecules to Tissues – Optical Tools for Cancer Research
http://www.leica-microsystems.com/science-lab/from-molecules-to-tissues-optical-tools-for-cancer-research/
(Disclosure: I have been involved in the launch of Leica Science Lab)


text:
What's the difference between mutation and substitution rates?
The Wikipedia section on substitution rates (shown below) isn't clear to me. What's the precise definition and difference between mutation and substitution rates, and how do they relate to each other?

Substitution Rates
Many sites in an organism's genome may admit mutations with small fitness effects. These sites are typically called neutral sites. Theoretically mutations under no selection become fixed between organisms at precisely the mutation rate. Fixed synonymous mutations, i.e. synonymous substitutions, are changes to the sequence of a gene that do not change the protein produced by that gene. They are often used as estimates of that mutation rate, despite the fact that some synonymous mutations have fitness effects. As an example, mutation rates have been directly inferred from the whole genome sequences of experimentally evolved replicate lines of Escherichia coli B.

Further context behind this question here.

@Tyersome's answer is correct if you consider that the only mutations that occur will result in substitutions. This is false for biology, if true for how the subject is commonly talked about. (I realize that I'm in the uncomfortable position of saying that Rich Lenski is being imprecise about his evolutionary terminology). In fact probably a rather larger proportion of mutations will result in other kinds of DNA modifications.
For those unfamiliar with the different kinds of mutations, substitutions (also called point mutations) are only one class of mutation. Other kinds include transpositions, inversions, insertions, deletions, and many many more.
In other words, the "mutation rate" is probably >2X higher than the "substitution mutation rate", and I suppose since I'm getting very involved with my terminology, we could then say that there is an "accepted substitution rate" (the same as the "substitution rate" that people talk about) and an "accepted mutation rate" which includes all substitutions but then also all other kinds of mutations that are incorporated as laid out in the quote above. (I have made up all the terms other than "substitution rate" and "mutation rate" to emphasize that I think the usage of terminology from the Barrick and Lenski article is extremely misleading).
We tend to focus on substitutions because they are easy to understand and our math works well for them. Thus when people write about the "mutation" rate they have a tendency to use it to mean the "mutations that lead to substitutions" rate. But that's an approximation for mathematical convenience rather than reflecting real biology.
It's good to recall that when Hugo de Vries wrote "The Mutation Theory" >100 years ago the mutations he was talking about were not substitutions but changes in ploidy- those are absolutely mutations, but they have nothing to do with substitution. In plants changes in ploidy are among the most phenotypically dramatic class of mutation, but those are invisible to analysis of substitutions.
Of course, the approximation for mathematical convenience has more or less taken over the field, so from that perspective @Tyersome's answer is perfectly correct, and it does directly address your specific question. But I think that there are problems with how the field in general thinks about this.
(Forgive me for being pedantic, I wrote a review on the topic: https://www.cell.com/trends/genetics/fulltext/S0168-9525(19)30012-5)

Thanks Maximilian. Very helpful. I noticed you introduced several terms here that would be great to define more precisely (e.g. you mentioned "substitution mutation rate", "accepted substitution rate",  and "accepted mutation rate", not sure if there are others). Perhaps this could be an answer with a preamble that describes the basic entities, mechanics and steps involved, followed by definitions with their corresponding Eqs. I would love to help if you can point me to the right info. This is a good time for people to learn more and become more interested inabout virology / genomics :).

updated answer to reflect that these are terms that I made up on the spot, to underline how Barrick and Lenski's "mutation rate" is actually just one way people use that term.

(I also clarify that "substitution" has a very specific meaning in terms of the kind of modification to DNA that occurs)

Ok thanks. That's helpful. I think I get it now. From what you are describing a substitution is just one type of change (a single point nucleotide change specifically). I somehow understood "substitution" to mean directly the "acceptance" (i.e. take over) of an entirely new chain, i.e. a whole new chain   "substituting" (displacing) a chain (e.g. a viral strain) that is prevalent in a population. What you are saying makes sense, i.e. there many other types of changes that can take place in replication that don't need to be simple single nucleotide substitutions.

BTW - This whole question spawned from a comment I got to this other question which still remains unanswered. I wonder what you think of it!

Ok, glad to have cleared that all up! I will take a look at the other question.

The mutation rate is the rate at which mutations happen — i.e. the rate at which "mistakes" are generated.
The substitution rate is the rate at which mutations are accepted — i.e. the rate at which "mistakes" become incorporated into a genome.
The difference is due to selection — if a mutation happens that results in an essential protein becoming non-functional that mutation will tend to be purged and thus won't be "accepted".
A relatively clear discussion of these differences:

Box 1
Mutation rates versus substitution rates
  It is important to distinguish between the rate at which spontaneous mutations occur and the rate at which genetic changes accumulate in a surviving lineage. The MUTATION RATE reflects the probability of a change in genome sequence between a parent and its offspring. It is the compound result of unrepaired DNA damage, polymerase errors, intragenomic recombination events, movements of transposable elements, and other molecular processes that introduce errors during the transmission of genetic information. However, only those mutations in lineages that persist — typically in the face of selection — contribute to the SUBSTITUTION RATE measured by whole-genome sequencing. The failure to carefully distinguish between these two types of rates is a persistent cause of confusion and misconceptions about whether mutations are random. In the same vein, the frequency of a mutant allele in a population generally does not equal the rate at which the corresponding mutational event occurs.

From: Barrick, J. E., & Lenski, R. E. (2013). Genome dynamics during experimental evolution. Nature Reviews Genetics, 14(12), 827-839.
You may also find the following article to be of interest:
Yi, S. (2013) Neutrality and Molecular Clocks. Nature Education Knowledge 4(2):3
.

When you say "accumulate", or "become incorporated into a genome", you obviously mean the genome of an entire population (e.g. species of virus in this case), not a single virion, right?

Also, is it fair to say that the substitution rate is the rate at which the mutation in question increases its population share (%) over the entire population? If so, what are the units for it?

Yes, you could think mutations as being accepted in the "gene pool".  2) No, I don't think that is correct. These are measures of new mutations either being generated (mutation rate) or being accepted (substitution rate). {I'll change the wording in my post since I see that accumulation is open to misunderstanding.}

Thanks - but on #2 - if the substitution rate is not the rate at which a mutation increases its population share (%), then what do you mean by a measure of "mutations being accepted"? Wouldn't the substitution rate be a measure of how successful a mutation is, where success would be defined as a fraction or growth over this fraction of the resulting (genetic) population?

This answer is not accurate. Probably only a minority of mutations that occur in any given genome would result in a "substitution" if "accepted"- a much larger proportion consist of expansion and contractions of satellite DNA. There is a bit of an ascertainment bias in how we think about mutations because substitutions are easy to "see" using most sequencing technologies.

I downvoted this answer because I was feeling grouchy and it touched on a pet peeve of mine, but upon reflection I decided that I was wrong to do so. The time window for changing that has passed, nonetheless I wanted to comment a symbolic +1 back in.

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text:
Difference between Diffuse Optical Tomography and Optical Tomography
What are there the differences between these two modalities?

Diffuse Optical Tomography (DOT)
Optical Tomography (OT)

Are there forms of OT that are not DOT?


text:
How many virus infections does the average human have?
According to the WHO:

67% of the population  are infected with herpes simplex virus type 1 (HSV-1)

Presumably there are other viruses as well that infect a lot of people. How many infections does the average person have?

What do you mean by "have"? Should we count short-term infections that can be caused by countless cold viruses from many different families? Or should we count persistent viruses only, such as HSV and HPV?

@EliKorvigo : I would call all of them.

There isn't really an average person; I doubt this can be answered as asked. If you live on a remote island, you won't have all that many; if you live in an overcrowded city, you'll likely have a ton; if you live in cold regions, your risk of many viruses is lower than in temperate or tropical regions. If you travel a great deal, you're exposed to many more than someone who stays put. Etc., etc., etc. Then there's everything in between. Maybe the only real way to get an answer to this is to look at rates for every known virus and add? I don't know. I think it's too broad.

You also need to make the distinction between being infected and becoming sick. The immune system can keep infections subclinical, but they will still remain present in the body.

This is likely very different depending on location. Most people live in Asia (China, India) or Africa. Most of the studies are done in North America or Europe.

Ignoring short-term (acute) viral infections, so only considering persistent viruses, probably on the order of 5-10-ish.  There are 8 human herpesviruses known, of which 6 (herpes simplex I, EBV, CMV, VZV, HHV6, and HHV7) are very common in humans, generally infecting 50-90% of a population.  There are over 50 strains of human adenoviruses, but only a few are very common and persistent; hAb2 and hAd5 are probably the most likely.  Then there may be a human papilloma virus or two persistently infecting many people, though the prevalence is lower than herpes or adenoviruses.  So, it's reasonable to assume that most people have somewhere around 5-10 persistent viral infections.
If you add in acute infections, and ask about all exposures during one's life, you're probably looking at thousands or tens of thousands of viruses, but the questions about what's a different virus and what's an "infection" become trickier.

I really like the this answer, but can you give a reason for "thousands or tens of thousands of viruses"?

About a hundred strains each of rhinovirus and enterovirus, plus multiple strains of influenza viruses, noroviruses, adenoviruses, RSV, parainfluenza, rotaviruses, reoviruses, coronaviruses, parvoviruses ... probably around a thousand already, and these are only the agents that have been identified and that are known to cause disease. New pathogens are still being discovered, meaning we're undoubtedly infected with many unknown viruses, and there's very little known about viral infections that don't cause disease, even though those are probably common too.

Thank you for this answer. I'm not an epidemiologist, so forgive me if I am very mistaken, but are you saying that we've all (on average) been infected by a hundred strains of enterovirus? Maybe we have, but that seems a bit high to me. With rhinovirus I won't disagree. I doubt that the "average person" has actually been infected by a great many influenza strains, and the numbers sound too high to me. But I repeat, I'm not an epidemiologist.

That's why I didn't want to answer that part.  Questions  of "what's a different virus" and "what's an infection" come down to shrugs and handwaving.  As soon as I say something, you focus in on the details, and they don't matter. It makes no difference whether we're infected with 10 or 20 or 50 enteroviruses, because the vast dark matter of viral infections outweighs all of them  If you don't like my answer (I'm not an epidemiologist either, just a virologist) then make your own; you can define strains the way you like, and come up with any answer you want.

I didn't intend to offend; I asked because that was the OP's question, and on SE, the answers are supposed to answer the question. If there isn't an answer, I'm certainly not going to try to give one. That was the point of my comments to the OP.


text:
How do I generate a phylometric tree given species names?
I have a list of species. I want to put those names into a tool and get back a visualized tree that includes names of shared order, suborder, family and genus.
Is there an existing tool that does this job for me or do I need to program my own solution?
(The solutuion in the other thread only shows the name of the species but not order/suborder/family/genus)

Possible duplicate of Visualising a subset of the tree of life

Biopython may have a module for this. I know it can parses phyloxml files and render a tree. You can query the ncbi database for the xml files. Here is some sample code that will render an ascii tree given a phyloxml file...
from Bio import Phylo
tree = Phylo.read("examplephylo.xml", "phyloxml")
Phylo.drawascii(tree)

There is also support for drawing more graphically rich trees using matplotlib. There is a .pdf book for Biopython that you can download from this url http://biopython.org/DIST/docs/tutorial/Tutorial.pdf
Hope that helps

There is support for other file types besides phyloxml, but I can only speak for the phyloxml files, because I have used them personally.

This is easily doable in the R package 'rotl' with only three simple commands.
E.g.
library(rotl)
taxa<-tnrs_match_names(names= c("Danaus plexippus",
                       "Sylvia atricapilla",
                       "Acrocephalus arundinaceus",
                       "Anas platyrhynchos",
                       "Oncorhynchus nerka",
                       "Hirundo pyrrhonota",
                       "Progne subis"))

tree <- tol_induced_subtree(ott_ids = ott_id(taxa))

plot(tree, cex = .8, label.offset = .1, no.margin = TRUE)

Full details outlined here: http://onlinelibrary.wiley.com/doi/10.1111/2041-210X.12593/full

As far as I am aware, there isn't an easy one-stop-shop solution for what you'd like to do.
My own solution for doing something similar (with the caveat that the NCBI taxonomies are not always up-to-date with the latest data) is to a) use NCBI's Common Tree page to build out the lineages you'd like to include and download it as a text tree (e.g. in Phylip format, which includes internal nodes), b) visualize the tree on a local computer using something like TreeView X or FigTree
It's a bit of a pain, but if you'd like to add additional metadata to the tree before visualizing it, you can edit the Phylip-formatted text file directly before opening it in one of the viewers.


text:
Experiments in vitro vs those with dead organisms and fixated tissue
Does the term in vitro necessarily imply that the organism/organs/cells of study are  dead?
If not, is there an alternative latin term to refer to studies of dead biological matter ? (e.g. in Connectomics where the tissue is biologically dead, and has been fixated and sectioned with a microtome)

Ex vivo perhaps? In mortum? :)

Does the term in vitro necessarily imply that the organism/organs/cells of study are dead?
No, in vitro studies are often carried out with living cells - just think of in vitro fertilisation. The nearest I can come up with for what you want is histology, but I think even this encompasses studies of living cells and tissues.


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L1 - L5 layers of the brain
I have read in some papers about the layers L1-L5 of the brain (e.g. in this paper). I could not find a definition of these layers. I have found information about the layers V1-V5 in the visual cortex.
Where exactly are L1-L5? And do these definitions vary across mammals?

V1-V5 are different (sub) regions of the visual cortex itself.

via http://www.tecsyn.com
The layers L1-L5 (some regions have a layer 6) refer to the different cellular strata in the depth dimension of the cortical mass.  This stratification occurs to some extent or another in various areas.  Different sections of the cortex, e.g., the primary motor cortex have a predominant level 5 (for the pyramidal tract).  Something like the visual cortex has more cells in layers 4 and 6.

 From http://www.unige.ch/cyberdocuments/theses2003/RivaraC-B/images/fig.2.jpg
Layers 2 and 3 tend to carry interconnections between different areas of the cortex, and the topmost layer is generally less dense.


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How many human proteins are very well characterized?
Following up on How many human proteins have a solved 3D structure?,is there a list of very well characterized human proteins / protein complexes?
My criteria for "very well characterized" includes, at least:

a high quality 3D structure
known activity in vivo
known associates in its activities in the cell
kinetics of its activity
regulatory elements for expression
etc..., and
(probably most importantly) a general consensus among experts that it is well described

This list would most likely include such proteins or protein complexes as:

P53,
polymerase alpha, and
the nuclear pore complex,

to name a very small number.

Don't you think that this question is a good match for bioinformatics community at SE, biostar.SE?

Sure, and I'll go see what's over there, too.  However, if there were a curated list of the kind described in the question, the answer to this question would fall squarely outside the domain of bioinformatics, except for whoever makes the list.

To address your list:

a high quality 3D structure: this you can easily get from PDB, using the answers to the question you linked as starting point. However, it is become increasingly clear that intrinsically unstructured proteins also play important roles in the cell, and for these you won't get a good 3D structure.
known activity in vivo / known associates in its activities in the cell: interaction partners can be found in databases like STRING, although just knowing the partners doesn't mean we understand what's going on :)
kinetics of its activity: I know of no good resource on this one except BRENDA for enzyme kinetics. But of course there are also kinetics to protein–protein interactions that would be interesting to know. (Update: There is AffinDB.)
regulatory elements for expression: there are databases like TransFac, but ChIP-Seq experiments show that we only know a tiny part of the regulation.

But, I think the key to a good answer lies here:

(probably most importantly) a general consensus among experts that it is well described

I would check how often the genes are described in the literature. The GeneRIFs from NCBI may be a good starting point, because these are snippets from the literature that are curated and shown on the NCBI Gene pages. E.g. p53 has >3800 of these. The length of the summary could also be a good proxy. (Or, the length of the Wikipedia page?)

Many of these questions can be answered by UniProt:

around 4,600 proteins with some 3D structure (this query)
of these 3,800 with annotated function in the Gene Ontology (this query)


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How do baby animals that primarily subsist on cellulose get their initial gut flora?
In the case of mammals like giraffes and koalas, is that bacteria common on the plants they eat so when a baby starts to try to stick something besides its mother's milk in its mouth, it can't digest the cellulose at all the first time, but along with the cellulose, into its mouth went some cellulose-digesting flora that then begins a lifelong colony in the animal's gut? Is that about how it happens?

I would not expect this to be any different than other animals - they get the flora from the environment. Key components of the environment for newborns are:

Birth canal
Den / living quarters
Skin / fur of mother, especially near the teats
Diet
Feces of family members (animals sniff this and aren't so clean)

I don't know about ruminants, but baby rabbits (and presumably other lagomorphs) apparently acquire the necessary intestinal flora by consuming their mother's cecotropes.[1]
[1] Johnson-Delaney, C.A. (2006), "Anatomy and Physiology of the Rabbit and Rodent
Gastrointestinal System" (PDF)

We now know that humans acquire not only their initial gut flora but also that of the skin from swallowing and touching mother's vaginal mucus. This doesn't apply to Caesarean birth, however.
For reference, see my answer at skeptics: https://skeptics.stackexchange.com/questions/9994/do-c-section-born-babies-have-worse-immune-systems/10078#10078


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Is it the sphincter that flexes when a human pushes a bowel movement?
Of course the sphincter muscle is at the exit point. To use a toothpaste tube analogy, if I want to squeeze out some toothpaste, it does me little to no good to jostle the nozzle; I need to squeeze the tube (which is analogous to the colon) to get the paste (payload) to come out.
So when a human is sitting on the toilet squeezing, is that squeezing flexing of the sphincter, or squeezing muscles along the sides of the colon pushing on it as one's fingers push on the tube to get toothpaste to come out.
If it's the sphincter that's getting flexed, how is that helping get a big log out?

Excellent use of the medical terminology!

The pressure that you apply when you push during a bowel movement derives from an increase in the pressure of the abdomino-pelvic cavity.  You generate this pressure by closing the glottis (the opening to the lungs) and contracting the anteriolateral abdominal muscles (i.e., the external oblique, internal oblique, and transversus abdominus).  This reduces the volume of the (now sealed) abdominopelvic cavity and increases pressure helping to drive feces from the rectum.  This is mechanism is also used to expel urine and during childbirth.
If you do this with the glottis open, then you forcibly exhale because the increased pressure of the abdominopelvic cavity is transferred across the diaphragm and into the thoracic cavity compressing the lungs.


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How are the gene sequences of individual sperm and egg cells "randomized"?
What I mean by "randomized" is, in the place where an egg cell or sperm cell is made, what is the mechanism by which each one is not made identically? Though I am a layman, I'm pretty sure that if the sperm cell that was right next to "me" had made it to the egg instead of the one that did, the resultant human would have a different genomic sequence and different features.

are you familiar with concepts like haploid, homozygos, alleles, chrossing over? I am trying to figure out how high scientific level my answer should be.

Meiosis is the type of cell division responsible for the diversification of genetic material among egg and sperm cells. The diversity comes primarily from crossing over (Prophase I) and the cell divisions (Telophase I & II) later on in the process.

Meiosis begins with one diploid cell containing two copies of each
  chromosome—one from the organism's mother and one from its father—and
  produces four haploid cells containing one copy of each chromosome.
  Each of the resulting chromosomes in the gamete cells is a unique
  mixture of maternal and paternal DNA, ensuring that offspring are
  genetically distinct from either parent. This gives rise to genetic
  diversity in sexually reproducing populations, which provides the
  variation of physical and behavioural attributes (phenotypes) upon
  which natural selection acts.

Further detail of the precise phases can be found in the Wikipeida article.

[picture from wikipedia]

I think we can attribute this to sheer probability. The human genome contains around 3 billion base pairs. When you consider recombination from chromosomal crossover that occurs in germ line cells, there is an astronomically huge number of possible unique combinations that can be made.
Of course, males generate many many sperm, so some of these are bound to be similar. But the number of sperm produced by any individual doesn't come anywhere close to the number of possible unique sperm that he could produce.


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Are B Cells unique to an individual's immune system?
I was wondering how the body "remembers" viruses after having once overcome them, and while reading this article on the immune system (page 14, Vaccinations), I read:

There are many diseases that, if you catch them once, you will never catch again. Measles is a good example, as is chicken pox. What happens with these diseases is that they make it into your body and start reproducing. The immune system gears up to eliminate them. In your body you already have B cells that can recognize the virus and produce antibodies for it. However, there are only a few of these cells for each antibody. Once a particular disease is recognized by these few specific B cells, the B cells turn into plasma cells, clone themselves and start pumping out antibodies. This process takes time, but the disease runs it course and is eventually eliminated. However, while it is being eliminated, other B cells for the disease clone themselves but do not generate antibodies. This second set of B cells remains in your body for years, so if the disease reappears your body is able to eliminate it immediately before it can do anything to you.

Which made me wonder, instead of vaccinating people with weakened forms of the disease, getting their B cells to activate as described, what would be wrong with growing large colonies of B cells for a given virus and injecting them into someone who has never had the disease so that one can go straight to the last sentence of that paragraph, having many of those B cells in place before the virus is ever experienced?

the problem is transplantation rejection - the body will reject the injected cells as foreign...

There is no other way than vaccination (besides the infection) to bring these B-cells in place.

That's essentially what the vaccines do ! In vivo !

Remember first that the human body nearly always, although there are exceptions, rejects any non-genetically identical graft placed into it, and therefore one cannot prepare a general colony of B-cells to confer immunity to the population at large. However, in principle, there is no impediment to removing B-cell progenitors in an individual, conditioning them to produce antibodies (which would be an artificial analogue of the natural process of 'Clonal Selection'), and re-injecting these differentiated B-cells into the patient. To my knowledge this process is currently beyond the capacity of our current cell culture techniques, as B-cell differentiation is controlled by an elaborate cell-signaling process, and even if it was feasible, it would remain impractical for several reasons. First, since the B-cell products, antibodies, can be transferred humorally, and should be tolerated by the general population, many existing treatments simply involve injecting antibodies into the patient's bloodstream. Examples of antibodies taken from volunteers' sera are the RhoGam preparations as well as IgG mixtures used to treat certain forms of immunodeficiency. There is a means of growing B-cells in culture to produce antibodies of precise specificity (i.e. monoclonal antibodies - note that clonal selection occurs in a living host for this technique, the B-cells are subsequently harvested then immortalized in culture). Adalimumab is a therapeutic monoclonal antibody.
There is however, very promising work being conducted involving T-cell vaccination, which is technically similar to what you described. The advantage in using T-cells is that these leukocytes can orchestrate an immune response, mobilizing the several, diverse elements of the immune system to respond to a specific antigen. These techniques are being principally researched as cancer treatment regimens.

And to clarify, the T-cells are coming from the pt, or in more extreme cases HLA matched donors, not just generic T-cells from a cell line or pool.

@AtlLED - Presumably. It is essentially adoptive immunity, which by definition would seem to indicate histocompatibility. Being an experimental procedure, there are several methodologies explored to produce these cells. I will try to keep an eye out for a good review article on the preparation methods. A promising aspect of this therapy is that in addition to inducing immunity, the possibility of producing T-regulatory cells may enable us to effectively treat autoimmune diseases and allergies.

@J.AlfredPrufrock When we have vaccines available, do you think what the author of the post describes is necessary ?

@biogirllajja - Direct antibody injection is currently more technically feasible and easier to control. However, there may be niche applications for B-cell adoptive immunity, perhaps if one needed antibody against a very specific epitope. Otherwise I believe T-cell adoptive immunity would initiate a more natural immune response. I have not seen an article that employs the method of B-cell adoptive transfer. I would presume that even if the clone of interest could be isolated, it would be difficult to ensure its proliferation in vivo.

Biogirl hit the nail on the head. Vaccines are one of the most beneficial medicines ever invented - in large part this is because they take advantage of a well evolved immune system rather than re-inventing the wheel.

There is also some work with programming a patients own stem cells to become long lived plasma blasts for broadly neutralizing antibodies against HIV (and other diseases I assume). Although you are essentially asking what is harder...eliciting these broadly neutralizing antibodies with traditional vaccine approaches (difficult), or working out the complex cell signalling pathways to get from stem cell to long lived plasma blast. Even the pathway from memory b-cell to plasma blast is still not entirely understood, so we are several years away from this approach.
It is so appealing though for so many reasons. Once you have a plasma cell secreting a broadly neutralizing antibody, you have it forever (or at least many many years). This circumvents the extremely expensive antibody therapeutic approach as large quantities of these proteins are indeed just expensive to make as with all protein therapeutics.


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Do any nonhuman species have effective ebola immunity?
I've read that ebola is an effective killer in humans because it has the ability to interrupt dendritic cells from manufacturing proteins that cause the immune system to destroy the dendritic cells when they're infected. Do any other animal species have different kinds of dendritic cells that don't get thus interrupted by ebola?

Recently some cases have sprang up in some African countries.

While at least some other primates are suspectible to Ebola, pigs appear to be immune. From the WHO factsheet on Ebola (1):

Although non-human primates have been a source of infection for
  humans, they are not thought to be the reservoir but rather an
  accidental host like human beings. Since 1994, Ebola outbreaks from
  the EBOV and TAFV species have been observed in chimpanzees and
  gorillas.
RESTV has caused severe EVD outbreaks in macaque monkeys (Macaca
  fascicularis) farmed in Philippines and detected in monkeys imported
  into the USA in 1989, 1990 and 1996, and in monkeys imported to Italy
  from Philippines in 1992.
Since 2008, RESTV viruses have been detected during several outbreaks
  of a deadly disease in pigs in People’s Republic of China and
  Philippines. Asymptomatic infection in pigs has been reported and
  experimental inoculations have shown that RESTV cannot cause disease
  in pigs.


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Is there a correlation between incidence of type 1 diabetes and vitiligo?
Does the data indicate that if you have one, the probability of you having the other is higher than that of someone who doesn't have the one?

Is there a particular reason for you to suspect that this might be the case?

This article ( http://www.ncbi.nlm.nih.gov/pubmed/16477262 ) talks about co-occurrence of type 1 diabetes with other autoimmune diseases, but not the autoimmune disease vitiligo.

It has been associated with polymorphisms with the CD4 gene, which is usually implicated in type I diabetes. The wikipedia article for vitiligo also mentions studies for the NALP1 gene. NALP1 is expressed at high levels in T cells and Langerhan cells, white blood cells that are involved in skin autoimmunity.

References to papers? If there isn't one on the wiki page with the statements, I would be less than happy to vote this up. Also, if CD4 mutations been found to cause both diseases, is there any observational evidence (epidemiology) you have found whilst reading? It does seem likely they are related as they are both autoimmune diseases of the T-cells, but they may have independent mechanisms of action via CD4 (etc), so disease incidence may not be correlated.


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What are current abiogenesis hypotheses for first food source?
What is the very first abiogenetic piece of reproducing life (small piece of RNA + ribosome that randomly occurred?) hypothesized to have used as an energy source? I'd be interested in sources to what experts in abiogenesis research have hypothesized on this subject, if any such researchers have spoken on the question.

In RNA world hypothesis, ribozyme is thought to play the role of reproducing molecule.  That may help you with more initial research, but I don't know the answer to your specific question.


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Why does regular exercise increase brain volume?
It has been shown in several studies that regular aerobic exercise increases brain volume in aging humans. The changes were observed in hippocampus and were correlated with dramatic reduction of age-related dementia. Interestingly, the intensity of training had little influence on the results: walking, climbing stairs, gardening were just as effective at reducing dementia as more strenuous exercise.
What is the biological mechanism behind this phenomena?

Fig. The aerobic exercise group showed an increase in the anterior hippocampus and no change in the posterior hippocampus.[1]

Erickson et al. Exercise training increases size of hippocampus and improves memory. PNAS. 2011.
Colcombe et al. Aerobic exercise training increases brain volume in aging humans. J Gerontology. 2006
Ravaglia, et al. Physical activity and dementia risk in the elderly. Neurology. 2008

Well, Erickson et al (2011) attribute the increase in brain volume in the aerobic exercise group to brain-derived neurotrophic factor (BDNF).
Specifically (p. 3020):

In fact, we found here that changes in serum BDNF levels were
  associated with changes in anterior hippocampal volume; an important
  link because the hippocampus is rich in BDNF, and BDNF levels increase
  with exercise treatments in both rodents and humans. BDNF is a
  putative mediator of neurogenesis and contributes to dendritic
  expansion and is also critical in memory formation. Our results suggest that
  cell proliferation or increased dendritic branching might explain increased
  hippocampal volume and improvements in memory after exercise

with the caveat:

however, increased vascularization (15, 16, 33) and dendritic
  complexity (34) may also be contributing to increased volume


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Is there an "evolutionary species similarity calculator"?
Is there a website where I can input pairs of species and get an "evolutionary similarity score"?
E.g. (numbers are completely made up)

Input: Chimp and Human, Output: 97%
Input: Cat and Human, Output: 85%
Input: Is Cat closer to Human or Chimp, or Snake, Output: Cat is closer to Chimp (87%), second is Human (85%) and Snake is last with 50%.

I have no idea what the actual scale should be, but I imagine there is at least one interesting scale, perhaps several.
Cross posted to Quora

Since the simple value of percentage of nucleic acid identity over whole genomes isn't very useful in taxonomy, you won't find these values published in a database, even if they were computed by someone in the process of other work.
One project that provides ready-for-consumption phylogenetic trees based on similarity metrics, by using orthologous genes between species, is OMA. They compute all orthologous genes between two species, and they are now at 1,235 species:
http://www.biorecipes.com/Orthologues/status.html
You could then read off the "distance" between cat and mouse from the eukaryotes tree. This value would then be more meaningful than the nucleic acid identity percentage.
Apart from the trees, using their OMAbrowser you can get for any species pair the number of common orthology groups, i.e., the number of common genes between those two species.

TimeTree gives you an estimate for time of divergence, which is also nice to know. But of course different species have different rates of evolution.


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How to find transcription factors?
I need to find master transcription factor(s) regulating secreted proteases in a fungus to be disrupted toward upregulation and overexpresion of extracellular recombinant proteins.
How can I detect transcription factors and preferably master TFs (master regulators) in an organism? Does NGS applicable to find TFs and preferably the novel ones? I know ChIP-seq is used to identify TF binding sites but how about detection of the TFs that bind to these sites?

How can I detect transcription factors and preferably master TFs (master regulators) in an organism?

The easiest approach to find transcription factors for any given organism would be based on sequence homology with other transcription factors. In order for this to work your organism of interest does have to be sequences, you can check this (e.g.) on the NCBI genomes page. By comparing the genome or the genes of your organism with other known (fungi) transcription factors, you can find most of the transcription factors of that organism.

Does NGS applicable to find TFs and preferably the novel ones?

Both NGS and ChIP-Seq only allow you to determine DNA (or RNA if you reverse transcribe first) sequences. Therefore these techniques alone will not help you in identifying which TFs act on your genes.

I know ChIP-seq is used to identify TF binding sites but how about detection of the TFs that bind to these sites?

I can't currently think of any 'classical' or standard experiments to determine which TFs bind to a given gene or promoter. One possibility would be to use CoIP (co-immuno precipitation) on the RNA polymerase complex and use Mass-spectronomy to identify the TFs in that complex. The problem with this is going to be, that you need a way to only get the RNA polymerase complex for your genes of interest and not all the other ones in the cell. Maybe you can use columns with DNA probes that can hybridise with your genes instead of standard antibody based CoIP.
Another way to determine which TFs bind the promoters of your genes is to analyse the respective promoter sequences. However, without knowledge of most (or at least some) of the binding sequences of the TFs in your organism, this will most likely not work very well. Edit: As @AlanBoyd commented there is a database for fungal transcription factors. However, it seems like they mainly annotate which fungi genes are transcription factors, but do not cover binding motifs of these factors.

Fungal TF database https://www.hsls.pitt.edu/obrc/index.php?page=URL1231356721

The best way is to determine the TFs in a specific organism with specific function first, then you need to check if they are transcription factors and find their domains on http://smart.embl-heidelberg.de/.

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


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Do large animals often evolve into smaller animals?
There are several examples where the largest animals were killed off preferentially due to a major ecological shift:

The KT extinction event
The Holocene extinction, as well as the major megafauna humans killed off

The common ancestor of modern mammals is thought to be "shrew-like" in size, and it differentiated into most of the large animal species in the world today.  I imagine that a similar statement can be made for dinosaurs.  In general it seems that a major extinction event is likely to be best weathered by smaller creatures which can later, over time, increase in size to fill the niche that larger animals, and evolution dictates it will be profitable to do so.
Does this limit large animals to only the branches of the tree of life?  Any given set of (Multicellular) species obviously share a common ancestor that is much smaller than them.  Is it possible for many species to share a common ancestor that is considerably larger than any of them?

@J.M. That would be a counter-example to my examples, and it could answer the question as yes, they do.  But we also need to establish that modern insects actually evolved from the past's large insects, instead of evolving from small insects that lived among the large insects.

Define "often"; island dwarfism is a seemingly-repeatable effect.

As written, it is confusing as to what you are asking.  In one sense you seem to be asking about the environmental factors that would drive the evolution of size but since evolution is never progressive then there can be no expectation of a evolution-based temporal trend.  I am not sure if the idea that large animals are more vulnerable to extinction is completely accepted, but if we accept it, then it reduces your question to a truism if applied to mass extinctions - if only small animals remain then non-directional evolution would give the impression of progression.

@DQdlM Is it common that an animal species decreases in size then differentiates into many other species?

@Zassounotsukushi I don't think there is much support for those kinds of generalizations.  Different ecological contexts would tend to apply selection pressure for body size in different ways and those ecological contexts will vary in space and time.  As Kevin points out in his answer the potential for large changes in body size have been shown so it is a plastic trait but it will respond to the selection pressures at hand (as Nick T points out in his comment on island dwarfism).

Your question brings up several important issues with regards to the evolution of body size. The rationale for concluding that the ancestral mammal had a small body size is that all of the taxa in that area of the tree tend to be small. In contrast, if all of those taxa had been cow-sized, then the most parsimonious conclusion would be that the ancestral mammal was cow-sized.
Identification of ancestors is difficult
Identification of a fossil species as the most recent common ancestor of a pair of sister taxa is exceedingly difficult. The way that different species are diagnosed in fossils in by their unique derived characteristics (autapomorphies). So if a fossil is found with no autapomorphies, then it is plausibly an ancestor (i.e., at the split between two sister taxa). Some would argue that if you don't find any autapomorphies, then you just haven't looked closely enough.
Cope's Rule
The idea that lineages tend to evolve toward larger body size is known as Cope's Rule, named for the paleontologist Edward Drinker Cope. The success of Cope's Rule has been highly variable, with some lineages following and others not (Polly, 1998).
Some clades following Cope's Rule

Early reptiliomorphs (Laurin, 2004)
Pterodactyloidea (Hone and Benton, 2007)
Most Cambrian-Devonian marine invertebrates (Novack-Gottshall, 2008)
North American canids (Van Valkenburgh et al., 2004)
Mesozoic birds (Hone et al., 2008)

Some clades not following Cope's Rule

Early stegocephalians (Laurin, 2004)
"Rhamphorhynchoid" pterosaurs (Hone and Benton, 2007)
Mesozoic birds (Butler and Goswami, 2008)

Note that many results depend on the methods used.
Evidence from experimental evolution
Several studies have addressed body size evolution in vertebrates both directly and indirectly. MacArthur (1944a, 1944b) directly selected for large and small body mass in laboratory mice. Within 8 generations, mean body masses had increased or decreased by over 50%. Even when body mass is not directly selected upon, mass can change in a correlated way. Selection for high levels of voluntary activity has led to an approximately 25% reduction in body mass.
Based on these studies, evolution of body size (larger or smaller) is certainly possible within relatively few generations.

i'd heard that miniaturization of animals is also a recognized effect of subpopulations on islands.  gigantism can also occur, but is the result of the organism differentiating into new niches.  the hobbits are examples of this effect, do i remember right?

It probably goes equally both ways. Examples of miniturization are balanced by examples of gigantism (e.g., lots of South American taxa during its "island" period).

yes - i think its a matter of niches being open for just a few critters to fit into and sizes can change drastically. in crowded systems, the time it takes to change size would be prohibitive.


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How are the paranasal sinuses linked with the capillaries in the ear canals?
Sinus congestion often seems to be accompanied by excess pressure on the outer ears (as anyone who has shared a transcontinental flight with an infant can attest to) or fluid buildup in the canals.  An increase the capillary pressure within the ear canals would explain the pressure, but what is the physiological connection between the sinus pressure and pressure in the ears?
The most obvious answer I can think of is that any direct drainage from the sinuses would cause a backup of fluid into the Eustachian tubes.  This would only explain pressure coming from the other side of the eardrum, but is such pressure simply relieved by blood pressure transfer to the capillaries in the ear canal, or is there a non-trivial mechanism by, e.g., a vagal circuit which governs the relationship between the sinuses and the outer ear?

There is no direct link between the capillaries in the sinuses and the ear.
The Eustachian tubes drain the middle ear (between the eardrum and the inner ear) into the nasopharynx, the part of the throat that is just behind the nose.

The para-nasal sinuses drain into the nasal passages themselves at different points. The sinuses and middle ear constantly produce some fluid, which is either reabsorbed or drained.

Often what happens is that in the case of a common cold or other upper respiratory tract infection, the nasopharynx and nasal mucosa are both infected. The inflammation causes swelling and blocks off the Eustachian tubes and the drainage pathways of the sinuses and the trapped fluid itself causes sinus & ear pain and can get infected causing sinusitis and otitis media. Alternatively a viral infection can also go up into the middle ear and sinuses causing direct infection.
The process that occurs when you go on a plane is slightly different. The Eustachian tubes and sinus openings collapse due to pressure and thus the natural fluid that is produced accumulates as well as there being an inability to neutralise the internal and external pressure (thus why making your ears 'pop' works- you force the Eustachian tubes open via positive pressure)

Regarding blood supply of the paranasal sinuses and the ear:
The ear is supplied by the posterior auricular and superficial temporal arteries of the external carotid artery.

The paranasal sinuses are supplied by various branches of the internal and external carotid artery including the maxillary artery, anterior and posterior ethmoidal arteries, ophthalmic artery, supraorbital and supratrochlear arteries


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Alternate genetic codes in newly sequenced organisms
Variations of the standard genetic code are pretty rare, but as the cost of high-throughput genome sequencing continues to drop, there is a greater possibility of discovering additional exceptions. That being said, there is a clear emphasis in genome projects on nucleotide (genome and transcriptome) sequencing, with much less (if any) effort put into proteomics work (correct me if I'm wrong there).
Let's assume we're sequencing the genome of a new organism and we're focusing completely on genome and transcriptome sequencing--no proteomics. Let's also assume this organism has slight variations to the standard genetic code. Would it be possible to annotate this genome (for protein-coding genes) completely incorrectly since the gene prediction software does not take into account these variations, or would it be pretty obvious? What would you expect to see in this case?

Your question is very vague.  Can you be more specific and/or more concrete?  There are a dozen sequencing technologies and even more variations to the genetic code.

Perhaps the vagueness comes from the fact that I don't know what to expect if I was trying to annotate the genome of an organism that uses an alternate genetic code. My basic question is: would I even be able to tell? Is that not clear from the original question?

I think that's a clear question.

If the organism uses an alternative code, the predicted protein sequences would always include the same type of amino acid substitution errors. This pattern should become apparent when you compare the proteins to other organisms.
In reality, the most common alternative code uses UGA for tryptophan instead of the usual stop. If you make the mistake of using the standard code for these genomes, the predicted genes would become highly fragmented so it is almost impossible not to notice.

You are correct to be a little concerned, especially with mitochondrial genomes (where non-standard genetic codes are more prevalent).  In addition to the use of non-standard codes you should also consider RNA editing (changed codons or deleted/inserted nucleotides to shift reading frames) and special amino acids (e.g., selenocysteine).  All together, the emphasis on DNA sequence to infer protein structure is safe in the bulk of cases, but don't be surprised by differences (for particular genes or for whole organisms).

The short answer is yes, you could end up with many errors.  See here for more detail:
NCBI: "The Genetic Codes"


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How does Haloxyfop control young grassy weeds in fields of broadleaved crops?
Haloxyfop (haloxyfop-P-methyl) is a selective herbicide used to control grassy weeds in young stages. The mode of action (iirc) is basically inhibition of acetyl CoA carboxylase (ACCase). Why does this affect the monocots, while not harming the dicots?

On the Botany department website of Purdue University (http://www.btny.purdue.edu/weedscience/moa/ACCase_Inhibitors/text.html) I found the following information on Acetyl-CoA carboxylase (ACCase) inhibitors:

[...] (ACCase inhibitors) inhibit the enzyme carboxyltransferase, an [...] Acetyl-CoAesterase which speeds the formation of malonyl-CoA from acetyl-CoA and CO2.
  Malonyl-CoA and acetyl-CoA are the building blocks of phospholipids and triacylglycerols [...] (that) combine to form lipid bilayers that serve as the cellular membranes. Affected plants cannot produce new cell membranes. This takes place in the grass’s meristematic tissue, which explains the mushy and disintegrated growing point. [...]
Selectivity [...] Monocots (grasses) [and] dicots (broadleaves) [...] both possess ACCase enzymes in their cytoplasm and chloroplasts. Dicots have a prokaryotic form of the enzyme in the chloroplast and the eukaryotic form in the cytoplasm. Monocots have the eukaryotic form in both their cytoplasm and chloroplasts. Only production of the eukaryotic form is inhibited.

So to sum up, ACCase inhibitors act on eukaryotic ACCase, not the prokaryotic type. ACCase is essential for cell membrane formation. Blocking ACCase results in a depletion of its product, namely malonyl-CoA. Malonyl-CoA is essential for the synthesis of long fatty acids used in the cell membrane. Without cell membranes, cells lose integrity and turn to mush. Tissue growth is impossible without ACCase activity. Since monocots only have the eukaryotic ACC in both cytoplasm and chloroplasts, they die. Dicots, on the other hand, express prokaryotic ACC in their chloroplasts, making them resistant to ACCase inhibitors.
After some literature search I also found that blocking (knocking out) acetyl-CoA carboxylase in Arabidopsis (a dicotyledon) results in dead plant embryos and, hence, non-viable seeds (Baud et al., 2003).

I am mobile, but here is my source: https://www.google.com.au/url?sa=t&source=web&rct=j&ei=nFnIVILZDoiU8QW72IGACA&url=http://onlinelibrary.wiley.com/doi/10.1046/j.1365-313X.2003.016010.x/pdf&ved=0CBsQFjAA&usg=AFQjCNGqIyW0fggl5kulKagsSzN29hjlAg&sig2=q7Q1EGkJvmGTvjO2xYBmuA

@J.Musser I am working on the others! Very I interesting material!


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Why are some plants frost tender?
Why do some plants have the ability to stand frost, while others can't? Does it have to do with the size of the water vacuoles in the plant cells?

Cf. How do individual plants adapt to changes in temperature

All cells are susceptible to cold, but freezing is particularly difficult.  If the water in the cells freeze, it would usually burst the cells (water expands when it turns to ice) and tearing the cell membrane (totally killing it).
Some plants and animals have adapted to colder temperatures by putting antifreeze proteins in their cells.  A lot like adding antifreeze to the radiator of a car, this lowers the freezing temperature of the water in the cell.
So the answer is that some plants have adapted to colder climates with the help of additional genes.  There are other things that have to change too - the chemical reactions in the cell will go haywire when temperature changes too, so lots of genes must make adjustment for a fully cold adapted plant.


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How does water move throughout plants?
I haven't yet found a decent explanation for how water moves throughout plants. It does seem to travel more efficiently upward than out or down. Why is that?  How does it travel through the plant?

Most water moves up through the xylem by capillary action. Imagine dipping a pipette into a small pool of water; the water would rush up into the pipette. Or, imagine dipping the edge of a paper towel in water. The water "runs" up the paper towel. This is capillary action.
As water evaporates out of the leaves and such in higher regions of the plant, a capillary force pulls up more water. If for instance, you were to dry the top of your saturated paper towel, more water would be pulled up from the pool below to wet that top section.
As for a molecular explanation, Wikipedia has a good explanation of Cohesion-tension theory.

Indeed it does. There is tension between the weight of the water and the force of the capillary action, which they think is what limits the height of trees (http://www.nature.com/nature/journal/v428/n6985/abs/nature02417.html). Remember that the xylem is like a very, very skinny tube, so it isn't like there is a single massive column of water flowing up.  With a narrow tube like that, the weight of the water builds pretty slowly.


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Could an animal with an open circulatory system survive in a near-zero gravity environment?
An animal such as a crayfish relies on gravity to keep its circulatory system running. If it is turned upside down, the gravity works against the system, suffocating the animal. Now if, instead of placing the animal on it's back, we were to take take it to a space station, gravity would not be working against it, and random blood flow plus capillary action should get some blood flowing. Would the animal survive this?

How does a clamfish clam?

I believe that fruit flies have been taken aboard the Space Shuttle for experiments. They survived and the adults have an open circulatory system.

Would a larger animal survive?

You'll have to dig a bit to see what is known. I vaguely recall that spiders went into orbit as well, likely to observe web-spinning behavior and characteristics. The link I provided may give you a place to poke around NASA's biology pages. If you're real serious about this, I could ask a Shuttle astronaut I know, but she is training for another mission and may not be able to provide any reply.

A list of animals sent to space also includes crickets, snails, sea urchins, brine shrimp, jellyfish, orb spider, silkworms, carpenter bees, ants (several species),hissing cockroaches, and various butterflies.


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Are there animal models for Clostridium difficile that better replicate human infection than hamsters?
So I'm looking for some information on the infectious dose necessary to colonize a human with Clostridium difficile. There's no human challenge studies, and since it's not a foodborne pathogen, little we can get from outbreak data.
Which leaves me looking at animal models, to at least get the shape of the probability of infection based on a given dose. But the papers on hamsters makes it appear that they're infected rather easily, and that this infection is particularly severe.
Is there another animal model that more closely mimics the infection dynamics of C. difficile in humans?

Hamsters are considered the best animal model, most studied.
C. difficile has been found in calves, ostriches, chickens, elephants, dogs, horses, and pigs, but its role in infection and its pathogenesis in animals are largely poorly understood and possibly underestimated


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Can any plant regenerate missing tissue?
I have not yet found a plant that, when an insect eats a hole in one of its leaves, it can regenerate the lost tissue. Many plants will grow a new stem if the old one is cut, but it is not a perfect regeneration, and has no likeness in form to the previous stem. Are there any plants that can, even to a degree, regenerate missing tissue?

Essentially the answer is yes, except that your qualification "but it is not a perfect regeneration, and has no likeness in form to the previous stem." is confusing me - I would consider all stems from a single plant to share a likeness in form. No, they won't be identical, but neither is a regenerated limb identical to a lost limb.

How about the leaves?

same for leaves, I used stem as an example

So if I punch a hole in a leaf, it can regenerate the missing tissue?

it will generate a new leaf

But can it regenerate the missing tissue?

@David I know that plants can sprout new stems, and sometimes new leaves. I am a gardener. But I haven't yet found a plant that can replace a missing structure exactly. Like regenerating the tissue lost if I punch a hole in the leaf.

In general, plant cells only undergo differentiation at special regions in the plant known as meristems. Two of the primary types of meristem are the root apical meristem (at the tips of roots) and the shoot apical meristem (at shoot tips)^. Within the shoot apical meristem the plant cells divide and begin to differentiate into different cell types (such as different cells of the leaf, or vascular cells). Later growth (of, say, a leaf) is largely a result of cell expansion (although cell division does still occur, but drops off as the leaf expands). Therefore, if you punch a hole in a leaf, it probably won't be filled in because the cells in that leaf have finished growing and dividing.
However, as a shoot grows, more meristems are created. These are found in the axillary buds, just above where the leaf meets the stem. The meristems in the axillary buds can grow to form branches. Different plants obviously make different numbers of branches, but there is a common control mechanism known as apical dominance, where the meristem at the tip of the shoot suppresses the growth of the lower axillary buds. This is why a shoot with no branches can be made to grow branches by cutting off the tip (gardeners often do this to make "leggy" plants more bushy).
All of that was a long explanation to say, no, a plant doesn't normally^^ regenerate in the sense of filling in cells that have gone missing. However, if you cut off a shoot, the next remaining bud might begin to grow and, in a sense, replace the part that was lost. In that case, an existing bud is recruited to form a new branch and replace lost functionality, but I wouldn't say that qualifies as regenerating missing tissue.
^There are other types of meristem as well.
^^If you torture plant cells enough you can force them to become "stem cells" and thereby make an entirely new plant, but this is rare in nature.


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How does Trifluralin kill newly germinating seeds, with almost no effects on established ones?
Trifluralin (2,6-Dinitro-N,N-dipropyl-4-(trifluoromethyl)aniline) is a pre-emergent herbicide used in landscape beds before the application of mulch (my use for it, anyway). It kills the weeds as they germinate, while not harming most established plants.

From what I understand, the mode of action is as a mitotic inhibitor, which disrupts the microtubules that pull the cell apart when it divides (stops cell division).
How does this only affect germinating weeds, while not noticeably affecting weeds that have emerged from the soil (I have to hit those with another herbicide)?

Mitotic (cell division) inhibitors in plants are pretty much what a chemo therapeuticum means for cancer, i.e., rapidly dividing tissues will be affected most. Germinating seeds depend on mitosis for growth. An established plant will also be affected (it will stop growing), but it will stand its ground. To push the analogy - chemotherapy is often commenced after surgical removal or irradiation therapy to remove the tumor, and then chemo is applied to make sure any surviving tumor cell will not start to divide. Your herbicide will prevent germination (cf. cancer re-growth), but will not grossly affect established plants (cf. existing tumor).


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Does arterial blood always flow away from the heart?
Is there a negative net flow of blood in human arteries at any point of the cardiac cycle? I realise that blood flow can be turbulent, e.g. in the aorta or around stenotic arteries, but then the average is still flowing away from the heart.
The question was provoked by this graph, which admittedly I haven't seen in its context:

A similar graph showed negative velocities in the aorta and innominate artery of humans.

oh no, which one should I accept?

Quick answer, no.
Imagine a balloon; as you compress the balloon, there will be a lot of air that leaves it. But as you let it relax, the balloon pulls in surrounding air even as you fill  it from another side. When the aortic and tricuspid valves are closed, there is blood flow forward but due to conservation of mass, the blood goes back to fill in the empty region.


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Why do plants' leaves become enlarged in low light areas?
Why do almost all plants in shade have a smaller stem structure and larger leaf than that same species grown in a well lit, sunny area?

I have no idea of the biological mechanisms behind what I'm about to propose. Consider this a hypothesis.
If the purpose of the leave is to collect sunlight for photosynthesis, then the behavior you mention is predictable. I order of trying to maintain a healthy flux of light in dim conditions, the plant adapts by increasing the area of its leaves. Once back in a well-lit environment, the need for larger leaves fades and new leaves are thus smaller, but still catch as much light. Of course, there must be limits to the extent of leaf area variation that one plant can handle.
As for the stem structure, I can only guess it's because plants spend more energy on leaf building than stem maintenance when under such stresses.

Also, plants that adapted to a "shady" ecological niche are competing less for access to direct sunlight, and therefore have less need to invest in height or the larger stem this requires.

The main factors that affect leaf shape are water and light needs. The plant needs a certain area of leaf to provide enough energy to live, so smaller leaves means more leaves(grasses), as opposed to one enormous leaf like a lilypad.
Generally, as light intensity increases water needs increase along with it. A thicker stem with a smaller leaf can support enough water flux to keep a grass blade hydrated in full sun, whereas a big tropical plant in high humidity has low water needs and can therefore use a thin stem to support a big leaf.
I would hypothesize that self-regulatory systems that affect leaf development as a function of available water and sunlight needs are responsible for the effect.


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How do mushrooms react to being grown in a microgravity environment?
I'll use Agaricus Bisporus as an example mushroom. If cultured in potato dextrose yeast extract agar, will the resulting growth grow in a normal pattern? Will the sporocarps emerge from the surface (assuming there is one) properly? Will they develop inside the agar, or emerge an an angle?
Will the plant develop at a normal rate, and to normal proportions?

There were some experiments done in microgravity in longer space shuttle missions. The reports show that the fungi develop relatively normal but grow in random orientations instead of orientating upwards. See this images:

The upper image shows fungi grown on earth which are subjected to normal gravity. The lower image shows fungi (actually only the fruiting bodies) which are grown during 7 day on the Spacelab D2 mission. The fungi obviously have a way of detecting gravity to let their fruiting body grow upwards. The image is from here, the article contains more information about this.
There is also a publication in this topic:

Mushrooms in microgravity - Mycology at the final frontier

Thank you Chris. I guess I didn't search long enough.


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T1D autoimmunity causes' possibilities
As far as I've learned about T1D, the prevalence of the disease and autoimmune disorders in general over the past 5 decades intrigued me to the point it made me wonder if it's really a genetic predisposition. I've read that it could be related to a virus but as far as I've read and came to conclude, could it be the EBV virus in the first place as a primary suspect infecting the beta cells in those with no genetic hisory of diabetes in their families?

I learned that EBV infects the human body then morphs itself into a human cell look-alike, could it be why the immune system attacks beta-cells if EBV infected them?
I also learned that there is a significant population with islets' antibodies present in serum yet over the years they never develop T1D and they stay within perfect glycemic control.

My question is, were there any studies done to examine that EBV possibility being the cause of T1D and if there were any studies done to explain why some of those with islets antibodies never go through the T1D autoimmune storm?


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Circulation through the liver in light of drug metabolism
I have a lingering question which stems from an answer that I gave to What hydrolyses aspirin within the digestive tract and blood stream?
When a drug or any other substance is absorbed into the bloodstream in the stomach or small intestine, it ultimately passes through the hepatic portal vein and into the liver sinusoids, where it is processed by hepatocytes and introduced into the general circulation via the vena cava.  In terms of metabolism, this is what causes a "first-pass" effect for drugs that are ingested.
For drugs that are delivered either by intravenous, intramuscular, or sub-lingually (as in the other Biology.SE question), this first-pass effect is avoided, and the drug is introduced into the general circulation without being metabolized by the liver first.
Even though the first pass is avoided, the blood in the body still makes its way back through the liver eventually via the hepatic artery, which is a branch off of the celiac artery.
The issue I still have is, does the incoming blood from the hepatic artery merge with the blood from the hepatic portal vein?  If not, does the blood from the hepatic artery still interact with the hepatocytes in some way? (it makes sense that it does, and I have also read that one of the main functions of the hepatic artery was to deliver blood supply for the liver's metabolic needs)  If this is not the case, where in the body would these drugs that were introduced via IV, etc., be metabolized?

Yes, the blood from the hepatic artery (proper) and the portal vein mix in the sinusoids of the liver. The hepatic vein supplies about 75% of the blood to the liver, and the hepatic artery the remaining 25%. Because the portal vein provides such a large part of the blood supply to the liver, then any disease that causes the blood to build up can cause portal hypertension.
The hepatic artery carries oxygen-rich blood from the heart. The portal vein is part of the portal system and connects the capillary beds of the gastrointestinal tract to those of the liver. Because of the larger volume through the portal vein, I think that each vessel carries about half the oxygen supply to the liver.
For drugs introduced through an injection, for example, metabolism occurs throughout the circulatory system and in the liver. Remember that it's all the same blood supply, but the first-pass effect just refers to the blood that goes to the liver before entering the systemic circulation (by which it can travel to its target).


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How does a brain distinguish stimuli?
If all the brain ever "sees" is action potentials, how do we know that one set of action potentials denotes a flash of light, another one signifies a loud sound, etc ?

The fundamental way in which this works is by geography: signals triggered by different stimuli travel by different pathways to different regions of the brain that are specialised for dealing with the sorts of information they contain.
For example, visual signals from the retina pass down the optic nerve and (after a few interesting twists and turns that, inter alia, send the left and right halves of each visual field to different brain hemispheres) wind up in the visual cortex, which contains neuronal networks adapted for recognising different structures and regularities in the image. Whereas sound information from the ears, after an even more tortuous sequence of processing steps, winds up in the auditory cortex.
Along the way, the signals will typically be split up across many neurons and reintegrated into new signals that pick out different kinds of information. So a particular stimulus will result in a complex spatio-temporal pattern of action potentials firing across many regions of the brain.
Conceptually, the further along this process you go, the more abstracted the signal probably becomes, so that it stands for a collection of events and ideas and thoughts rather than for excited photoreceptors or vibrating hair cells. But exactly how this parsing of the sensory content eventually turns into perception and conscious recognition is essentially unknown.

In short, one action potential denotes a flash of light and another one signifies a loud sound by occurring in different neurons.

Also, the frequency and the pattern of the action potentials are very important for information processing. A neuron firing short bursts of action potentials is not the same as one continuously firing.

For a human brain to differentiate signals from different locations of the brain, it must be able to perceive itself. And you commented how it is done is essentially unknown. But do you know any papers that attempt to figure out this how?

@jachilles it doesn't have to perceive itself, the brain is not homogenous, a signal entering the brain from one pathing is entering a different part of the brain and a different network of neurons than one entering from a different pathway.  there is no homunculus.

Just adding some metaphors in support to the excellent answer by walkytalky.
Our brain is like a huge processing center that can be seen from techni's prospective as a sort of a data center with parallel processing of hundreds of thousands of inputs with processing cores scattered throughout the complete brain.
Human brain (medulla) is connected with the rest of the body through special types of nerves that convey the information to brain (sensory, centropetal nerves) or deliver information from brain to the target organs (motor or centrofugal nerves) or both (mixed nerves).
I intentionally use the term "medulla", because this word comes from origin where it is applied to somwwhat more than brain: the spinal cord is also "medulla" (medulla spinalis), as well as the part that connects the spinal cord with the brain itself (medula oblongata).
The nerves that come directly from the brain are called cranial nerves. There are only 12 pairs of them in humans, numbered using Roman numbers (from I to XII) and every pair has a specific function: I bringing olfactory information (about smells), II -- the optic one, III -- moving the eyes etc.
The counterparts of these nerves in spinal cord are spinal nerves, which go through the holes between single vertebrae.
Brain and CNS in general can locate the information input and determine the information type judging by the input source using these nerves.
Besides the classical sensory information, like those from eyes coming via optical nerves into CNS, there is also some sensory information that is conveyed through autonomous nerve system, that is less specific and can not be localized as well as in case of sensory information coming via sensory input. Pain, for example, or the feeling of pressure belongs to the type of information coming via vegetative nerves.
The complete brain surface (so-called cortex) is mapped into special zones, called Brodmann zones, depending upon prevailing neuron types and (secondary) role in information processing.


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How does herpes (HSV) infection suppress HIV?
HIV compromises the human body to defend against infection. Yet people who are infected with herpes are at less risk of developing AIDS.
How does this work?
This question comes from this paper, which is hard for me to follow since I am uneducated on this field. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1716975/

I think HSV is sufficiently descriptive enough to characterize and generalize herpes.

@bobthejoe I don't think it is. For example, HSV-1 and HSV-2 are massively different infections, and both are extremely common in humans.

Also, can we have a citation on this claim? Most of what I've seen suggests that HSV-2 is a risk factor for the acquisition of HIV, and that is is the suppression of HSV using acyclovir that helps prevent HIV.

Yes, sure. Give me a moment

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1716975/ Here is one. Its hard for me to follow, no where near that educated on the matter.

Alright, having read the citation linked, and doing a little poking of my own, here's my approach at an answer:
Some human herpes virus infections may compete with HIV infection. Essentially, some strains (not the ones you normally think of) infect CD4 cells - the same cells targeted by HIV. These strains down regulate transcription in CD4 cells, which in turn interferes with the HIV infection process. This pertains, it appears most notably, to HHV-7.
However the actual impact on HIV disease isn't clear. Strain competition triggers some fascinating evolutionary pressures, but HIV is notoriously prone to mutation, and competition for CD4 cells might not impact HIV infection on a clinical - rather than microbiological - scale.
Additionally, the two most commonly thought of forms of herpesvirus infection, HSV-1 and HSV-2 are associated with increased acquisition of HIV infection. The clearest reasons for this are genital lesions and inflammation at the site of HIV infection. There's also some interesting dynamics in play for active coinfection, such as the impact of acyclovir treatment for HSV impacting HIV, or HAART treatment for HIV impacting HSV.


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Is there any documented evidence for suicide among vertebrates other than humans?
Is there any documented evidence for suicide among vertebrates other than humans? Lemmings not accepted !

Does whales beaching themselves count as suicide? Wikipedia defines suicide as "the act of intentionally causing one's own death", but, in my opinion, it's hard to determine intentions of non-human creatures.

Supposedly Tarsiers will commit suicide when in captivity by banging their heads against a wall.  But I think it is difficult to distinguish between "that animal went crazy and lost its sense of self preservation" from "that animal committed suicide".

Hmm... Lemmings? :)

He said the L- word ...

I heard of a boar species where one boar will face the attacker and fight a losing battle, buying time so that the group can safely evacuate the area.

@aland That's the problem isn't it? How do we know thatt whales are really intentionally beaching themselves?

I would be curious to check if unicellular organisms commit apoptosis.

Here's a short piece about animal suicide from Time: http://www.time.com/time/health/article/0,8599,1973486,00.html

From Wikipedia: "It is not a mass suicide, but the result of their migratory behavior. Driven by strong biological urges, some species of lemmings may migrate in large groups when population density becomes too great. Lemmings can swim and may choose to cross a body of water in search of a new habitat. In such cases, many may drown if the body of water is so wide as to stretch their physical capability to the limit. This fact, combined with the unexplained fluctuations in the population of Norwegian lemmings, gave rise to the misconception." Misconception.

Well, there are certain behaviors that may qualify. The clearest example I know of would be sexual cannibalism, and more specifically (source):

The redback spider is one of only two animals to date where the male
  has been found to actively assist the female in sexual cannibalism. In
  the process of mating, the much smaller male somersaults to place his
  abdomen over the female's mouthparts. In about two of three cases, the
  female fully consumes the male while mating continues. Males which are
  not eaten die of their injuries soon after mating.

That sounds pretty suicidal to me...
A less flagrant but commoner example is that of mothers dying to nourish their offspring. Again often seen in spiders, the best example I know of is the giant pacific octopus (Enteroctopus dofleini). The female will chose a den and lay her eggs. She will then spend her last weeks tending her young, never leaving the lair to hunt. Eventually she dies of hunger and her body nourishes her young. My source here is the wonderful BBC life documentary series.
Neither of these are vertebrates of course but still, I thought the suicidal little spider was interesting.

is right - basically animals care less about their lives when they have reproduced or when there are lots of near relative (like a bee hive, an ant colony or a clutch of cockaroaches or guppies).  They may not overtly be committing suicide, but they will defend their nests to the death or take what would seem to be tremendous risks just for some food.

@shigeta, yes this question got me thinking about social insects. I would have mentioned it but for the fact that the question asks for vertebrates (and I already mentioned two invertebrates :) ) and that, for hive insects, it might be more correct to see the hive as the individual. That raises other questions of course...

I did say vertebrates since that was the original discussion I had, but evidence for "suicide" in any organism is interesting..

Ostensibly, its the conditions of selection that cause this not as much the branch of the family tree you come from.  On the other hand there are fewer animals whose lives are cheaper than insects. Lizards will eat their own eggs... that's not suicide tho.

There's a cool new paper that documents for the first time a male spider (dark fishing spider) whose physiology causes death upon mating.  its a one time deal for these boys. http://rsbl.royalsocietypublishing.org/content/9/4/20130113

@shigeta, ouch!

According to this article whales could kill themselves by swimming to the beach and even when pushed back to the water, they return or dogs can drown in the water when suffer a lot.

The problem is that committing suicide, using the commonplace definition of it, would require an understanding of death. I am sure that an animal can have a basic understanding of the death of others, so far as they realise the difference between a living companion and it's dead body. But if they understand that this lifeless body will never go "back to normal" again and that there is also future death for themselves, I am not convinced.
So, without the understanding of the own, irreversible death, there is (following the definition) no suicide.

Totally not an answer. He's asking for evidence, not philosophical stuff.

The problem is, he did not ask if there is evidence for other vertebrates killing themselves. (As I would guess by the "Lemmings not accepted.") There is. So, the question is really can we classify any of these occurrences of them killing themselves as suicide.

Answer: Yes.
As Zoobiquity points out, gorillas sometimes die from self neglect (starvation) caused by clinical depression. These, besides humans, are likely the only animals to do so through self-neglect.
Then again, one could call scrapie (a prion disease in sheep) or tail-plucking disorder (in parrots and other birds) and other self-mutilative disorders as a form of suicide, but the actual wounds themselves aren't liable to kill the animal.