text:
Dimethyltryptamine and Sigma 1-type opioid receptor interaction
Where exactly do dimethyltryptamine and sigma 1-type opioid receptor interact? I read in this When the Endogenous Hallucinogenic Trace Amine N,N-Dimethyltryptamine Meets the Sigma-1 Receptor but it does not say where exactly they interact only that they do.

From your article:

Sig-1Rs localize at the interface between the endoplasmic reticulum (ER) and mitochondrion, which is known as the mitochondria-associated ER membrane (MAM).

Consequently, they are found in a variety of areas within the central nervous system as well as in other types of cells throughout the body (notably cardiac cells).

An important biological activity of sigma receptor activation is the inhibition of ion channels, which operates through protein-protein interactions without mediation by G proteins and protein kinases. In addition to modulating various types of voltage-activated K+ channels, the sigma-1 receptor associates with the Kv1.4 K+ channel in posterior pituitary nerve terminals, as well as in Xenopus oocytes. Sigma receptor ligands also modulate N-, L-, P/Q-, and R-type Ca2+ channels in rat sympathetic and parasympathetic neurons. Sigmareceptor ligands modulate cardiac voltage-gated Na+ channels (hNav1.5) in human embryonic kidney 293 (HEK293) cells, COS-7 cells, and neonatal mouse cardiac myocytes. To evaluate the capacity of DMT to induce physiological responses by binding to sigma receptors, we examined the action of DMT on voltage-activated Na+ current.

From:

Fontanilla D, Johannessen M, Hajipour AR, Cozzi NV, Jackson MB, Ruoho AE. The hallucinogen N,N-dimethyltryptamine (DMT) is an endogenous sigma-1 receptor regulator. Science. 2009;323:934–937.  [DOI]
  (reference 24 in the article that you cite)

I would not bother If i haven't been looking for it for 5 days trying solve it, but: Could you please have a glance at my question: http://biology.stackexchange.com/questions/14731/pharmacodynamics-of-ethinyl-estradiol-drospirenone-and-interactions-with-istot


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What Freshwater Fish Are Affected By Magnetic Fields
I am interested in knowing which freshwater fish are affected by magnetic fields.  I've heard that Lake Sturgeon are, but would like more references. This is for a project that will have buried 3 phase power cables.

Sockeye salmon species definitely do, although admittedly the interesting salmon are those that spend significant time in the ocean.
Here's some evidence that carp can.
Raindbow trout are also capable.
Zebrafish are also able.
Japanese eels too, of which some are freshwater.

source: Stack Exchange

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

sort: votes


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Non-fatal / low-harm measurement of Drosophila traits
I am trying to generate some candidate traits to measure in a fitness assay of wildtype outbred (lab population) flies. The key trait I will measure is lifespan.
I am looking for some additional traits which can be measured from the same flies as those in the lifespan assay without harming or killing the fly in the process. For example, I could measure wings using a technique devised by the Houle Lab called WingMachine. I think I could also do some other measures with the same equipment, leg length etc.
The traits should also be present in both sexes (can be monomorphic or dimorphic) and quick to measure; I'm aiming for 200-250 measures/collections/images a day. Traits that can be measured properly in a fly which has died of old age would also work. Traits can be morphological, behavioral etc..
What other traits can be done like this?

You could do negative geotaxis (climbing) assay, (larval or adult) locomotion assays, % brain vacuolisation (after the flies die), maze tests. There are probably much more but these are all I can think of that are no-lethal and can be applied to males and females and some larval work too.
You could maybe consider doing starvation assays and longevity in some of your populations.

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


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Which is harder to contract - HIV or AIDS?
I am working on mathematically modeling HIV and Tuberculosis Co-infection dynamics, and am working with 12 differential equations describing the behavior of all of the compartments and parameters.
Anyway, I just have one question:
Which is harder, in general: For a susceptible person to contract HIV, or a HIV+ person to contract AIDS?
Please pardon my ignorance.
Thanks.

infection rate constant is much higher than disease progression constant. The rates will depend on how many infected individuals are present and how much are they interacting..

This is rather broad...

Your question depends hugely on the factors at play.

The rate of transmission depends on the route of infection.  Wikipedia has a good breakdown showing the wide variability.  Are they getting a blood transfusion?  90%.  Mother-to-infant?  25%.  Male-to-female vaginal sex?  No higher than 0.3%.  Not to mention that the incidence varies massively between countries, as does the most common route of infection.
The rate of progression to AIDS also depends on a large number of factors including age, viral load, various genotypes, access to medical treatment, and, of course, long-term nonprogressor (LTNP) status.

The incidence of LTNPs is around 1 in 500, or 0.2%, which overlaps with but is at the low end of transmission rates for some routes of infection.


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Is it true that there is a spider that eats parasites from caterpillars
I think I once saw a video of a caterpillar that could get infected by a parasite, and could die of that, unless a specific kind of spider would eat the parasite, and so once the caterpillar is infected it goes looking for that spider. I can't find that video anymore though, nor any reference on this, so I'm beginning to doubt myself. Does this behaviour really exist?

Oddly enough it is a bit difficult to find good field studies where the diet of spiders was studied.  I have a feeling it's a hard thing to get funding for.  Luckily some do exist.
Peucetia viridans has been shown to eat from the Chrysididae family and Lepidoptera order, but I didn't find an explicit statement that it ate the larvae out of the caterpillar.  Likewise Oxyopes globifer was found to have eaten from the Braconidae family and Lepidotera.
At this point you might be wondering why I'm looking for spiders that have been shown to eat both parasitoids (Chrysididae and Braconidae) and caterpillars (Lepidotera).  It my assumption that in the scenario you describe a spider that would normal eat ether the caterpillar or the larvae would be just as happy to eat them both if it was lucky enough to find them.
I could find one example where it seems wolf spiders under the right conditions might seek out larvae, and I found a fun photo of a wolf spider eating larvae (though not the kind in the study).
I never saw the video you were talking about, and I too could not find it.  It is not unreasonable to assume that an opportunistic spider wouldn't just take the opportunity to feed on both, or that it might find the larvae more tasty and just eat them.  I've not found a spider seeking caterpillar as of yet.

That's no fun photo! Thanks for the search. Actually the way I remember it it was actually even more crazy than the spider looking for the caterpillar; it was the caterpillar looking for the spider. It was a rather small spider, couldn't eat the caterpillar, but the larvae was a good meal.

@JasperKennis Again I would be very interested if someone could pull that up. Under the right pressure I could imagine such behavior evolving, but I am unaware and couldn't find an instance where it is true.  It might be worth noting that plenty of insects/spiders eat pray that are larger than they are.


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What is the physiological difference between snorting/swallowing cocaine
I know that mucosa inside the nose absorbs cocaine molecules when snorting cocaine, but what difference is there compared to swallowing?
Also more cocaine administration equals more cocaine molecules in the brain equals more inhibition of repute equals more serotonin–norepinephrine–dopamine in the synaptic clefts equals more work for receptors equals more intense effect, right?  What about the duration of a particular molecule which inhibits reuptake? How long this particular molecule stands there?

You can easily google for this question and find plenty of disreputable sources, but this is another case where Wikipedia does an okay job.  There are some misleading and erroneous sentences, but this one basically sums it up:

Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects.

Mainly, take a look at this 1981 article.  The researchers gave participants cocaine, measured drug activity, and did then did a great review of the literature.  They found that, like plenty of other drugs, ingesting cocaine results in a slower but longer-lasting effect.
Your stomach is not an efficient route of absorption for things besides water, alcohol, and aspirin; besides, it's highly acidic.


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How much natural genetic variation is there between bacteria of the same species?
There are lots of questions about how and why there is genetic variation between organisms of the same species, but I haven't been able to find a numerical value for the expected amount of genetic variation.
Let's say we have two different samples of MRSA252. We sequence these samples and get the full genomes of ~3 million base pairs each. What percentage of these bases would we expect to be different (assuming there is no sequencing error)? I figure it will be about 1%, but I haven't been able to find a source.
I'm sure the answer will depend on the specific species, but I'm looking for a ballpark figure for bacteria. An academic source would be much appreciated.

I'm sure the answer will depend on the specific species, but I'm looking for a ballpark figure for bacteria.

Yes indeed it will.  Bacteria are a huge domain of life; you might as well ask for variability between all plants or between all animals.  Bacteria can live in very different environments, and the whole things is made more complex by widespread horizontal transfer.
Still, for bacteria, you can't do much better than E. coli, and boy are they a mess.  Here's a paper from 2010 that blew my mind.  The authors sequenced 61 E. coli genomes and found:

...that any given E. coli genome sequenced will have only roughly 20% of its genes part of the E. coli core, and the remaining 80% are not found in all other E. coli genomes.

20% variability within a species.  20%, one species.  E.coli is an extreme example, but still, species is a stupid concept.  Here's a 2006 paper finding that plenty of unique Campylobacter proteins simply aren't in plenty of Campylobacter species.
On a more broad scale, here's an excellent (and free) paper you should look at.  It examines islands of "microdiversity" among various species, finding that some species are easily 50%-75% different.  A simple way to estimate this is too look at gene number for bacterial species, which should make it clear that some of these bugs vary by up to an order of magnitude.
In short: A lot.

There is a database of Multi Locus Sequence Typing (MLST) data for E. coli at http://mlst.ucc.ie/mlst/
These data are limited to sequences at seven genes: adk, fumC, gyrB, icd, mdh, purA and recA. Furthermore for each of these genes only part of the sequence (in the range 452-536 bp) is characterised.
Each strain tabulated is represented by a genotype consisting of the alleles present at each of these loci. There are many different alleles found for each locus ranging from 240 variants at recA to 431 variants at fumC.
I ran a pairwise comparison (87398 comparisons -nowhere near the maximum possible, but I didn't have time to let my script run all pairwise combinations) and found that the average total divergence at these loci was 1.3%
Although this is a very different perspective from the one described by @Amory, I think it is nicely complementary, and it reveals that even at genes shared by all strains of E.coli there is a degree of sequence divergence that is quite close to your guess of 1%.

Thanks for the resource and info, this was really helpful. I accepted the other answer because there are links to a few papers.


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How was the heritability of IQ tested?
I have read that IQ is highly heritable.
How could this be tested?
For honest testing, it seems to me that only children who were abandoned should have been tested, to exclude education effect. Was it really done?
UPDATE
Intelligence is one of the traits, that can be inherited both by genes and by education. You can't educate your children to have blue eyes, but you can educate them to count or to read.
So, to study heritability of intelligence, educational inheritance should be excluded.
I know that usual way to study heritability is to compare variability for monozygotic and dizigotic twins. Being sufficient for other traits, this method is highly insufficient for intelligence (which is obvious). Having identical perception system, monozygotic twins will respond identically to an education, so they will be more closely educated, even if IQ is completely independent of genes.
So, to study IQ heritability, subjects should be studied under different education conditions. I.e. they should be abandoned by parents and/or adopted separately.
My question is: was this done or not?
If not, then the question is, how education effects were eliminated?
Also I would like to know, if my reasoning about why just studying twins is insufficient is wrong.

I don't really know what you mean by "abandoned children".  Adopted children?  Children in the wild?  Have you read the Wikipedia article on the subject?  If you want to know how it was studied, just take a look at the references, it's pretty straightforward.
Heritability simply means how much variation in a trait is due to genetics, which is usually easiest to test in monozygotic twins.  Here's a good example where they did just that - they compared identical (monozygotic) and fraternal (dizygotic) twins raised apart or separately, finding:

General cognitive ability yielded a heritability estimate of about .80 in two assessments 3 years apart as part of the Swedish Adoption/Twin Study of Aging. This is one of the highest heritabilities reported for a behavioral trait. Across the two ages, average heritabilities are about .60 for verbal tests, .50 for spatial and speed-of-processing tests, and .40 for memory tests. For general cognitive ability, the phenotypic stability across the 3 years is .92 and stable genetic factors account for nearly 90% this stability.

Here's another example doing basically the same thing.  The rest of the enWiki article gives a good breakdown of all the various factors involved in making this such a complex issue, as well as what was studied.

My question is how verbal (educational) inheritance was excluded. Your answer is it wasn't at all? Comparing monozygotic and dizigotic twins does not help to exclude education. Monozygotic twins can show lower variation just because they respond to education similarly.

P.S. Explanation about what is child abandonment http://en.wikipedia.org/wiki/Child_abandonment

I know what child abandonment is but I don't see how it's useful to your question.  By studying children raised in the same environment, you remove the educational/verbal barrier.  As stated above, they looked at twins raised together (same education) and twins raised  separately (different education).

A classic study of IQ heritability is Skodak & Skeels (1949). They studied heritability of IQ in children who were adopted at a very young age, with IQ data of the children, of their biological mothers, and of their adoptive mothers. It is important to keep in mind that heritability is a measure of the proportion of variance that is attributable to genetic inheritance in the population; it is formally the ratio between genetic variance in a population to the phenotypic variance in a population. The above mentioned study found a high heritability between biological mothers and their children (0.88), but no heritability between adoptive mothers and their children. Yet the mean IQ of children were similar to adoptive mothers, and much higher than their biological mothers.
This is not a contradiction. High heritability does not mean that environmental factors are not important. Indeed, environmental factors (such as upbringing, education, socioeconomic status) may have a large effect on mean values, hence why the children had IQs similar to their adoptive mothers. However, heritability explains variance not mean; in the above study, there is a high correlation between where children fell on the normal distribution of IQ scores among the children and where their biological mothers fell on the distribution of biological mothers, but no correlation with where their adoptive mothers fell on the distribution of adoptive mothers.


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What is the origin of viruses? How could they get both living and non-living characteristics?
I read that viruses are called intermediate between living and non-living particles. Well, if so, then where did they originate from?  From living or non-living? If they originated from either living or non-living then how could they have both the characteristics of living and non-living?

Here is a somehow similar post that might interest you. But it does not answer the interesting question of their origin.


text:
issues with MultiPipMaker
I would like to use MultiPipMaker for testing a genome alignment between two sequences, each sequence is in .fasta format, but the problem is that when I submit the couples of file that I need, the web browser sends an email that the blastz has timed out. Does anybody know why is the that?
The address of the program is:
http://pipmaker.bx.psu.edu/cgi-bin/multipipmaker
thanks

How big are the sequences that you are submitting?

they are 4 Mb each one approximately


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What is the relationship between sexual and natural selection?
In Evolutionary ecology: Novelty makes the heart grow fonder, they say:

Thus, it seems that the diverse coloration in this species is promoted by both natural and sexual selection.

I had always thought of sexual selection as a subset of natural selection. What's the right way to think about the relationship between the two?

sexual selection is a set of special cases within natural selection.  clearly any living thing which does not have gender will not undergo sexual selection.

You're not wrong, per se, but in practice they refer to two different concepts.  I honestly think the Wikipedia article does a good job, in particular this sentence:

In summary, while natural selection results from the struggle to survive, sexual selection emerges from the struggle to reproduce.

It also cites Darwin:

The sexual struggle is of two kinds; in the one it is between individuals of the same sex, generally the males, in order to drive away or kill their rivals, the females remaining passive; whilst in the other, the struggle is likewise between the individuals of the same sex, in order to excite or charm those of the opposite sex, generally the females, which no longer remain passive, but select the more agreeable partners.

The whole argument is moot when dealing with individuals that aren't reproducing sexually, of course.

I just thought of even another way to see it... Doesn't all selection end up coming down to sexual selection? i.e. If you get killed by a bear, you're not going to be reproducing sexually. In other words, the struggle to survive is only a means to an end, which is reproduction. I guess I'm wondering what the benefit is to science in distinguishing between natural and sexual selection.

@Sancho It's a different mechanism, so why shouldn't there be different terms?  The two are certainly not always the same: a good example alluded to below is when a trait, such as a long tail, is attractive to a mate but is a negative fitness attribute.  Besides, having more terms allows us to be more precise.  It'd be no fun saying every scientific field was really just physics or applied math.

I don't agree, SS and NS are not different, separated mechanisms. They were considered as different concept by Darwin (and it is indeed your reference) but our understanding of these processes have changed and although different definitions still exist, SS is considered as a subset of NS.

To Darwin's point of view, sexual and natural selection are two different mechanisms. Then, we tended to consider that sexual selection is part of natural selection. The part of natural selection that is not attributed to sexual selection is sometimes called ecological selection. Today, our understanding of these mechanisms brought us to consider the meaning of these words slightly differently.
Natural selection is not anymore the result of a struggle for survival. It is any process yielding to a change in allele frequency through a long-enough term difference in fitness. Fitness is a index of how much an individual, a gene or whatever, leave copies of itself after a long and short enough amount of time (one might not agree with this definition I guess). Take two strains of bacteria in two petri dish, consider they are one population and let the bacteria grow. One strain will grow faster and the allele frequency will vary over time. It is the result of natural selection although there were no competition, no struggle at all given that they were not in contact.
Sexual selection is a type of natural selection that involves sexual competition. There are two types of sexual competition, the so-called inter- and intra-sexual competition. Inter-sexual competition means that one sex chose the other one, while for intra-sexual there is no choice from the other sex. For example, if you see two animals fighting, they either fight to have the physical acces to the other sex (intra-) or they fight and then, let the female decide which one is the best to mate with (inter-). These two concept of intra- and inter-sexual competition might somehow overlap in some specific case. I would argue that the concept of sexual competition and therefore of sexual selection have never been accurately defined. Therefore, I would not complain if one prefers to give up the concept of sexual selection to use only the concept of natural selection.
Many articles state that sexual and natural selection act on a trait with the same or opposite directions. Given the above argumentations, you could as well say that there are two different forces of natural selection. if the trait is at state 'A', then the individual is very attractive to the other sex but is likely to not be able to escape a predator. This is the case of most of the trait we think of when talking about trait evolving through sexual selection. See Zahavi's handicap principle for more information.

I have not posted or read much on this forum before but thought I would throw in my two cents.  Perhaps a more accurate and comprehensive term is "reproductive selection".  This would include "sexual selection (eg qualities making an individual more attractive to the opposite sex) and "survival selection" - to the extent that survival allows one to produce more offspring.  (Dead organisms don't tend to reproduce).  Reproductive selection would correctly exclude fitness traits promoting post-reproductive survival that did not contribute to the reproductive success of progeny, eg a longer lifespan spent away from mates or offspring.  Reproductive selection would apply to a range of replicative mechanisms,  spanning sexual, asexual, mitotic and even possible early-stage RNA-strand replication.  It would also include both natural and artificial selection.  Finally, it has the advantage of being a more intuitive term that IMHO gets more at the core principle driving this aspect of evolution (as opposed to genetic drift, etc).  Not sure if this term is in common usage.  As a clinical physician I am not very familiar with the literature on evolution.

According to a theory proposed by Amotz Zahavi (formulator of the so called Handicap Principle), and others, sexual selection can be seen as a subtype of signal selection, which in it's turn is a subtype of natural selection.
The well known example of a signal that is selected for is the tail of the peacock, which signals the high quality of it's owner.  The interesting thing is that to maximise fitness it would be better for the peacock to have a smaller and less colorfull tail.  Signal selection and efficiency selection (for want of a better word) hence often work in opposite directions!
Some quotes from the abstract of the article "The Logic of Analog Signaling and the Theory of Signal Selection" by Amotz Zahavi & Avishag Zahavi:

... evolution by natural selection is a consequence of two selection mechanisms: the selection for efficiency on the one hand, and signal selection that reduces efficiency in order to provide reliability on the other hand.

The fundamental difference between signal selection and efficiency selection is that

when the investment required for signalling is reduced to the extent that everyone can signal alike, the trait loses its value as a signal. This loss of value is unique to biological analog signals

For example, lace used to be a signal of wealth, but it's effect as a signal diminished once lace machines took over manual production.
The exciting thing about this approach is that it could explain the evolution of features that would be hard to explain by efficiency selection only:

We further suggest that the interaction between the selection of signals and the selection of other traits enabled the evolution of new traits that require the accumulation of many mutations that reduce efficiency before they can start contributing to new efficient adaptations e.g. antlers and feathers.


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Dimethyltryptamine binding site on Sigma 1 type opioid receptor?
I asked this question Dimethyltryptamine and Sigma 1-type opioid receptor interaction but it seems that I didn't express myself well. I was looking for the place on Sigma 1 type opioid receptor where dimethyltryptamine binds rather than the location of Sigma 1 type opioid receptor.

There is no definitive answer to this question since the 3D structure of the receptor has not been determined. In this paper;

Laurini et al. (2012) Another Brick in the Wall. Validation of the σ1 Receptor 3D Model by Computer-Assisted Design, Synthesis, and Activity of New σ1 Ligands. Molecular Pharmaceutics 9:3107-3126

the authors report the analysis of their molecular model of the receptor. They design 33 new ligands for the putative binding site with binding affinities across five orders of magnitude and then go on to show that the experimentally-determined affinities are in very good agreement with their in silico studies. The paper provides lots of information about the proposed binding site. The paper also describes the use of in silico alanine scanning mutagenesis to assess the relative importance of residues proposed to form the binding site: these are D126,I128,T151,V152,E172,Y173 and L182. Of these D126 and Y173 seem to be critical.
I must stress that this work does not directly investgate the binding of dimethyltryptamine, and the ligands that are used are not based on an indole ring structure. The molecular model used by the authors was first published in an earlier paper.

Laurini et al. (2011) Homology Model and Docking-Based Virtual Screening for Ligands of the sigma(1) Receptor ACS Medicinal Chemistry Letters 2:834-839

I tried to find out if that paper looks at dimethyltryptamine but unfortunately there seems to be a broken link at the source. Here is the abstract of that paper:

This study presents for the first time the 3D model of the sigma(1) receptor protein as obtained from homology modeling techniques, shows the applicability of this structure to docking-based virtual screening, defines a computational strategy to optimize the results based on a combination of 3D pharmacophore-based docking and MM/PBSA free energy of binding scoring, and provides evidence that these in silico models and recipes are powerful tools on which virtual screening of new sigma(1) ligands can be based. In particular, the validation of the applicability of docking-based virtual screening to homology models is of utmost importance, since no crystal structure is available to date for the sigma(1) receptor, and this missing information still constitutes a major hurdle for a rational ligand design for this important protein target.


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What does fitness really mean?
Fitness is certainly the most important concept in the theory of evolution. My question does not have to do with practical measures of fitness but with the theoretical definition of it.
I am a bit lost with the concept of fitness. Below I give some possible definitions of fitness and I am hoping to get critics for these definitions. The broad question is What is the definition of fitness?
In the following, to make things easier I will consider only one bi-allelic locus. For simplicity, I will assume a panmictic population of infinite size evenly distributed into age classes.
1) Let the variable $M$ be the mean time of a generation in the species of interest. Measure the allele frequency $p(t)$ and measure the frequency $p(t+M)$. By comparing the two you get the ratio of fitness of the two different genotypes. Obviously it does not work if we have sexual reproduction or diploid selection.
2) Genotype the individuals and wait until they die by counting the number of offspring they had and take the mean per genotype ($W_{AA}$, $W_{Aa}$, $W_{aa}$). This method would not work if they have different lifespan. One individual might make two babies in 8 years and the other would make two babies in 2 years but they would have he same fitness.
3) Do the same that at 2) but don't wait until they die, wait 1 month, Or 2 years?, or $M$?, or $2\cdot M$?, or...? What is the right decision? The more you wait, the closest you will be to the long term effect of natural selection. The less you wait, the more probable you will suffer of genetic drift.
4) Fitness is just a measure of natural selection that is not perfectly accurate because it is measured at short-term. In some circumstances, our measure on this short term is representative (Wright-Fisher equation) enough of what will happen on the long term.

What's wrong with "ability to survive and reproduce?"

Over what time amount of time should one measure this ability? One generation? His measure would suffer from drift! And not everybody has the same generation time. Over 10 years? It does not give the same result if you make this measure over 5 years. It seems rather arbitrary the time one should consider, isn't it?

fitness has no definition if the selection criteria are not specified. Having specified it, the fitness is a measure of reproductive potential.

@WYSIWYG Could you develop your comment?

@Remi.b.. I meant that something is said to be fit for some condition. Therefore fitness is conditional. There is nothing like absolutely fit. Unless you know what the selection pressure is you cannot measure fitness.

"As I said I don't want to talk practical issues but theoretical ones, therefore we will assume to work on a panmictic population of inifinite size evenly distributed into class age." infinite versus finite population is not a practical concern, but a very important theoretical distinction in particular if you have stochastic events.

I don't understand your four points & I feel they should be fleshed out for clarification if you're still interested in the question (I see you asked it three years ago). You might have already come across this, but in The Extended Phenotype, Dawkins' wrote a passage about the various meanings of the term "fitness."

I must have 50 reputation to comment.

Fair enough.  Seems you should be a moderator (if you want).  You're carrying the site.

I appreciate it.

I don't see how #1 wouldn't work, given sexual reproduction.

The concept of fitness is very general. An adequate definition of fitness is hard to specify in the same way that a definition of "species" is hard to give. To be useful, scientific or technical definition of such broad concepets will often need to be so narrow that more than one is needed. A uselessly broad definition of fitness might be:
"Fitness is modeled as a utility function, where higher fitness is indicated by a higher score"
Here every important detail about whatever's fitness is being tested, how that fitness is measured, and the environment in which that fitness is determined are simply wadded up together and transformed into a different question that is no easier to answer.
The hypothetical problems you raise with various definitions are not (in essence) problems with the definitions, but problems with the definitions not being applicable to the domain in which such problems matter. You have to define your criteria for success, and then these constraints can be translated into a "fitness" function that allows the desired predictions.
Some issues that might matter are:

Are predictions about populations, or individuals.
Are predictions about dynamic fitness (snapshot at some time) or long-run steady state fitness.
Are predictions about quantitative values (like heights) or discrete values (like sex).
How do you want to present error in your predictions - p value, sensitivity/specificity, confidence interval, etc.

I'm sure this is not the kind of answer you were looking for, but I think part of your question revolves around a confusion that there is "one" technical definition for fitness. Part of the process of learning is comparing different presentations of the same concept, and realizing where they are different. A full walk over all the different ways one could evaluate and apply fitness would be a book, not a short answer. Perhaps some other people can provide good links to more detailed information.
I just found a blog posting, by Dr. John S. Wilkins, which says some of the same things. His perspective comes with a good pedigree; his PhD work was on trying to define "species" and he has authored a couple of books on the subject.

This answer will also give some hints about the various definitions of fitness

As I see it, your question is also encompassing an inquiry for a theory of fitness.
In recent years the inclusive fitness theory has seen its share of interest, which can be applied to social entities.
Freely citing from wikipedia here:

An organism is judged by the number of offspring it has, how they support them, and how their offspring could support others

As for the mathematics and informatics this paper

JY Wakanoa et al. "A mathematical description of the inclusive fitness
  theory", Theoretical Population Biology, Vol84. March 2013. pg 46–55

explains:

Recent developments in the inclusive fitness theory have revealed that
  the direction of evolution can be analytically predicted in a wider
  class of models than previously thought, such as those models dealing
  with network structure. ...

It takes a Markov chain approach.


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Radial Basis Function Network (RBF Network)
In the Wikipedia article on radial basis function network, I didn't understand what was meant by "center vector for neuron i", in other words "center of the RBF units called also prototype".

In RBF networks each neuron in the hidden layer applies a computation that is related to its "center vector".
First consider the set of input neurons as a vector $\mathbf{x}$, and that each hidden layer neuron receives the complete input vector as its own input.
Second, each hidden layer neuron $i$ is parametrised through a vector (center vector) $\mathbf{c_i}$ of equal dimension than $\mathbf{x}$.
The computation of each hidden layer neuron $i$ consists of:

Evaluate the distance (according to a metric, which may or may not be Euclidean) between the input $\mathbf{x}$ and the center vector $\mathbf{c_i}$. When the input is equal to the center vector, the output for that neuron will be maximal (see 2).
Evaluate a Gaussian function that decays with increasing distance between the vectors. That's the output of each hidden layer neuron. In the following equation, $\beta$ is a parameter that specifies the decay rate of the Gaussian (converse to the standard deviation in a regular Gaussian distribution).

\begin{equation}
\rho_i(\mathbf{x})=\exp{[-\beta\Vert\mathbf{x}-\mathbf{c_i}\Vert^2]}
\end{equation}
Now combine linearly the output of all hidden layer neurons to obtain the total neural network output. For that, you need an additional set of parameters or weights $a_i$ (one $a_i$ for each hidden layer neuron, but the $a_i$ values are scalars while each $\mathbf{c_i}$ is a vector).
The final equation, that yields the total network output (a scalar value), is:
\begin{equation}
\varphi(\mathbf{x}) = \sum_{i=1}^N a_i \rho(||\mathbf{x}-\mathbf{c}_i||)
\end{equation}
And that's it.

I have all the honor if you can response me to the question "ventral stream architecture" asked now in this site :):)


text:
Transitivity of Species Definitions
There are many definitions of "species" which usually take the form

Two individuals are of the same species if ...

An implied (rarely made explicit) property of any sensible species definition is that the relation "is the same species as" should be an equivalence relation (the reason why this is sensible is that only such a relation partitions the set of all individuals into equivalence classes, that is, separate species). In particular, it should be transitive, that is

If A and B are of the same species, and B and C are of the same
species, then it follows that A and C are also of the same species.

It appears to me that all species definitions in use violate that property.

Example
Are the Chihuahua  and the Great Dane  of the same species?
Not according to the "biological" species definition, which states:

Two individuals are of the same species if and only if they can produce fertile offspring.

Since that is (presumably) not true of Chihuahua and Great Dane, according to that definition, the two dog breeds are not of the same species.
However...
Let us say that the Chihuahua can produce fertile offspring with the Dachshund...

... and the Dachshund with the Golden Retriever...

... and that at last with the Great Dane as desired.
Then, if we assume transitivity, Chihuahua and Great Dane are of the same species - contradiction!

Another Example
Are the Chimpanzee  and the White Oak  of the same species?
Intuitively, they are of course not, the very idea seems ridiculous. Sure enough, with the definition (a variation of the "genetic" species definition)

Two individuals are of the same species if and only if their genome differs in less than 0.5% of base pairs.

the two are indeed not of the same species.
However, we can again construct a "chain" of intermediate individuals, each of which is similar enough to its predecessor to satisfy the definition, eventually connecting Ape and Tree and violating transitivity again.

My question to biologists: How is this problem resolved in practice? Are there any species definitions that preserve transitivity?

Does the criterion "produce viable offspring" include physical reasons? I'm assuming that the Chihuahua and the Great Dane could produce viable offspring by artificial insemination. Since species is a genetic term this is what matters. Otherwise you might say that a Great Dane in the USA and a Great Dane in Europe are different species because they cannot mate (due to physical separation).

@AlanBoyd: Interesting question, I don't know the answer. It is, however, irrelevant to the presented problem of transitivity, which would still apply when more remotely related individuals are chosen (and also applies to other species definitions, such as genetic similarity).

Added another example using a different commonly used type of species definition.

I'm not convinced that you could form a chain of connectivity between a plant and a mammal using the criterion of 0.5% sequence divergence. In fact if you started with a human you would fail at the first hurdle (approximately 1% difference from human to chimp at the most conservative estimate).

I think there could be a viable question in here, but you've started with some false equivalencies.  The answer to your questions is clearly "yes" as it's been shown that both statements you took to be false are indeed true.

don't confuse the schoolbook definition with the scientific definition.

I am pretty sure you cannot jump from an oak tree to an ape with whatever common definition of species you're using. But this is some kind of practical implication of your question.
The concept of species was already being used by Aristotle and was kept up to now although the grouping of living things into species might not be a clever thing to do. I don't think there is any non-arbitrary, logical way of making groups out of living organisms. Here is a podcast (It is in French, sorry!) that is interesting for those wanting to learn about how the concept of species evolved.
The case you describe is called Ring species. There has been lots of discussion in philosophy about the concept of species. The concept of species is unclear and if accurately defined, then in practice we don't really follow this definition to improve efficiency in how we name lineages. The term lineage has a much more rigorous meaning and is often of greater usefulness.
Ensatina eschscholtzii (a salamander; see DeVitt et al. 2011 and other articles from the same group) is a classic example of ring species.
You should definitely have a look at the post How could humans have interbred with Neanderthals if we're a different species? which discuss the concept of species. Some other sources of info include:

Species problem wikipedia
Reduction of species
The evolutionist view of the species concept: ESU
Stanford dictionary

"Species" is a human rule-of-thumb, often useful but having indefinite boundaries and not a thing that actually exists. See this short section of the Wikipedia article mentioned above for a good summary.

Membership of nominal species is certainly an equivalence relation. For instance, membership of Canis familiaris, or domestic dog. Dogs are not wolves, and wolves are not dogs. But all domestic dogs are the same species. But of course, some taxonomists recognize the dog as a subspecies of the wolf, as in Canis lupus familiaris. In that case, dogs and wolves are members of the same species. So it just depends on whose definition you are using.
Reproductive compatibility is not an equivalence relation, as you correctly note with respect to Great Danes and Chihuahas. It is not always transitive.

dogs are actually a subspecies of wolf in most usages.

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

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


text:
Does endo- and (or) exocytosis require energy? Do they belong to active / passive transport?
I expect vesicle formation and fusion to require energy input; however, I'm not sure about which of endocytosis and exocytosis require energy and how they use the energy input.
Do they belong to active or passive transport?

Wikipedia is your friend:

Exocytosis... is the durable, energy-consuming process by which a cell directs the contents of secretory vesicles out of the cell membrane and into the extracellular space.

and

Endocytosis is an energy-using process by which cells absorb molecules (such as proteins) by engulfing them.

Emphasis mine.  Here's a nifty paper which gave some evidence a few decades ago for some basic intracellular thresholds for budding and fusion, and this paper shows that endocytosis definitely requires ATP, using a novel assay.  Check the sources, too, some of them are excellent.

What on earth does 'durable' mean in the context of that first quote?

@AlanBoyd Durable=long lasting, survives wear-and-tear.  I interpret it to mean that exocytosis doesn't just pop in and out of existence, quantum mechanics style, it's "intentional" and can last.  That's my guess anyway, it's a weird word choice to be sure.

Just to extend the answer from @Amory slightly, I think that the terms active and passive transport are best kept for describing transmembrane movement of molecules.
In the case of exocytosis the only transmembrane event is when a secreted protein is first inserted (usually cotranslationally) across the endoplasmic reticulum membrane. I'm not aware of any evidence that this uses more energy than that already expended during polpeptide elongation by the ribosome. At that point the secreted protein is topologically extracytoplasmic, and everything else is achieved by rounds of vesicle formation and fusion of vesicles with target membranes.
The same is true in reverse for endocytosis. Any molecule that is internalised in an endocytic vesicle is still extracytoplasmic unless some process specifically moves it across the membrane of the vesicle, or a downstream organelle such as the endosome. At that point whether the transport process was active or passive would depend upon the properties of the carrier system.


text:
What does it mean for a distribution to be "consistent with a two rate-limiting stochastic steps"?
I'm reading a study (full text here) that examine the dynamic of nuclear translocation of a transcription factor in budding yeast, in response of calcium stress. They found that it occurs in bursts, which distribution of durations is plotted on this normalized histogram:

In the text they say:

Normalized histograms, $h(t)$, of total burst duration at two calcium concentrations are both well-fit by $h(t)=te^{-t/\tau}$, with $\tau$ = 70 sec (black line).

And also

This distribution was consistent with two rate-limiting stochastic steps, each with a timescale of ~70 sec.

Can someone explain me the second sentence cited?

WYSIWYG is almost there, but you need one more piece of information to make this explicit.
The distribution cited in the paper is $h(t)\propto te^{-t/\tau}$ (we're going to ignore normalizing constants today). We can recognize this as a particular case of the Gamma distribution, with PDF:
$$f_{\mathrm{Gamma}}(t\,\big|\,k,\theta)\propto t^{k-1}e^{-t/\theta}.$$
In particular, $h(t)$ looks like the PDF of a $\mathrm{Gamma}(2,\tau)$ random variable,
$$h(t)\propto f_{\mathrm{Gamma}}(t\,\big|\,2,\tau)\propto te^{-t/\tau}.$$
So the authors of the paper are claiming that the burst duration $\tau_{\mathrm{burst}}$ is a random variable with a $\mathrm{Gamma}(2,70\,\mathrm{ sec})$ distribution.
How do we get from that to "This distribution was consistent with two rate-limiting stochastic steps?"
If we recall from our stats class (or look up properties of the Gamma distribution on Wikipedia), a Gamma distribution with integer values of $k$ is the distribution of the waiting time for $k$ events to occur in a Poisson process. The setup of a Poisson process is that you are tracking the occurrence of unlikely/infrequent events in time, so the fact that the distribution $h(t)$ of burst times looks like a $\mathrm{Gamma}(2,\tau)$ suggests that the burst duration $\tau_{\mathrm{burst}}$ is determined by the occurrence of 2 stochastic events (with the same "frequency" $1/\tau$). In other words, this distribution is consistent with the following scenario: a nuclear localization occurs, and then will stop after two particular events, where the timing of the events is governed by a Poisson process (which, as WYSIWYG pointed out, is a reasonable model for the occurrence of chemical reactions with reasonably slow kinetics, i.e. you can count individual reactions in time). If this is true, the distribution of $\tau_{\mathrm{burst}}$ will look like $te^{-t/\tau}$.
The authors generalize that statement somewhat by saying that technically there could be more events/reactions required to terminate a localization burst, but all but 2 of those reactions happen extremely rapidly, i.e. there are 2 rate-limiting steps in the decision process (both of which happen to have the same value for $\tau$).

Edit: I realized that one more mathematical point might make this more clear: The statement about the Gamma distribution and Poisson processes above is equivalent to the statement that the sum of $k$ iid random variables with distribution $\mathrm{Exponential}(\tau)$ is a random variable with a $\mathrm{Gamma}(k,\tau)$ distribution. Thus $h(t)$ is literally (up to normalization) the distribution of a sum of 2 independent exponential random variables. If you read up on the connection between the exponential distribution and waiting times that might make the claim in the paper seem more transparent.
Source: https://en.wikipedia.org/wiki/Gamma_distribution#Special_cases
http://en.wikipedia.org/wiki/Exponential_distribution

A very thorough answer, now is truly clear. Thank you!

Do you have any speculations about the identity of the two rate determining steps? Is it plausible that one of them is the binding of the molecule at the DNA (it's a transcription factor) and the other is the translocation process itself?

The article mentions that Crz1 nuclear localization is controlled by phosphorylation and dephosphorylation. If I had to speculate I'd hazard that at least one of the steps is based on phosphorylation (see well-studied examples like the Pho2/Pho4 system in yeast). But I would caution against reading too much into this statement in the paper; without more rigorous tests of the properties of the empirical distribution, it's quite possible that this distribution that fits well "by eye" is not at all related to the process generating the empirical distribution.

The rate limiting step of a reaction is the slowest component of the reaction. So if there are two steps in a reaction, each of these steps will have a rate, and the slowest of those two rates will determine the overall rate of the whole reaction.
As a simple example, consider the equation
$A + B + C\rightarrow AB+C\rightarrow ABC$
If the rate of $A+B \rightarrow AB$ is fast, but the rate of $AB+C \rightarrow ABC$ is slow, then the overall reaction will still be slow.
The figure in your question is showing the distribution of the burst durations, and highlighting the fact that the calcium level has no effect on the burst duration. The second quote is a bit confusing, this is my interpretation:
The functional form which they fitted to the distribution indicates that the expected burst duration is about 70 seconds. I'm not completely sure which stochastic steps they are referring to, maybe translation and subsequent localisation (I think transcription would happen on a different timescale and so could be ignored in this case).
By the way, this paper is a really excellent example of an organism harnessing stochasticity to its advantage in order to synchronise its response to a stimulus (calcium in this case). I just think that it is so cool that the mean response to the signal level can be different to the response to the mean signal level - so counter-intuitive to me. And so much fun!!

Well.. First assume the chemical reactions to be a Poisson's process (which is a right stochastic approximation for processes such as chemical reactions and radioactive decay etc).
While the event of a burst follows a Poisson's distribution, the time interval between two reaction events follows an exponential distribution. (See wikipedia page on Poisson's distribution for details)
Since the both two mentioned steps have approximately equal time scale of ~70 sec we can expect that the mean delay between two reaction events to be equal to 70 sec.
The exponential distribution with a mean τ is:
p(t)=e^(-t/τ)


text:
How does smoking, an environmental factor, cause cancer, fundamentally a genetic disease?
If cancer is fundamentally a genetic disease, how might an environmental factor such as smoking cause cancer?

Cancer is fundamentally a disease of genetics(it involves genes and genetic damage), but it's not a genetic disease in the way you might be thinking (strictly heritable). You cannot inherit cancer the way you inherit Huntington's. You can inherit an increased risk of cancer, though. Once you are born your genes are not fixed in stone forever. They can be changed with carcinogens or other processes.

Because cigarette smoke contains many carcinogens.  Carcinogens can cause cancer by directly affecting the genome.  Wikipedia has a list of those present in cigarette smoke, which includes classics such as lead, benzene, and formaldehyde, not to mention radioactive polonium.

There are carcinogens in smoke but they've not been shown to be the cause of cancer in smokers.  Note that some smokers never develop cancer or heart disease; some have lived more than 100 years.
Just because something is classified as a carcinogen doesn't mean it causes cancer in everyone and doesn't mean a given exposure to a particular carcinogen has any effect at all.  All smoking does is increase one's risk of developing cancer.  That it increases risk is not a fact but the association between smoking and cancer is significant, statistically.  (This means it meets certain mathematical criteria and is, therefore, not mere opinion).
Chromosomal replication is not perfect and a healthy cell can replicate only a limited number of times.  Cancer is characterized (in part) by a loss of this control.    When DNA mutates in a way that results in the loss of this control an otherwise-healthy cell (now a mutation) results.  Smoking increases cell turnover and the increased turnover increases the likelihood this type of mutation will occur.
You can think of skin cancers in the same way.  This is the reason an exposure resulting in a color change (sunburn, tanning including that from a tanning booth) increases the risk of skin cancer.
Over a typical lifetime we develop a handful of cancerous tumors.  They're killed by our immune system.  Symptoms of malignant cancer develop when the immune system hasn't been effective.

The fact that not everyone who smokes develop cancer does not rule out that those carcinogens be (amongst) the causes of cancer in those people who do.

Just out of interest - how could it ever be shown that the carcinogens in cigarette smoke caused a specific case of cancer? My feeling is that this is impossible, and that the chain of potential causation from smoking>carcinogens>increased risk of lung cancer is as good as we can get.


text:
Correlation between genome size and mutation rate?
Martin Nowak in his book "Evolutionary Dynamics" talks about a given correlation between genome size and mutation rate.
What correlation does exactly exist between these two concepts?

Is it a linear correlation?
What is the coefficient of correlation?
Does this correlation exist in many different taxa?

One will need to make whether we talk about mutation rate per base per generation or for the whole genome.
Some references to accompany claims are welcome!

Could you provide a reference for the first sentence of the question, or is it an opinion? And what are the units of mutation rate- is it mutations per bp per generation? Or are we talking somatic mutations?

I read about this correlation in Nowak's book "evolutionary dynamics". I am sorry I don't have a better reference right now. Good point! Yes I meant mutation rate per base pair per generation. And generation time is correlated with genome size. Let me rephrase completely my question in order to not assume this correlation.

@AlanBoyd I'll ask the "why" part of my question in another post depending on the answer to this post.

its probably not a linear relationship to genome size because larger genomes don't necessarily have

Drake proposed an inverse correlation between genome size and mutation rate A constant rate of spontaneous mutation in DNA-based microbes.. His rule seems to be true for DNA viruses (this is probably also interesting for the other thread on this). The paper has some kind of a follow-up for higher organisms (I have so far only read the abstract):"The mutation rate and cancer."

I missed this question somehow. Well, when comparing mutation rates many more hidden variables come into picture- general biochemistry, habitat etc. Also, eukaryotes should not be compared to prokaryotes.

Bradwell et al. report RNA viruses with the smallest genome may have particularly high mutation rates. A particular bug was shown to have about 1.4 x $10^{-4}$ substitutions per nucleotide per round of copying (high for viruses generally) and the authors suggest this is to optimize adaptibility. Correlation Between Mutation Rate and Genome Size in Riboviruses: Mutation Rate of Bacteriophage $Q \beta$, Genetics, vol.195 no. 1 243-51 (2013).
Cuevas et al. report a phage with 1.0 x $10^{-6}$ mutations per base per round of copying (m/b/r), which conforms (they state) to Drake's rule of 0.003 mutations per genome per round of copying in DNA-based microorganisms. They indicate that DNA-based microorganisms range between $10^{-10}$ to $10^{-6}$ m/b/r. They state that RNA viruses vary between $10^{-6}$ and $10^{-4}$ m/b/r, consistent with the result above. Point Mutation Rate of Bacteriophage $\Phi X174,$ Genetics, vol. 183 no 2 (2009).
Drake's paper often-cited paper (one of them) is available at this link.
He has a remarkable graph on p. 7163 of this paper in which based on his observation of seven microorganisms with a wide range of genome size (bp) he plots the log of the mutation rate per base pair against the log of genome size (bp). The resulting (fitted) line has a slope of roughly negative one.
In a nutshell, Drake shows that over a wide range of genome size, as the genome size climbs exponentially the mutations per base per round of copying drops exponentially. This relationship is roughly log-log linear.
In his discussion he says that the factors influencing mutation rates (in either direction) are so general that they seem to have imposed a small range of variation of mutation rate per genome in microbes that have a large range in genome size and mutation rate per base pair.
As for more complex organisms, I have read very little. There is a recent review article in Nature about a report that a hypothesized inverse correlation between genome size and mutation rates in certain plants (angiosperms) is untrue. Genome size is positively correlated with genome size. Plants with the larger genomes have higher mutation rates than those with smaller than average genomes. I don't have access to this pay-walled article or the methods involved so I am quoting the abstract. Tasci, Nature Reviews Genetics 13, 148 (March 2012).
As usual an expert in this area could correct/expand these few details I've found but it's an interesting question. Drake's paper gives a remarkable result.
As for the question about correlation coefficient, I think that Drake's graph suggests a strong correlation between linearized functions over a certain range.
I suppose we could attach a number to that...

I'd clarify the above that the mutation rate is probably linear with the number of bases in the cell, since they are caused by random collision with ionizing radiation most of the time.
The number of mutations retained will vary though by organism which may reflect the trend that @daniel is describing.  Certainly larger prokaryotes will start to have more DNA and mutation repair genes when they have larger genomes, on the average.
Eukaryotes, including metazoans will have more elaborate selection mechanisms such as diploid recombination and social selection to throw out mutations for many of the genes.  This may explain the additional dropoffs for even larger genomes, who tend to be eukaryotes.
As an example of the points above, take a look at Deinococcus radiodurans, a prokaryote found in cans irradiated with gamma radiation as a means of sterilizing and preserving the food.  This bacterium can withstand a half million rad of gamma radiation - one thousand times the human lethal dose.  D radiodurans has multiple copies of its genome and several times the number of DNA repair pathways, and probably all the tricks in the book to keep its DNA intact and break/mutation resistant.  It would be way off the mean slope in your chart.

The plant article seems to support your idea. I think Drake's finding is interesting in part because it is counterintuitive. The info on Deinococcus sort of reinforces that the niceness of Drake's result is due in part to the narrow range of bugs involved (although I think he mentioned a couple of outliers).+1

thanks @daniel!  Its always important to remember the underlying assumptions and a constant mutation rate from the environment is important.  viruses also have their own requirements - they favor variation because they have no replication genes to protect and it helps them evade immune systems - its not entirely a matter of size.


text:
Why were dinosaurs not as smart as humans are?
According to http://en.wikipedia.org/wiki/Dinosaur, Dinosaurs were the dominant terrestrial vertebrates for 135 million years.
They had a lot of time to evolve. My question is: why were dinosaurs not smarter than us, and why was their society not complex like ours is?

Because inteligence is not necessarily selected for.
A population evolves to get smarter if being smart is beneficial over being stupid. Big brain are costly in terms of energy. For example the human's brain consume 20 percent of all the enery we have. This is a pretty big cost!

@Remi.b So why are we so much smarter than animals or any dinosaurs?

"Smart" is an extremely subjective thing...

"Smart" here is probably just talking about brain volume in cubic centimeters, complexity of tools and complexity of social systems.

@nico I don't want to debate about words, you and your friends can write comments on this human created page, but your dog can't do this work. So I think, your are smart

@Пуя Proving that you can select two examples and chose whether they should belong to the group "smart" or "not-smart" does not prove that the word "smart" is well defined. To take an example: some birds have a way better spatial memory than humans does. Are they smarter? What about people that are not able to tie their shoes but can solve incredible square roots in 5 seconds

@Pooya the best guess as to why we are as smart as we are is a perfect storm of the few pressures that can favor intelligence combined with runaway sexual selection. It also may have a lot to do with the evolution of art.  Your question to Remi would make for a great question by itself.

We are all equally evolved
All life that exist on earth today had the exact same amount of time to evolve (3.5 billion years). Therefore, one cannot say that one species is more evolved than another one. It just makes no sense (at least if "more evolved" means "have evolved for more time").
Being a dominant species/clade for some time (whatever dominant may mean to you) doesn't make this species/clade more evolved than any other one.
Your question need not be specific to intelligence
You can think of any other phenotypic trait (wings, toxins in the skin, good eyes, good smell, strong leaves, etc...) and ask this same question. You seem to assume that being smart should be some kind of goal or necessary direction toward which species should evolve. Following your reasoning I would rather ask why the hagfishes, the oyster, the lampreys or the turtles are so dumb although they exist for so long (once again remember that this notion that some lineages have existed longer than others is flawed).
You might also want to have a look at: Why evolution should not be equated with progress?
Being clever is not a goal of evolution
Most of these trait have associated cost to the benefice they might bring. For example having a big brain asks for much energy (20% of ATP in humans) and it also has a cost due to its weight. The sperm whale for example has a brain that weights 7.8 kg. Obviously it is not a big cost for such a big animal to carry heavy organs while it would be impossible for a migratory bird to carry such a brain.
taking different evolutionary path This part is not complete!
Now the question of why Homo sapiens are smart while Tyranosaurus rex are not or why wings evolved in bat and not in mice is rather interesting and hard to answer. I can think of 2 main causes:
1) The newly arising trait (which is usually not the trait you can observe today. Big brain did not appear suddenly, first there were individuals they had slightly bigger brains than the other individuals in the population) is not beneficial over the wildtype trait. There are so many parameters that will affect if a trait is beneficial or not. You can think of the predators, the humidity in the environnement, the social structure, the population size, the type of reproduction, the genetic background etc...
For example, think of a species that is fixed, has no social contact, has nothing it can really predict in the environnement. What would an individual from this species do with a brain? Think of a bird that needs to make food stock for the winter. This bird needs to remember where it hide something. It has been found by the way that some birds have an awesome spatial memory, way better than humans.
2) The trait never happen to occur (or never in a strong enough individual, or never in a population big enough to not suffer from to much drift while the trait is at low frequency) just because the necessary mutation never happen. Mutation is just a random process.
For example. It seems rather hard for a tree to have the necessary mutations to have develop a brain! But we don't need to go to such a extreme example. If you split a population of clone mice in two, the two subpopulation will evolve differently (even in absence of genetic drift (infinite population size)) just because  some mutations occur on one side while some others occur on the other side. Or maybe the same mutation might occur but once in an individual that has low fitness and once in a very fit individual.
Evolution of human cognition abilities
So what are the factors that drive humans to evolve big brains? This question is not solved yet. We have many models to explain this but I don't we have much solutions to test these models. The 2 most common models explain big brains

for social purposes (understanding relationship between other individuals, being able to coordinate the movement for a hunt, etc...)
due to sexual selection. Being intelligent would be a proxy for having good genes.

For more information concerning the evolution of human cognition, this wikipedia article might be a good start.
UPDATE

Why do you think mutation is a random process?

Our genetic data are encoded into a succession of 4 types of nucleotide bases (A,T,C and G). A mutation results from a modification of this sequence such as a replacement of a T by a C. These mutations are due to mistakes usually while duplicating the DNA. Most of these mistakes do not affect the fitness (survival + reproduction ability) of the individual, very often these mutation are deleterious and rarely these mutations are beneficial. Some mutations are more probable than others but nevertheless some individuals have a higher mutation rate than others. In order to make things slightly more complicated, some sequences have a higher mutation rate than others. For example, the sequence AAAAAAAAAAAA is more likely to mutate than the sequence ATGTGCATCTA. But even if some mutations are more likely to occur it is still a random process (we couldn't talk about likelihood otherwise!). Two clones living in the exact same environment that both have a baby at the exact same time wil not create babies with the exact same genome given the randomness of mutations. One baby might have a very bad mutation that will make him die, while the other baby might synthesize (=construct) a new enzyme that increases its digestive capacity.

We created very complex languages, we write and read, we created computers, we have philosophy, we have maths, we have religions, we can send spaceships to the other plants. Why there were no species in dinosaurs in 135 million years,that evolved to read and write and think about philosophical thoughts?

@Пуя I think your comment has already been answered above. Can you try to pinpoint what seems unclear to you? Or try to pinpoint why I did not answer your question.

Why do you think that the mutation is a random process?

@Пуя Do you think that mutation isn't a random process?

@Пуя See update in my answer. Please let us know if anything else is still unclear.

@Пуя You will find many introduction to evolutionary biology with a simple google search. Here is a video from Khan Academy that might give you introductory knowledge in the science of evolutionary biology (I haven't watched these videos!).

So what are the factors that drive humans to evolve big brains? This question is not solved yet., Why? Why is human smartest among billions of other species?

Around 200,000 years ago, Homo sapiens first appears in East Africa. It is unclear to what extent these early modern humans had developed language, music, religion etc. They spread throughout Africa over the following 50,000 years or so.

@Пуя The last paragraph of my answer gives you two different models to explain the evolution of human intelligence. It is a very broad subject for which we have several hyopthesis but we can't really test them. have a look on this link: http://en.wikipedia.org/wiki/Evolution_of_human_intelligence (it is the same link I gave you in the answer) and then if you have specific question I suggest that you ask it in another post.

While mutations happen randomly, its important to understand that evolution isn't random


text:
Examples of virus originated from a living system
Do you know some examples of virus or a viroid (or a prion) that originated from a known living organism? How does the virus/viroid/prion lives? Does it paratize the organism from which the virus originated?
UPDATE
Thanks to the first answers I have examples of newly originated prions. Does someone know such an example about viruses?

Retrograde evolution is not an impossible concept, I know examples of unicellular parasites (in a way) evolving from multicellular lifeforms (See Devil Facial Tumor Disease and Canine Transmissible Venereal Tumor). A related question would be: how ancient the viruses are. Retrograde evolution of a eukaryotic cell to a virus would be a huge evolutionary jump.

Prion diseases are still very poorly understood, but one of the dominant theories is that they are misfolded proteins that cause disease by catalyzing the misfolding of more proteins of the same type.  If that is the case, then they arise from the organism that they affect simply by protein misfolding.  In the case of bovine spongiform encephalopathy (mad cow disease) being transmitted to humans and resulting in new variant Creutzfeldt-Jakob disease, it seems like it might be transmissible between species, but it probably needs to infect a closely related species so that the protein has a homolog it can act upon.
Can't say I know of any examples where people have shown the de novo creation of a virus from a living organism.  There are definitely virus protein homologs in the genomes of organisms, but directionality is hard to argue since its common for viruses to pick up host genes, or leave behind viruses genes.

Prion diseases arise spontaneously fairly often.  There are only ~170 total cases of human infection by mad cow disease, but there are ~50 cases/year of Creutzfeldt-Jakob disease, which is a spontaneous strain of prion diseases in humans. There is a strong case that Alzheimer's and Parkinson's diseases (among others) are similar in nature, in which case it's a much more frequent occurrence.
However, they are the consequence of a misfolding and aggregation of a naturally occurring protein produced in our brains.  In this sense, they are nothing like the complexity required to produce a de novo virus. The closest viral analogy would be retroviruses, which could insert their genome into your DNA, die off, and then possibly spontaneously revive at a later date.


text:
Function of an VEGF inhibitor in the treatment of macular degeneration
I'm working on a short presentation of treatments of macular degeneration for a biomedical
optics seminar on macular degeneration.
Since I don't have any relevant medical or biological background (B.Eng. Electrical Engineering, now M.Sc. Biomedical Engineering w. a major in Biophysics) I need some help with
understanding the function of VEGF inhibitors, and how they work.
It doesn't need to go into all details as it is one of three treatments that I'm supposed to present, but enough to explain how it works, in about roughly 5 minutes.
Could anyone help me please?

The Wikipedia page for vascular endothelial growth factor (VEGF) looks pretty useful - it explains that VEGF stimulates the growth of blood vessels. If this gets out of balance, for example in diabetic retinopathy and wet form age-related macular degeneration, one treatment is to attempt to reduce levels of VEGF in the circulation, using monoclonal antibodies directed against VEGF, or to antagonise the action of VEGF using drugs that target the VEGF receptors.
Two milestones in anti-VEGF therapy are described in these papers:

Ng et al. (2006) Pegaptanib, a targeted anti-VEGF aptamer for ocular vascular disease. Nature Reviews Drug Discovery 5: 123-132 (This paper describes the first approved aptamer drug: an RNA directed against VEGF.)
Ferrara et al. (2006) Development of ranibizumab, an anti-vascular endothelial growth factor antigen binding fragment, as therapy for neovascular age-related macular degeneration. Retina 26:859-870 (This paper describes a therapy based upon an antibody fragment directed at all isoforms of VEGF-A.)

A very recent review of anti-VEGF therapies is:

Freund et al. (2013) An update on the pharmacotherapy of neovascular age-related macular degeneration. Expert Opinion on Pharmacotherapy 14:1017-1028


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What is the difference between local and global sequence alignments?
There are a bunch of different alignment tools out there, and I don't want to get bogged down in the maths behind them as this not only between software but varies from software version to version.
There are two main divides in the programs; some use local alignments and others use global alignments. My question is threefold:

What are the fundamental differences between the two?
What are the advantages and disadvantages of each?
When should one use either a global or local sequence alignment?

The very basic difference between a local and a global alignments is that in a local alignment, you try to match your query with a substring (a portion) of your subject (reference). Whereas in a global alignment you perform an end to end alignment with the subject (and therefore as von mises said, you may end up with a lot of gaps in global alignment if the sizes of query and subject are dissimilar). You may have gaps in local alignment also.
Local Alignment
5' ACTACTAGATTACTTACGGATCAGGTACTTTAGAGGCTTGCAACCA 3'
             |||| |||||| |||||||||||||||
          5' TACTCACGGATGAGGTACTTTAGAGGC 3'

Global Alignment
5' ACTACTAGATTACTTACGGATCAGGTACTTTAGAGGCTTGCAACCA 3'
   |||||||||||    |||||||  |||||||||||||| |||||||
5' ACTACTAGATT----ACGGATC--GTACTTTAGAGGCTAGCAACCA 3'

I shall give the example of the well known dynamic programming algorithms.
In the Needleman-Wunsch (Global) algorithm, the score tracking is done from the (m,n) co-ordinate corresponding to the bottom right corner of the scoring matrix (i.e. the end of the aligned sequences) whereas in the Smith-Waterman (local), it is done from the element with highest score in the matrix (i.e. the end of the highest scoring pair). You can check these algorithms for details.
You can adopt any scoring schemes and there is no fixed rule for it.
Global alignments are usually done for comparing homologous genes whereas local alignment can be used to find homologous domains in otherwise non-homologous genes.

Global alignment is when you take the entirety of both sequences into consideration when finding alignments, whereas in local you may only take a small portion into account. This sounds confusing so here an example:
Let's say you have a large reference, maybe 2000 bp. And you have a sequence, which is about 100 bp. Let's say that the reference contains the sequence almost exactly. If you did a local alignment, you would have a very good match. But if you did a global alignment, it may not match. Instead, it may look for matches throughout the entire reference, so you'd end up with an alignment with many large gaps. It does not matter that it matches near perfectly at one particular region on the reference, because it's looking for matches globally (i.e. throughout the reference).
If you have a really good match it may not matter what type of alignment you use. But when you have mismatches and such it starts to get important. This is because of the scoring algorithms used. In the example above let's say that there is a 100bp region in the reference that matches your 100bp sequence with 85% accuracy. In local alignment it's very likely it will align there. Now let's say that the first 30 bp of your sequence matches a region in the beginning of the reference 95%, and the next 30bp matches a region in the middle of the reference 85%, and the final 40bp matches a region at the end of the reference about 90%. In global alignment the best match is the gapped alignment, whereas in local alignment the ungapped alignment would be best. I think in general gap penalties are less in global alignments, but I'm not really an expert on the scoring algorithms.
What you want to use depends on what you are doing. If you think your sequence is a subsequence of the reference, do a local alignment. But if you think your entire sequence should match your entire reference, you would do a global alignment.

Take look to the attached image file. It will clear your doubts about difference between local and global sequence alignments.

Please do not post text answers as image files on SE Biology. This discriminates agains people with vision defects who use screen readers, and does not allow proper indexing.


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Is an antivenom venomous?
What happens when someone takes an anti-venom for an animal they weren't bit by, either for incorrect identification of the animal they were bit by or if they weren't bit at all?
I am looking for the immune system reaction, and possibly why it reacts as it does.

@jonsca Why the edit to change antivenom to antivenin? From Wikipedia: "The name "antivenin" comes from the French word venin, meaning venom, which in turn was derived from Latin venenum, meaning poison.
Historically, the term antivenin was predominant around the world, its first published use being in 1895.[2] In 1981, the World Health Organization decided that the preferred terminology in the English language would be venom and antivenom rather than venin and antivenin or venen and antivenin."

@AlanBoyd Feel free to roll back.  I was always taught that "antivenom" was incorrect.

It seems like there's a mixture of both in the literature, and Webster's defines "Antivenom" as "Antivenin".  I will leave it be, though.

@jonsca I searched for both words as title terms at Web of Science: antivenin has total hits 190, 104 (54.7%) since 1981 whereas antivenom has total hits 598, 561 (93.8%) since 1981. It looks like the WHO decision was pretty influential. Incidentally I have no axe to grind on this, I was just curious since I don't recall ever seeing the word antivenin before your edit.

@AlanBoyd I guess who can really argue with the WHO, then?  I have enjoyed learning more about the usage of the word, so thanks for enlightening me.

usually the antivenoms are antibodies raised against these protein based venoms. Serum injections may cause anaphylactic reactions but should otherwise be safe.

https://books.google.com/ngrams/interactive_chart?content=antivenom%2Cantivenin%2C+ANTI-VENOM&year_start=1800&year_end=2000&corpus=15&smoothing=3&share=&direct_url=t1%3B%2Cantivenom%3B%2Cc0%3B.t1%3B%2Cantivenin%3B%2Cc0 @AlanBoyd

Although it is fancy to think of antivenom as a poison for the poison, technically it is a poison only for the poison!
Antivenom is developed in horses (equine) by hyperimmunizing them against the particular venom at a non-lethal dose, followed by collecting the serum. Venoms are complex and have many enzymes and hence are proteins. So, antivenoms are just antibodies against the venom proteins.
Moreover, the antivenoms are classified into monovalent and polyvalent. This signifies whether the sera was prepared by hyperimmunizing the animal with the venom of a single species or many common venomous snake species together.
Usually, a snake bite is an emergency and the victim or the attendants rarely identify the snakes (In our place, patients sometimes to our surprise, even bring the killed snake to the casualty!). Hence, to avoid confusion polyvalent sera are used.
I've written all this just to make an impression that polyvalent sera also carry antibodies against the wrong snake too, but at the end of the day, it's the right antibody that does the job.
As mentioned in the comments, apart from occasional anaphylactic reactions or serum sickness, they are pretty safe (cost/benefit) to use.


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Humidity for wood rotting
If I put a piece of wood in a humid environment (basically humid air), it will start to rot. Does the humidity influence the rotting speed, and if so, what is the relation between the rotting speed and humidity?

Rotting is a biochemical reaction: basically catabolism (breaking down of complex compounds to simpler compounds). Cellulose or lignin or any other structural polysaccharide will not undergo spontaneous hydrolysis. This reaction is catalyzed by enzymes produced by the microorganisms like fungi and bacteria (the term for these decomposers is saprophyte). Saprophytes prefer to grow in humid and warm environments.
So the primary role of humidity is to promote the growth of decomposers. Simultaneously it provides the water required for the hydrolysis.

I'm afraid this is not a topic of chemistry, the main degradation process in wood decay is a matter of biological attack, of course life needs water so if the ambient is very humid the wood decompose very well if the ambient is dry the wood can be conserved easier.
However wood is not a substance but a complex material, you have to investigate the degradation process for all the components. Chemically holocellulose is the most degradable part of wood, his microcrystalline structure improve the resistance but cycle of imbibitions can blow up the structure leading to a larger surface more suitable for degradation. The hydrolysis of cellulose however doesn't occur at normal temperature only peeling off can occur under 100 °C.
Lignin is more and more durable if a little bunch of micro and macro organism wouldn't decompose it we would be sub-merged by a large quantity of lignin.


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How does ultraviolet light influence the decay process of wood?
Given a piece of wood, how does putting it in the sun or not influence the rate of decay due to rot (assuming that it's in an otherwise humid environment)?

its not going to degrade the lignin in the wood directly that's for sure!

Ultraviolet light is microbicidal. See this post.
As I answered in this previous post, micro-organisms are essential for rotting. Since UV kills these microbes it will reduce the rate of rotting. The heat from sun will also dry the wood and further decelerate rotting.


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Why did the yeast rise?
Here are the notes I made for an experiment I was doing (I didn't put it here as it is too long)
(please ignore the numbers at the end of the pdf file)
The graph looks like this:

As you see on the graph, the numbers are the same as the ones below
1. The effect running out of glucose has on the yeast growth
Our yeast increased in number by dividing rapidly. They use glucose to respire and release energy. They need energy to grow.
2. Why the yeast starts to grow again
The yeast  starts to decrease in volume when they ran out of glucose.
3. Describing patterns in graphs
The yeast breaks down the starch to glucose
The problem is, why did the yeast rise at the end, I forgot?
Thanks in advance

I just would like to say that the teacher never talked about the production of Co2

What did your growth medium contain? Only glucose? Or other substances as well?

@Chris only glucose

So you added glucose and some salts into the medium? Or did it also contain some complex materials like yeast or tryptone extract?

What do you mean by Volume. Volume occupied by yeasts? Then it is not the cell number.

First, the glucose is reduced by anaerobic fermentation to ethanol and carbon dioxide. The yeast uses the produced energy for a fast growth and division (1). As soon as all glucose is consumed the metabolism of the yeast changes from anerobic fermentation to aerobic respiration (oxygen is required). This is called diauxic shift. During this time the yeast stops growing (2). After this shift the yeast further reduces the ethanol to carbon dioxide and water. The generated energy is used for the second growth phase (3).
Hope this answers your question.
Best
Vanessa

Ethanol is toxic for yeast, it cannot metabolize the large amounts produced during fermentation. This is the reason why most wines are not stronger than 12-14% alcohol.

Welcome to Bio. Some references would be appreciated.


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How does blue white screening work in selecting E coli that have taken up a plasmid vector?
The plasmid vector I am referring to is pCR 2.1 - TOPO. I added the vector to the E coli and plated them up onto LB+amp+X-gal plate, then incubated. After incubation the plates had two types of bacterial culture on them, one white and one blue.
I think that the blue cultures have accepted the plasmid as they are able to grow on ampicillin, so have the ampicillin resistance gene, and are able to convert the X-gal substrate to blue via the lac Z gene. What i'm confused about is the white colonies. If the colonies are able to grow on ampicillin, surely they have accepted the gene because they have the resistance, and surely they should to be able to convert the X-gal?
So why are these not expressing the lac Z gene? Is it that the lac Z gene and ampicillin resistance aren't on the same plasmid, or is it that the lac z gene didn't make it into the plasmid?

What was the strain of E. coli that you used? Was this a TA cloning kit? Did you also add insert DNA of any kind?

I believe it was the k12 strain, yes it was a TA cloning kit, and I added DNA from Aequoria victoria to the vector that caused the bacteria to fluores

The traditional blue/white screening is set up so that blue colonies are considered negative for the insert, and white colonies are positive for recombinant DNA. The gene responsible is the lacZ gene, or beta-galactosidase. This enzyme converts a synthetic substrate, X-gal, into an insoluble blue compound.
The pCR2.1 TOPO plasmid is a blue/white selection plasmid in which white colonies are considered positive for the insert. The way this works is by inserting the DNA sequence to clone inside the coding region for lacZ. By having any inserted DNA interrupting the sequences of lacZ, so that the enzyme has lost its function (because it is no longer being translated correctly in the bacteria). On the other hand, no insert present means that lacZ is ligated back together, and the entire enzyme is correctly made, and therefore can metabolize the X-gal substrate to form an insoluble blue dye.

This makes a lot of sense, however, if the E coli is growing on the plate, surely by default this means it has taken up the plasmid because it has the ampicillin resistance? How are the blue colonies surviving on the ampicillin if they haven't taken up the plasmid?

The ampicillin resistance gene is encoded on the plasmid in a different region. Every plasmid, with or without insert, contains ampicillin resistance. Every colony growing on the plate has taken up a plasmid, that's how they survive, but not all necessarily have a plasmid with the insert.

Oh I see, so it's a test to see if the plasmid has ligated together with the insert, not to see if the plasmid has been successfully inserted into the E coli?

That's correct! After all, the antibiotic is spread over the entire plate, so any bacteria growing must already have the resistance gene.


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What in neurons and their connections changes during the process of learning?
I'm not sure if this question belongs more in physics or biology (or maybe even computer science)... but biology seemed to fit more.
What changes in the state of our brains when we learn things?  Because I looked on the internet and I learned about artificial neural networks, and every resource I've found teaches of neural networks that have weights that are trained/evolved and then are static at runtime; you simply train the weights and then once you use them in simulations, they never change.
Purely feedforward neural networks that rely on this can't react to new situations differently if they've experienced it before.  They react exactly the same each time.
I suppose that theoretically, a recurrent neural network that was big enough could really learn, but in practice, these have been used as purely memory slots for an existing method defined by the weights, not as storage of new methods of doing things.
So my question is, physically, chemically, biologically, what changes in the neurons and the connections between them when we learn things?  I don't think we really understand how it comes together on a grand scale yet, but I'm pretty sure we've figured out that much.  I want to learn how to model a simplified version of it mathematically/programmatically.

What changes in the process of learning:

The connections (the way one neuron is connected to another). New synapses can form or dissolve in the process of learning. The glial cells such as astrocytes and microglia can facilitate this process.
Strength of connections: Existing connections can be made weaker or stronger in the process of triggering the same circuit. This happens by up/down regulation of the ion channels at the synaptic junctions.

This process is not fully understood and is an active area of research. You can find some mathematical models too for learning processes such as Long Term Potentiation etc.

During learning, LTP (long term potentiation) or LTD (long term depression) can result in post synaptic neurons altering their responses to neurotransmitter release by the pre synaptic neurons. This is achieved at the post synaptic cell by increasing or decreasing the amount of neurotransmitter vesicles, moving them closer or farther away from the axon terminals, and increasing or decreasing the density of sodium channels. All of these factors can lead to changes in the tendency of the post synaptic cell to undergo an action potential as a result of stimulation by the pre synaptic cell, as well as changes in the amount of neurotransmitter released by the post synaptic cell as a result of that action potential. Further, neurons can also establish or degenerate synapses with other neurons, leading to modifications of neural pathways as a result of learning.


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Attaching suspension cells to coverslip during mycoplasma contamination detection
I am planing to screen my cell cultures for mycoplasma contamination using the Hoechst 33258 DNA staining method.
This method is suitable for adherent cultures. Is this method suitable for suspension cultures?
If yes, what is the procedure to attach my suspension culture on coverslip and prevent washout of cells during staining.

microscopic methods require some experience in cell culture (to see and identify things). You can use other techniques too such as PCR based methods.

Related: How to convince suspension cells to adhere more tightly?

If you are working with suspension cells, it's always easier to use Flow cytometry but if you want to use microscopy then I would suggest using chamber slides. You just have to put your cell suspension inside the chamber and then stick the cells to the microscope slide. After that you can do whatever treatment you want just by putting in the chamber the proper solution and wash afterwards. The more the steps the more cells you'll lose mostly because of pipetting so try to pipette always at the same corner and be gentle. To stick the cells to the slide your best option is to centrifuge the slide. Unfortunately in my lab that wasn't an option so I just fixed the cells with methanol while there were suspended in PBS and it worked very well. Most of the cells were attached to the slide and the staining was perfect.
Hope I helped. Good luck!

Contamination detection in suspension cells
For contamination detection in suspension cells, use the culture media of these cells: (with no antibiotic)
NRK, 3T6, A549, VERO Cells
These cells are good hosts, especially for Mycoplasma then contamination is easily detectable using optical microscopy after staining. check host cell culture for contamination before transferring suspension cells.


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Are there any enzymes in cytoplasm to help the newly-synthesized polypeptide to form tertiary structure?
Polypeptides made by ribosomes which attach to rER will go into the rER to form the tertiary structure. Those polypeptides made by free ribosomes usually stay in cytoplasm. So are there any enzymes in cytoplasm to help them to form tertiary structure?

What about the chaperone?

There are several types of proteins that do this, all of which fall under the category of molecular chaperones. In particular, chaperonins such as GroEL/GroES complex in E. coli, sequester newly-formed polypeptides to allow them to fold their tertiary structure and avoid aggregation. Another widely studied class of these proteins are heat shock proteins (Hsps): these are involved generally in acclimating cells to stresses (such as heat), and some of these Hsps have been specifically implicated as chaperones. I'm a new user, so I can't post a 3rd link, but just google Heat shock proteins and you'll find plenty of information.