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Looking for protocol to produce a drosophila primary cell line
I'm looking for a general (and easy, this is going to be for an undergrad class) protocol to isolate and culture primary cells from fruit flies.

Do you want primary cells or cell lines since they are different. My response should however aid with both.

We are time limited. We have about 3 weeks for this project im guessing stables takes up to months

This is the original 1972 paper describing the isolation of the S2 cells from Drosophila. However it would be best if you specify what application you are planning to pursue with the cells, which would make it easier to suggest which ones to isolate. I have personally isolated garland cells, which are visible with the naked eye and highly suitable for endocytic assays. It takes a few minutes to isolate them and all you need are two grade 5 or grade 4 sharp tweezers and 2nd or 3rd instar  Drosophila larvae and a dish and some PBS to submerge the larvae in. You don't even need to pin them! If you are interested I can edit this response and write their isolation technique as I can't find a good technique online.
EDIT:
I have not personally isolated S2 cells although I have extensively worked with S2 and S2R+ cell lines (which are embryonic). Garland cells are excellent to work with for endocytic assays using Dextran (fluorescent dye used for bulk endocytosis assays) and Dynasore [dynamin inhibitor] (and infact they were used to characterise Drosophila dynamin homologue, shibire, here and here and its temperature sensitive behaviour in Shi[ts] mutants and shi role in endocytosis) as an example shown here in fig 6 using S2 cells. I have never cultured the garland primary cells so I do not know their PD and how they behave in Schneider+FBS (since I only isolated them and performed andocytic assays with them while they were in schneiders) and I don't think anyone has (but have a look) so it would be a great protocol to stablish and publish in a methods paper. I'm more than happy to share the isolation technique with you, tried looking on jove or youtube for a video but failed to find one, and let you know what to look for if you wish. Just as a cautionary note, garland cells are multi-nucleated (i have seen up to 4) so it might not divide very well or at all so just bear that in mind.

So this is why I love stack e...thanks for this. So the end result is pretty open ended as of now. At that point in the course they will be learning about fluorescent microscopy. Last semester we had a lot of success using lysotracker in s2 cells and would like to expand the work they did with established cells, now in primary. I would love to have them make stables but I'm concerned about time (and serum). Im very interested in the method you used. Approx How many doublings a did u observe after isolation? We would acknowledge you if the manual goes in press. Thanks @bez I'm open to advice!

I have edited my reply. Please let me know if you require the isolation protocol for garland cells and I shall write it as an edit to my response.


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Global Acidification or Warming
Which poses the greater threat to ecology Global Ocean Acidification or Warming?

Although I'm not an expert in either field but I imagine this is a highly philosophical argument, leading to a fairly high degree of opinions being presented since for example the word threat has to be defined. Please consider highlighting specific concerns/issues/questions you may have about the above topics.

which will kill us and the planet soonest is not an opion

The issues of global ocean acidification and global warming are two symptoms of the same disease, too much carbon in the atmosphere. And they have 1 solution, put less carbon into the atmosphere. It doesn't really matter which aspect is the more harmful one, you can't treat one without treating the other.
If reducing carbon output were simple, we would have done it by now. However, it will most likely require radical changes to our energy infrastructure, with moves away from coal, oil, and natural gas and towards solar, wind, and nuclear power. It will probably require changes to our agricultural practices, and you should really watch Allan Savory's TED Talk for how those changes should be implemented.
People are very slow to change their habits, and short term profit is a powerful motivator against change, but I believe these we can and must solve these problems if humanity is to continue to thrive on Earth.

No if we artificially explode a few volcanos to block radiation with sulfur...acidification becomes a problem but global warming basically ends

Geological engineering is pretty risky. 1: How to trigger volcanoes? 2: How to stop volcanoes? It sounds like a good way to cause more problems than it solves.

Hans Lechner thinks he can stall one into oblivion with magma chambers...meh...starting one would be pretty easy bunker buster bomb somewhere around magma chamber...might need to trigger a small series of quake events...no big deal

If we were to use sulfates, we'd probably deliver it by airplane, but the questions about how much and when to stop remain. Climate is hard to model, and intentionally messing around with it can cause a lot of issues. That said, sulfate delivery is one of the better ideas out there. But if you try to bandaid global warming with sulfates while not reducing carbon emissions you have to come back every few years with more and more sulfate. Look at Venus, it has a lot a sulfate, it has a lot of carbon, it's still hot. I don't think we can get that bad, we'd die first.

with that i can agree...but sulfates and iron (regardless of delivery method) would stem the tide until politicians could get their act together on emissions.

Also sulfate a by plane unbalance ecosystems which are not designed to handle acid rain where as a artifical eruption does not hurt as bad

@caseyr547 It is possible. But it is also possible that we cause negative effects by influencing factors we yet don't know. It is risky.

@Chris agreed but the planet is going to hadies at the moment as the world cannot make laws to keep china from being stupid...its going to get bad with all these north atlantic hurricanes and midwestern tornadoes and blizzards...and at some point it will be beyond this quick temporary fix...

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What would happen if a person had the right side of their body totally removed (including the brain)?

What would happen (in reality or theoretically) if the entire right side of a human's body was removed?
Could they live (aside from all the probable infections and such)?
I would guess that humans can live without part of the liver or brain.
The left brain controls the right side of the body.
What do you think (or know) will happen?
Thank you very much in advance!

in the odd chance that the person survives, (s)he would be totally immobile as the right half of brain controls the left half of the body and vice-versa. The only part of the body that the person can control would be the upper half of face which is supplied by both halves of the brain!

This reminds me of a joke: Q. "What happens if a person has the left side of the body totally removed?"  A. "I think they'd be alright!"

They would die.
Let's imagine that we perfectly cut a person down the middle. That would mean cutting the spinal cord in half, probably damaging the tissue so much that the remaining half wouldn't work well. The liver would be gone. The intestines and bladder would just be open. The heart would have to be adjusted to the left. The surgery would probably cause so much blood loss that they wouldn't even survive to die of other organ failure.
And you already alluded to the mismatch between what side of the brain controls what side of the body, so if you kept the pseudocorpse "alive" on an IV, heart lung machine, and hemodialysis, they'd probably still be paralyzed.

We humans are not perfectly symmetrical. Some organs exist only on one side of the body which are critical for life.That said you can however live without half your brain (if you call that state living) and some other organs also have distributed function over thier surface.

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Enzyme Assay, absorbance change to concentration change
I have a few issues with this question.
An enzyme assay is performed and the kinetic data graphed. The y-intercept of a Lineweaver-Burk plot is 0.6 min/ΔA. The substrate being assayed has a molar absorbance coefficient (ε) of 4500 L/mol.cm.
What is the V max of the enzyme in mmol/L.min?
My working:
Vmax = 1 / 0.6min/ΔA = 1.66ΔA/min (the units switch back I believe?)
And then 1.66ΔA/min / 4.5L/mmol.cm to get 0.37 mmol/L.min?

This looks correct to me, although it odd not to relate the activity to the amount of enzyme that was added to the reaction - the Vmax that you have calculated is a property of the exact assay conditions used.

see here.
y-intercept = $\frac{1}{V_{max}}$
To convert absorbance to concentration, plot the standard curve and get the linear relationship between the two quantities. Make sure that the line that you fit (for standard curve) passes through origin.

No need for a standard curve if you have an extinction coefficient, as in this case.


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What should be the distance between plant promoter and gene?
I am trying to clone a rice gene under a different endogenous rice promoter.I will be cloning the CDS of the rice gene.So I wanted to know what is the minimum or maximum distance I should put between the rice and the promoter so that I can get good expression levels.
Should I check the expression of the construct in E.coli before transforming it?
What should steps should I follow before finally transforming the construct into rice?

where do you want to express the protein?

I will be overexpressing the protein in rice.


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How do nicks in the DNA strand affect the success of Long Range PCR?
Long Range PCR using NEB Master Mix - Hot Start Taq was working fine for me (amplicon sizes of ~10kb) but stopped working all of a sudden. Is it possible that many freeze-thaw cycles on the DNA template introduces nicks into the DNA strand that hamper the polymerase activity ? In certain cases, I am getting no amplification and in some I am getting very weak amplification. Because the integrity of the DNA should be intact over the entire length in case of long range PCR, am I right in thinking nicks in DNA will be especially detrimental if we are trying to amplify large fragments ?
The concentration of the DNA templates I used was 90-140ng/ul in a 10ul PCR reaction, DNA eluted in TE buffer after a magnetic bead method of DNA extraction.

It is not unlikely that nicking is causing trouble. The question is if repeated freezing and thawing is causing the problem, there is an article which has been published in B.R.L. Focus in 1983 which disputes this effect. You can find the PDF with the article here, the article itself starts on page 10 in the PDF. On the other hand there is this paper ("Impact of long-term storage on stability of standard DNA for nucleic acid-based methods."), which shows that sstorage conditions do have an effect on the effciency of qPCR standards. Whatever causes nicking, it is a problem in (long) PCR. The following quote is from Sigma in their long PCR enzyme mix:

Template High quality and adequate length of the template are
  essential for reliable amplification of larger fragments. Extreme care
  must be taken in the preparation and handling of the DNA target for
  long PCR. Nicked or damaged DNA can serve as a potential priming site
  resulting in high background. Avoid freezing, or, alternatively,
  freeze only once to minimize damage. The condition of the target DNA
  is critical. Depurination during cycling is minimized by use of
  buffers with a pH greater than 9.0 at 25 °C.

This paper ("Effect of Highly Fragmented DNA on PCR") shows that induced nicks affect the efficiency of PCR (although they do a much shorter amplification than you). So to overcome this problem I would make small aliquots of fresh DNA preps and then see, if this helps.


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How to identify the genes that distal enhancers pair?
I am writing a project proposal and I have to talk about this problem: how to identify the genes that distal enhancers pair?
I am really new to this topic and I don't know what it is all about. I have been searching the literature but I did not find anything useful. Can someone explain to me what it is all about?
Maybe suggest some papers to me.

To make sure I understand your question right: You want to know how distal enhancers of genes are identified?

@Chris Yes, and how enhancers regulate distal genes. Thanks.

Check this technique called Chromosome Conformation Capture (3C). Its variants exist such as 4C, Hi-C etc.
Basically, the principle of this technique is based on the physical interaction between the enhancer and promoter that is bridged by a transcriptional modulator(protein).

The chromatin is crosslinked
DNA is sheared
The protein is pulled down (Optional)
The fragments of the promoter and enhancer are ligated together and then sequencing/qRTPCR is done.

Sequencing (low throughput- sanger) can be used to identify enhancers of a given promoter. qRTPCR can be used to quantify the strength of the association.
What I just said is not a high throughput technique. Hi-C is high throughput variant of 3C. See the protocol here.


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NMR spectroscopy detection methods for proteins
I've stumbled upon a table comparing the sensitivities of different detection methods in NMR spectroscopy: "Direct", "DEPT" and "Inverse", where "Inverse" seems to be the most sensitive.

What exactly are those different methods are and how do they differ?

In most cases when you perform NMR experiments on proteins you detect the signal on the protons. Even if you're looking at other nuclei, in the end you transfer the magnetization to a proton and detect that signal. This is simply the most sensitive method due to the high gyromagnetic ratio of 1H, and this is the method that is labeled "inverse" in your figure. This is pretty much the default way to measure heteronuclear spectra.
Direct detection means that you directly observe the less sensitive nucleus like 13C. This has certain advantages especially for large proteins where you often have to deuterate the protons to be able to measure anything useful.
DEPT is a type of experiment where magnetization is transferred from the directly attached protons to the heteronucleus. This increases the sensitivity and allows to distinguish CH and CH3 groups from CH2 groups


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Is it possible to convert nerve signals or electrical pulses into a readable format?
Can we have the technology to recreate the informations (like images, sounds etc.)[as in the form of signals in our mind] from human mind to human understandable format? In short, can we read human mind?

Ist of all, i am posting this question again because i have asked that question but my account was not linked to it earlier, so i m unable to comment on it.

Thus i am adding all the previous comments here

The question is slightly unclear to me. Although we can measure brain electrical activity and do things like fMRI but we can't read the human mind which is why I said the question is vague since the definition of reading the human mind is required. What I essentially mean is mind is the construct of the brain and although we can measure brain activity but mind reading is not yet possible unless we can have a highly exact knowledge of the brain activity to know how it is perceived, which I do not know if we have reached that stage yet. –  Bez Aug 20 at 13:09

For clarity, Let me ask in two ways: Our Eyes sees anything (e.g. an image of a tree) then convert into a signal/electric pulses; to be processed in mind and then stored in mind. Now, 1. Do we Have the Technology or machinery to read that image before conversion? and 2. Do we Have the Technology or machinery to read the signals after conversion? –  Khushhal Aggarwal Aug 22 at 21:23

In between these 2 questions, what happens is -- "CONVERSION" of that Information. That conversion method must be a "TECHNIQUE". Thus if we are able to design a machine to convert the same information by the same "TECHNIQUE" as used by the human mind, then it will be helpful to understand the signals after conversion. In short, can we define/design the mechanism to convert the the informations into signals/electric pulses? –  Khushhal Aggarwal Aug 22 at 21:47

for 1, I would say no. For 2 I would say fMRI is addressing this and it is at its infancy but the problem is an image, which produces lets say fMRI machine data analysed/visualised by a computer, is usually associated with many things in the human brain such memory and experience and one image can provoke another depending on the individual so its not as easy as signal A equals object A. Don't know much about fMRI but it measures neuronal activity. Apologies if i cannot be of further help. –  Bez Aug 22 at 22:51

This is what researchers are trying to do with machine learning algorithms. There have been certain successes but the field is still in its infancy. Typically one tries to decode ("read the mind") between few simple classes, e.g. does the person see a happy vs. sad face. The input to the algorithm can be EEG, MEG, fMRI, etc.
See e.g. http://www.nature.com/news/brain-decoding-reading-minds-1.13989
Things like decoding content of dreams, visual imagery, or moral judgements have succeeded this far.

I think the researchers are trying to understand/develop the converted informations (i.e. signal/electric pulse) but i am asking from a different view; i am focusing on the method by which our mind converts it. I am symbolising it as "TECHNIQUE" to convert the informations into signals/electric pulses. Thus, i want to understand/define/design that "TECHNIQUE". –  Khushhal Aggarwal Aug 22 at 22:00

Mr. Bez, Ist of all Thank you for all your support and no appologies are required but please look again at the matter with a different view. I am actually trying to understand the method to convert images into signals which i think no one else has thought of. Everybody is trying to read the signals already converted and stored into our mind. But what if we developed the Technique  by which our mind converts the informations.

This is the third post that asks exactly the same question.

Dear WYSIWYG sir, This is actually the 2nd post because i posted it again due to account problems. Please do continue to answer here. And i request you to please take a look at all the comments. Thanks

I would suggest that you edit your question to add the details that you mention in the comments.

I will follow your suggestion in all the next questions but since i had copied this question from my older post i have to mention these comments separtely because these are the comments posted by others like Mr. Bez etc. But i sincerely thanks for this kind suggestion. Now if you can give some views on the question, i will be obliged.

Sorry Mr. Bez, I am unable to understand what you are trying to say by the comment "possible duplicate of ...".


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Modelling how much cadmium a cell will be able to chelate with phytochelatins
I am involved in a synthetic biology project where I have to do modelling with ODEs. The biological process I want to model is the chelation of Cd2+ with phytochelatins, to know how much can be chelated. I know the basics of ODEs and I already did other modelling tasks, but I never studied anything related to chelation (I am a computer scientist) so any hint about how these kind of biochemical reactions are modelled would be helpful to get started.

If you know the stoichiometry and dissociation constant of the binding interaction this should a straightforward task. If the aim is to discover the stoichiometry via modelling, it's unclear to me how that could work. I'm probably missing something - maybe you could expand your question, and/or make it more specific?

would this be more suited for the chemistry stack exchange? Chelation is a wide field, and there may be existing models based on EDTA, siderophores, and others that could serve as decent starting points.

One of the best ways that I have found for modeling reaction pathways is to set up a boolean network for that specific pathway. The boolean will give you an idea of the possible different states in that pathway (dependencies) and while not really necessary I find it helps orient you to the system.
The next step once you have yourself oriented is to set up Michaelis-Menten equations which you can then use to run you ODEs. Here is a great primer on how to set up these equations: http://depts.washington.edu/wmatkins/kinetics/michaelis-menten.html
The subsequent modules provided in that link are also helpful in explaining how to set-up quadratic velocity equations and do different sequential models.
Also, I'm sure you know this but, it bears saying: these are all steady-state kinetics. If you are looking for a more accurate model of what is occurring in that reaction you are going to have to set-up stochastic models of your system.
Hopefully, that answers you question. Good luck!
EDIT
I have found a paper that seems to relavent to the process you are trying to model. It goes into a bit more detail than I think you are looking for but the basics seems sound. Mendoza-Cozatl and Moreno-Sanchez, 2006

would michailis-menton really apply here? phytochelatin is a polymer that chelates metal ions and gets transported to the vacoule. I guess you could treat it like 2 enzymatic reactions, with chelation as step 1, and transport to vacoule as step 2. But you might get complex cooperativity as more metal ions bind to the phytochelatin.

Michaelis-Menton is only relevant to a simplified system that only has explicitly two variables. It seems from the original posting that this is the case. The original poster appears to be only trying to observe chelation and not transport to vacoule which makes this method a valid option. You are correct that you can treat the pathway as individual reactions but those reactions you mention must be considered independently for the Michaelis-Menton approximation to work. Additionally, cooperativity can be identified by a sigmoidal curve as in the classic case of hemoglobin.


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19th century Latin species description
While reading a 19th century text of new species description, I'm confused by some Latin phrases.
The case here is:

Corp. long. 8 poll., caud. 9 poll.

I guess 'corp.' and 'long.' are abbreviations of some Latin terms, and the whole meaning of the combination of these two words is probably "body length". But I still can't figure out what "caud." and "poll." (the number seems like is in inch though) are stand for.
The species described is a rodent species. Full text could be found here (p.185).

"Caud." refers to the tail (lat: cauda) and, judging from the description, "poll." seems to be another word for inch. So the translation should be something like:
Body length: 8 inches, tail length: 9 inches.

The pollex was a Roman length measurement, approximately equivalent to an inch. The pollex was also known as the uncia, which is where the word "inch" comes from. There were 12 unciae in a pes ...

Thanks for the further explanation. Sorry don't have enough rep to upvote.


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Does E. coli survive at any pH level?
Does E. coli survive at any pH level? If I was to incubate it in agar of different pH, would it still form a bacterial lawn as it's called?

I assume you are asking if E. coli can survive extreme pH conditions and according to this study E. coli K-12 W3110 survives at pH 1.2 – pH 2.0 under low oxygen. This study cultured different strans overnight and exposed to pH 2.0 for 2 hours before diluting 1:80,000 and 1:400,000, under anoxic and aerated conditions. Dilutions where then plated allowing colonies to grow up overnight at 37 oC so this study measured survival as far as I can tell. E. coli can demonstrate robustness and E. coli survives and grows 'accustomed' at pH 7-8 based on the paper here. However it would be great if you clarified your agar pH and the E. coli genetic background you are interested in if you have a specific question about its particular limits (growth or survival).

Also you need to clarify - grow, or merely survive?

@AlanBoyd I made further clarification/amendments to my response to state what the studies mentioned have measured, as requested to clarify my response. Many thanks for the pointer.


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can a bacterial protease inhibitor cocktail be used for Western Blotting involving HUVEC cells and HT-29 adenocarcinoma cells?
Dear fellow biochemists,
I need some advice on Western Blotting, more specifically the use of certain protease inhibitors with the RIPA cell lysis buffer and protease inhibitor cocktail. A Millipore technical representative recommended my using "539134 | Protease Inhibitor Cocktail Set III, EDTA-Free - Calbiochem" as a good general protease inhibitor cocktail.
I have another protease inhibitor cocktail which includes: AEBSF, bestatin, E-64, and pepstatin A (E.coli protease inhibitor cocktail) but it does not include the aprotinin or the leupeptin inhibitors. Is there a risk of proteolysis in a mammalian cell lysate without these latter 2 inhibitors? The specific cell types which we are using are: HUVEC (human umbilical vein endothelial cells) and HT-29 adenocarcinoma cell line.

In general, leupeptin (a cysteine, threonin and serine protease) and aprotinin (sometimes called Trasylol; trypsin inhibitor) are included in most mammalian cell lysate buffers. Whether you need them is really up to your protein of interest: if you know how it gets degraded in vitro, then you should be fine with inhibition of just those proteases. If instead you want to preserve as much protein as possible, then you should add them. Should you not use them, then yes, those proteases will degrade some of the cell proteins.
The good news is that you can buy aprotinin and leupeptin individually and supplement them to the necessary concentrations for a working lysis buffer.


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Can viruses that normally infect eukaryotic cells also infect bacteria?
Can standard viruses infect bacteria?  I'm not speaking of bacteriophage but typical RNA and DNA virus such as influenza and Ebola.

That's a very human-centric view.  There are more bacteriophages floating around this planet than anything else.  Phages are your "typical" viruses, Influenza and Ebola are the weird ones.

I like this question is fine and should stay open. Lots of good things are correcting misconceptions.

All viruses that infect bacteria are known as bacteriophages. In your question you mention the "typical RNA and DNA viruses", however, bacteriophages also contain DNA, which is often double-stranded DNA.

Some viruses even infect other viruses! There are still very few examples and in addition to that those examples involve host species that are on the boundary of the definition of what is a virus. You may want to have a look to mamavirus and its parasite: sputnik. Also one may want to have a look to Marseillevirus (named after the University of Marseille), Lausannevirus (named after the University of Lausanne) and mimivirus.

I'm not so sure about my answer. But I think "bacteriophage" is a polyphyletic name of which was defined by the ability of infecting bacteria, but not defined by the genetic, evolutionary, or morphological relationships.
It seems that if a species (or a taxon in a higher taxonomic level) of virus is infectious to bacteria, it will be classified as a member of the bacteriophage.
Here is a review article about the phage classification.

this is a fine answer to a fine question

Tailed phages (Caudovirales) are an ancient monophyletic viral taxon, and include species that infect bacteria and species that infect archaea. People often use the term bacteriophage as a synonym to them. Caudovirales are the most abundant biological entities on the planet. There are three families: Myoviridae, Podoviridae and Siphoviridae, which are characterized by linear dsDNA genomes and unique head-tail morphology. Eukaryote-infecting Herpesviridae are believed to be related to Caudovirales.

The word infect is an encapsulation of several activities: transcription, translation, viral entry, budding, lysis, etc. When you ask if a eukaryotic virus (influenza, ebola) can infect a prokarytoic cell (bacteria) you are asking if these viruses can do the same activities. The answer is no.

Translation is mediated by ribosomes, which are different in
prokaryotes/eukaryotes.
Transcription is mediated by viral RNA polymerase which may be contained in viral nucleic acid. This is possible, but useless without translation of the mRNA.
Viral entry is mediated by cell surface features and would be incompatible for eukaryotic viral entry into prokaytoic cells, and the reverse.
Viral budding is mediated by viral proteins inserted into the cell membrane. This is prohibited since a eukaryotic virus is unable to enter a prokaryotic cell/translate its proteins.
Lysis is mediated by excessive buildup of viral particles inside a cell. This is also prohibited by an incompatibility of eukaryotic/prokaryotic cell surface, translation machinery.


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What is this creature?

Since it has six legs, I believe it's some sort of insect, but I could be wrong.
I spotted it in my Central Texas backyard (Austin area). It was very slow and not at all skittish.
For size reference, it's standing on a 2x4. It was a good 3-5 inches long, not counting antennae.

I don't know anything about Texas insects, but it almost looks like a species of walking stick or other phasmatodea. I don't think I can get any closer than that.

I think you may be right. I looked into it a little more after posting this, and the nearest match I've found is the Two-Striped Walkingstick: http://www.insectidentification.org/insect-description.asp?identification=Two-Striped-Walkingstick. Thanks for your input!

yes walkingstick is what we would have called it in texas but i dont know if it fits the scientific classification...it sure is fat though

It is the Two-striped walking stick

Walkingsticks, like that in your photo, belong to the insect order Phasmida (also sometimes called Phasmatodea). The species in your photo belongs to the family Pseudophasmatidae. Texas has two species documented for this family. One is Anisomorpha ferruginea, commonly called the dark walkingstick or northern two-striped walkingstick.  The other species is Anisomorpha buprestoides, commonly called Florida stick insect or two-striped walkingstick.
According to W.S. Blatchley's Orthoptera of Northeastern America (1920), pg. 145, A. ferruginea has narrow stripes and is a bit shorter than A. buprestoides, which has broad stripes. Based on the appearance of the stripes in your photo, I'd say you have A. buprestroides.


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What is a membrane potential?
I know this may be silly, but I am confused to what a membrane potential actually is. I understand that at resting membrane potential is -70- -80 mV. But what does that exactly mean and how does this all tie into diffusion potentials and equilibrium potentials.

The existence of membrane potential is just that: as long as they are alive, cells try to keep their cytosol different from the outside soup, mainly by expelling sodium ions. There is a longer story, with cells pumping other ions in or out, or leaking ions due to the imbalance, but resting membrane potential really revolves around sodium. There is an imbalance in sodium across the membrane, and that makes sodium naturally try to balance out, by trying to leak back in.
I am sure you have heard about the famous sodium/potassium ATPase. It expels sodium ions, while letting in fewer positive ions. It is just the most studied way the cells are going about making sure their innards poorer in cations, that is, negatively charged when compared to their environment.
All these pumps are ATP-dependent, and you would know ATP is the main energy store. So as long as cells live and make ATP, they can maintain this difference between their innards and the environment. Once they die, ATP is gone, pumps stop, and there is no sodium disequilibrium - no membrane potential.
Diffusion potential is an artificial concept that we use in order to make sense of the membrane. We imagine a membrane that opposes sodium movement alone, and we calculate how hard will it be (how much energy must be spent) to keep the asymmetry of low sodium inside - higher sodium outside, were a hole punched in the semipermeable membrane. Luckily, we can use some physics and maths, and figure that this energy is dependent of the ratio of sodium concentrations ([Na]in divided by [Na]out). For typical cells, there are 150 mM Na outside and 15 mM Na inside a cell; physics tells us it will take 62 milli-electronvolts to hold a Na ion out once some hole is found.
If you don't provide those 62 meV and you don't close the doors for leaking, sodium ions will fly in. And that is indeed what happens in depolarization, when sodium gets a chance to move.
These electronvolts are a unit of energy, or work. We can think of a few ways of performing this work on a Na ion that tries to leak in: heat the cell until ions stop caring about direction of movement, hold the outside Na in some tight  chemical structure etc. But the simplest way is to apply an electric field. If you add to the concentration imbalance a 62 mV electrical difference in electrical potential, you stopped the flow of sodium either way. Get a bit less than 62 mV, and the Na ions will carry on their old ways and try to no avail to leak into the cell. Get a bit above 62 mV, and the flow of sodium will be force in the opposite way. Stay on 62 mV and you achieve equilibrium potential: neither direction will have the upper hand.
The picture is way more complex once you factor in the other ions, but the facts are:

resting and action potentials are voltages one can measure across membranes, quite often during cells' lives
diffusion potentials are part of an abstract model
equilibrium potential is something one could impose on a cell - not something that you'd find in natural frequently, yet not plain fiction.

To understand what a membrane potential is, you should understand the units for -80mv. The negative sign is relative to the observer, yourelf, to the inside of a cell. From your perspective, the inside has an excess of negative ions. On the outside of the cell, there is an excess of positive ions.
Unlike electricity, where charge separation is quantified by electrons, action potential is quantified by ions. Ions are matter, like Na+, K+, Cl-. When electricity flows through a wire, electrons are flowing from excess negative charge to a deficiency of negative charge.
When a cell establishes an action potential, it moves Na+ outside the cell, which moves the potential from 0mv, negative. The number -80mv, or whatever potential that may be observed, is the point at which a net flow of positive ions are not leaving the cell.
Na+ is actively pumped outside a cell, using energy. K+ is passively driven into the cell by simple diffusion to neutralize the charge imbalance. Opposing the outward flow of Na+ and inward flow of K+ is their diffusion gradients. Ions flow from a high concentration to low concentration.
At -80mv, the Na+ concentration is high outside the cell. Intracellular Na+ is being pumped out to counteract any leaking back in. The K+ concentration is high inside the cell from its passive diffusion to cancel the electrical potential.
The physics of why K+ does not neutralize the -80mv is in its concentration gradient. K+ is being pulled outside the cell by this gradient and driven inwards by an electrical potential. The net electrical potential across the cell membrane is -80mv for a given cell's capacity to maintain the concentration of its intracellular ions.

Membrane potential AKA the membrane electrochemical potential,  may be thought of as the voltage that is experienced across the membrane, analogous to a battery.
The extracellular side is typically positive, while the cytoplasmic side is typically negative. This induces the electrochemical gradient with ions having a preference for a particular side depending on their charge.
An equilibrium of ions can be maintained by transport pumps which "force" a difference in electrochemical potential on either side of the membrane potential. If the membrane is permeable to a certain type of ion, the the diffusion processes occurs as ions diffuse to their "preferred" location dependent on ion concentrations.
Wikipedia has a nice succinct definition of the functional advantages of maintaining a membrane potential:

First, it allows a cell to function as a battery, providing power to operate a variety of "molecular devices" embedded in the membrane. Second, in electrically excitable cells such as neurons and muscle cells, it is used for transmitting signals between different parts of a cell.

This is an advanced concept, so perhaps a few video tutorials might explain better than my words. Start here perhaps.

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


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Does osmosis take place in prokaryotic cells?
As far as I know, osmosis occurs in Eukaryotic cells, and I'm wondering if it could take place in prokaryotic cells too.

Since osmosis is a physical-chemical phenomenon, it happens along all concentration gradients.

So that means, it could happen in prokaryotic cells too ?

yes, even happens across non living membranes if they let water across, that's how dialysis works.

Osmosis works across every cell membrane along a concentration gradient as its a physico-chemical principle. Water can cross the membrane (or cell wall), while the substance dissolved in it (for example salts) can not. Because eukaryotic cells only have a cell membrane, they will burst eventually, while bacteria (and also plant cells) have a more rigid cell wall, which will mostly prevent bursting. However the influx (or outflux) of water creates a pressure which is called turgor pressure. How this works is shown below (figure from here), bacterial cells and plant cells work pretty much the same way:

That's a good explanation of osmosis, but most bacteria have a cell wall to prevent too much swelling.

You are right - I took the wrong turn here. I corrected the answer.

The force driving osmosis exists in any system with an imbalance of solute molecules across a semipermeable membrane.
Think of a concentration gradient as an electrical potential, where high concentration is negative charge and low concentration is positive charge. In the case of electricity, its the magnetic force which causes the interactions leading to charge equilibrium.
In osmosis, there is no communication between solute molecules by an 'osmotic force'. Osmosis is a result of entropy. In chemistry, a separation of solute concentrations is called a chemical potential. As entropy increases in the system, this chemical potential is decreased, either endo or exothermically.
Here's a chart showing the change in heat for the dissolution of substances. Negative numbers mean a system loses heat (enthalpy) and is exothermic. Cold packs use ammonium nitrate, which absorb heat as they are dissolved in water.
The processes of osmosis, entropy are fundamental to our universe, not to a specific domain of life.
Enthalpy change of solution for some selected compounds
hydrochloric acid   -74.84
ammonium nitrate    +25.69
ammonia             -30.50
potassium hydroxide -57.61
caesium hydroxide   -71.55
sodium chloride     +3.87
potassium chlorate  +41.38
acetic acid         -1.51
sodium hydroxide    -44.51
Change in enthalpy ΔHo in kJ/mol in water at 25°C[1]


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Can microdialysis be made in Drosophila melanogaster?
I've asked this before in stack overflow's cognitive science community, and someone recommended me to ask here:
I've found a couple of studies using microdialysis on insects, but didn't found any in Drosophila. I've found that the membrane diameter are from 240um, and it seems that Drosophila melanogaster brain must be between 200-300um , but I was wondering if the lack of studies of perfused drugs in Drosophila is due to this technical constraint, or is just I'm searching wrongly.
--
Edit: I specified the original target, Drosophila melanogaster, since there are bigger parients like Hawaian D. heteroneura and D. cyrtoloma. that could be subject to MD with current probes.

This is a great question! I was not aware microdialysis was used in Drosophila since most use feeding (compounds dissolved in Drosophila food) to administer different drugs to Drosophila. Is the microdialysis used on the adult Drosophila or larvae? why not inject the larvae?

@Bez , I didn't find microdialysis use in Drosophila but I thought that maybe it could be made on heteroneura and cyrtoloma since they are bigger, that's what I meant to say :P sorry for the missleading comment.

It seems highly unlikely to me. The smallest microdialysis probes I've ever seen are about 250 µm in diameter, so about the size of a Drosophila hemisphere. You can deliver drugs by microinjection (well, I assume you can, seeing as a) you can do it in honey bees and b) you can perform whole-cell patch clamp recordings in Drosophila).


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What is the best current understanding of how yeast transformation works?
I would like to get myself up to speed with what is currently known to science about yeast transformation. Specifically, transformation of plasmids and linear DNA fragments. I am particularly interested in practical aspects, such as:

What is salmon sperm for? What if I don't use it? What if I use more?
What is the relationship between number of cells, amount of transforming DNA, and transformation efficiency?
How does choice of electroporation cuvette gap size affect efficiency?
What can I do to get more colonies after transforming my yeast?
What steps can I skip to make the transformation quicker if I am doing an easy transformation?
How do different genetic backgrounds and media affect efficiency? Are there any common ones that reduce efficiency substantially? Are there any uncommon ones that increase it substantially?
What is the effect of post-transformation "recovery" time (eg. culture 12 h without selection and then plate on selective medium)?
Is making spheroplasts worth it?
Does the same transformation protocol work for different species (S. cerevisiae, S. pombe, C. albicans, etc.)?
Is there a coherent theoretical framework for understanding what actually happens when yeast are transformed, as opposed to "you mix some chemicals with DNA and throw cells in, abra kadabra, transformants come out"? The sort of theory I'm asking about would be useful in predicting conditions for better efficiency.

I am not expecting you to comprehensively answer these questions in your answer. This would make for a very long answer, and each of these could be a question here in its own right.
Instead, I want the answer to name reference materials which can be studied to learn more about the points above. For example, recent reviews or textbooks by established experts in the fields would be quite useful.

If "what should I read to learn more about concept X" is not an appropriate question for this site, I would be happy to delete this and split it into many smaller questions.

I think the question is absolutely ok. However, collecting a number of references takes time...I can look into this tomorrow when I have a little spare time.

I have never worked much with yeast, but I can still give some answers:
Salmon sperm is used as a the so called "carrier DNA". It is thought to bind to the yeast cell wall and thus prevents that the DNA which shall be transformed does so. This raises the transformation efficiency. See here for more details: "Transformation of yeast by lithium acetate/single-stranded carrier DNA/polyethylene glycol method.".
Effect of the recovery time: In this time you typically give the cells the chance to recover from the relative rude treatment and to express the resistance gene (when used) before moving them to a selective medium. This raises the efficiency of the transformation.
Spheroblasts: As far as I remember they are terribly fragile and painful to handle. However, when you succeed making them, you have cells which take up high quantitaties of DNA which makes them pretty efficient.
I think these reviews are definitely worth looking at (they also contain a lot more references):

Genetic Transformation of Yeast
Transformation of Saccharomyces cerevisiae and other fungi - Methods
and possible underlying mechanism
Foreign gene expression in yeast: a review

If you have a chance to get hands on a copy of "Methods in Yeast Genetics: A Cold Spring Harbor Laboratory Course Manual", I think this will be very helpful.


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How are isopotential maps computed from EEG channel data
I have some EEG recordings of $1$ minutes, with $500$ samples per seconds and $63$ channels. For each recordings, this effectively yields a $30,000\times 63$ matrix $M$.
How do I extract isopotential maps from the data?
My first try was to simply take each row $m_i\in M_{i,j}$ such that $m$ has length $63$ and plot them with respect to the $x,y$ coordinates given by the location of each of the $63$ channels... However, I seem to get bad plots...
I also tried to bandpass the data first. For alpha waves, my Mathematica code looks like this:
BANDPASSALPHA[x_] :=
 BandpassFilter[x, {8 Pi, 13 Pi}, SampleRate -> 500]
bpalpha = Map[BANDPASSALPHA, dataz];

I bandpassed the columns of the matrix $M$. That is the signal $x$ that is used in BANDPASSALPHA[x] is one of the columns of $c_j\in M_{i,j}$ and are of length $30,000$
According to Wikiepdia: http://en.wikipedia.org/wiki/Isopotential_map, the spatial derivative needs to be computed first...
Does anyone know how isopotential maps from EEG recordings?


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Microsatellite shifts (peak calling) GeneMapper! Thesis help!
I'm a masters student attempting to conduct a parentage analysis on a population of fish for my thesis. My advisor and post-docs haven't been very helpful, so I need some help! I have dinucleotide microsatellite markers that I've run on a set of individuals.
I'm using GeneMapper 4.0 to score the alleles of said markers but something isn't making sense. My alleles are shifted to where they are not evenly distributed in their sizes. For example, at a given locus for one individual I have one allele peak at 152 while the other allele peak is at 161 (It's an obvious heterozygote).
This "shift" doesn't make sense considering my markers are dinucleotide and should be spaced 2 bp apart, right? So either 152 is actually 151/153 or 161 is actually 162/160. How can I score these and resolve this issue while keeping consistency for my analysis later? I see this shift everywhere and I've already ruled out contamination and I'm positive these peaks are real. Any pop gen people out there that have a clue what to do?
I've been stuck on this for weeks, no amount of web searching/paper reading helped.
Thanks!

@MikeTaylor
Thanks so much! I'm really glad to hear that. My peaks are beautful, but there are so many shifts that I'm not sure which way to score either allele. Should I make the odd even or the even odd? I'm using GeneMapper if you have any experience with that, I'd really appreciate some advice!
Thanks again!

You don't need to change the allele size. Is there a reason why you can't use the sizes as they are called by the software, regardless of odd or even size?

Here's another way to think about it. Assume the ancestral alleles all had even sizes but you don't know what the sizes were. An indel occurs after the repeat region. If a deletion, the size will decrease by one. If an insertion, the size will increase by one. In general, you can't tell whether the change was due to an insertion or deletion. That's why you shouldn't change allele size. You're changing data based on unverifiable (and unnecessary) assumptions.

@MikeTaylor Thank you SO much for your replies! I don't trust the automatic binning and calling of the peaks on the software only because the same allele is inconsistently called different sizes if it's shifted ever so slightly. I know I have to keep the same peak across all my samples called the same throughout, but the odd/even thing worried me for the sake of inconsistency. I'm not as hesitant now to call an even peak even when the rest are odd, so long as I call that peak that size consistently, I guess. Thank you for all your help Mike!

Your markers are probably fine, especially because you keep seeing the same allele in multiple individuals. Dinucleotide repeats do not always copy perfectly. More likely, remember that the primers you use to amplify your microsatellites bind outside of the actual repeat region. You could have an insertion/deletion in the region between the primers and the repeat region, changing your allele sizes from to even to odd (or vice versa).

I like this answer but I think you should have mentioned gene flow


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Genome-wide methylation analysis: sources of technical error?
We are doing a genome-wide analysis of methylation via bisulfite sequencing for an insect species. Previous experimental techniques have suggested the presence of methylation in this organism, including an AFLP analysis using methylation-sensitive restriction enzymes and a differential expression analysis using a methylation inhibitor.
Our bisulfite sequencing data, however, is giving us essentially no evidence of methylation. If this finding is true, it will be a pretty big deal. But before we go down that path, we want to make sure we've counted out all sources of technical error.

First, we wondered if the bisulfite treatment failed, but quickly determined that this would not explain the result. If the C --> T conversion had failed at an extremely high rate, you would expect to see methylation all over the place. That's the opposite of what we're seeing, which is essentially no methylation.
Second, we wondered if there was some kind of "overexposure" issue in the bisulfite treatment that caused even methylated Cs to convert to Ts. We found a paper describing this phenomenon[1], but reports we can find suggest this happens at a low (<10%) rate, which cannot explain our data.
Third, we wondered if perhaps there was an issue with the reads mapping to the genome, we got at least 70% mapping efficiency for each BS-seq sample, so that can't be it either.

Are there any other sources of technical error we should consider and check for before believing this result?

Genereux DP, Johnson WC, Burden AF, Stöger R, Laird CD (2008) Errors in the bisulfite conversion of DNA: modulating inappropriate- and failed-conversion frequencies. Nucleic Acids Research, 36(22):e150, doi:10.1093/nar/gkn691.

This sounds very interesting. Could you provide a link to the paper that found methylation? "Previous experimental techniques have suggested the presence of methylation in this organism,"


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Pharmacokinetics: why do certain drugs follow zero-order kinetics?
I understand that alcohol and phenytoin are two examples of drugs that follow zero-order kinetics. Why do these two particular drugs follow zero-order kinetics as opposed to first-order kinetics?

Hi and welcome to Biology.SE! We encourage making a decent attempt to answer questions before we make new posts - could you let us know some of your thinking that led to this question, and what part of it you couldn't find easily by searching the web?

Zero-order kinetics is linear, and the rate of metabolism of a particular drug is constant despite the amount of drug present. I was curious to know if there were any biochemical processes involved that would cause alcohol and phenytoin to follow zero-order kinetics.

You would observe zeroth order kinetics when the metabolism is dependent on a catalyst (enzyme) that is limiting. Very low $K_m$ and low enzyme concentration compared to substrate would show this kind of effect.

Basically any compound in concentrations sufficient to saturate its metabolization machinery will show zero-order pharmacokinetics. This reflects the fact that metabolization is taking place at full speed while facing a comparatively enormous amount of substrate (just as @WYSIWYG pointed out). This effect can also be shown in vitro with pure substrate/enzyme solutions.
But the above is a rather simplistic model, valid only in specific situations.
Most of the time in humans, zero-order kinetics stem from the fact that liver enzymes are saturated. However, for most drugs the redistribution phase is much more important than metabolization/elimination in defining the duration of effect. A good example of that would be sodium thiopental. As a single iv bolus dose, it will induce loss of consciousness for a short time due to redistribution. However, continued infusion will allow blood and tissue concentrations to equilibrate, and then the metabolization/elimination rate will become much more prominent in defining the duration of effect. And as sodium thiopental happens to have zero-order metabolization kinetics in continued infusion, it will take you a loooooooooong time to wake up! This is why in human pharmacology, we use context sensitive half-life to better represent drug kinetics.

Alcohol is a drug that is cleared by an enzyme. This interaction is what follows zero-order behavior. However, initially alcohol follows first order behavior because the ability of the enzyme to clear the alcohol exceeds the concentration of alcohol. That means clearance is constant and does not depend on the alcohol concentration.
Now what makes alcohol zero order is that the desired effect of alcohol (the therapeutic effect) occurs when the dose is greater than that enzymes ability to clear the alcohol. Once the alcohol concentration is greater than a certain point the body begins to struggle to clear the alcohol (roughly near the Km of the clearance enzyme) because of a physical limitation on the quantity or quality of the enzyme. So now when you increase the concentration of alcohol, the rate of clearance is not able to account for that increase proportionally because it is saturated. Therefore the alcohol you consume after a certain point (Km of the clearance enzyme) has a greater toxic effect. One drink too many is a very real thing.


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Does isolation have any effect upon mouse behavior?
I work with a lot of mice. I don't do any behavioral analysis, I just inject DNA or RNA and do imaging assays. However, I have noticed some effect of isolation on mouse behavior. Normally, the mice are housed in our university's animal facility with no more than 5 mice to a cage. Sometimes, 1 mouse will be put in a cage by itself. When I go to get these lone mice from their cages, they seem more skittish, harder to grab, and more likely to bite me than mice kept in groups.
Additionally, our Office of Animal Resources, which is responsible for getting in the mouse shipments and putting them into cages, has recently changed how our mice are caged, with a group of 4 mice being normal, any leftover mice are put into cages with other mice, making a 5 mouse cage. This means I haven't seen a single mouse in a cage for a while. So I might not be the only one to have noticed an effect of isolation on the animal's health.
I have heard of studies on monkeys by B.F. Skinner, where he induced very severe depression and other psychological issues by isolating them, so I suspect similar studies have been attempted on mice using far more quantitative methods than I've been able to do.

Yeah, it's not good:

Social isolation (SI) rearing in rodents causes a variety of behavioral changes, including hyperlocomotion, anxiety, impulsivity, aggression, and learning and memory deficits. These behavioral abnormalities in rodents may be related to the symptoms in patients with neuropsychiatric disorders, such as attention-deficit hyperactivity disorder, obsessive-compulsive disorder, autism, schizophrenia and depression...

Also:

Our findings suggest that [social isolation]-induced behavioral abnormality is a psychobehavioral complex relevant to various clinical symptoms observed in neuropsychiatric disorders, including ADHD, schizophrenia and depression, and that SI-reared mice are a useful animal model to study the pathophysiology/pathogenesis of these diseases.

There's this:

In contrast, long-term social isolation is a model to study the behavioral and neurochemical consequences of depriving rodents of social interaction. Many of the symptoms caused by long-term isolation resemble those seen in depression and anxiety disorders. Furthermore, long-term isolation of male mice is known to induce offensive and aggressive behavior, such as attacks.

And this:

These data suggest that long-term isolation may induce functional changes in the sensitivity of alpha 2 receptor in the noradrenergic system...

And this:

In the present study, we found that social isolation elevated the anxiety levels of mice...

Emphasis all my own.
There's a lot more meat in those studies, and especially the paper they cite in their introductions.  Some of them, as well as others also explore the effect of isolation in addition to other substances.  It can absolutely affect your studies, in particular behavioral or expression-based studies.  Your mouse house is good to change their practices.


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Evolution of sexually concordant genetic variation on the X-chromosome
It was theorised in 1984 that sexually antagonistic genetic (SA) variation should more easily evolve on the X-chromosome. This is partly because female beneficial/male deleterious mutations face less powerful selection against them; the X is in females twice as often as in males so mutations will persist up to the point where male cost is <2x the females gain. Furthermore, male beneficial/female deleterious recessive mutations (p) will always be expressed in males and, when rare, only very occasionally in females; if the frequency of p 0.1 then 1 in 10 males will express that trait and only 1 in 100 of the females.
It is therefore expected that the X-chromosome should become a hotspot for SA variation in comparison to the autosomes. A result would be increased persistence of genetic variation on the X- within sexually antagonistic loci. However, how would a sexually concordant (male & female beneficial, or male & female deleterious) fare in the X- compared to the autosomes? Just eyeballing it, it feels like the X- should be better able to select on recessive mutations because they are always expressed in males; removing deleterious and spreading beneficial mutations more rapidly. Should there then be less genetic variation on the X- than autosomes?

I dont really understand what Sexual Antagonism means. However this article may be relevant to your question. Just happened to see it some days back.

@WYSIWYG - I briefly touch on sexual antagonism in my answer to this question. See the last part where I talk about conflict.


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Premise of life cycle synchronization between predator and prey
While reading about the predator satiation hypothesis of the periodical cicadas' 13/17 year life cycles, I started wondering about its premise. By the way, I understand the math behind the prime number life cycle. 13 and 17, being prime numbers are only divisible by themselves and 1, and thus have as few divisors as possible. But my question is about the premise of why a predator would even want to synchronize its life cycle with a divisor of the prey's life cycle in the first place.
If the predator has a set life cycle, but its individuals are evenly distributed in regards to their development within that life cycle at any given time (for example there could be roughly even amounts of mature and immature predators at any given time), then what difference does the life cycle make? Here I am assuming that eating cicadas is most beneficial to a specific developmental stage of the predators, which is the only reason I can think of why there would be an advantage to this synchronization. By the way, is this even a correct assumption in regards to this hypothesis?
To be clear, my main question is why life cycle synchronizations between predator and prey matter when/if predators aren't all undergoing the same stages of their life cycles simultaneously.
edit: To be even more clear, I am asking what the benefits are to the predator to synchronize its life cycle with the prey (the cicadas, in my example).
My reference: Wikipedia says the following: *It was hypothesized that the emergence period of large prime numbers (13 and 17 years) was a predator avoidance strategy adopted to eliminate the possibility of potential predators receiving periodic population boosts by synchronizing their own generations to divisors of the cicada emergence period.
Goles, E.; Schulz, O.; Markus, M. (2001). "Prime number selection of cycles in a predator-prey model". Complexity 6 (4): 33–38. doi:10.1002/cplx.1040.
I have interpreted "synchronizing their own generations to divisors..." to mean synchronizing the length of the life cycle. I am happy to hear of another interpretation.

Thanks for your edits. I've updated my answer. I hope it proves a bit more satisfactory than my first attempt.

New Answer, based on first comment by user2686410 and subsequent edits to the question.

I have interpreted "synchronizing their own generations to divisors..." to mean synchronizing the length of the life cycle. I am happy to hear of another interpretation.

First, the overall goal of Goles et al. (2001) does not seem to test hypotheses related to the evolution of life cycles in the cicadas per se. It seems their overall goal instead may have been to explore the generation of prime numbers from numerical theory, using biologically-based models. For example, from the abstract they state,

The model marks an encounter of two seemingly unrelated disciplines: biology and number theory. A restriction to the latter, provides an evolutionary generator of arbitrarily large prime numbers.

and at the end of the discussion they write,

Although there are traditional methods for prime number detection (see e.g., Ref. 23) that are faster than the methods presented here, it is remarkable that the generation of prime numbers can be performed using a biological model.

To more directly address your question and if I understand their models, Goles et al. (2001) do seem to allow the the life cycles of both predators and prey to co-evolve yet this is not always clear.

We compare now a prey mutating to a cycle Y' with the resident prey (cycle length Y ) at constant X. Analogously, we compare mutant cycles X' with resident cycles X at constant Y (Goles et al. 2001, pg. 34; emphasis added).

Here, they seem to be saying that the life cycle of one (predator or prey) can change while other other remains constant (prey or predator). The life cycles don't coevolve.  Subsequent formulas and statements imply an interactive effect between the predator and prey life cycles. (Honestly, their writing is somewhat opague to me and they do not define all of their mathematical terms, making it difficult to follow the logic of their models.)
Regardless, the results of their initial models, shown in the figure below, shows the prey converging on a 17 year life cycle while the predators converge on a 4 year cycle. Somewhat more complex models tended to converge on 13 and 17 year cycles, although other primes like 11, 19 and 23, had similar probabilities of evolving.

Goles et al. (2001) admit at the outset of their paper that there is no evidence for predators with periodical cycles that align with the life cycles of cicadas. This would be consistent with general ecological observations. Most predators consume multiple prey items. Highly specialized predators would be more vulnerable to extinction if their prey source went extinct.
Another numerical model, developed by Tanaka et al. (2009) explicitly to explore life cycle evolution of cicadas, does not include predator life cycles at all. Their results still converge on 13 and 17 year life cycles although they restricted the possible range of life cycles to between 10 and 20 years. Thus, it does not appear to be necessary for predators to evolve a life cycle that coincides with prey life cycles for the predator satiation hypothesis to work. Of course, this is consistent with the real world observations that cicadas do not appear to have predators with concommitant life cycles.
Original answer, lightly edited
In the case of the cicadas, they are the prey, not the predators. They are not synchronizing their life cycles with the predators (if I am interpreting your entire question correctly). The argument is that cicadas have evolved synchronized life cycles to maximize survivorship.  By having a large number of individuals emerge within a very short period of time, the very high density means most individuals will live long enough to reproduce because the predators (birds, small rodents, etc.) will be satiated (see Williams and Simon 1995 for a review and pointers to early literature). Some predators of cicadas will be always present so the cicadas are not synchronizing to any specific predator.
Goles et al. (2001) used numerical models to argue that such life cycles will tend to converge on prime numbers. (As discussed in the update above)
Tanaka et al. (2009) recently argued, again using numerical models, that the prime number-based life cycles of cicadas evolved as a result of the Allee effect. The Allee effect basically states that there is a positive association between the fitness of individuals in the population and the population size or density. Below a certain size, a population is unable to sustain itself and is vulnerable to extinction. Tanaka et al. argue that the Allee effect results in prime-based life cycles under varying environmental parameters. They further argue that maintenance of alternate life cycles minimize hybridization between groups with different life cycle timings.
What seems to really remain to understand the evolution of cicada life cycles is to unravel the genetic mechanisms involved with timing.
Literature Cited
Goles, E. et al. 2001. Prime number selection of cycles in a predator-prey model. Complexity 6: 33-38.
Tanaka, Y. et al. 2009. Allee effect in the selection for prime-number cycles in periodical cicadas. Proceedings of the National Academy of Sciences USA 106: 8975-8979.
Williams, K.S. and C. Simon. 1995. The ecology, behavior, and evolution of periodical cicadas. Annual Reviews of Entomology 40: 269-295.

I am not sure where you read that I said cicadas were predators. I was referring to the life cycle of the predators of the cicadas, and its synchronization with the life cycle of the cicadas. At one point I even mentioned "eating cicadas." Thanks for your links, though. It looks like the models needed to explain this aren't as simple as I thought they might be.

@user2686410 - Sorry, I completely overlooked that phrase in your question. I interpreted sentences like "If the predator has a set life cycle..." in light of the cicada life cycle, which is why I thought you were thinking of cicadas as the predator. Later this evening, I'll try to edit my answer to better suit your question.

@user2686410 - would you please provide a citation you found that suggests the predators are synchronizing to their prey, especially for interpreting the predator satiation hypothesis. I'm interpreting your question in light of that hypothesis. However, no predator has synchronized it's life cycle to the cicadas (that I am aware of).

OK - I have added a reference to my question.

@user2686410 You're welcome. I hope you found it useful.

Mike Taylor's answer is well-researched and inspired the following thought experiment that might help you.
Imagine a predator of the cicada which takes several years to reach maturity(say, five). The population of this predator is distributed evenly across all the different stages of its life cycle, at least at first.
One year there is a cicada eruption and all the members of this predator species are incredibly well-fed for a month or two. If the effects of this prey glut aren't perfectly evenly spread across all ages of the predator species, there will be a fitness advantage to one age group or another. Maybe the young ones grow faster, or the old ones spend more time looking for mates instead of eating. It doesn't matter which(it can even be both) as long as it's not even across all members of the predator species.
Now examine the next generation, five years down the line. The effects of the prey glut are felt here too (more parents-> more children, bigger parents->stronger children, etc etc). If the cicada cycle is five years, or even ten, every predator generation(or every other generation) that coincides with the cicada eruption gets a fitness/population bump. After many iterations, the age group of predators that matures or spawns or whatever in time to get the maximal benefit from the cicada eruption dominates. Instead of evenly distributed age ranges, you get a big group of predator species that are synced up to benefit optimally from the cicada eruptions, which is bad news for the cicadas.
The thing that regulates the predator life cycle length is the time to sexual maturity, or the generation time. If this is a factor of the cicada hibernation time, cycles develop and the cicadas are in trouble. If the cicadas use a large prime number, the number of cicada generations between matching predator generations is very large. (a five year predator cycle and 17 year cicada cycle only overlap once every 85 years.) For every predator generation that benefits optimally from the cycle, 17 of them have to live without the benefit.
Generally speaking taking a long time to reach sexual maturity is bad news for a predator species(all other things being equal), so no species to my knowledge has evolved to sync up its generations with the cicadas.

Thank you! Very helpful and reasonable sounding explanation.


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Is there a specific word for bacterial death?
What do you call it when a bacterium dies? Cellular death is apoptosis, necrosis, and bacterial is ...? I don't simply want to write in a paper that it - well dies!

Death is an appropriate word to describe something dying. Perhaps more descriptive terms are dependent on how the cell actually dies. Lysis comes to mind…

Is non viable ok? e.g. "after the treatment of cells with X, bacterial cell death occurred. The non-viable population of cells were determined ..." since you presumably did some viability tests to determine whether they still divide or not i.e. dead or not or looked at some viability markers.

Death is appropriate. Using this word to describe both unicellular and multicellular organisms places them in the same hierarchy. This hierarchy is the domain of life.
Both prokaryotes and eukaryotes have unicellular and multicellular species.
If you choose another word for death I would suggest not using it exclusively for bacteria. If a reader finds the idea of bacterial death esoteric, they may be inspired to dig deeper into the subject. Encouraging an informed reader would seem to be an effective device in a paper for communicating scientific information.
You could qualify the word 'death' to be more precise. Senescence is the natural process of deterioration of life with age.
Google has a great tool for tracking word popularity. Here's a Google graph for 'senescence'.

Senescence is not death - it is related to deterioration with age. It may lead to death, but so can a thousand other things. I don't think you should be confounding the two.

This is why I suggested he qualify death with the word, not replace it.

Apoptosis and necrosis are only two ways by which eukaryote death is achieved. Certainly there are other ways. Say, if a tissue or organism burns, death is achieved before any nuclear changes, cell swelling or shrinking.
Same thing goes with bacteria. Death is the generic term. If you have more details, you can be more specific. In laboratories, cells die by lysis induced by the human experimenters, either by fancy P1 buffer or by the less sophisticated bleach. Sporulating bacteria autolyse the mother cells in the process of spore release. Overcrowded bacteria may decide to relieve some the pressure by having some individuals commit controlled suicide, called autolysis. For example, lytA is an autolysin stimulated by crowding in the pneumococci. The couple ccdA-ccdB sitting on the E coli plasmid F help ensure that daughter cells that did not inherit any plasmid copies commit programmed suicide. Details about these and some other described mechanisms of death in bacteria are to be found in http://www.ncbi.nlm.nih.gov/pmc/articles/PMC99002/
But if you are looking at some bacteria dying, and you have no evidence about the molecular mechanisms, death is good enough.

The word bacteriocidal is commonly used when describing agents that kill them, as opposed to agents that slow their growth which are said to be  bacteriostatic.

This doesn't really answer the question at hand.


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Does scratched Teflon coated frying pans contain carcinogens which can cause cancer?
Is it true that using scratched Teflon-coated pans contain carcinogens, and if so, can they be consumed through the food cooked in them?
E.g.

The deadly toxins from non-stick frying pans

I think the moderators didn't like the way you worded your question, but I think its answerable.  I tried to edit it, but it was hard to edit and not lose the intent of the question so I will try to answer it...

Thank you, eventually you can post your re-phrased question, I'll update.

i know what you mean, but the moderators would appreciate it. lmk what you think of my answer :)

Hi there, I've tried to re-word your question to be more objective about the concern that Teflon (or some part of the pan) may contain possible carcinogens. I hope you are happy with this edit.

You should ask your question on Skeptics.SE.

Very close to: http://biology.stackexchange.com/questions/9343/are-there-dangers-to-teflon-and-aluminium-cookware

Improved the question, please check.

Teflon is a polymer of perfluorooctanoic acid (PFOA) and related compounds.  PFOA is thought to be a carcinogen.
I think there's an urban legend that if you really heat teflon up or burn it (it doesn't burn as flouroxides are not stable in air) that you might get some of the constituent chemicals out into the air.
Once the flourocarbons are polymerized into fibers and surface coated a metal pan, they are chemically inert and aren't carcinogenic.  Teflon can be made to burn and some noxious fumes produced, but they are not especially carcinogenic.
Even after all this, this paper reviewed PFOA exposure and points out that most people in industrialized countries have some PFOA in their blood and this does not seem to be related to a strong incidence of cancer as the level of exposure is so low.
Flouro-carbon compounds are terribly inert - thats why teflon is so tough.  If PFOA is dangerous, then Teflon is > 10 million times less dangerous.  If PFOA is dangerous, crossing the street is many more times dangerous.
Even PFOA will be eliminated from Teflon production, supposedly next year (2015).

The question and link imply that if cooking with Teflon generates carcinogens that carcinogens then always lead to cancer. This is not always true. In some cases exposure to carcinogens may signal protective pathways. Oncogenesis and exposure to both genotoxic and non-genotoxic carcinogens are not always positively correlated. Cooking with Teflon influences how you cook, and it's how you cook that has the greatest effect on the levels of carcinogens in food.
Cooked food contains carcinogens in the form of reactive oxygen species. This is related more to the heat its cooked at than the type of cookware used. Carcinogen exposure in the heating of biological material is an interesting subject.
Carcinogens can be classified in 2 categories (1):

Genotoxic carcinogens (Reactive Oxygen Species/ROS)
Non-genotoxic carcinogens (PFOA is thought to be here)

Genotoxic carcinogens facilitate the formation of cancer through alterations in a cell's DNA.
Non-genotoxic '...carcinogens have no direct interaction with DNA; they are believed to cause tumors by disrupting cellular structures and by changing the rate of either cell proliferation or of processes that increase the risk of genetic error. (1)'
The molecular mechanism most often thought of for cancer formation is genotoxic oncogenesis, damage to DNA. Here, genotoxic oncogenesis often involves a reactive oxygen species (ROS). ROS may generate free radicals which, when reacting with other molecules, generate more free radicals. Another example of a reaction involving free radicals is a fire. Human cells contain genes for antioxidant enzymes, like glutathione and superoxide dismutase, which catalytically converts the free radical superoxide into hydrogen peroxide.
The abundance of ROS in our cells has 2 components:

Production of ROS
Depletion of ROS by upregulation of antioxidant enzymes

Intracellular levels of ROS positively regulate levels of antioxidant enzymes like glutathione and superoxide dismutase (2). This means that more oxidative stress leades to more protection from ROS by antioxidant enzymes. This is why exercise, while increasing ROS levels, actually protects against them.
ROS are also produced during the cooking of food, especially meat (3). This applies to any type of cookware, any method of heating of any food: protein, carbohydrates, fats.

'For example, it only takes a few hours at 70C to have the same extent of autoxidation which at room temperature requires months (4)'

Intracellular ROS are unavoidable. They are produced by normal metabolism, exercise, cosmic radiation, during the consumption of food. Balancing this are endogenous antioxidant enzymes. The antioxidant power of glutatione exceeds any known nutritional supplement (5).
Exercise is an extremely effective upregulator of antioxidant enzymes, eclipsing any antioxidant supplement or change in cookware. Regular physical activity will most likely be the best prevention one can take against ROS induced genotoxic oncogenesis.

This does not answer the question.

Carcinogens in cooked food come mainly from the cooking process not the cookware.

Right. The question is whether the pans themselves contain carcinogens, not whether it's possible to generate carcinogens by cooking foods in the pans.

There is mixed data suggesting PFOA may or may not be genotoxic. If it functions as a ROS, it's important to know that total levels of ROS in the body is not a good indicator of risk for developing cancer. The question implied that carcinogens - > cancer. This is not always true. In some cases a raise in the levels of ROS or other carcinogens may signal protective pathways. Oncogenesis and exposure to both genotoxic and non-genotoxic carcinogens are not always positively correlated.


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Why are human children more likely to get lice (nits) than adults?
By my own experience, lice seems to be prevalent in the hair of human children, but not in adults.
My question is Why are human children more likely to get lice than adults?
Assumptions:

Can be referred to lice/louse/nits

I would say it is a simple psychologic phenomenon: Kids come in much closer contact than adults usually do. So there is much more chance for spreading lice.

i think its only because there is more human to human contact - heads touching, hugs and full contact jostling in a school (and locker rooms) than at an office or other typical adult days.  I simply touch fewer people than my 5 year old...

Thanks guys - add that as a full answer - and if no one has a better explanation, then I'll mark it as answered.

"Children are most likely to get lice because of the close physical contact they have with playmates in school and day care centers." - http://healthvermont.gov/prevent/lice/headlice.aspx

Additionally, adults get aware of the lice earlier and will then (hopefully) avoid close contact with others until it is cured.

I will second Amory's comment.

Children generally don't care about their hair as much as adults do. So unless parents insist, they don't care for their hair as much (reference). Kids generally get lice because they are in close contact with each other during play-dates, slumber parties, and sports activities. They are also prone to exchange hair brushes and other personal items more often than adults (reference).
An interesting difference I came across between articles is that one article says that its

theoretically possible to get infested if your hair makes contact with
  items such as hats, combs, or brushes (reference).

Another article insists that

You’re extremely unlikely to get head lice by sharing hats, combs or
  pillows – a louse’s lifespan is very short once it’s removed from your
  head (reference).

Between the two, I believe that it is extremely likely that lice would spread if you use a infected hairbrush immediately after it was used by someone harboring the parasite since the time span is short.

Can't lice larva lie dormant in a comb or jacket as a means of transmission?

@aitchnyu Yes, but they can only stay alive upto 48 hours from the body

Lice prefer clean hair, so in addition to closer contact among children, adults seem to use more hair product (gel, hair spray, etc.) than children in preparation for their day. Lice have difficulty moving through hair strands that are stuck together with product, so this may also contribute to the prevalence in children.

It would be great if you could provide references for your response.


text:
Is it essential to add cholesterol to agar or liquid culture for C. elegans?
In preparing agar plates with NGM, and also liquid cultures for growing c elegans, how essential is the addition of cholesterol and heavy metals? I have prepared both. I can't notice any obvious difference and I hate having to add all these supplements.
I'm using yeast extract and peptone as the primary components of the base.
Isn't this just supposed to be a moist semi-soft substrate for them to crawl around, their nutrients come from the bacteria they eat.

C. elegans needs cholesterol, but can't make it. Since bacteria don't make cholesterol either, the food bacteria aren't a source. As explained in the linked paper,  lack of cholesterol affects normal development.

And without supplementing there is enough in the peptone and yeast extract to already. I wonder if this stuff is only essential for   cholesterol biosynthesis studies?

Just FYI @alan Boyd's I upvoted and would like to keep open for a few days to see what else out there but this is prob best foreseeable response

No, it's not just for sterol biosynthesis studies. You don't need to add the metals to NGM. There are enough in the peptone, yeast extract, and agar. But they will be visibly abnormal (although alive) if you don't add cholesterol. Believe me, I have done it :-/


text:
Pharmacology: Drug Administration
Why is the enteral route seem by far the most common way to administer a drug to the body?

Who says it is the safest route?

Question seems valid to me. It appears difficult to deny that the oral route is the most common administration route. However, it is true that any answer given to this question will be partly opinion-based...

Let's review drug administration routes, and see for yourself:

transdermal/ionophoric: expensive, unreliable release concentrations (which makes it expensive because of the extensive research needed for controlled release), noticeable to others ("why do you have that skin patch, mom?" Er...)
Sublingual: quite similar to oral route, however absence of first pass hepatic metabolism can result in completely different blood concentrations between the two routes. Impairs speech. Could cause mouth irritation (quite disabling). Requires patient compliance.
intravenous: quite unpractical in outpatient settings. Invasive measure.
intramuscular/intradermal: hurts. As all things using a needle. Usable, but impractical in the outpatient setting. Can lead to skin lesions (insulin injection in diabetes, for example)
rectal: culturally unacceptable to some, unreliable release.
vaginal: similar to rectal, but only for women obviously
spinal/epidural: very invasive, only in inpatient settings.
topical: usually only acts locally, can cause discomfort (eyes)
oral/enteral: well known pharmacokinetics, mostly invisible to others, practical in the outpatient setting, requires limited patient compliance, well known excipients. Of course there can be secondary effects, but that is the case for all administration routes. Most common side effects are abdominal discomfort and nausea, but no one can see you in the water closet. Plus people are used to see pills as medication, something which might not be the case for other routes, depending on the cultural background of the patient.

This answer is of course somewhat subjective, however the importance of the patient's perception and his/her view of what the administration route implies socially cannot be overemphasized.

Also IM (Intramuscular).

i've done the sublingual with powerful medications and its not really that bad as long as your mouth doesn't blister and your oral nerves are not so affected. the taste can be abominable though.

Pill, tablet and time release are great enteral treatments because of their ability to control dosage by the patient at home. Compared with an IV and oil/sublinguals they are less effective at due to the greater risk of causing toxic damage to the liver and kidneys but there is little chance of overdose by reason of mechanical failure. That is the reason that viagra and metformin are first lines of defense; followed by insulin and alprostadil if they so fail. You do not infect yourself typically with a pill but with an injection its possible for a needle to be dirty. Likewise also there is the ever fear of an air bubble.

I would say that tablets are actually one of the hardest methods to regulate dosage over time. The drug release rate can be modified by the pH of the gut, how much food the patient has eaten, and other factors. The drugs hit the liver first, and experience first pass metabolism, usually losing most of the drug in the process. Metabolites can be excreted in the bile and reabsorbed in the intestines. While the IV route requires a needle, it guarantees the exact dose gets into the blood, and allows more of the drug to avoid the liver and hit the target site.

@user137 is that better?

I would say that the reason sildenafil is typically preferred over alprostadil is largely due to Viagra being a nice friendly tablet and alprostadil being a particularly daunting injection into a sensitive area for patients.  Perhaps this goes some way to indicating one of the main reasons many drugs are enteral in administration - patients find it easier.

I think the edited answer does suggest that pills are preferred because they are easier to take, and the patient can do it by themselves. Patients can do their own injections, but must be trained and compliance is harder. However, pills are not foolproof. Taking too many pills is a common method of suicide, which is why the UK switched to putting acetaminophen in blister packs. And people who like to cut pills in half to swallow them easier inadvertently defeat the extended release mechanism, and cause drug levels to spike too fast.

@RoryM yes agreed

@user137 yes agreed

@caseyr547 BTW, the amount of air needed to cause embolism when injected in a vein is debatable, but clearly is above 10 ml, which is in fact a quite large quantity.

@Raoul that would be several cc's right? i did not know that thank you


text:
Is there any evidence that soft tissue can be preserved for 65m+ years and if not what hypotheses exist to explain it?
I read an article on howstuffworks.com and they mentioned how we have found soft tissue in dinosaurs. According to the article even Mummies and Mammoths have no soft tissue left. Is there any evidence that soft tissue can remain intact this long even under perfect conditions? and if not what are some hypotheses that could explain it?

Science is not at the stage of imaginative hypotheses. We have the natural experiment of DNA recovery from geological strata that are easily and precisely dated, for example by 14C. From the fact that, as you look at older rocks, you see less useful DNA, the highly likely conclusion is that DNA is unstable in time. There is less fossil DNA in warm, humid places, pointing to a few explanations. There are DNA fossils dating more than those 65 million years, but they were in places where mammoths could not get (say, salt deposits that form today's mines).

Schweitzer et al. (2007) studied soft tissue preservation in a number of specimens, including an 800-1000 year old moas, 300,000 year old mammoth and mastodon, and 65 million year old *T. rex. and Triceratops. The oldest specimen was a 78 million year old Brachylophosaurus. Their goal was to try to find common environmental conditions that favor soft tissues preservation in fossils. As of this study, they have not been able to identify a single common environmental factor that seems to favor soft tissue preservation. They did note, however, that the specimens from which they could extract soft tissue (with varying success) were from fluvial sandstone environments, meaning sandy rivers. They (so far) could not extract soft tissue from terrestrial mudstone or marine environments.
Note that Schweitzer et al. did successfully extract soft tissue from the mastodon. The conditions required for mummification are probably not conducive to soft tissue preservation.  Here is a good blog article on one of Schweitzer's previous studies of soft tissue preservation.
The importance of extracting soft tissue from fossils cannot be overstated. Based on Schweitzer's work, her and her colleagues (Organ et al. 2008) were able to develop a phylogeny that incorporated both mastodon and T. rex. The used the amino acid sequence from collagen, a protein that is abundant in soft tissue. She and her colleagues repeated the analysis (Schweitzer et al. 2009) and included Brachylophosaurus, a hadrosaur. As predicted by morphological and other evidence, the mastodon was most closely related to modern elephants and the two dinosaurs were most closely related to modern birds and alligators.
Here is the phylogenetic tree derived from Schweitzer's 2009 study. Mammut is the mastodon. Brachylophosaurus and T. rex are the two dinosaurs.

Literature Cited
Organ, C.L. et al. 2008. Molecular phylogenetics of mastodon and Tyrannosaurus rex. Science 320: 499.
Schweitzer, M.H. et al. 2007. Soft tissue and cellular preservation in vertebrate skeletal elements from the Cretaceous to the present. Proceedings of the Biological Society of London B: 274: 183-197.
Schweitzer, M.H. et al. 2009. Biomolecular characterization and protein sequences of the Campanian hadrosaur, B. canadensis. Science 324: 626-631.


text:
Can ants sense food from a long distance?
I recently had ants find and then swarm to a food container that I put down on a desk. I'm curious as to whether an ant would have needed to get lucky (i.e., discovering the food after crawling up the desk) or ants have the ability to sense food from a distance.
I'm skeptical of believing that ants simply scout around until finding food; I'll use this case as an example:

My room has had no food or drink in it for weeks, so the area wouldn't be a "hotspot" for ants to be interested in.
I put the mostly empty food container down on my clean desk and turned my lamp off to work on the computer. No more than 2 hours later did I turn my light back on to discover a trail of ants swarming to the container I put down. It happened pretty quickly.
The desk is high, standing on four thin legs. I find it difficult to believe that an ant would crawl up the desk as often as a 2 hour time frame to scout for food, for the message to be passed to the colony so quickly.

I've been curious about this scenario for a long time. So my question:
Can ants sense food from a long distance? If so, how does it work? If not, how is the phenomena (ants locating food quickly in unlikely places) explained?

You can detect food at a distance too, it is called smell.

Ants follow odor cues in the wind.  A study by Wolf and Wehner (2000) manipulated ant antennae and wind direction to show that ants followed odor plumes on the wind. A more recent study by Buehlmann et al. (2014) showed that desert ants of the genus Cataglyphis cued in on linoleic acid, a so-called necromone (death scent) released by dying insects. Here's a popular article that summarizes the latter study.  Chances are good the ants are followed the odor plumes coming from your mostly empty food container.
Literature Cited
Buelhman, C. et al. 2014. Desert ants locate food by combining high sensitivitty to food odors with extensive crosswind runs. Current Biology 24: 960-964.
Wolf, H. and R. Wehner. 2000. Pinpointing food sources: Olfactory and anemotactic orientation in desert ants, Cataglyphis fortis.  Journal of Experimental Biology 203: 857-868.

I'd also like to point out that ants leave a trail which they patrol so the food need not be detected from a far only by a single worker patrolling near a region. Once found they have various means to initiate a swarm.

I'm actually a programmer with interests in developing some of the brain's intelligence in computing (Think Siri, but taught, not programmed) and the Ants Swarm Like Brains Think article that you linked just, in a few paragraphs, helped me understand more about the working of the brain than any article or chart that I could have studied. Neat reading, thanks!

@jt0dd if you would like to collaborate on a general intelligence Turing machine that's fine it's doable I'm at gmail but it's 10 or 20 years man hours requiring multiple programming paradigms

As well as being a system interface designer, and back-end software engineer, I'm a web developer. My skill as a programmer is in advanced JavaScript, now whether or not that's the best language for the job is debatable. My thing is planning the infrastructure and then envisioning a brilliant user interface for it. So I lack C++ or C# or Java programming skills that you're likely accustomed to. Email jonathan@evisiion.com, if you'd like to talk.


text:
Species identification, tree from Ecuador
This tree is recently photographed in Quito, Ecuador. It grows everywhere. I'm new to South American flora, so I'd like to know what the species it is?

Your plant appears to be Chionanthus pubescens, the pink fringe tree, which is native to Ecuador and Peru. The genus has a number of species. It belongs to the family Oleaceae, which includes well known plants like jasmine, forsythia, ash trees and olives. I could not find much biological information on the pink fringe tree but plantlist.org contains a number of links to various databases that may be helpful if you want to dig deeper.