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A question about entropy and Thermodynamics
According to the Second Law of Thermodynamics (also known as the laws of conversation of energy and mass), anything is an isolated system cannot increase in complexity. For example, a wearing suit will eventually decompose.
Now we know the sun (and Earth mantle) is pumping energy into the system so the earth is not a closed system. However, the sun sends dangerous radiation that harms and even kills bacteria.
I am an advocate of evolution, but how can entropy begin when raw energy, unshielded from the sun, is ultraviolet light. As biological molecules require amino acids, proteins, DNA, and RNA is untenable when radioactive UV light kills simple bacteria.
I am well aware that the human body is a very complex machine. That is not the issue. My question concerns the first cell (inorganic material) from which life would sprout, as we know it. This inorganic material (soup that came alive) would not have been very complex at all. How did it survive the various heat of the sun in which all primitive life forms decay?
Source, please.

There are some  misconceptions here. The second law of thermodynamics is not known as the "law of conservation of mass and energy". And the second law of thermodynamics makes no mention of the word "complexity".

@Cell I heard that according to the 2nd law of thermodynamics progression is always downward, a law.

The second law of thermodynamics states that the change of entropy of an isolated system, under a physical or chemical process, is never a negative quantity. It is not an equivalent formulation for the energy and mass conservation laws.

In my opinion, the question should be rephrased, since what @Turk Hill wants to know is how did early life cope with UV radiation. There is not an special connection to entropy and thermodynamics.

@LuisSierra Do you think it is a natural law that everything progresses downwards or progresses upwards, but gradually.

If by everything you mean entropy, in regard to an isolated system, it increases with respect to time.

@LuisSierra I agree since the earth is not an isolated system (ie the sun is pumping energy).

What is "up" or "down"? Define complexity in mathematical terms for clarity, please.

Perhaps research "probabalistic density" and "disorder" on the topic of entropy and use that info to redefine complexity.

https://www.youtube.com/watch?v=Tr_gv5CKB1Y

The blanket statement that UV kills bacteria is wrong, the huge number of earth bacteria that thrive in sunlight would be evidence of this. UV mostly just causes mutations, this could actually accelerate the evolution of early life.

@AlexReynolds I meant "up" and "down" in complexity in an isolated system. But of course, this 2nd law cannot be applied to everything since the earth, for example, is not an isolated system, since the sun (as well as its mantle) is constantly pumping energy into the system.

@com.prehensible Yes, that is correct. Thank you for the link.

@John Yes, I agree with you. The answer below explains that life likely formed in the deep ocean, which would be further from the sun but not far enough to receive its energy.

@John I would have to disagree, a mutation in an essential gene could easily converge into cellular death. One can presume that early bacteria did not have DNA damage associated mechanisms (e.g. SOS response), so they were indeed vulnerable to UV-light induced mutations. Eventually, they had to develop such mechanisms, which is bacteria can thrive in sunlight exposed habitats.

@LuisSierra vunerable to mutations is not the same thing as killed by, especially at early stages when the genome would be very small. As I said that could actually lead to more rapid evolution. would it kill some of course would it kill all of them no not in the least.

It's unclear how the laws of thermodynamics relate to the dangers of UV light in your question, but if I understand correctly your reasoning is the following:
1) The laws of thermodynamics say that order cannot increase in an isolated system, precluding life.
2) Life exists anyway because the Earth is not an isolated system: it receives energy from the Sun
3) Therefore, the energy received from the Sun is necessary for life
4) However, the Sun's rays also contain UV light, which would be fatal to primitive life forms
5) This leads to a contradiction, how do we resolve it?
The answer to the question as posed this way is that there is a flaw in items 2 and 3. It is true life needs inputs of energy to exist. It is also true the Earth receives energy from the Sun, and that this is the main source of energy that powers the modern biosphere. However it is not the only source of energy life can use to function; some organisms generate energy from chemical reactions such as the oxidation of hydrogen sulfide into sulfur. You yourself bring up "the Earth's mantle" as a possible source of energy, which is... The answer to your question :)
https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_Introductory_Biology_(CK-12)/02%3A_Cell_Biology/2.24%3A_Chemosynthesis
I believe it is generally agreed upon that however the first organisms got their energy they would not have used photosynthesis, and thus could perfectly well have developed away from sunlight and damaging UV radiation. See for example this article on the evolution of photosynthesis, which describes the consensus that it is a very ancient process that evolved not long after the origin of life:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2949000/
Here is a hypothesis of the origin of life that suggests the first life used chemosynthesis, and in fact would have occurred in hydrothermal vents - about as far from sunlight as you can get:
https://m.youtube.com/watch?v=3jW9dH6NOQ0

I agree with what you stated, and it seems that early life developed far from the archean ocean surface, where UV radiation would be several magnitudes of order above the radiation you would get now. Early life must have survived in certain depths such that the radiation dose would be very low, atleast until DNA damage response mechanisms were developed.

Thank you for your answer. @LuisSierra I agree with what you wrote about the ocean. Oosaka, thank you again for sending the links.


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weird growth pattern of tree, grafting?
Whats the most likely explanation for following structure
2 Aesculus hippocastanum trees that merge into a third one, I guess its man made but what was the process?
Edit: Just found out about inosculation. Natural process by which trees merge mostly over their braches which after rubbing against eachother heal stuck together.

Probably grafted together but that sure does look weird.

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How do you re-adjust gaze coordinates after bad eye tracking calibration using Matlab?
As a beginner with oculometric data pre-processing (in children from 2 to 12 years old), I would want some advice from the community! :)
Using a Tobii Pro Fusion Eye tracker (250Hz), children are asked to watch stimuli like objects, avatars, and faces (4s per stimulus). My goal is to calculate, in a series of areas of interest which correspond to an x-y coordinate range for each trial, when and where the first fixation occurred, the duration of the first fixation, and the total visit duration/the total time spent of each corresponding AOI, for example. AOIs are, for example, the nose, the mouth, and the eyes of faces.
As I work with young children, I sometimes have lousy calibration (even with our best effort with the child!), and the recording takes place without calibration or with "bad calibration".
With Matlab, I am trying to re-adjust the gaze position to be the most loyal to where the child looks during the apparition of the stimuli because "bad calibration" affects where the children look.
I was wondering if the best way was to either re-adjust the gaze position as a function of the precision and validation (in degree) of the calibration or as a function of the interstim, considering that children look at it correctly (the interstim is a black cross appearing 2 to 3s before the stimuli).
As I am new to this, I am all ears for some tips :)
Thanks to all the community for future advice!
Best, Camille

Unfortunately I worry that not many people in this community will have expertise here! Which is too bad as it's a good question. However, there is a Neuroscience Stack Exchange that seems to have a variety of questions/answers on this topic. I'm going to flag your question for migration there.

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Will Fst (inbreeding coefficient) always be a value close or at 0 in asexual populations?
FST is the average inbreeding coefficient of a total population. The equation is:
$F_{ST} = \frac{Var(S)}{Var(T)} $
$Var(S)$ = variance in the frequency of the allele between different subpopulations, weighted by the sizes of subpopulations
$Var(T)$ = variance of the allelic state in the total population
If $F_{ST}$ equals 0 that means there is no population differentiation and there is no heterozygosity in the population. The ceiling for $F_{ST}$ is one so there is population differentiation and the population is all heterozygotes.
If the population is asexual, meaning they are parthenogenetic, would $F_{ST}$ be at or close to 0? Can this not be assumed?
In the context of this question I am considering the whole genome or just one allele.

It depends on whether mutation exists. Generally mutation is happening in biology, but in its absence, yes it will be at or near zero:

Note that in the absence of any mutation, $F_{ST}$ would be defined but equal to 0, as all the genetic variance is within individuals and none between individuals and subpopulations.

From that paper, see this figure:

So, basically, the exact level of $F_{ST}$ in such cases will be controlled by the mutation rate. That figure shows a value above zero at 100% clonal reproduction because it does have a nonzero mutation rate. There is also nonzero migration between populations, so that will have the effect of reducing $F_{ST}$ somewhat. So here the value is controlled by those 2 factors. Another thing worth noting is that, if there is no initial variation between populations before the split, that will tend to increase $F_{ST}$. So it does matter how much variation exists overall.


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Would it be possible to create logical circuits out of insects?
Could one organise ants, bees or any insects to do addition using logical gates:

AND,
OR,
NOT,
XOR.

As inputs/signals one could imagine for example that 1 would be food and 0 would be no food.

http://dx.doi.org/10.1162/artl.2009.15.3.Michael.008

@Roland Can you please turn your link into an answer?

@jakebeal Link only answers are not allowed and I won't invest the time to summarize the study. Feel free to do so.

@Roland Done; it's not so hard to do a simple version.

Could you please explain why this is a problem in biology. Is it akin to one on whether you can train elephants to dance?

@David You just answered your own question. Logical gates can built from a lot of things, not just electric circuits, I was curious how they translate into insect behaviour.

In which case I would suggest it is really not on-topic here, as the Help makes clear.

@David How about this: "is there an insect with a special natural behaviour that resembles a logical circuit?"

How about it? Sounds on-topic. But a bit strange. I would have thought certain aspects of insect behaviour might qualify, but not the insect itself.

In short, yes, it appears to be possible, and a number of people have performed investigations in this area. For example, see the "Ant-Based Computing" article suggested by @Roland, whose abstract explains the concept at a high level:

A biologically and physically plausible model for ants and pheromones is proposed. It is argued that the mechanisms described in this model are sufficiently powerful to reproduce the necessary components of universal computation. The claim is supported by illustrating the feasibility of designing arbitrary logic circuits, showing that the interactions of ants and pheromones lead to the expected behavior, and presenting computer simulation results to verify the circuits' working. The conclusions of this study can be taken as evidence that coherent deterministic and centralized computation can emerge from the collective behavior of simple distributed Markovian processes such as those followed by biological ants, but also, more generally, by artificial agents with limited computational and communication abilities.

Whether such a computer is good for anything besides curiosity is another question, but curiosity and art are fine starting points for any investigation.

As an aside, this idea was explored by the sci-fi/fantasy author Terry Pratchet in his 1996 book Soul Music, prefiguring the actual research here.


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Price Equation in Evolution
I am trying to solve for $\text{cov}(w_i,z_i)+E(w_i\Delta z_i)$ as it apears in Price Equations in terms of the mean $\overline{w}$ and variance $\sigma_{w}^2$ of the fitness of a population where I am given the relation $\Delta z_i=-cz_i$. I don't understand how we can solve this because I do not know how I have any knowledge of the values of the $w_i$s given what I know about the $z_i$s. Any hints would be appreciated.
The Price Equation is defined as:
$\Delta z = \frac{1}{w} cov(w_{i}, z_{i}) + \frac{1}{w} E(w_{i}\Delta z_{i})$

It would help to know if you are working from data ("what I know about the $z_{i}$s", "values of the $w_{i}$s") or just as a theoretical exercise. If you have data, getting an example would be helpful. Usually my understanding is that the Price equation is applied when we have knowledge of trait values and of fitness. It does not sound like you are doing theoretical work but it's hard to say based on the question.

The question was intended to be theoretical. The problem I was given was to first find the expectation in terms of the mean and variance of the fitness, and then to compute the right hand side of the Price equation (which I presumed also meant to compute $\text{cov}(w_i,z_i)$. This was all the information I was given, and I am not sure if I misunderstood some element of the Price equation or if there was not enough information given.

Seems like it might be better to ask for clarification from the person giving you the assignment (and edit this into your question, if it's helpful). Of course, if you do come up with an answer on your own it's perfectly acceptable to self-answer your own question.

I'm not an expert here so I won't answer in much depth (and for homeworks we want to see some evidence of work usually, see here for more info https://biology.stackexchange.com/tour), but I would suggest the standard algebraic tricks. E.g. look into the definition of covariance, consider a case where covariance approaches zero,  consider a case where covariance is complete.


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Why increasing the vector concentration does not increase the effeciency of bacterial transformation?
I was reading some old description of the protocols used for the transformation of bacterial cells.
In the description I read that the transformation works best with low amount of DNA, and if we increase the amount of DNA used the amount of transformant cells does not increase proportionally.
I just wonder why, since in my eyes the process of entering the cell is mainly related to the diffusion principles, and therefore concentration dependent.

If there are many times more plasmids than cells, increasing their concentration when the cells are already saturated would therefore not increase the transformation ratio.

Thanks, but then it is similar to a enzymatic kinetic. So in theory I will have an increased transformation at higher concentration of plasmid till a saturation point that, I would guess, depends from the strain I use to transform?

According to the Hanahan transformation protocol (one of the highest competencies published), a transformation of 200µl will contain $1×10^8 - 1.7×10^8$ cells.
Assuming that the pBR322 plasmid is used, 1ng of plasmid will convert to 0.36fmol of plasmid, or $6×10^8$ plasmid copies.
As we can clearly see, even at very low quantities of DNA used, there are multiple plasmids per cell. Since transformation is thought to be mediated by DNA channels, massively increasing the quantities of DNA would not equally increase transformation efficiency once all of these channels are saturated.
The example from NEB Turbo DH5α cells seems to show this quite well, that once DNA quantities exceed 1ng, the transformation efficiency drops precipitously.

This being said, if the amount of plasmids available is very large, there is no reason to avoid adding more than 1ng of DNA, as they would not reduce the total number of transformation colonies, but only the efficiency.

Thanks very much for your nice answer. I am thinking though that in the example you do there will be around 6 copy of plasmid available per each cell. For my understanding there could be hundreds of possibilities (e.g.DNA channels, electroporetic generated holes) for the DNA to go in. SO in theory if we create a saturation curve we can see that the number of transformant is increasing with the amount of plasmid we add, at least at the beginning. When saturation is reached he amount of DNA is not influent. It would not make sense to add more DNA from the start to have higher transformant?

@efrem I am not sure if Michaelis-Menten kinetics (in the sense of the saturation curve) apply in this case due to the mix of many different means of plasmid entry, but the general concept of channel saturation should still apply.

thanks! So the efficiency drops, but the number of transformed cells increase exponentially. Therefore, if someone is not limited in terms of plasmid amount, and has cells that do not transform so well, it would be better to increase the amount of plasmid to get a higher number of transformant, even though with less efficiency.

@efrem The increase is most notably NOT exponential. It is in fact worse than linear, considering the X axis is log but the Y axis is linear. However, in most cases of bacterial transformation, you are using high concentration plasmids in any case. I can't think of a way to reduce the number of total transformation colonies by adding too much DNA.

right, sorry. It is indeed linear. Anyway, it seems to me that there is not any major drawback in adding too much DNA (plasmid), in terms of total number of transformed cells.

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Taxonomy for plasmids
I liked the question about F' and R plasmids.
What is a good resource that describes what is known about the functions and diversity of plasmids in the wild? Prokaryotes or eukaryotes?
Wikipedia points to five kinds of plasmids (fertility (F), resistance (R), col plasmids (offensive genes that let a bacteria kill other bacteria), degradative function plasmids, and virulence plasmids). There is a brief section on yeast/euk plasmids too. It seems like plasmids could actually convey nearly any gene. Restriction enzymes are found mostly on plasmids and they would seem to be defensive - maybe those are degradative.
Are there references that are more detailed and nuanced?

Not sure if generalized plasmid taxonomy is going to be relevant any longer. A lot of these old names were created before the exact sequence and function of the various DNA sequences were known. This is becoming especially true as synthetic biology allows us to mix and match parts of plasmids at will. If you want to dig through a lot of the old plasmid classification papers, a lot of them are published before 1980.
Back then I'd imagine conversations went more: "oh look, I found an R plasmid conferring ampicillin resistance", instead our more modern understanding: "oh, I have a plasmid conferring ampR via bla "
That being said, I think the more specific / specialized plasmid classifications will stick around for a while as they confer a lot of domain specific meaning.  Check out Ti and Ri plamids which have very specific meanings in plant pathogens and are used in the genetic engineering of them.  You'll notice that the classification for these plasmids comes from a lot more than a single gene.
There have been some modern attempts to classify plasmids, but rely a lot more on the structure / lineage of the plasmid rather than the payload genes (replication origin, size, etc.). Check out [1] for an example.
[1] Wang, et. al. 2009. Plasmid.

This makes a lot of sense - plasmid categories are probably highly artificial.  would you say that new categories of plasmid function are also being discovered as well as blurred boundaries between the plasmids functions already described?

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Why do many fruit trees have five-petaled flowers?
Peach, pear, apple, cherry, and many other fruit trees seem to have flowers comprised of five petals. Assuming there is no evolutionary advantage to confusing students of trees, is there a plausible reason (evolutionary or otherwise) the morphology is so regimented? Are the trees related? Do they like the same pollinators?
Thanks for any insight.

Peach, apricot, plum, pear, apple, cherry trees are plants of the same family, Rosaceae, so they are closely related. They share many more aspects than the five petals. In fact, other plants in this family, and even many other dicots have five petal, simply because their share a common ancestry.

@BBM: The answer might also be that "it just happens to be like this". Not every trait of an organism confers an advantage, and much less is "optimized". You could be interested in reading: http://evolution.berkeley.edu/evolibrary/misconceptions_faq.php#b8

@BBM: early flowering plants had indeterminate petal numbers. The general trend has been towards fewer petals, with fixed numbers. The specific number probably isn't important. However, having a consistent number within a species might confer an advantage in terms of developing a stable relationship with pollinators. Having a consistent number of petals, along with consistent colouring, would enable more controlled & targeted advertising.

It is hard finding answers to this question, which also interests me a lot. The most satisfying answer I have found is detailed in this paper http://www.ijpam.eu/contents/2012-78-3/6/6.pdf.
From the abstract : "This article examines why many flowers are five-petaled through the use of a five-petal model that draws insight from the location of cell clusters at a shoot apex, rather than from concepts such as the Fibonacci sequence or the Golden ratio which have been referred to in the past. The conclusions drawn are that flowers are most likely to be five-petaled, followed by six-petaled flowers, and that four petals are unstable and almost no flower can be seven-petaled."
As for the alternative theory alluded to at the end of this abstract, you may want to check out the work of mathematician Michael S. Schneider (Master's Degree in Mathematics Education from University of Florida). His answer revolves around this idea where, much like what Plato proposed, geometry is seen as the fundamental building block of the universe and where geometric patterns (therefore numbers) are given different meanings based on observational data. In this theory the number five is seen as the "flag of life" if you will. Look-up an image of a DNA strand viewed along axis, I find it interesting that it's mostly in series of five.
That being said, the article I linked certaintly contains a more satisfying answer to your question.
Hope this helped.

If possible add in the main conclusions of the paper you referenced, helps just in case the link doesn't work in the future

This was a in interesting and entertaining article, thank you. It is true that many more flowers than those mentioned in the first answer or my question have 5 petals.

I just edited my answer to include the main conclusions. Also, I would like to put an emphasis here on the following quote from the paper : 'I do not deny the Fibonacci sequence theory in every aspect, but it does not sufficiently explain why a flower is five-petaled.'
I think it could very well be that both the fibonacci sequence theory (in nearly all flowers, the number of petals is a Fibonacci number) AND this new theory can co-exist in a way.
Anyways, glad this helped.

An asymetrical number of petals might offer an advantage: when wind blows there is a clear direction of rotation. Thus the flower turns in one direction only. There is less oscillation that could damage the flower.

This is sort of ingenious. You should be able to test it. +1 for the suggestion.

I cannot explain the downvote. People like to see a reference but sometimes someone has a testable hypothesis with no evidence either way. I think that's worth something.

Didn't downvote, but the fact that this is completely hypothetical with no references probably contributes.


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Were there lifeforms before LUCA?
This question got me thinking about something. LUCA is the last universal common ancestor of all current living organisms, which is a very different definition from the first-ever living organism. Is there any evidence that LUCA had evolved and diverged from a now-extinct, more primitive lifeform?
To rephrase, is there any evidence to suggest that at some point, the first-ever living organism(s) had diverged into two phylogenetic groups, one being now-extinct and the other describing all current life?

It is logically possible, however there is no hard evidence for it, and parsimony suggests against it.

@Galen I disagree that parsimony suggests against it. "Parsimony" isn't about having fewer things, it's about having fewer independent assumptions about how the world works. And life through evolution shows constant branching and extinction. Assuming this happened after but not before the LUCA isn't parsimonious. (though it would depend on where the LUCA is in the history of life and evolution to be fair)

@RozennKeribin I think you may be using a different usage of "parsimony" than I was. In evaluating trees via parsimony (in the context of evo-biol), we count the number of evolutionary steps required for each tree, and select the set of trees (ideally there is only one) requiring the minimum count of such steps. Adding branches at the root of the tree (before LUCA) will mean more evolutionary steps, ergo its smaller counterpart will be selected preferentially in this process. I like your usage of 'parsimony', but it may require demarcation when discussing the topic of evolution.

@RozennKeribin ... and it would have been helpful for me to demarcate the usage I was using. It is a recommendable practice in general. Although not the exact same type of example as what we're considering above, here is a pedagogical example of parsimony (in evol-biol) being used. http://evolution.berkeley.edu/evolibrary/article/phylogenetics_08

@Galen that's fair, I know phylogenetics has its own use of the concept of parsimony. That said I think it's used in cases where you're building a phylogenetic tree based on actual data, traits or entities we're trying to order. I don't think this is really what the [original] question was about; the question seemed to be about whether pre-LUCA side branches could/would have existed. I think one can give an answer without satisfying the much stricter standard of building a phylogenetic tree with such branches (which requires knowing what the side branches were like)

@RozennKeribin Agreed, it requires data to build trees with parsimony, and I find data to be an agreeable requirement for assessing evolutionary relationships. The original question is asking for if evidence exists for pre-LUCA branches, and to my knowledge there is no substantial evidence of this. Our models of descent with modification expect there to be such branches, but I think it is arguable whether to call that 'evidence'.

@Galen Absolutely, as far as the post's main question goes on whether there's evidence I think your original comment was 100% correct. I was just reacting to the last clause, which I felt made an additional claim and that's the one I disagreed with. (I'm mostly making this comment so the record shows I do agree we have no evidence of LUCA cousins, in case this long conversation made it look like we disagreed more than we do)

Well, what you seem to be suggesting is "Did life evolve twice on Earth?"
Your original question has an answer: Probably yes. It's not unlikely to think that the original cell evolved into two different paths and then one went extinct. However, that doesn't address LUCA. If we found fossil evidence of what we thought was LUCA, and then fossil evidence that LUCA had a genetic cousin - all that would do is push the application of the term "LUCA" on more evolutionary step backwards until both shared a common ancestor which would then be called LUCA. You can do this indefinitely until all life originates from a single cell, with countless offshoots which have gone extinct.
If you mean was there a whole other type of life - one that did not originate from LUCA and existed - then the best answer we have right now is "No." All life we know of, no matter how different and old, is still based on RNA/DNA and proteins. Fossil evidence supports this premise until about 3.5 BYA.
If there was an 'alternate' construction of life, we have not found the fossil evidence for it, and might not know what it was if we did. If the alternate form didn't utilize cells, we might not be aware we had it. If it did, but utilized different metabolisms or structures for proteins and storage - that evidence would be long gone by now.
Our best bet for answering if life can evolve differently than what we have today is out among the stars.

I actually wasn't referring to "a whole other type of life" as you describe, or if abiogenesis had happened twice on earth, but the first paragraph (not counting the first sentence) is exactly what I was looking for, and now seems all-too-obvious in retrospect. As you suggest, if we knew of evidence which described this early now-extinct lifeform, we would have to revise our definition of LUCA. Thanks for the epiphany!

I'd like a reference to rna world 3.5 years ago.  what is the evidence like?

@shigeta - RNA acts as both storage of genetic information, and can fold into proteins/enzymes (Ribosomes utilize rRNA, for instance). DNA has never been observed to naturally act as an enzyme, indicating a specialized role (and it is orders of magnitude more stable than RNA). So RNA is thought to occupy the area between Proteins and DNA, and since proteins have not been observed storing genetic information, RNA is hypothesized to be the first form of genetic storage, enabling Evolution via Natural Selection.

I'm aware of the RNAWorld hypothesis and so forth - but what is the "Fossil Evidence" you refer to in your answer?

@shigeta - www.paleosoc.org/Oldest_Fossil.pdf
Cyanobacteria, which are an extant species, have been traced to about 3.5 BYA.
Recently (http://www.sciencedaily.com/releases/2011/08/110821205241.htm) some fossils were found of sulfur using bacteria with a very confident date of 3.4 BYA. The latest one is probably the most sophisticated, as it utilizes chemical analysis to look for organic components that wouldn't be found in natural mineral formations.

LUCA was the LAST universal ancestor not the first.  Naturally it competed with other extinct species.   My reseach suggests that LUCA was resulted from the fusion of 2 genomes.  The evidence for this is that on reconstructing the amino acid sequences for LUCA enzymes we find some contain no cystine but do contain tryptophan or the opposite.

Some references to support your response would be great!

Can you please add some references? Actually it is more a comment.

No. LUCA is a construct based on comparative analysis. Because LUCA is defined as the last universal common ancestor, no genetic evidence can be use to determine what's LUCA's ancestor looked like. The only way such a question can be answered is if by some luck, you found a fossil..or a time machine.
Given that horizontal gene transfer is all but certain in the time frames we are looking at, LUCA is unlikely to be a single organism. But more like a community of organisms, sharing a pool of genes. And a subset of these shared genes became the core of all descendants of that community. These shared genes is LUCA


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What negative effects can pinhole glasses have on the body?
While shopping in the local supermarket yesterday, I was surprised to find this display on one of the shelves.

I also realize that I should have taken a pamphlet with me, as well as a picture of the boxes for the glasses, as seen in the picture to read more about it.
This answer at Skeptics.SE shows that there are in fact probably no long-term benefits of wearing pinhole glasses, but my question is...
What potential harm/side effects can be caused in the short and long-term from wearing this type of eyewear?

They forgot the point: "make you look like an idiot"

Did you try them on by any chance?

@Luke, I didn't. I had a feeling that they were just an alternative healing scam, and so didn't bother.

Probably not many side effects except in specific instances, but no benefits either. My guess is that there are potential side effects because these glasses reduce the amount of light that the eye receives and restrict the visual field. Therefore, the restricted visual field would be bad for activities such as driving, in which you need your peripheral vision. And the reduced light makes objects appear dimmer, so it is harder to see with them at night. I also imagine (just a guess) that they would be bad for very young infants, who are almost always born without perfect vision and require some visual stimulation to correct.
There are probably many reasons why optometrists use a pinhole occluder for diagnostic purposes, but never prescribe it as treatment...

interesting answer, well reasoned, but do you have any references (e.g. for the infants being born without perfect vision)? I agree that these could definitely be argued to reduce your field of vision, and thus be unsafe for driving, but if you can find a study into this that would be ideal

A good reference by someone who studies child vision is here, and a less technical one is here. The infant brain is highly plastic. Completely patching the eye (24/7) will cause form-deprivation myopia, but interestingly, patching a few hours a day (in young children) can correct myopia. But I don't know how pinhole glasses will affect them. And as for studies, well, everything I can find online sounds like a scam.

Oops, I meant that patching in children can correct amblyopia.

I believe I saw a documentary (years ago) that stated that these glasses are illega for sale to the public.
Wikipedia says making any medical claim at all is illegal. This is the result of a legal settlement made with the Federal Government.
They can cause blindness when worn regularly outside as Sunwear.

It would be better if you could provide some citations on your claims.


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Convert flux value in nmol/min/mg protein to nmol/min/cell?
This is a question about unit conversion. I found an experimental measurement of the saturation uptake of glucose in yeast:
$$V_\textrm{max} \approx 650 \textrm{nmol}/\textrm{min}/\textrm{mg protein}$$
See Table III of Diderich et al. (1999)*. Actually the paper reports a range of measurements, I just picked an intermediate value.

Table III
Maximum velocity (nmol·min−1. mg protein−1) and Michaelis constant (mm)
of glucose transport by cells grown in aerobic glucose-limited
chemostats at various dilution rates and in batch culture on glucose

I want to convert this to nmol/min/cell, that is, to units of flux per individual cell.
These are my questions:

What exactly is the meaning of the units reported?
It wasn't very clear to me after reading the paper, so I suppose these are standard units. I presume that "mg protein" refers either to the milligrams of transporter protein, or to the total cellular protein content, but I don't know which.
If that's the case, what's the advantage of these units instead of
grams of dry weight (which I think are more common)?
Finally, how can I convert this to flux per cell?

* Diderich, Jasper A., et al. "Glucose uptake kinetics and transcription of HXTgenes in chemostat cultures of Saccharomyces cerevisiae." Journal of Biological Chemistry 274.22 (1999): 15350-15359.

I think the reported unit refers to the maximum specific activity of the enzyme.

@WYSIWYG So you guess that the "mg protein" refer to "mg of enzyme", not total protein content?

@WYSIWYG I read the experimental section in more detail. They determine "protein content" using the biuret protein assay, which I looked up and I think only determines the total protein content. That is, it is not specific to a particular protein. But I am not sure, and I still think this is a weird way to measure it? Isn't gDW better?


text:
Do white Australians have a distinct look?
Background
I've heard from many people working in tourism or similar industries that, white Australians can be recognized as Australian solely by their facial features. Being Australian myself I've heard variants of the claim quite often and lean towards the claim being at least, a possibility.
While it's true that people tend to see patterns when there are none or incorrectly attribute, why they correctly recognize something. I don't necessarily think that is the case here. Australians don't tend to dress in a distinguishing way when overseas, and people have recognized them before hearing them speak. Given the extent to which I hear this claim made, I can't completely dismiss it.
Examples of claims
This article from an Australian newspaper in 1943 interviews an artist who when asked if Australians have a racial type, says he thinks that it was generally possible to distinguish an Australian [from other Caucasians] due to differences in the nose and differences in the jaw.
Googling for terms like "look Australian" returns examples of the claims strewn around the internet, such as this forum thread and this blog.
Also of note is the art project to show the average face of Sydney, of which the following quote is relevant:

In many cases, however, the likeness is so strong that it's possible
to guess the nationality just by taking a cursory glance at the photo.

Reasons for thinking it may be possible
I'm fairly ignorant when it comes to biology, although there are a few reasons I think this might be possible. The (relatively) small gene pool from when Australia was colonized could have led to features from a small group being inherited in a large population.
There seems to be some evidence that environment can play a large role in influencing genetics more so than ethnicity. I can't find the paper investigating that, although will update this question if I am able to.
It seems possible to me that facial features belonging to the original colonists could have spread through subsequent populations, becoming a defining characteristic for some Australians.
I don't think most immigrants are relevant to this question as they will not have inherited distinguishing features (if they exist), nor will they or their parents/grandparents have been able to be influenced by the environment - if that is even a relevant factor.
So...
Do a significant number of white Australians, excluding 1st or 2nd generation immigrants, have distinct facial features unique or generally only found in Australia?
Is it reasonable that some white Australians could be recognized as Australian, going only by facial features?

Why the downvote? How can I improve the question?

Our brains are incredibly good at two things. 1) Seeing patterns, even when there is none 2) recording hits and discarding misses. It is very likely that the people who told you that had either recognized Aussies from other features (e.g. wearing flip flops in the middle of winter :P) or that they just recalled the times when they recognized Australians just by their looks, conveniently forgetting the times when they did not.

@nico that may be likely, although as an Australian who spent an inordinate amount of time overseas, I do feel like I can sometimes tell Australians by face alone. Aussies don't tend to dress like the cliche when overseas, so dress isn't really a distinguishing factor.

I don't understand the downvotes. I'm asking if it is possible or not. Is the question really so ridiculous that it doesn't merit an answer?

I actually upvoted it, I think it is a good question, too bad there is no Anthropology SE :D.

@nico thanks, I just get miffed when downvoters downvote without giving a reason.

"I do feel like I can sometimes tell Australians by face alone" -- and you can also sometimes tell what way up a coin is before seeing it. 50% of the time, in fact. Which is why the only way to answer the question is a study of the actual task, which is to measure whether anyone can distinguish between (for example) white Australians and white New Zealanders better than 50/50 :-) If we knew whether it was true or not, we could worry about whether it's reasonable and what facial features are involved.

@Steve, my claim on being able to identify some Australians by face alone is nothing like being able to correctly guess the side of a coinflip. I absolutely agree a study would be needed to see if there is anything to my question, however I thought a question checking the plausibility of my claim was in order first.

@SonnyOrdell: sorry, but if you only get it right 50% of the time when asked to state the nationalities of an evenly-mixed group of Antipodeans, then yes it is exactly like guessing a coinflip. So make sure that's not what's happening. Which is why I say that "sometimes" getting it right is worthless, that just means you don't always get it wrong. To protect yourself from the natural human tendency to perceive a pattern where none exists, you should establish that you get it right better than guessing.

@SteveJessop Your argument is based on a flawed assumption, that I only get it right 50% of the time. Try 90%. Note, I'm not saying I can identify all Australians by facial features, only those that I perceive to have facial features distinct to Australians.

I didn't assume anything, I merely said that "sometimes" isn't good enough. Most people would not describe 90% as "sometimes", but if that's what you meant then that's great. I'm not saying you can't do it, I'm saying that (until just now) you'd given no indication that there's any real phenomenon here. But fine, if 90% of Australians are recognisable to you as such because you perceive distinctive features, and the other 10% aren't because you don't, from a "big enough" sample, then that's an extremely strong result.

@SteveJessop fair enough, my apologies. That is a result of my trying to make the question more conservative so that it could even be asked on Skeptics.SE, although the mods at the time we rather difficult to work with so it ended up on here. When I worked in the tourism industry, it was pretty common to be able to spot Australians, something my colleagues do frequently also. They don't tend to be wearing anything that would signify Australian nationality and it is often before they speak.

I'm surprised this question has so many up-votes. The sources cited are forums, bad journalism, and an art project. The reason you might think there is a difference seems purely cultural. Even the studies cited below in answers have no empirical data, or are purely hypothetical, and the facelab haven't published anything on this. This is a very subjective question and I am going to open a close vote.

Sun exposure - Lots of it over years make people look distinctive.

Yes, it is possible (on some average basis, i.e. with chance better than random).
Take a look at average women faces from 41 different countries (AFAIK created with Face Research software; sadly no picture for Australia). Clearly, even from small and nearby European countries you can spot differences (which work on the average). I guess the case of Austriala vs other countries isn't an exception. Similar face averages are also on the project Face of Tomorrow.
However, when dealing with a single subjects it it may be not a reliable method to tell of his/her nationality or country of origin, as:

even within an relatively isolated group there is variance in genotype and phenotype,
people do move (especially now) and do mix (so unless you are comparing isolated islands you should't expect to have homogenous genotype).

Moreover, when identifying a person we may (even subconsciously) look at different features (including clothes, accent, behaviour, context, ...).

As much as I like that "average face" link, it only remains an exercise in style. Obviously averaging different faces will give different results. What you would have to do to make it meaningful is getting different subset of faces from the same country and show that all the subset give similar results (I guess we could call that face bootstrapping). Then, as a negative control, take various faces from different countries and show that those characteristics do not show up anymore.

@nico I am hoping that someone may explain why or why not what I propose in my question would be possible, although average a decent sample size and looking for patterns would also give a good indication.

@nico I agree with your scrutiny, as the result is not cross-validated. However, it is not hard to design a test when people see two faces (single, not averaged) and two countries (and their task is to match them). I bet that even for nearby countries (e.g. Germany and France) one can guess with >50%.

@Piotr Migdal: sure, that would also be another very good way to do it.

I think this answer deals with the general case of recognizing someone by their nationality and not Australia specifically. I think that Australia is a special case as most people would not believe white Australians could have a distinct look, as they simply look white.

@SonnyOrdell Yes, it is a general case and here is nothing special about Australians. Perhaps there is something special about Caucasian Australians but I doubt.

@piotr but that is the question I am asking is about, if there is something special about white Australians. Your answer should be specific to that, not a general case.

It seems unlikely, but it's possible.  The mechanisms that might occur (that I can think of) are:
1) if the Australians had some rare genetic traits that became more common in the australian gene pool than in the UK gene pool, it is possible.  This is what happened with eastern Asia and the Y chromosome, which something like 40% from a single individual.
For this to be the case, it would be necessary that:  Australia's gene pool must be isolated - very little immigration to the company and mixing with other gene pools.  (i think not- what do you say?)
2) the diet of Australians caused their general body or face to be distinctive.  As there is a lot of fast food in Australia now (and obesity) I'm guessing that this is simply not the case, at least compared to the UK and US.
Since there is no direct study (that I can find) all we can go on is anecdotal thought experiment.
As far as cognitive bias goes, I'm Asian American and I've heard many many (maybe most Asians say that they can tell one nationality vs another just by appearance).
Whenever I have tested myself or others I have not found anyone who can tell that i am 100% Japanese genetically.  This is probably because diet in the midwest where i grew up was so corn rich and I've been mistaken for nearly everything, including Latino backgrounds.  Most people think I'm Filipino, which is great except that I am not :)
Even when I ask Asians to look at other Asians and guess, it seems pretty rare that one can be consistently correct.  There has been a lot of gene migration between countries there, even though the national groups are much much older than Australia.  This is why I really doubt that Australians have been genetically isolated long enough or strongly enough for this to really be likely.
It would be pretty simple to get a bunch of pictures together, say 100, and test this if you really want to know.

Do you know about alllooksame.com?

ha - good one! I hope I wasn't trying to subliminally prove a point, but for faces I scored 6/16.  the average is 7.

Could you maybe expand on point 1 and 2 showing that what you say is possible? There is no direct study with Australians but there should be for your underlying points?

RE Australia's gene pool being isolated, it surely was at the formation of the country and likely stayed so for many years, perhaps this could have had an effect?


text:
How do different tissue culture matrices affect background in fluorescent microscopy?
In response to my previous question, I've been reading up a little bit on poly-D-lysine, Collagen I, Collagen IV, laminin, and other tissue culture coatings that promote cell adhesion. I've always assumed that anything other than standard TC-treated plastic or glass would significantly increase background, but perhaps my views on background fluorescence are a little outdated. Does anybody have experience with these in a fluorescent microscopy/high-throughput screening environment?
Specifically in my case, I'm looking at endocytosis and trafficking of a labeled protein into the lysosome. I'm labeling the protein with the pH-dependent dye pHrodoTM from Molecular Probes, which supposedly has very little fluorescence at neutral pH, but becomes very bright as the pH drops when endocytic vesicles become lysosomes. This theoretically means that a final wash step is not needed, but with a matrix coating on the plates I'm worried about background.
So, what is the current thinking as far as background fluorescence of the various TC matrices is concerned? Does the background come from the matrix itself, or by the fluorescent dye becoming adsorbed to it? Is it wavelength-dependent? Fortunately I may not be stuck with my poorly-adhering cells, and I may not need supplemental matrix at all in the end, but I still want a better understanding of how it works.

Extracellular matrix (ECM) fluoresces, especially Collagen and Laminin. The maximum is in the DAPI and FITC channels and the fluorescence becomes weaker towards longer wavelengths. However, since the coat on the TC flasks is very thin, I would not expect this to be a problem. The best thing is just to try it. There is also a quite famous document available which might be of help:
Autofluorescence: Causes and Cures


text:
Disadvantages of unihemispheric sleep
Is is well known fact that marine mammals and some birds can sleep with one brain hemisphere at a time, since it's essential for their survival.
However, at least in my opinion, such mechanism would give significant advantage to many other species (e.g. to antelops) because it helps avoiding predators.
While answers to this question explain why sleep is necessary, animals with unihemispheric sleep mode does not seem to suffer from any of mentioned drawbacks of non-sleeping (except maybe increased energy consumption).
Are there any particular disadvantages of unihemispheric sleep versus "normal" sleep?
EDIT: I've stumbled upon the following paper:  Rattenborg N., Amlaner C., Lima S.. 2000. Behavioral, neurophysiological and evolutionary perspectives on unihemispheric sleep. Neuroscience & Biobehavioral Reviews 24: 817–842, which discusses several possible reasons for absense of unihemispheric sleep in most mammals, but does not present any evidence to support their hypothesis. The main reason (from authors' point of view, at least) is the need for very loose coupling of both hemispheres to allow them sleep independently, which might negatively affect overall brain effectiveness.

Along these lines, sleep may play a role in integrating the
  functions of different brain regions. Thus, BSWS1 in terrestrial
  mammals may be superior to the BSWS in animals with USWS2
  because it allows integration within and between hemispheres, rather than
  just within a particular hemisphere.
...
Specifically, the reorganization of the central nervous system
  required for USWS may interfere with other adaptive brain functions,
  such as integrating the functions of both hemispheres.
1 Bihemispheric Slow Wave Sleep; 2 Unihemispheric Slow Wave Sleep

They also argue that the unihemispheric sleep might have been present in first mammals, but wasn't giving any advantages on first stages of evolution.
However, this paper was published more that 10 years ago, so there might have been some advances in the field since then.

I would assume that to give your brain the rest it needs you would have to spend double the time sleeping when resting one hemisphere at a time. For humans at lest that would be kind of disastrous.

@UltimateGobblement I agree that it might be bad for humans, but I doubt that most low savannah animals have more complex lifestyle than dolphins, so using one hemisphere most of the time might be enough, and enhanced alertness during night increases chances of survival during attack of nocturnal predators. Giraffes and elefants, e.g., sleep approx. 4 hours a day, so reduced sleep time is likely very beneficial to them.

that would make it easier to work as a night watchmen or some other jobs like working in a toll booth.

I am pretty sure one hemisphere of my brain is asleep when I watch TV...  ;)

Interesting note, seals which can sleep both on water and on land, employ unihemispherical sleep in water but whole brain sleep on land, so this suggests unihemispherical sleep is non-optimal

I thought this was an interesting subject and I had some time to do a little search around today.  I can't find anything better than the review you point out. All I can do is add a few interesting notes since 2001.  Nothing really turns over Rattenborg et al.
Sleep is itself a poorly understood process and most of the theories of the necessity of sleep can teeter precariously with discoveries like this report that baby dolphins and killer whales and their mothers simply don't sleep at all for the first few months of life.
The Rattenborg review is only guessing, but I think its clear that there is a cost to unihemispheric sleep, even if we don't know what it is.  Cetaceans and birds and perhaps reptiles having unihemispheric sleep are all cases where there are perpetual and strong selection forces that maintain the ability in these animals.  Without constant predation experienced by tasty ducks or the vagaries of being an air-breathing underwater mammal, animals quickly lose their ability to sleep with one half their brain, one assumes because the ability to maintain it is particular and easily lost with variation.  Modelling work of the hemispheres in sleep indicates that the connections between the hemispheres are modulated between the two modes of sleep - there may be advantages to such brain structures for instance.
This blog post is a good read though and a bit more recent, though most of the references are from before 2001. Dolphins do use both hemispheres to sleep, but just not very often (about 15% of the time), indicating there is some advantage even for these animals.  Seals may alternate between bi and uni-hemispheric sleep when they are on land and at sea.
If you were wondering if there was something you were missing - I'd say no.  At the time of this writing THIS web page is the sixth hit on a google search for the term 'unihemispheric sleep'....


text:
Human Body "Fat" Equilibrium
Here's my theory:

If you consume x calories each day with y amount of caloric expenditure each day you gain zero weight, regardless of x and y being out of balance.
If you then mechanically remove a large percentage of body fat (surgically), the fat should not come back.

Is this a true theory or not? It seems to me that if the body is stable at the current consumption of x and expenditure of y then the removal of excess weight/fat should not affect anything.
Anyone have thoughts on this? Is my thinking flawed? Why? Even if x and y were equal why might the fat come back if there is no net gain when the fat exists?

The fat that you removed has some non-zero metabolic cost that you need to account for. Your x-y=0 balance will be off.

What makes you think your theory is true? Definitely your first premise is false, otherwise nobody would ever gain weight...

Kevin- so if you consume less calories after the removal with all things being the same the removed fat should not return right?

Nico- true- but generally, very very generally, most people stay the same regardless of x and y. Within a range of course.  this is what I would consider the equilibrium point. If the fat is removed, why would it come back if it wasn't increasing before?

@nico Some people have very different metabolisms: i.e., gaining weight although they are eating healthy or staying skinny although they eat garbage. This definitely isn't the case for everyone, but I'm okay entertaining the premise that some people can maintain weight equilibrium even though x and y are somewhat out of balance.

@helicopterjeff I would, however, recommend clarifying your wording. Currently, it sounds like your assumption is that x and y can be completely off balance and yet you always maintain weight equilibrium. I don't think this is what you're trying to say. If I understand, you're suggesting that for some, weight equilibrium is possible even if x and y aren't balanced. Is this correct?

@DanielStandage: that is exactly my point. As it stands it looks like with any combination of x and y you will never gain weight. I am not doubting that SOME people may not gain weight for y<<x but that would definitely not be the norm.

I guess my ultimate question is why do people who have had liposuction or some other kind of fat removal surgery gain the weight back if their diets remain the same?  Usually, from what I can tell the body before the surgery was not gaining/losing weight. it was just there. After the surgery it eventually comes back. That doesn't make sense to me.

I'm not quite sure what you mean by

regardless of x and y being out of balance.

Surely it would make more sense to assume you gain 0 weight if x and y are balanced? The prime reason why people get obese is probably because x and y are not balanced for them (there are other reasons though, as well as reasons why people can have it imbalanced and still not gain weight).

Even if you consume exactly as many calories as you expend in a day, you may gain weight depending on how (ratio of protein/fats/carbohydrates) and especially when you consume the calories. The body may for example store consumed amounts as fat after eating and then use carbohydrate storage from liver and muscle when starving, so long term you would still gain weight.
Adipose (fatty) tissue requires energy too. If you consume in the same manner after as before cutting a large amount of it away, you may just regain it until x=y again.
Also consider: if people ate just half an apple a day more than the exact amount of energy they need, they should gain more than a kilo on average every year. But they don't, and you can hardly assume that people manage on average to consume the exact amount their body needs.

The reason for that is probably leptin. It is a hormone produced by adipocytes (fat cells) and essentially indirectly reduces food uptake and increases expenditure, among others by decreasing your appetite. This has been regarded as a sort of "adipostat"; your leptin system creates a genetically determined level of body fat that you will tend to obtain. Dieting or cutting away fat will cause a drift to return to the previous weight because of a lower level of leptin (due to reduced fat cells). Of course it's not as simple as that though, so it's also possible that you will actually long-term reduce weight through those methods. E.g. exercise seems likely to be an exception somehow.

x and y being out of balance meaning that most of us, in the USA anyway consume WAY more calories that we expend. Yet in many cases no weight gain is seen. I am personally in that boat. Despite diet, I'm not gaining or losing.
So I am wondering why then if the fatty tissue is removed why does it come back?
The leptin system is probably what is at work. The body wants to be at a certain weight. If you starve it you're at a lower weight.

There are many reasons why that can happen. Regarding leptin, something could be wrong with its production or its reception at the target sites. The same is the case for me though even though my leptin is probably ok. It's most likely due to a kidney malfunction which my dad and brother have as well (we're all slim the same way). There's probably other different causes as well.


text:
Are (baseline) high blood levels of melatonin associated with either circadian rhythm or mood disorders?
(Exogenous) melatonin is administered at night for treatment of circadian rhythm disorders, but melatonin taken during the day is linked with depression.
I would like to know if high blood levels of (endogenous) melatonin (at a steady state, throughout the day) might be linked with mood or sleep disorders (or have any effect at all), or if the body's response to melatonin adjusts accordingly.
I think the answer to this SE question is related, but I can't find the source using a reverse image search.

This question isn't fully answered - I found nothing on circadian rhythm disorders.

I found a recent PLoS article that said that none of hypochondriasis, depression, hysteria, psychopathic deviate, masculinity-femininity, psychasthenia, schizophrenia, or social intraversion (on the MMPI-2) "were associated with any melatonin parameter."
However, it does appear that "increases scores of Hypomania and Paranoia were associated with a shorter DLMO-DLMOff interval" (duration of melatonin production).
The only thing that concerns me are the significance and the effect size of the latter two results.  I can't tell whether they corrected for multiple comparisons or not.
Reference:  Burgess HJ, Fogg LF (2008) Individual Differences in the Amount and Timing of Salivary Melatonin Secretion. PLoS ONE 3(8): e3055. doi:10.1371/journal.pone.0003055


text:
Is it possible to repopulate lactase in the stomach?

Possible Duplicate:
Can an adult without genetic lactase persistence still develop a tolerance for dairy foods?

In my younger years, I don't seem to have a problem drinking milk.
Nowadays, when I drink milk, I keep farting away.
After searching around the Internet, this site claimed that it is due to lactose intolerance. They have a product that claims to be able to repopulate the enzymes in the body so that it can digest milk. Is this product based on sound principles?
Can someone (other than the Dairy Care company itself) refute or support its claims?
Thanks!

Although the other question is not specific to this product, the answer does answer your question.

I think the other question answers this and is a better written question.

How does "repopulating the lactase enzyme" and "tolerating milk" mean the same thing?

If you read the answers you will see they describe essentially the technology which is in the product you asked about. The supplemented lactobacteria produce the lactase enzyme, and the tech fundamentally is sound. Whilst the question isn't worded the same, the answer you're looking for is there. Anyone answering this question would basically be repeating all the info in those answers.


text:
What chemical or biochemical agents do plants use to inhibit each other's growth?
As I just learned, allelopathy is the action by which plants regulate the growth of other nearby plants.
I have hear of ethylene is a general signal for growth and fruit ripening in particular, but I would like to hear about more specific compounds or proteins that are known to be allelopathic agents and how specific can they be - lots of plants ignore each other and just grow over each other.
@AlanBoyd has pointed me to a journal, but as its not open content, I'm hoping for a next level review of the mechanisms and actors in this topic...
thanks in advance!

A classic example is juglone from Black Walnut tree roots. This review from 1973 discusses juglone and allelopathy, inhibiting growth of other trees. This 1961 paper describes juglone's effects as able to sedate or at depress movement of Daphnia magna, leopard frogs, perch, catfish, goldfish, mice, rats and rabbits. That led to work testing juglone on cancer cells.

As with the massive variety of compounds that serve to protect plants against insect and animals, resulting in a wide range of poisons, antibiotics and other natural insecticides, allelopathic compounds are highly varied with different methods of action: some merely prevent germination while others are effectively herbicides.
One example is Alliolaria petiolata. In that species the allelopathic substance is not known, but is thought to ahve a fungicidal effect that impedes mycorrhizal development, which would seriously affect the development of many species.


text:
What causes feeling of feet falling asleep to be delayed?
This answer explains the sensation of extremities "falling asleep" as a result of sustained pressure on a nerve. The answer links to an external web page that says that the feeling "quickly goes away once the pressure is relieved."
In my experience, however, it doesn't usually go exactly like this.  For me at least, usually what happens is I will start feeling a tingling sensation in my feet after sitting in an awkward position for an extended period of time. If I ignore the sensation for long enough, it continues to get worse until I finally do stand up.  But after I stand up, rather than the sensation quickly disappearing, I find that usually it suddenly gets much worse for a period of time.  What started as an annoying tingling when I was sitting quickly turns into something quite uncomfortable upon standing up, even to the point where I am not able to walk around properly until the sensation passes a few minutes later.
But once I am standing up, the nerve shouldn't be pinched anymore, so why does the sensation of my foot being "asleep" remain for a few minutes after standing up, and why does it actually seem to briefly get worse after I have already stood up and "unpinched" the nerve?

This is a personal medical advice question. I should be aware of many other factors to answer such a question satisfactorily. Has this kind of behaviour occurred in you all your life or started just recently or during your university years?

I believe this sensation can be generalised to everyone. It's the feeling you get when you fall asleep with arms/legs crossed and wake up with the strange tingling feeling.

@wysiwyg why was my answer deleted?

@majid This question is different because it is asking about the delayed feeling.

This paper, while mainly dealing with chronic nerve compression, appears to explain the effects of nerve compression on the blocking the transmission of neural impulses (causing the "sleeping limb" syndrome).
This paper describes how the application of pressure on a nerve causes a miniature case of compartment syndrome, where the pressure causes the intraneuron pressure to increase, leading to paresthesia. Edema also occurs within the neuron, causing pain signals to be sent out. In the experimental rats which were unable to relieve this pressure, permanent nerve damage resulted.
When the effects from the nerve compression exceeds a certain level, the pain/tingling will result in you releasing the pressure from the limb in order to prevent nerve damage.
However, the nerves are still blocked from transmitting their impulses due to the  compression blockage described in Paper 1. When the blockage is resolved, the neurons are now capable of transmitting their pain signals, which continue for a period of time until the pressure within the limb falls sufficiently below the pain threshold.

Paresthesia is defined as the abnormal sensation of the skin, such as numbness, tingling, pricking or burning. Paresthesia is a diverse medical condition and the definitions seems too vague. Most of the books define Paresthesia as a symptom of some other disease. Mostly Paresthesia is categorized as transient or permanent. Paresthesia can arise from several causes like artery related, nerve related, migraine, vitamin B deficiency, brain related and may cause from side effects of other drugs.
Classification of transient and chronic Paresthesia is described in detail here.

Nerve impulses require a healthy energy supply, known as the axonal transport system.  This well developed micro-vascular distribution method provides the blood flow needed to maintain the cells in good working order. If pressure is put on the correct spot, though, all the tiny arteries, veins and capillaries that supply the nerves’ nutrients become pinched off and the nerve cells begin to function abnormally.
Compression isn’t the only thing that can cause limbs to fall asleep. Excessive vibration will also lead to paresthesia. Operating hand-held vibrating tools is an extremely common cause of this
Reference

As simulation level increases transient Paresthesia may occur, usually disappearing with in a few second

Localized paresthesia or pain occasionally results from a specific
mechanism. Mechanical irritation of a peripheral nerve can project
such sensations to their periphery.If the pressure on a peripheral
nerve provokes paresthesia, then a neuroma or chronic compression
occurs. If the pain is initiated by the movement of a joint, there may
be a ganglion affected by the process.
Reference : Neurological Differential Diagnosis -- Marco Mumenthaler

The paresthesia mentioned in the question is transient, mostly paresthesia can happen in cold weather conditions or can happen when sitting in a particular position for long time. Several types of paresthesia exist and there are several reasons for the occurrence. But most of them are attributed to the strain in  peripheral nerve. When we stand up, the itching effects get increase and it slowly fades out, this is because when the nerve resulted in the formation of paresthesia is stressed more when we take a stand up poster. As some paresthesia is caused by the lack of blood supply, blood supply itself is not always causes paresthesia but there are cases when blood circulation to the nerve is interrupted and this may result in stress of nerve and which may cause paresthesia. These kinds of paresthesia is common and it only last for minutes. So when we stand up the tension to the nerve increases, also the blood pressure increases and blood is slowly available to the nerve. When we try to stand, the nerves are burdened with more tension and paresthesia increases but after sometime the blood flow become natural and paresthesia  diminishes slowly. Paresthesia   can be reduced by massage or applying pressure on the affected areas, all these are helpful for people having transient paresthesia. Chronic paresthesia and paresthesia due to other medical conditions need more complex treatments.
Causes for paresthesia

References
Clinical Guide
Clinical Neurology of the Older Adult --  Joseph I. Sirven, Barbara L. Malamut
Paresthesia and Dysesthesia

why does standing up cause tension in the nerve to increase? If that were the case, I would expect my feet to fall asleep whenever I was standing and spotting awkwardly would make it better.

According to the post you linked, paresthesia causes the "falling asleep" notion. According to Wikipedia, there are two types of paresthesia, transient and chronic. Transient paresthesia is the type you are describing.

Paresthesias of the hands, feet, legs and arms are common, transient symptoms. The most common, everyday cause is temporary restriction of the blood supply to an area of nerves, commonly caused by leaning or resting on parts of the body such as the legs; other causes include conditions such as hyperventilation syndrome and panic attacks.

Other places like this link mention that parethesia is caused by:

• Obdormition: Obdormition is a numbness caused by prolonged pressure on a nerve,
  such as when a leg falls asleep if the legs are crossed for a prolonged period. It
  disappears gradually as the pressure is relieved (1).
• Whiplash: Paresthesias in the upper extremity may occur after
  whiplash injury (2), a type of cervical soft tissue injury (3). Pujol
  et al showed that 13% of patients with whiplash had associated
  paresthesias (4). Recovery usually arises within 6 months after injury
  (5).
• Hyperventilation syndrome: Paresthesia constitutes 35% of presenting
  complaints in patients with hyperventilation syndrome (6) and may
  begin after as little as threeminute of hyperventilation (7). After
  increasing the depth or frequency of respiration, www.intechopen.com72
  Paresthesia the alkaline shift produced selectively increases Na+
  conductance and ectopic discharges in normal cutaneous afferent nerves
  can be induced (8). Other electrolytes, i.e. magnesium, potassium,
  chloride, phosphate and bicarbonate, also demonstrated significant
  changes in concentration (7).
• Panic attack: Paresthesiae of the mouth, hands and feet are common,
  transient symptoms of the related conditions of hyperventilation
  syndrome and panic attacks. Ietsugu et al demonstrated that
  paresthesia can be used as a reliable indicator of severe panic
  attacks (9).
• Transient ischemic attack (TIA): TIA may be manifested by
  paresthesias. Several reasons may cause TIA such as thrombosis,
  embolus, intravascular debris and blood vessels disruption. Perez et
  al. reported the initial manifestation of cardiac myxoma can be
  paresthesias caused by TIA (10). Post-ischemic paresthesia occurs when
  hyper polarization by the Na+/K+ pump is transiently halted by
  elevated extracellular K+. The electrochemical gradient for K+ is
  reversed and inward transport of K+ triggers regenerative
  depolarization (8).
• Seizures: Paresthesia may happen during and after a partial seizure
  (11). Treatment of seizures with vagus nerve stimulation can also
  trigger paresthesias and is considered an adverse event associated
  with this treatment modality (12).
• Dehydration: At around 5% to 6% cumulative water loss, paresthesia
  may occur.
• Insufficient blood supply: Circulatory disorders could lead to
  transient or chronic paresthesia.

As you can see, there are many causes for paresthesia. The most common is the pressure on the nerves and the loss of loss supply.
Usually, the feeling quickly goes away once the pressure is relieved. But in your case, the paresthesia is delayed because it's caused by restriction of blood flow. Because it is caused by restriction of blood flow, it may take time  for the blood the reach the area and oxygenate the nerves.
Why does it get worse? Well, because the action of standing up causes the blood pressure and heart rate to increase, decreasing blood flow to the nerves (read the abstract of this). Another reason is that when standing up, there is increased pressure on the nerves, causing paresthesia. Together, these effects, may increase paresthesia for a few seconds. But when the blood flow becomes normal and the pressure on the nerve decreases, the paresthesia goes away.
There you have it! Nice and concise hopefully... @Daniel if you have more questions, you can ask them by adding a comment to this post.


text:
How can a three-base codon evolve from a two-base codon?
Inspired by this question among others.
It's widely suggested that the current 3-base codon system of encoding protein sequences in DNA evolved from an earlier 2-base codon system. This makes sense if you look at the coding sequences themselves but I fail to understand how it can evolve? Wouldn't any shift wreck the coding of all existing proteins?
Perhaps they could overlap, but wouldn't even that produce nonsense and how would it shift to non-overlapping codons? Perhaps both systems could run in parallel, but how would anything useful come from that in the short term? What selective of advantage of 3-base coding could be strong enough to overcome any disruption?
Has anyone developed a coherent model of what intermediate stages might look like?

It is not suggesting a 2-base->3-base code in the way you are thinking, but of a non-coding, two-coding triplet pattern occurring first.
This means you would have 16 different coding sequences with 4 possible spacing bases in between.
Later, the spacing bases could become used as part of the code.
Does that make more sense?
Instead of AA,CG becoming AAT,CGT; AAX,CGX becomes AAT,CGT etc.
Its also likely that between 2 and 3 base codes a 2 base pyrimidine/purine system was used. Today the third base can often be switched for its pyrimidine/purine pair without changing the resulting amino acid.

Yes, that does make more sense. Thanks, Nick. Do you have a source for this, though?

Erives' paper is interesting:
A model of proto-anti-codon RNA enzymes requiring L-amino acid homochirality.

Why is it interesting?  Try to include a summary of anything you're linking to in your own words.


text:
By what mechanism does elevated homocysteine level accelerate thrombin formation?
It has been stated that elevated homocysteine level accelerates thrombin formation. By what mechanism does this happen?

According to a heavily-cited paper (below), homocysteine reduces the expression of thrombomodulin on the surface of endothelial cells.
Thrombomodulin binds to thrombin, and the resulting complex does not promote coagulation, but instead activates protein C. Protein C has an anticoagulant effect. Thus reduced levels of thrombomodulin will result in increased levels of free thrombin (promoting coagulation) and in reduced levels of protein C (also promoting coagulation).
I haven't found any evidence that homocysteine has an effect upon thrombin formation directly.

Lentz,SR and Sadler, JE (1991)Inhibition of thrombomodulin surface expression and protein-c activation by the thrombogenic agent homocysteine. J. Clin. Invest. 88:1906-1914
Abstract Elevated levels of plasma homocysteine are associated with both venous and arterial thrombosis. Homocysteine inhibits the function of thrombomodulin, an anticoagulant glycoprotein on the endothelial surface that serves as a cofactor for the activation of protein C by thrombin. The effects of homocysteine on thrombomodulin expression and protein C activation were investigated in cultured human umbilical vein endothelial cells and CV-1(18A) cells that express recombinant human thrombomodulin. Addition of 5 mM homocysteine to endothelial cells produced slight increases in thrombomodulin mRNA and thrombomodulin synthesis without affecting cell viability. In both cell types, thrombomodulin synthesized in the presence of homocysteine remained sensitive to digestion with endoglycosidase H and failed to appear on the cell surface, suggesting impaired transit along the secretory pathway. In a cell-free protein C activation assay, homocysteine irreversibly inactivated both thrombomodulin and protein C in a process that required free thiol groups and was inhibited by the oxidizing agents diamide or N-ethylmaleimide. By inhibiting both thrombomodulin surface expression and protein C activation, homocysteine may contribute to the development of thrombosis in patients with cystathionine beta-synthase deficiency.


text:
By what mechanism does elevated homocysteine level cause endothelial dysfunction and damage?
It has been stated that elevated homocysteine level causes endothelial dysfunction and damage. By what mechanism does this happen? Why is it the endothel where elevated homocysteine causes problems?

In addition Alan Boyd's answer homocysteine interferes with Glutathione synthesis by reducing the catalytic efficiency of GCL (Glutamate–cysteine ligase), the enzyme which performs the rate-limiting step in GSH synthesis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267299/
Results of the present study are the first to suggest that the relatively high levels of homocysteine that accumulate during aging can interfere with de novo GSH synthesis. Although the precise nature of the underlying mechanism is at present unclear, our results demonstrate that physiological concentrations of free homocysteine can inhibit the efficiency of cysteine utilization by GCL in a competitive manner. Homocysteine has been shown to bind GCLc at the active site in vitro [25] as well as in vivo [35], forming γ-glutamylhomocysteine [36], which is then rapidly degraded enzymatically. An additional mechanism by which an age-related increase in free homocysteine can inhibit the catalytic efficiency of GCL in a competitive manner is described in [35]. It is possible that an aging-related increase in the competition between cysteine and homocysteine for the cysteine binding site of GCL might lead to a decrease in GC synthesis.

Low glutathione means a reduced ability to detoxify and deal with oxidative stress and a more oxidised redox state which has many implications
Further reading:
Inhibition of glutathione synthesis in brain endothelial cells lengthens S-phase transit time in the cell cycle: Implications for proliferation in recovery from oxidative stress and endothelial cell damage
http://www.sciencedirect.com/science/article/pii/S2213231713000244
Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability
http://content.onlinejacc.org/article.aspx?articleid=1125915

Short answer: homocysteine promotes elevated levels of reactive oxygen species which interfere with signalling via nitric oxide.
There is an extensive literature on this topic: a Web of Science search using [TITLE: endotheli* AND homocysteine] produces 567 hits.
The prevailing view seems to be that homocysteine causes oxidative stress in cells because autooxidation of the sulphydryl group of homocysteine promotes the production of reactive oxygen species (ROS): superoxide, hydrogen peroxide and hydroxide radical. There is also evidence for decreased levels of glutathione (GSH) and glutathione peroxidase (GPX) (McCully, 2009). The classical pathway for dealing with ROS is conversion of the primary species,superoxide, to hydrogen peroxide (by superoxide dismutase) followed by reduction of peroxide to water by GPX using GSH as a reductant. This pathway rapidly destroys ROS and importantly avoids the generation of the damaging hydroxide radical. Reduced glutathione is regenerated at the expense of NADPH.
Endothelial cells use nitric oxide (NO) to signal to surrounding smooth muscle, resulting in vasodilation. ROS react with NO, inactivating it. There is also evidence that NO production by epithial nitric oxide synthase (eNOS) is affected, and Leung et al., 2013 present data indicating that the phosphorylation level of eNOS is reduced by homocysteine. Phosphorylation is a key regulator of eNOS activity (Mount et al., 2007).
Leung SB et al. (2013) Salidroside Improves Homocysteine-Induced Endothelial Dysfunction by Reducing Oxidative Stress. Evidence-Based Complementary and Alternative Medicine 20: Article ID 679635
McCully, KS (2009) Chemical Pathology of Homocysteine. IV. Excitotoxicity, Oxidative Stress, Endothelial Dysfunction, and Inflammation. Annals Clin. Lab. Sci. 39:219-232
Mount, PF et al. (2007) Regulation of endothelial and myocardial NO synthesis by multi-site eNOS phosphorylation. J Molec. Cell. Cardiology 42: 271-279


text:
Can Naegleria fowleri enter through the eyes ( example rinsing/splashing eyes with water)
I understand that it primarily enters the body through the nose by by "feeding on the olfactory neurons in the nose" as answered here in a different question. Would the nerve cells in the eyes present a similar entryway?

@Gabriel could you perhaps opine on this?

In a 1987 article "Nonenteric Infections Acquired through Contact with Water", the author mentioned that "Infection of the ears, throat, respiratory tract, and cornea are also encountered" by virulent strains of Acanthamoeba and Naegleria fowleri. The only reference that implicates Naegleria fowleri is this one, but it doesn't mention modes of infection.
The long and the short of it is that Acanthamoeba infections can be acquired through contact with the cornea, but it's not clear whether Naegleria infections can also be acquired in this way.
n.b. The first link takes you to the JSTOR page.  In the event you do not have access, here is the PubMed page.

Is the extract you quoted specific to Naegleria fowleri or just water borne pathogens in general? Thanks for your input.

@Jarnal: I edited the post to answer your comment-question, but I am aware that this doesn't answer the original question. I cannot provide that answer; I only delved into the article posted by ohcanada.

@dd3, thanks, your input provided helpful clarification.


text:
Dimensionless number for blood volume
Comments from the question How is the blood volume of a living organism measured without killing it? by @Nico discussed that the time of blood recirculation scales with the size of the organism. I was curious if there were a series of dimensionless numbers that characterize blood flow, blood volume, and time of blood recirculation?
Such dimensionless numbers exists for stride length and drug penetration.
Edit
I like @Nico's comment so much it's going to part of the question. Any description of the circulatory system doesn't necessarily have to be dimensionless. However, I would imagine that one could develop a characteristic time (lets call it Tau) based on blood flow (L/t), cross-sectional area (L^2), and circulation time (t). From that characteristic time Tau, interesting observations and appropriate comparisons about the various ratios and how they vary amongst species.

Why would it need to be dimensionless? Blood flow is a speed (mm/s), blood volume is a volume (ml) time of blood recirculation is a time (s).

By the way, to further expand my comment, I was considering that the ratio between cardiac output and the volume of the circulatory system would vary between species. I wasn't necessarily implying that it would be higher in smaller animals, although re-reading my comment it looks like I was saying exaclty that!! :)

The trouble with miles/gallon is that it has square-cube problems. Motorcycles get far more miles/gallon despite being less aerodynamic, because they are smaller. So if you wanted a measure of how efficient motorcycles as a design independent of their size were, a dimensionless measure would resist scaling problems. It's especially important in biology because nothing is the same size as anything else.

What blood volume can be normalized to is body volume. Since body volumes is slightly difficult to measure you can assume the density to be equal to that of water and calculate volume from body mass (bad approximation when comparing species with different bone and muscle densities).

Blood volume is not a dimensionless number - it's a volume. Historically we used to measure this in patients or volunteers by giving a large carbohydrate molecule like a starch that is not digestible or harmful to the body. Just like every other body fluid compartment volume (i.e. plasma, interstitial fluid, intracellular and extracellular) that we have, blood volume is estimated by intravenously injecting a known concentration of a particular compound. Once that compound equilibrates you take a blood sample and measure the compound's concentration again.
Initial Concentration * Initial Volume = Final Concentration * Final Volume
When you inject a known volume of a known concentration that only fills the "blood" component, and then you measure a final concentration - you can then solve for the "Final Volume" for "blood volume".

Great that you dug up this old question and answered it. +1

This does not really answer the question. The OP wishes to know if blood volume can be non-dimensionalized. My opinion is that it can be normalized to body size (which seems quite reasonable; larger people would perhaps have higher volume of blood) but I haven't seen any literature on that.

I see what you are saying - larger individuals would have larger volumes of blood. Similar to energy expenditure, though, that's a nonlinear relationship that you would need a large, diverse sample size to measure empirically (not sure if that's been done yet). The numbers we use clinically, like blood volume being 7% of total body weight, only holds in a 'normal size' or near normal weight individual around 70-80kg. Even though the numbers don't hold at the extremes of weight they remain "close enough" for clinical estimation when needed.

@VanceAlbaugh So like there is BMI, is there not a blood volume to body weight ratio such that a range of that factor may be considered healthy?

There is no unit that I am aware of for an index of blood volume for research purposes.  Clinically we use the historical values of 7% of total body weight - but realize that is based on 70kg males from 50+ years ago. Obese and morbidly obese individuals have different values because the relationship is nonlinear.  Check out this for one model (but definitely not the only one) that has been 'attempted' to model blood volume.  http://www.ncbi.nlm.nih.gov/pubmed/16756741

Thanks for answering but at @WYSIWYG mentioned, it doesn't really answer.

@bobthejoe that's because volume is not dimensionless

@vancealbaugh, neither is time and length yet we frequently find ways to nondimensionlize those properties.

Like? @bobthejoe

@VanceAlbaugh, Tau, Damkholer, f-number, Knudsen number, Radians, etc. Nondimensionalization is pretty standard in a lot of engineering fields. I would guess that BV is a good factor to normalize against. That way you can say that a "heart contains 0.05 BV" or "there is a flux of 0.01 BV/minute through this artery".

@bobthejoe - cool... we don't use any of those types of numbers clinically when treating patients. On the research side the bioengineers might use numbers like those you mention for modeling purposes. Clinically we have estimates of blood volume that are "close enough" for treatment purposes. 50+ years ago when you wanted to experimentally measure a volume of any fluid within the body, you used the dilution technique that is shown in my answer above.


text:
What is this fruit?

There is a hairy hard shell (looking like a small kiwi), which naturally breaks, and under it there is brain-shaped red sweet flesh, half-covering the smooth black seed.
Picture taken in the Mediterranean coast of Israel in August

Kinf of Morus : https://en.wikipedia.org/wiki/Morus_(plant)

I think this tree is not native to the Mediterranean (cause I've never seen it). Was it located in a garden? Can you ask the owner of the house?

@RHA I have seen it mostly in public places, along roads, in a hopital, etc.

Might it be Alectryon tomentosus?
To me, the fruit looks the same and also the leaves have the same look.
It is an Australian tree whose common name is "wooly rambutan" and is used as a street tree as you observed. I did not find instances of this tree in Israel, though.

Kind of Morus, I have seen this in Morocco and it is delicious : https://en.wikipedia.org/wiki/Morus_(plant)

No. Morus has many small seeds, this one has one big seed. Morus has no shell around the fruit.

@Anixx I didn't say it is Morus, I said kind of Morus, which means Morus Family