text:
What does self-preservation stem from?
Self-preservation, or preservation anyway, probably happens throughout the animal kingdom, and perhaps through the plant kingdom as well (some plants/trees, apparently, produce chemicals to repel bugs).
Where does self-preservation stem from? Is it only about a biochemical imbalance?

Could you expand on your question a bit please? I cannot understand what you are asking here.

self-preservation in what sense?

Saving one's own life by avoiding starvation/discomfort(extremes of temperatures for instance)

This is a prototypical case of evolution by natural selection. Any trait that prevents the organism from being eaten or destroyed will probably make that organism more likely to reproduce* than similar organisms that do not have that trait**. This results in self-preservation traits becoming more prevalent in the population and eventually ubiquitous.
* Or they reproduce more, or are able to provide for their offspring better, etc. Self-preservation behaviors that reduce reproductive success are not selected for and generally aren't common (unless they are a special case of some general trait that has a net reproductive benefit).
** Assuming that the trait is reproductively favorable after considering any trade-offs such as increased energy expenditure.

I would argue procreation is a side-effect ...

A side effect of what?


text:
Parse PDB using DSR-PDB Library
I'm trying to parse ATOM section of a PDB file. I'm using the dsr-pdb library for this purpose.
I've encountered a problem. This library interprets CD1 atom of ILE residue in the PDB file as AL_CD instead of AL_CD1*. Does it have a particular reason?
It's maybe helpful that within the source code, in Residue_data.cc, there is a mapping between atom lebels:
Atom_fallback_data atom_fallback_data_[]=
      {{Residue::AL_CD1, Residue::AL_CD},
       {Residue::AL_1HA, Residue::AL_HA},
       {Residue::AL_1HB, Residue::AL_HB},
       {Residue::AL_1HD, Residue::AL_HD},
       {Residue::AL_1HE, Residue::AL_HE},
       {Residue::AL_1HZ, Residue::AL_HZ},
       //{Residue::AL_1HH, Residue::AL_HH},
       {Residue::AL_1HD1, Residue::AL_1HD},
       {Residue::AL_2HD1, Residue::AL_2HD},
       {Residue::AL_3HD1, Residue::AL_3HD},
       {Residue::AL_INVALID, Residue::AL_INVALID}};
It means that AL_CD1 is deliberately converted to AL_CD or for example AL_1HA to AL_HA.
Thanks.

In general, in dsr-pdb library, AL_X is the atom label of atom X.

Isoleucine only has one delta carbon, which we can just call CD. But it seems like some PDB files still name it CD1, and hence programs map CD1 to CD in this case. (E.g. see this tutorial where this practice is shown.)

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text:
Using ion-exchange chromatography to purify DNA from a cell extract - Is DNA more negatively charged then RNA?
When applying this method we have a glass or plastic column of resin which is positively charged. Then we pour cell extract into the column in order to capture the negatively charged particles which include DNA.
After that we gradually add salt which neutralizes the molecules. But it does this gradually so strongly attached DNA molecules fall last while RNA and proteins fall first.
The question is why does DNA have a greater negative charge than RNA ?

Perhaps this could be due to the size of the molecules? DNA is double stranded vs typically single stranded RNA and DNA is also more stable so would probably be longer.

A longer or duplexed Nucleic acid will have more charge per mole of the molecule. But generally it is not the overall charge that matters in electrophoresis or MS or chromatography; it is the charge density and specific charge (z/m) that matters (charge density of a longer RNA will be almost same as smaller RNA. they will also have same specific charge)
The properties of stationary phase  is very important in controlling the separation process. Without knowing what resin is used, it will be difficult to comment about why RNA is not retained.
Sometimes the strong basicity of the stationary phase, such as in quaternary ammonium resins, degrades RNA by alkaline hydrolysis.
If yours is a commercial resin then you will have a tough time finding out what exactly it is made of. Unless of course you break the column open and do a molecular analysis of the resin :P

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What's the name of the fibrous strands that hold the seeds in a pumpkin?
If you cut open a pumpkin, the seeds are suspended inside the pumpkin by some fibrous, slimey strands. You can see them in the middle of this sliced-open pumpkin:

I'm writing a post for the Cooking.SE blog, and am trying to find out the proper botanical term. Someone suggested that might be called the endocarp, but I want to make sure and also see if there is a more specific term.
Edit
In "Morpho-Physiological Aspects of Productivity and Quality in Squash and Pumpkins (Cucurbita spp.)" §C.1, I see this:

In the central portion of the fruit, a mass of tough fibers, together with vascular strands connected to the seeds, comprise the placental tissue. The endocarp is made up of small, thin-walled cells that form a membranous tissue that adheres to seed, becoming a transparent skin on dried seeds. (emphasis added)

Am I reading correctly that the name for this part of the pumpkin is "placental tissue", and that the endocarp is just a thin layer on the seeds themselves?

I have also found some sources that suggested this is the placenta, but couldn't find a good example like a figure with an arrow pointing to that and saying "placenta". Googling "pumpkin placenta" gives bubkes.

@Bitwise if you try "fruit placental tissue", you get more results... I think pumpkins are fruit from a botanical standpoint, right?

They are indeed berries.

This part of the fruit is called "Endocarp". It does not become more specific as that, as far as I know.
http://en.wikipedia.org/wiki/Fruit_anatomy

From the article I quoted in the edit, it sounds like the endocarp is actually the thin film directly attached to the seed, not the fibrous stuff around it. Am I reading the article incorrectly?

According to this site, the stringy bits inside a pumpkin is called the endocarp ( http://www.cls.zju.edu.cn/sub/fulab/plant_Antomy/plant/fruit/index.html )

@leonardo Where do you see that on the site? I can't find pumpkins mentioned anywhere. Wikipedia lets me know pumpkins are berries, and that site describes the mesocarp and endocarp as the "fleshy or juicy tissue", so that sounds like the part of the pumpkin you eat...

I was looking at squash in general.

Also, Wikipedia would inform you that pumpkins are indeed squash (not berries).

@leonardo http://en.wikipedia.org/wiki/Berry lists pumpkins. http://en.wikipedia.org/wiki/Squash_%28plant%29 says that squash are berries. So now I'm even more confused...

@derobert - odd, the first sentence of http://en.wikipedia.org/wiki/Pumpkin is that it is a gourd-like squash. I don't really know.

"Berries" are just a certain classification of the anatomy of a fruit, it has, as far as i know, nothing to do with the phylogeny. Apples are also berries, as well as Bananas and Oranges.

"Berry" is a good example of a perfectly normal English word that has been used with a different but related meaning by scientists (in this case botanists), and that pedants delight in pretending therefore doesn't have it's original (less precise) meaning. So pumpkins are certainly a kind of squash, and squash are generally considered berries by botanists AFAIK. Obviously they aren't considered berries by civilian English-speakers, but that's because normal English-speakers aren't interested in their anatomy.

... so in everyday English they're squash (not berries), whereas to a botanist they're squash (and also berries).

Each strand connected to a pumpkin seed is a funiculus (plural funiculi). The funuculus attaches the seed to the fruit placenta. This photo shows three areas of placenta, the spongy areas that the three clusters of seeds are around. The endocarp is the inner fruit layer; I'm not sure but here it either blends in to the mesocarp (the main flesh of the pumpkin) without a distinct boundary, or it helps make up the spongy tissue in the very center (or both!).

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text:
What is the purpose of measuring both VS (volatile solid) and TS (total solid)?
In the biogas process you often measure Volatile solid and Total solids. Can any one explain these concepts more accurately and why it is interesting to look at these properties.
The biogas process I refer to is a process of fermenting waste food materials and slaugther house waste in to bio fuels, consisting largely of methane. The fermentation is conducted in anaerobic milieu in large plants.
Total solids and Volatile solid are measurements on the sludge the currently fermented waste,(the gooey stuff that is in the bio-reactor).

Can you elaborate on what the "biogas process" is?

Total solids (TS): The part of the sludge that remain after drying at 105$^{\circ}$C for 20 hours:
$$ TS(\%) = \frac{\textrm{weight dried at } 105^{\circ}C}{\textrm{wet weight} }\times 100 $$
Volatile solids (VS): The part of the sludge that is combusted at 550$^{\circ}$C after 2 hours:
$$ VS(\% \textrm{ of TS}) = \frac{\textrm{dried weight at }105^{\circ}C -
 \textrm{dried weight at }550^{\circ}C}{\textrm{dried weight at }105^{\circ}C}\times100$$

For the definition, see Pelle's answer.
For the reasons, both are easy and cheap to measure and can tell you a lot about your material if you have similiar mterial to compare. TS is often used to asses howa material can be handled (pumpable, stackable)
In agricultural biogas applications for example, a sometimes used assumption is 1g COD = 1,6 g VS
In AD, VS is broadly associated with digestible biomass, and depending on input one third to one half of VS will be converted to gas. In fact, gas yields are often given per mass of VS because of this.
Note that solutes that are actually volatile, like alcohol, will be evaporated when testing for TS. Laso note that the points give na bove only work if you compare similiar materials.

VS and TS are very important parameter when it comes to Biogas production, in the following ways.
VS = Represent organic matter of the feedstock (excluding the inorganic salts, ash). Having in mind that bacterial action is on Organic mater and not Inorganic. meanwhile,
TS = Denote all the organic as well as inorganic matter in the feedstock.
Finally, VS/TS for different feedstocks can be model to give the biogas production.


text:
What are the biochemical interactions between human body and Polyethylene?
Our waterways and oceans are showing increased levels of plastic contamination. These plastics are breaking down into smaller pieces. When one goes to the beach and plays in the surf they often swallow some seawater and thus some amounts of plastics, including Polyethylene.
What are the biochemical pathways or effects of plastic, specifically Polyethylene, in the human body? I am looking for toxicity of both a large amount scenario (plastic bag milkshake) and a small amount (some in ocean water).

PE is not bothered by acids and there is no way humans have a pathway for it, except that for choking or being obstipated. But neither do bacteria or fungi make a dent in the molecule. That's why it's not degraded and collects in the oceans.


text:
Advice on Cell Biology texts by Alberts
I am currently reading "The Chemistry of Life" by Rose. It's a great book (to me as a lay reader at least) and an interesting topic so I am interested in pursuing some of the further reading he suggests.
The first book he mentions in the bibliography is Alberts' "Molecular Biology of the Cell". Looking at the description and the reviews it seems that this is a pretty advanced bio-sciences graduate level text, and I am very much not that. I see that Alberts has also written "Essential Cell Biology" which looks more accessible. Before I buy this I wondered if anyone can explain the difference, which would be a better read for an enthusiastic amateur?
If it helps at all I am a science grad and I typically read authors such as Dawkins and Matt Ridley, but I'm looking for something a little bit more rigorous to expand my knowledge in cell biology.

Don't know about "Essential Cell Biology" but "Molecular Biology of the Cell" is the classic textbook for Biology undergraduates. If you start at the beginning you should be all right :).

Ah, right. I think undergrad level is what I'm after. Thanks!

Might as well make it into an answer. As I said in the comments, Albert's  "Molecular Biology of the Cell" is the classic textbook for Biology undergraduates. It has been so for decades now.
It starts from the basics and builds up. Anyone with a high-school science education and willingness to learn should be able to understand it. Just work your way through it :).

I'd agree - it seems like a graduate text, but there isn't really a simple way to break down Mol Bio.

I've actually got a copy of Essential Cell Biology on my desk currently, it's one of our core textbooks.
When comparing with the "look inside" feature on Amazon for Molecular Biology of the Cell (remembering I only have access to the first few pages) I would suggest that Essential Cell Biology certainly takes a slower pace, but I wouldn't say that it was less detailed.
It goes into great efforts to explain how we know things experimentally, which I personally find quite helpful.  The pictures in Molecular Biology of the Cell look almost identical, however I would say they are more copiously used in essential cell biology.  Essential Cell Biology also comes with a DVD including very useful animations of cell processes.
Comparing the glossaries, I would still be inclined to say they are covering very similar levels of material, however Essential Cell Biology is using more 'entry level' language.
The key difference between the two in my opinion is the copious use of images in Essential Cell Biology - it's almost half a picture/diagram book.  In your situation (pretty much identical to mine) I'd probably recommend Essential Cell Biology just as a start then move on to Molecular Biology of the Cell as everyone else rates it so highly.
Finally, Essential Cell Biology certainly has some kind of sense of humour:

Geek Spoiler:

 The bottom line reads C A G T whilst the top line reads G T C A in semaphore, two complementary strands of DNA bases acted out for your amazement...

Nice answer. Unrelated to the content of the answer, I was wondering how you created that spoiler that only showed text when one rolls the mouse over it.

Hi @Pete - just add a <! before the paragraph, similarly as for a quote :)


text:
What evolutionary pressures pushed Galápagos tortoises to mature so slowly and live so long?
I read that they take up to 40 years (in the wild) to reach the age of reproduction and are thought to live over 100 years, with one in captivity reaching over 170 years.
Can someone explain in layman's terms how taking longer (especially spending years as a small tortoise) to reproduce was a winning trait, and how their biology delays the processes of senescence to the extent that it does compared to most other species?

This isn't so precisely focused on tortoises, but a general theory in evolutionary biology for why some animals live longer is K vs r selection theory.
The idea here is that animals will make a sort of evolutionary 'choice' and configure themselves to breed as numerously and quickly as they can.  This is called 'r' selection, named after the constant that is proportional to the rate or speed of breeding.  r selected animals adapt quickly to a rapidly changing environment and their lives are pretty cheap.  Many insects that lay hundreds or thousands of eggs every few weeks are examples of r selection. They do not care for their offspring (and may even eat them!).
K selected animals breed to be highly competitive in the environment.  They tend to be highly optimized for success and this often means they are larger, they live longer and require more investment as newborns.
By this theory the galapagos tortioises live longer because their environment changes very slowly and the tortoises are so optimized for that particular way of life that they have no predation or any competition at all.  Islands like the Galapagos are studied in fact because they are so isolated by the water that new species rarely ever arrive.  Such new arrivals may cause drastic changes in their ecosystems because islands are stable environments because migration happens so rarely.
There are other theories that emphasize other factors in the evolution of larger, longer lived animals, but I think r/K selection may describe the environmental pressure on the Galapagos tortoise.


text:
$S_{0.5}$ vs $K_m$ values in enzyme kinetics
What is the difference between $S_{0.5}$ values and $K_m$ values in enzyme kinetics?

What do you mean by S0.5? $K_M$ is the concentration of substrate at the point when the rate of the reaction is 0.5 of the maximal rate ($V_{max}$).

I edited the Mathjax into the title as well, as it seems to yield an appropriate URL slug: http://biology.stackexchange.com/questions/5004/s-0-5-vs-k-m-values-in-enzyme-kinetics

Km applies to a data set exhibiting MM kinetics, i.e. it has a "mathematical" underpinning. Presumably S0.5 is simply the observed substrate concentration for 0.5 x Vmax regardless of whether the data fit MM?

probably worth looking at http://biology.stackexchange.com/questions/3147/is-the-ec50-of-an-activating-protein-for-an-enzyme-a-good-indicator-for-the-bind

This expands my comment on the question to an answer.
If an enzyme exhibits Michaelis-Menten kinetics, then it is valid to define a KM and this equates to the substrate concentration when reaction velocity is 0.5 * Vmax.
However, many enzymes do not exhibit Michaelis-Menten kinetics. One example is when the enzyme shows a co-operative response to substrate concentration. In these circumstances the substrate concentration when reaction velocity is 0.5 * Vmax is still a useful parameter, but there is no KM.
See this paper for a discussion of the kinetic properties of the glucokinase of pancreatic β cells, which acts as the glucose sensor. This enzyme shows positive co-operativity with respect to its substrate glucose, and the authors develop a kinetic analysis in terms of various parameters. These include an S0.5 value for glucose, but a KM value for ATP (presumably because the kinetics with respect to ATP are simple Michaelis-Menten).


text:
How is evolution possible in contemporary humans?
I would like to know if evolution is continuing to happen in modern humans, assuming things like existence of the nuclear family structure, fidelity to one partner, etc. It seems to me the answer would be NO because evolution depends on differential reproductive rates, but in the modern world, all male humans have roughly 2.5 (or whatever the number) kids. Add in the process of culturally modified selection pressure, and it seems to me that even an "unfit" male would end up having a couple of offspring. The fittest male (or female) is no better off than his or her contemporaries because of this "leveling" effect.
However, the impression I get from the popular science media is that scientists think evolution is continuing to happen. I would like to know what the actual scientific consensus is, and why. Thanks.

Time rate of evolution is multiple orders slower than time rate of our sociology science perception. If nuclear war will happen, which is probable, then entire humanity appear to last for 30000 years. This is zero in evolution scale. So, evolution DOES continue, but it goes so slow that we cant see it.

I am tempted to say that "contemporary" (rather ambiguous time-frame) humans are under evolutionary pressure in much the same ways as we were in posterity. Humans still have sex which is the major mechanism of evolutionary diversity, which creates genetic diversity. This diversity is causes selective pressure in social, physiological and intellectual domains. All I would argue that "modern society" has done for us, when compared to ancient humans, is change the weight placed on us by each selective pressure.

This might be a perverse theory, but what if what we identify today as "development disorders" like autism, is actually evolution responding to modern information age pressures

@GabrielFair you should read David Brin's Existence it suggests exactly that!

No I haven't. I will add Existence to the top of my reading list. While we are on the topic have you heard of any research or peer reviewed studies referencing a theory like this one?

cesarian sections are increasing the tendencies to have babies that are too large for the woman's hips.

It is certainly not true that "all male humans have roughly 2.5 (or whatever the number) kids". First of all, male and female humans have exactly the same reproductive rate. For obvious reasons, every time a male has offspring, a female must have had also. Last I checked neither male nor female humans are capable of parthenogenesis (certain popular religious beliefs notwithstanding).
Second, let's assume that the 2.5 number is correct. That would be the average number of children per couple. That does not mean that all couples will have 2.5, or even that most couples will have 2.5. It just means that the average will be 2.5. If, for example you have one couple with 6 children, one with 2 and two with 1, the average will be (6+2+1+1)/(1+1+2)= 2.5.
On to the main point. What does selection mean? In its simplest form, that the individual most likely to survive (the famous "fittest") is also most likely to reproduce. This is a very simple concept, the longer you live the higher your chances of managing to have offspring. If you die two weeks after birth it is going to be hard to manage to reproduce yourself. This has not changed.
So, what does "fitness" mean? It can mean many things. If you are a warm blooded creature at the beginning of an ice age for example, it could mean being better at regulating your temperature than your peers. If you are a 21st century human, it could mean being funnier on twitter than your peers. The two are not fundamentally different. They can both be selected for or against. As long as one mate is chosen over another, selection is happening and the "fittest" (in each particular context) is most often selected.

Add in the process of culturally modified selection pressure, and it
  seems to me that even an "unfit" male would end up having a couple of
  offspring. The fittest male (or female) is no better off than his or
  her contemporaries because of this "leveling" effect.

"Culturally modified selection pressure", as you call it, is still selection pressure. Cultural factors can change what it means to be "the fittest" but there is no objective gold standard of "fitness". While it may be true that in modern human society, different characteristics are selected for than was the case with early Homo sapiens, this does not mean that "evolution is not occurring". On the contrary, it is occurring but perhaps it is moving in a new direction. In fact, this is essentially a circular argument. By definition, "fittest" means most likely to survive and reproduce. It does not mean strongest or fastest or prettiest. It just means whoever is better at reproducing. If that happens to be those individuals who are best at square dancing, then it is they who are the fittest.
Take the example of a modern human with diabetes. Medicine allows diabetics to lead fully productive and largely normal lives. So, perhaps diabetes is no longer a selective criterion. This does not mean that the diabetic cannot be selected for or against based on their fitness on other scales.
Whatever the selective pressure, whatever it may be that defines a "good mate", if selection is present then so is evolution. The only way to remove a species from the process of selection would be to have all (or none) individuals of each and every generation reproducing at the same rate. This is clearly not the case with humans. Surely not everyone around you has, or will have, children? There you go, selection!

UPDATE:
In answer to your comment, yes indeed, in order for a selective pressure to make itself felt and affect phenotype (at the species level), it needs to be constant across several generations. However, even the absence of selective pressure affects evolution. As others have mentioned below, active selection is not the only mechanism of evolution.
Your main question however seems to be the following: If modern society (medicine etc) allows individuals that would not survive in the wild to reproduce, how does that affect evolution? The main points in my answer, and all others here, are:

Even if we accept that modern humans have removed themselves from the purely "biological fitness"-based selection pressure (an assumption I am not at all sure is true), and assuming that this removal is constant enough over many generations (again unclear), even if all this is true, evolution is most certainly still occurring. It may even be faster since genotypes that would not survive in the wild persist in the gene pool, thereby increasing its diversity.
As you point out in your comment below, for such social pressure to make itself felt, it needs to be constant across many generations. We are probably not there yet.
Most importantly, as I said above, there is no such thing as an absolute biological fitness. When the ecosystem changes, so does the definition of fitness. Modern humanity's ecosystem, our habitat, is intimately connected with our culture and society. If an individual is better at reproducing in that context, then that individual is more fit.

Thanks for the answer. A follow-up: It's true that not all couples have the same number of children, but it seems like whether or not they have more children than average is no longer strongly dependent on biological fitness. Therefore, given that reproductive rates are fickle from one generation to the next (due to cultural factors), the signal would not have time to develop, right? It seems to me that there should be a persistent multi-generational selection pressure for the phenotype to develop, which is missing in the modern context. Maybe evolution is occurring, but significantly slower?

Very thorough answer. +1

I doubt that the distribution of reproductive success is exactly the same for men and women.  you are assuming that women and men have the same partners all through their lives, which is not so true at least in the US. In a society where a large percentage of children are born out of wedlock men and women do not need to have the same reproduction distribution. Also in polygamous societies or where there is gender based infanticide it doesn't hold. No judging here, just saying. Overall the point holds, but not sure you needed this base assumption.

@shigeta, for every child a man has, somewhere a woman has had one also and vice versa. Wedlock has nothing to do with it, nor does infanticide or anything else. This holds true for all (exclusively) sexually reproducing species. By definition.

@joebevo "It seems to me that there should be a persistent multi-generational selection pressure for the phenotype to develop, which is missing in the modern context. Maybe evolution is occurring, but significantly slower?"
... Evolution IS a slow process which has been occurring over billions of years, gradually fumbling its way along to the many species we know & others that have existed. Selection, though not constant, will have a temporary consistent tendency over a time frame which to us is huge (possibly hundreds or thousands of generations) but in an evolutionary sense it is very short.

Can I just add here that evolution would happen even without any directional selective pressure? You're all talking about fitness and directional selection, whereas selectively neutral processes (drift, migration) can also dramatically change the allele frequencies in a population ergo evolve the populations (think asteroid and the dinosaurs).

@yotiao, you're quite right of course. That's what I mean by "active selection is not the only mechanism of evolution" and it was also mentioned in DQdlM's answer below.

"That does not mean that all couples will have 2.5, or even that most couples will have 2.5." In fact, it's safe to say that no couples have exactly 2.5 kids.

@BruceAlderman well yes, I was going to make that point but then I figured that I might be belittling someone's personal tragedy. Do you know that no one has ever given birth to, say, a fine set of legs and attached pelvis alone? :)

+1 For noting that that the average number of kids per male is insignificant

I think that it is possible that the average number of kids per male to be different from the average number of kids per female. Consider this situation: Suppose the world has only one human male and two human females. If a male has exactly one kid from each of the two females, then the average number of kids per male is 2, while the average number of kids per female is 1

Let us not forget the effect of contraceptives and family planning, which is quite new. Now evolutionary very "fit" people can decide to have fewer kids.

Evolution is defined as the change in the allele frequency of a population through time.  In other words a change in the genetic diversity of the population through time.  This change can be the result of 4 processes, known as the mechanisms of evolution:
1) gene flow - this is the movement of individuals into or out of the population.
2) genetic drift - this is the removal of individuals due to random events (such as accidents).
3) mutation - this is the spontaneous change in the DNA, which instantly increases genetic diversity.
4) selection (natural, sexual or artificial) - this is the increase in the frequency of alleles (traits) that confer a fitness advantage (i.e., those with a given trait will leave more offspring). Most adaptive changes in gene frequency are the result of selection.
Even if one presumes that your analysis is correct and natural selection is no longer operating on modern humans (although this is suspect, as is pointed out by other answers), evolution would still be occurring due to mechanisms 1 - 3.  If we go further and consider the Earth's human population as a whole (eliminating gene flow as a mechanism) you would still have evolution via genetic drift and mutation.
In other words, yes, evolution is not only possible but inevitable in modern human populations.

In the US, different races have significantly different birth rates.  Obviously race has a genetic component, though I'm guessing that the racial differences are mostly due to cultural and economic reasons.  Still in this sense, the US population is evolving: alleles associated with some populations (African Americans, Hispanics) are becoming more common, while those associated to other populations (white non-hispanic, etc) are becoming less common.  So the US is definitely evolving to become "less white".  Note that this is true even though the overall birth rate reported in the study is not much above the minimal replacement rate of 2.0.
Another example: religiosity is associated with increased fertility, and there is some evidence that religiosity has a genetic component.  In that sense, the population may be evolving to be more religious over time.
Similarly, there are genetic factors to obesity, which has a negative effect on fertility.  These genes may even have been actively selected for in the past (the thrifty genome hypothesis), but are probably being selected against now.
We are currently undergoing one of the biggest shifts in human fertility in the history of our species: in the past century, we've developed technologies which allow people to more carefully choose when to become pregnant (condoms, abortions, hormone birth control).  Any genetic factor which has an impact on use of birth control could lead to evolutionary changes: this could range anywhere from ethnicity associated with economic or religious status (poverty, Catholicism), impulse control, etc.
This is all somewhat speculative (except for the first example), but it's certainly possible for evolution to occur in modern human society, and it likely is occurring.

I just want to emphasise that "races" is more of a social construct than a scientifically strictly defined category (see Razib Khan's comment here: http://blogs.discovermagazine.com/crux/?p=1350#.UR45L1qcYVo) . So while I agree with a term "alleles associated with some populations" the other terms you use ("race has a genetic component", "less white") are more murky (unless, in the latter example, you're talking about alleles associated with skin color - but then again, they do not necessarily correlate with ancestry).

I mean that there are differences in allele frequencies among the census bureau race/ethnicity categories.  These are probably self-identified groups, but there are differences in allele frequencies between the group of people who self-identify as hispanic vs those who self-identify as white/caucasian.  Alleles common in the former group are becoming more frequent relative to alleles common in the second group. Those would presumably include some alleles for skin pigmentation, among others (like variations in lactose tolerance, renal sodium channels, sickle-cell anemia, etc).

To rephrase that paragraph in more PC language: some self-identified ethnic groups have higher birthrates than others. To the extent that allele frequencies in high-birthrate ethnic groups are different from the mean frequency for the population as a whole, the US population is "evolving" to increase the frequencies of those alleles. I added "race has a genetic component, but..." to specifically avoid an interpretation that genetics were the cause of increased birthrates.

Darwin used the term “descent with modification” to describe evolution. That means a change between generations in the characteristics, or traits, of a population. It is a process which occurs by four processes - mutation, migration, drift, and selection. The conditions for evolution are i) a population must be able to reproduce, resulting in a descendant population, ii) offspring must tend to resemble their parents and this occurs because traits are determined by heritable information, e.g. DNA, and iii) that heritable information must have the potential to change from one generation to the next. It does not require selection.

Here is a paper about evolution and adaptation in humans:

"Despite popular misconceptions, natural selection does operate in
  modern human populations. New studies even show that changes
  associated with modernization are deeply reshaping selection pressures
  and, perhaps, bits of our biological nature."

Selection is still occurring in humans too, leading to further adaptation (a subprocess of evolution) (e.g. here and here). Many people naively think and suggest that selection has been halted in humans, the fact is, it hasn't. We still have variance in reproductive success based upon the genes individuals possess, e.g. some people die from genetic diseases before reproduction.

Here are some illustrations describing the mechanisms of evolution. Note that drift and selection both cause variance in reproductive success among individuals in a population, for drift the variance is independent of the genes, while for selection it is a tendency for the carriers of one allele to have higher reproductive output than another.
Mutation:

Migration:

Drift:

Selection:

Modern humans are continuing to evolve. Let me give you an example.
Before cattle were domesticated over 99% of all adults were lactose-INtolerant (i.e., they did not produce the enzyme needed to break down lactose (lactase) and could not digest it, i.e. got diarrhoea if they drank milk). All infants produce this enzyme, but in lactose-intolerant people the gene that codes the enzyme responsible for breaking down lactose becomes suppressed after the age of 1 or so. Before domestication of cattle, lactose-intolerant people were by far the majority in any human population. Why? Because if you never consume milk, constantly producing an unneeded enzyme is a huge waste of protein, especially in conditions of limited food supply. With the domestication of cattle, people who could utilize lactose suddenly had a huge advantage - they had another source of protein and calcium. They quickly became bigger and stronger than people who could not consume dairy products in adulthood. Thus, people in Europe and Africa (where cattle were domesticated) quickly became lactose-tolerant, unlike people in Asia, where to this day most people are lactose-intolerant. The evolutionary pressure at that time was huge - people in Europe and Africa went from mostly lactose-intolerant to mostly lactose-tolerant in 10 000 years or so. Interestingly enough, in this respect cats evolved in parallel to humans and now cats in Europe are predominantly lactose-tolerant, whereas cats in Asia are mostly lactose-intolerant.
Of course, this is not the only change that has occurred within the last 10 000 years and it surely is not the last one that will take place. It is just an illustrative (and hopefully interesting) example of evolution and natural selection in modern humans. In what direction humans will evolve in the future is very speculative.
As requested, a couple of references: http://evolution.berkeley.edu/evolibrary/news/070401_lactose
http://www.smithsonianmag.com/arts-culture/lactose-tolerance-and-human-evolution-56187902/?no-ist

can you please add some references to this answer

Evolution is possible for the same reasons it has always been possible (and I'll let the other answers' details comment on the mechanics, as they have done already...
I would like to offer a *slightly more philosophical point of view on the term, however.  I think that we have arrived at a point in our evolution where our prefrontal cortex is impeding our biologically driven urges, somewhat (which would have us evolving in similar ways to all the creatures less aware of the consequence of their actions).
I think it's impossible to say to what extent our evolution will now be driven by conscious choices we make about what traits we value vs. the traits that our biology drives us towards.  Certainly innate biological drivers are incredibly powerful, but as is evidenced by our desire to promote our intellect, and our progressive urge to help even the sickly and mentally challenged to get the most out of life (up to and including procreating), rather than to evaluate our potential partners purely based on physical traits and our brute strength, these purely biological imperatives are governing our reproductive choices less and less.
There is also much (reasonable) speculation as to what our new found understanding of genetics will allow us to artificially do to ourselves in the near future.
I think it's important to consider both these factors when speculating about how we're evolving, but I think it's not even slightly controversial to suggest that we're definitely evolving in a different way now than we were 500k years ago.


text:
A mathematician's confusion regarding parametric $t$ tests for gene expression data
I'm a mathematician trying to test some things on gene expression data, and I'm thus skimming over various articles such as Sotiriou et. al. to understand what is typically done with such data sets. Several things confuse me; in particular, a paragraph in Sotiriou et. al. reads:
"Clinical parameters such as ER status, [...] affect the behavior of breast
cancers. We asked whether these clinical/pathologic characteristics were
associated with differential gene expression. Parametric t tests identified 606
probe elements of 7,650 elements represented in our array that could segregate
ER+ and ER- breast tumors (P < 0.001)."
As segregation of ER+/- based on gene expressions is one of several things I'm
interested in attempting to achieve through novel methods, I have been trying
to understand what precisely is meant with the above paragrah. To recap the
article, there are 99 patients with 7,650 probe expression values, and one
ER+/- value each. The article sets out to determine which of those 7,650
probes successfully segregate the dataset into ER+ and ER-.
I've run the above paragraph by a nearby statistician, and he could not for
the life of him figure out what was done, and had not even heard of such a
thing as a "parametric t test". This leads me to suspect that the term is
specific to biology, so I ask: what is meant?  It is also unclear to me (and
him) what the P-value means in this context.
I hope the scope of this question isn't too broad. Of course I want to avoid
asking "explain this article to me, the outsider, please"; I do believe the
paragraph above is relatively self-contained in the context of gene
expression.
References:

Sotiriou et. al., Breast cancer classification and prognosis based on gene
expression profiles from a population-based study.

I understand this in the following way:
For each probe you have two sets of measurements, one for ER+ and one for ER-. What you do is a T-test (to my understanding is that the "parametric" just emphasizes that T-test is a parametric test) on these two sets, testing if their mean is significantly different (they refer to this as "separated"). You repeat this test for all 7650 probes, and you get a set of 7650 p-values. You then do some multiple testing correction, such as a Bonferroni correction (I haven't checked in the paper if they did it, but they obviously should). Finally, they find that 606 of the p-values are significant (for some choice of threshold), suggesting that they can "separate" ER+ from ER-.
As a computational biologist I would advise you to look specifically at bioinformatics papers if you are looking into developing new methods, since the analysis in "pure biology" papers can often be lacking and would not give you a good perspective of state-of-the-art analysis methods. Specifically for the question of separating groups from gene expression you should look into the field of Machine Learning, as it had been widely applied to this problem.

After checking the paper, the only adjustment they made (without explanation) is to lower thejr critical alpha value to 0.001, instead of the usual 0.05. With ~7600 t tests, these results are highly dubious. Even with a relatively straight-forward Bonferroni correction, the critical alpha value should be 0.05/7600 ~= 6.6 * 10^-6.

@leonardo sounds fishy... as I said, I wouldn't take this as an example of good data analysis. Although I believe that in the time since that paper was published some aspects of analysis in biology papers have become better, including multiple test corrections.

Thanks! Do any of you know of published clustering analysis of microarray data where the actual data that was fed into the big black box is available? As I am no biologist, processing "raw" data is quite difficult and seems to be a research area in its own.

@M.B. - I know of two databases (there are likely more). EMBL's ArrayExpress (http://www.ebi.ac.uk/arrayexpress/) and NCBI's GEO. There is a more comprehensive list over at Wikipedia actually: http://en.wikipedia.org/wiki/Microarray_databases .

This isn't the answer you're probably looking for, but I'd recommend not bothering with what they mean about their test in particular ... maybe they were really using a mann-whitney but their software (SPLUS) labeled it as a "non-parametric t test" for the non-formally-trained-statistical-end-user
[update]: I misread the text and thought you (and the paper) wrote "non-parameteric t-test" which is why I suggested a possible mann-whitney -- mistake on my part, sorry. The second part below still stands [/update]
Anyway, it has been nine years since that study has been published and the bioinformatics community has pretty much nailed down microarray analysis. Unless you have a specific reason not to, you should almost always prefer to use limma first for your analysis of such data (gene-level expression data). It has an extremely thorough user's guide to help you get started.
If you're looking for places to go to for follow up questions on your analysis, consider subscribing to the bioconductor mailing list, or head over to the biostars QA site.


text:
Filamentous algae - what exactly am I looking at?
I have just taken some images with my light microscope at 400x of  (what I think is) some form of filamentous algae from a local pond.
Now, I think I am looking at a single cell (centre) with some sort of arrangement of chloroplasts. Is this correct? Can anyone give me some more information on these structures?
I also have included a higher-constrast image of the specimen.

beautiful micrographs!  the chloroplast(s) look filamentous.

thanks @shigeta. I currently don't have a camera attachment so I had to hold my SLR up against the eyepiece!

Everything of our "common world" looks absolutely different when we look through a microscope :) try versatile materials like dusts, talcum powder, paper, section of foam-dishes, etc etc. beside biological things like fish scales, insects etc.

It looks indeed like a Spirogyra, or at least a member of the Zygnematales.
And yes, the green things are the chloroplasts (or one long chloroplast?), and they are arranged in spiral.
The "empty" space in the middle is likely the nucleus, and the darker circles within the chloroplast(s) could be the starch accumulated at the periphery of pyrenoids.

one long chloroplast? to my eye it looks 4 and that is quite clear from the photograph.

Almost certainly it is a filament of Spirogyra sp.

Cell at center outlined. Thick black line indicates chloroplast. Dotted black line is portion of chloroplasts shielded (hidden) by some other portion of chloroplasts. Chloroplasts are helical (spring-like). Some of the pyrenoids (nearmost to eye, not shielded) marked with blue ring. Other pyrenoids not shown to avoid complication. The grey bubble-like thing outlined and dotted with red, may be the nucleus (nucleus is usually difficult to see when not stained). Cell wall marked with brown. Septum between 2 successive cells, seems to be plain septum.
Number of chloroplast in Spirogyra depends upon species. The number can range from 1 to 15* or 16. In the cell at center, There are 4 chloroplast being seen.

Reference (*)
Algae /B.R. Vashista, A.K. Sinha, V.P. Singh/ S. Chand Publication / 2-colour revised edition.

Spirogyra. Apologies for the terse answer, but I think it does qualify.

also the name of a pop-jazz band of the 80s.

...and a 70s UK prog rock band before that!

ha no that's the one - i'm only remembering it from my uncles record collection, not from personal experience.  it was so progressive it didnt' sound like rock to me!

Further research reveals that they are now classed as " acid folk" which, as far as I recall, didn't exist as a genre back then. That's probably what confused you.

pond slime to 70's rock - i love it.


text:
How quickly can the human heart rate rise and fall?
How quickly can the human heart rate rise and lower?
For example lets say a human heart rate is rested and is at 60BPM and that person is suddenly scared to trigger their fight or flight reaction. Lets say their heart rate rises to double (120BPM).
From the above example their rate has gone from 1000ms between beats to 500ms between beats. Can the human heart instantly in one heart beat go from the 1000ms to 500ms between beats or does it need to ramp up? If yes how quickly can the heart rate ramp up?
I understand that each human heart is different, and that the speed increase and decrease will be different from person to person. What I'm looking for is a value that I can safely say the human heart won't exceed.
Similarly the same question goes to your heart going lower.

Heart rate is controlled beat by beat by the brain. Infact the native rate of the heart (the sinus nodal rythym) is around 100 beats per minute. The parasympathetic supply to the heart (through vagus nerve) supresses the rate to around 70-80. So if the parasympathetic flow is supressed, the heart rate will accelerate. Nerve conduction speed will then be the limit of speed at which the heart rate can be regulated.

According to the Wikipedia page on Supraventricular tachycardia the heart can go to a new faster rate in the space of a single beat, and then come down again just as quickly, as shown in this image taken from the Wikipedia page.

Thanks for the evidence. I was hoping the above not to be the case so I could apply some sort of validation off the readings from the pulse sensor I am using.


text:
What are the distinctive structural features of single- or double-stranded xRNA, or where can I find them?
I am interested in the structural differences caused by benzopurines and benzopyrimidines at the oligonucleotide level between RNA and xRNA, both in single-stranded and double-stranded form.
I am aware of RNA's tendency to be found in the A-form, of which the details are found here. However, other than the obvious nucleobase expansion, I can't seem to find any details about xRNA's secondary structure.

The only paper I found that examined the question is "Structural, Dynamical, and Electronic Transport Properties of Modified DNA Duplexes Containing Size-Expanded Nucleobases". They state

The results confirm that the structural and flexibility properties of
  the canonical DNA are globally little affected by the presence of
  benzo-fused bases. The most relevant differences are found in the
  enhanced size of the grooves, and the reduction in the twist.

They also have a picture comparing the structures of conventional DNA and xDNA:

So while the basic structure seems similar, the difference in diameter and twist look rather large to me.
This is for xDNA, I would assume that xRNA behaves comparably if double-stranded. It would have to somehow fit the larger nucleobases into the helix like xDNA. And the structure of single-stranded RNA is variable, helical parts would probably look similar to xDNA, hard to say how the modified nucleobases would affect tertiary structure.


text:
How are atoms in benzopyridines and benzopurines numbered?
I am well-aware of the numbering system used for the traditional bases, as seen below.

My question is how are the atoms in the size-expanded bases seen in xDNA and xRNA numbered?

This is a question of chemical nomenclature and the principle source for this is the IUPAC (IUBMB in case of biological molecules; but not in this case). You can find all hetero-ring nomenclature references on the IUPAC web site:
http://www.acdlabs.com/iupac/nomenclature/
http://www.acdlabs.com/iupac/nomenclature/79/r79_702.htm
(I'm skipping the actual naming step)
Numbering is actually done according to
http://www.acdlabs.com/iupac/nomenclature/79/r79_72.htm
That means, if you take the skeleton without hetero atoms, you start

in a clockwise direction commencing with the carbon atom not engaged
  in ring-fusion in the most counter-clockwise position of the uppermost
  ring, or if there is a choice, of the uppermost ring farthest to the
  right, and omitting atoms common to two or more rings.

Now, if there are more than one possibility due to symmetry, you chose the numbering that gives the heteros the smallest possible numbers (this means your purines would be actually wrongly numbered if they weren't an exception---see the List of retained names).
So, we have finally in dxC and dxT the start at the lower nitrogen, going anti-clockwise (the other N at 3, methyl at 6, ribose at 8), and in dxA and dxG similarly the start at the lower right N, going anti-clockwise with other Ns at 3, 6, and 8, and ribose at 8, as well.


text:
Slow-oxidative fibres vs fast-glycotic fibres
Why do slow oxidative muscle fibres contain more mitochondria compared to fast-glycolytic muscle fibres?

If I remember correctly, the slow oxidative fibers compose mostly structural muscles (thing multifidus, longissimus, capitus muscles) which are "on" a lot of the time but don't retract quickly like fast glycolitic fibres. Because the SO muscles need to be active most of the day, they probably have higher energy requirements - whereas FG muscles can get by with less because you can store enough energy for occasional activation (you're not doing pushups all day). It's been a while, though.

This is well-explained at the Wikipedia page on skeletal striated muscle.

There are two principal ways to categorize muscle fibers: the type of
  myosin (fast or slow) present, and the degree of oxidative
  phosphorylation that the fiber undergoes. Skeletal muscle can thus be
  broken down into two broad categories: Type I and Type II. Type I
  fibers appear red due to the presence of the oxygen binding protein
  myoglobin. These fibers are suited for endurance and are slow to
  fatigue because they use oxidative metabolism to generate ATP. Type II
  fibers are white due to the absence of myoglobin and a reliance on
  glycolytic enzymes. These fibers are efficient for short bursts of
  speed and power and use both oxidative metabolism and anaerobic
  metabolism depending on the particular sub-type. These fibers are
  quicker to fatigue.

In the terms used in the article, the Type II fibers rely on anaerobic, glycolytic metabolism, whereas the Type I fibers use oxidative metabolism which, of course, requires mitochondria for the TCA cycle and oxidative phosphorylation.The Type I fibers also contain myoglobin which promotes rapid movement of O2 through the cytosol to the mitochondrial ATP synthase.


text:
Does the speed of electrical impulses through neurones decrease with age?
From what I read on the NatGeo app, it stated that the speed of the electrical impulses that are sent by a neurone will be approximately 332 kilometers per hour.
Will the speed of this electrical impulse decreases over the years as we age?

I'm too busy right now to write a properly referenced answer... but you may want to have a look at this paper A theory of the effects of fibre size in medullated nerve - Rushton, J. Physiol. 1951, which gives very good explications (on a side note, look at the amazing aknowledgments at the end of the paper... precious!). Also, have a look at http://en.wikipedia.org/wiki/Action_potential#Propagation and http://en.wikipedia.org/wiki/Conduction_velocity

Myelination of neurons decreases with age, and that should reduce the speed of conduction.

As @Armatus notes, it is now generally understood that age-related cognitive decline is related to loss of myelination and axon damage (see, for example, Kohama et al, 2012). Myelin degeneration is also likely the cause of some age-related peripheral neuropathies. Loss of myelination (due to inflammation) is also the mechanism behind multiple sclerosis.
Myelin allows for fast and reliable transmission of action potentials by a mechanism known as saltatory conduction. This is necessary to compensate for axons which have small diameters (unlike the squid giant axon) and travel long distances. Degraded myelin will reduce conduction velocity and can result in propogation failures. The links @nico provided in his comment above are useful references.

Kohama, S.G., Rosene, D.L., Sherman, L.S., 2012. Age-related changes in human and non-human primate white matter: from myelination disturbances to cognitive decline. Age (Dordr) 34, 1093–1110.


text:
An unexpected mushroom in my garden
My grandma is a great fan of mushrooms and knows quite a lot about them. About 10 years ago, she started throwing out mushroom remnants in one special place, in order to grow her own mushrooms. In fact, for last three years we found some parasol mushrooms (Macrolepiota procera).
Today she found something, that nobody at home can classify. From what I searched, it might be  Cortinarius privignoides, but it is marked as almost extinct here in Poland, so I doubt this classification. Maybe you have seen this or know what it really is:

The hat is light brown with faint violet shades, the leg on the outside is partly violet too, but the inside is all white.
Some more photos:
All three
The gills are lighter brown, also with a violet tone
The cut through the leg
The cut through the hat
At my parents' house I found one more mushroom atlas, and a new candidate: Cortinarius traganus, but one thing is not right - the ones that I have don't have a smell and gassy webcap should smell and taste bad.

You might be better off asking this at gardening.stackexchange.com instead of Biology, unless a Botanist happens by here. :-)

Ooo! I did't even know about gardening :) Thanks!

If you know the german language, another good page is http://de.wikipedia.org/wiki/Wikipedia:Redaktion_Biologie/Bestimmung

Thanks to MCM's advice I know for almost-certain that this is Lepista personata.


text:
Why glycoproteins are better than non-glycoproteins in fulfilling biological tasks?
I have just an intuition that the carbohydrate part of glycoproteins help them to fulfil those tasks like in plasma membranes.
You can also get many more receptors if you can use carbohydrates too.
For instance, glycoproteins are necessary in recognising white blood cells. Antibodies are examples of glycoproteins. So they play a crucial role in our innate and adaptive immunity: MHC interaction with T cells in adaptive immunity.
Other examples: necessary in platelet aggregation and adherence, components of zona pellucida and connective tissue. Some hormones are also glycoproteins so necessary in humoral adaptive immunity: FSH, LH, TSH and EPO.
But why glycoproteins are "better" than proteins without carbohydrates moiety in fulfilling biological tasks?
I still see that both are important, but why the one is better than the other one.
In other words: Are there any biological tasks that only non-glycoproteins can fulfil, not glycoproteins? Are non-glycoproteins necessary in some essential biological tasks?
I think the answer to the last two questions is "yes", so why would one say that glycoproteins are better in fulfilling biological tasks than non-glycoproteins.

Essentially all cytosolic, nuclear and mitochondrial proteins are non-glycoproteins, so I think that the premise of the question is flawed. In fact, it isn't really clear what you mean by "better".

@AlanBoyd I completely agree with you. The thing is that the teacher wants explanations why some thing is better than other. I however do not see any sense in it. It is like comparing bananas with apples.

@masi, there are good reasons why membrane bound glycoproteins are suited for certain tasks. You cannot generalise though, it depends on the task in question.

The central reasoning is flawed because it places some intrinsic value on glycoprotein modification. The general intuition is that, if the protein is glycosylated, then it's likely for a reason, whether it be to help fulfil antigen recognition, adopt a correct conformation, or help in molecular tethering. Beyond, that, many (perhaps a majority) of cellular proteins are not glycosylated. Two important examples of cell membrane proteins that are not glycosylated would be endoproteases (eg, furin) and chemical transporters.


text:
Is There An Initiative To Sequence The Genomes Of Critically Endangered Species?
I realize that there are many isolated efforts to sequence the genome of a particular endangered species such as the orangutan or the snow leopard. However is there a concerted effort to sequence the genomes of every species on the brink of extinction? Also, is there an effort to sequence the genetic diversity of the surviving populations, since it would be very difficult to re-create alleles that would be needed if the species were to ever be resurrected.

Not an answer but I remember watching a documentary about a huge, international, "seed bank" containing cells from various species. So, not their genomes as such but the species themselves. I'll see if I can find a reference.

It seems like genomes are more valuable than spaceships.

It doesn't seem like there's a crowd-funded solution. That might be something to look into if you're interested.

The seedbank terdon mentions is the Norwegian Svalbard Global Seed Vault located at Spitsbergen island:
http://en.wikipedia.org/wiki/Svalbard_Global_Seed_Vault
However, the closest thing to a concerted initiative for sequencing animals I know of is the Genome 10K project:
http://genome10k.soe.ucsc.edu/
Their list of first 101 vertebrata proposed for sequencing contains 29 species with status RED from the red list. Most of them are only proposed, but the sequencing of the following are already in progress:

crested ibis (Nipponia nippon)
Amur tiger (Panthera tigris altaica)
cheetah (Acynonyx jubatus)
lion (Panthera leo)
domestic yak (Bos grunniens)
bactrian camel (Camelus bactrianus)

and that of the Chinese softshell turtle (Trionyx sinensis) has funding secured. Already complete are the giant panda, the chiru, and the polar bear.
And some surprising fact: where the funding is secured it is/was funded by the Beijing Genome Institute. A shame if this would remain the only one.

http://www.arthropodgenomes.org/wiki/i5K


text:
What do breeders call the effect when a breed resists modification?
It is impossible to breed a blue rose or a cat with a bulldog shape. This is because breeding is limited by gene variations in the population.
What do breeders call this effect?
UPDATE
I guess this term is from medieval and/or handicraft breeders, not modern and hi-tech.
UPDATE 2
I am speaking not about principal impossibility but just about observable or tangible barrier. We can be sure that it is possible to turn dog into cat in billion years, but it is much harder than turn German Shepherd to Yorkshire Terrier, which is possible for hundreds of years.
So, there are are two main types of changes, ones take hundreds of years, others take hundreds of millions of years. Former require genetic recombination while latter require genetic mutation.
This barrier was felt by breeders in practice and caused some versions of anti-evolution beliefs.
I need to know how this barrier is named.

I'm honestly not sure if one exists. They simply lack the gene/allele - the only specific term I can think of when it comes to lacking a gene is referencing Knockout variations where a researcher purposefully removes a gene from a subject in order to observe the effect.
However, "Knockout Mice/etc." imply intent on behalf of the researcher, not a result of breeding or natural lack of an allele. Perhaps "Genetically Incapable" would be a phrase meaning the same thing - but I'm not aware of any 'official' shorthand for 'Cannot because it's not in their genes.'

There must be a point where a desired trait cannot be obtained by selective breeding or by evolution at all!  Why can't there be viruses the size of houses or elephants as small as a flea?
Those may seem like absurd examples, but that's just to point out that not all traits can be obtained in less than infinite number of adaptive steps.  Jerry Fodor pointed this out (among other things) in his essay "Why Pigs Don't Have Wings".
Exactly what you can get and what you can't get is open to effort.  For instance I suppose you could turn a pig into a pigeon if you had a few million generations to do it - something similar to the evolutionary time back to the time they diverged.  That would be difficult, but you could basically run evolution for another billion years to get small hollow boned pigs with bats wings on their forearms.  you probably wouldn't recognize it as a pig, but then again youd be dead of old age several times over too.
Could you breed a human where bullets bounce off and they can fly?  not so sure of that.


text:
Do foods with preservatives become less toxic in the gut?
Do foods with preservatives stay digestible for longer in the gut by not rotting as much (producing less toxins)?

Hi @Jo Rijo, I edited your question to have better grammar and is now clearer. I'm not sure what you meant by the last sentence, from "doesn't start becoming toxic as fast thus the gut doesn't expel it as fast?" Can you clarify this please? Also, conservative is a poltical party, and preservatives prevent food spoilage. ;)

Please note that expulsion of feces is NOT at all due to food spoiling and becoming toxic.

@leonardo thx, I edited again, hoping it's clearer now. to clarify what you requested: I mean if the food has preservatives, then maybe it prevents the food decomposing as much as it would if it didn't have preservatives, thus not becoming as toxic as fast, thus the gut doesn't expel it as soon. hope that is clearer. But in the mean time nico has said what he said, but I don't really agree, I thought it was common knowledge that the intestines expel "stuff" that is sufficiently toxic, at least certain toxins, so...

@JoRijo no, that isn't the case :-)  I think your question is interesting but you might not get the answer you're looking for as your premise is incorrect.

what a mess :P I've done some more research and it was believed that food in the gut putrified and became toxic up until early 20th century when advances in science showed no evidence of such. source:http://www.ncbi.nlm.nih.gov/pubmed/2668399.

Do foods with preservatives take longer to digest?
Food preservatives are either antimicrobials (e.g. sorbate, sulfite) or antioxidants (free radical scavengers such as butylated hydroxyanisole).
Digestion is initiated in the stomach by hydrochloric acid and pepsin. It continues in the small intestine with the action of numerous other enzymes including amylases, lipases and proteases. There is no obvious way that these digestive processes would be inhibited by preservatives.

Can you please provide any proof of this? It is by no means obvious that and antimicrobial could not have an effect say, on intestinal blood flow...

You can only exclude specific effects. And you're right in suspecting that not all is well with food additives. Lots of people have intolerance/allergies to them. In general however, the answer is correct and if it weren't, the food industry would be buried with paper by lawyers.

@rwst: not necessarily. An additive can modify absorption of food without having necessarily negative effects. For instance, EDTA is sometimes used as a preservative, and it does halve absorption of non-heme iron. http://www.ncbi.nlm.nih.gov/pubmed/818893

Absorption isn't digestion.

Hum... well the antimicrobials, if they kill some of the helpful gut bacteria then It'd be expected that they affect the absorption rate negatively, right?

The OP referred to digestion. Digestion is the mechanical breakdown of food stuffs into small particles. To that end, @AlanBoyd has already mentioned how digestion occurs. There is nothing to suggest that food additives interfere with acid hydrolysis or other enzymatic breakdown of food materials. Whether these compounds inhibit intestinal absorption or uptake by gut microbiota is an entirely different question. Either way, as long as food can be mechanically broken down, there's nothing to suggest a healthy person cannot defecate normally.

Still, this does not exclude that a preservative could act as an inhibitor of an enzime (again, I can see how a calcium chelator such as EDTA could easily do that). I continue to say that this needs proper scientific sources.

If preservatives inhibit gut bacteria which aid in absorption, then preservatives could affect the body's ability to produce the digestive acids and enzymes in the first place.  That, in addition to the potential for more direct interference, it seems they are much more like to interfere in some way than to not interfere.


text:
Is there a circadian component to hunger?
I'm wondering what produces the feeling of hunger in humans. Checking Wikipedia revealed that leptin and ghrelin are two hormones involved. I've also read that the digestive system produces its own melatonin.
Because melatonin is related to circadian rhythm and the biological clock,Is melatonin involved in feeling hungry? Is there a circadian pattern to the levels of leptin and ghrelin in humans?

Many hormones aside of melatonin show circadian rhythms. I doubt melatonin is directly involved in this, but I would bet cortisol is for instance.

This question demands an answer that is tissue specific. Leptin is produced by skeletal muscle as well as adipose. Production of a hormone or signaling molecule may be under circadian control in one tissue but not another. In addition, a complete answer will talk about aging as circadian rhythms in peripheral tissues break down with aging.

Yes, absolutely. A major focus of understanding obesity, diabetes and other metabolic disorders are targeted to understanding the circadian (and other cyclical nature) systems in neurobiology and endocrinology. I can speak within the study of diabetes, there is an observed diabetic "dawn effect" in which there is an early morning (dawn) spike in blood glucose. The exact mechanism for this spike in blood glucose is not fully known, but the general circadian nature is intriguing and would suggest a dominant hormonal cause.
Some other review articles may be found here. An overall review of homeostatic balance as it relates to the central nervous system and apetite regulation. The second review more closely focuses on the biochemistry and endocrinology of central and peripheral regulation on food intake and physical activity.

Berthoud HR, Morrison C. The brain, appetite, and obesity. Annu Rev Psychol. 2008;59:55-92.
Lenard NR, Berthoud HR. Central and peripheral regulation of food intake and physical activity: pathways and genes. Obesity (Silver Spring). 2008 Dec;16 Suppl 3:S11-22.

I found additional information on the subject. Apparently Serotonin is also involved in feeling hunger and the motivation to eat. It also follows a diurnal/circadian pattern as described below:
Serotonin as as Gauge of food availability (appetite)

The expression of 5-HT2C receptors in the hippocampus follows a diurnal rhythm,[13] just as the serotonin release in the ventromedial
  nucleus, which is characterised by a peak at morning when the
  motivation to eat is strongest.[14]


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Screen brightness for reading in dark room
While searching online I did not find any conclusive article on whether it is good or bad for one's eyesight to read on a computer screen in a dark room. Most mention that it will cause strain that will go away after some rest (sleep).
My question is does reading in dark room has any long term effect on one's eyesight and what screen brightness setting (low of high) should one prefer if trying to read in a dark room?

This is rather close to personal medical advice, which is off-topic here. As written now, it's not really a biology question.

Not an answer, but just a suggestion:
If you are in a position where you must read off of a computer monitor without ample ambient light, I'd suggest you try setting your monitor/reader/whatever to have a dark background and light/wight text so it doesn't feel like you're staring into the sun.


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Do all sea creatures that have scales have to have fins?
Do all sea creatures that have scales have to have fins?
Do we know of any sea creatures that have only scales without fins?
I'm especially interested in fish that have scales but no fins.

The 'fish' part of this question may be circular, since fishes are a paraphyletic group. From wiki: "A fish is any member of a paraphyletic group of organisms that consist of all gill-bearing aquatic craniate animals that lack limbs with digits". In that definition, 'lacks limbs with digits' is a near-synonym of 'has fins' (the alternative being 'has lost all limbs'). If the group 'fish' were defined in the normal way (i.e., by phylogeny), then all of the groups mentioned in @Alan Boyd 's answer would count as fishes!

Very interesting question. It is stated in the Mishna (Ancient Jewish Texts) [Chullin 3:7] that there are no fish that have scales and not fins. Of course the definition of fish they were referring to was the swimming variety (not slithering or crawling). Later commentaries say that it was thought that the scincus marinus actually had scales and not fins. But it was redacted, due to the "skink" having legs, making it more of a lizard than a fish. So to answer the question, currently there is no fish (using the commonplace definition) that has scales and not fins. Plus a bunch of Rabbis put the

How about marine reptiles? Sea snakes have a paddle-like tail, so perhaps you would claim that as a fin, but maybe marine iguanas would qualify? And, of course, sea turtles.

Thanks Alan. Maybe you know of fish that answer the criterion?

Definitely not. Since the tail is the caudal fin, this hypothetical finless fish would have no means of locomotion.

Eels, but they have caudal fins... Would you consider rays to be finless?... Just checked, a ray's wings are considered fins...

Chitons have scales,but not like fish.


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Is there any evidence that a virus can modify human evolution
I was just reading Evolution of lactose tolerance, and in it one line says "But there was a time in human history when our diet and environment conspired to create conditions that mimicked those of a disease epidemic".
Something I've always wondered is rather than natural selection occurring and survival of the fittest and so on, is that a viral epidemic caused a mutation in the survivors, i.e. DNA was inserted from the virus that modified the survivors genome. There is some evidence that a significant percentage of the human genome comes from viruses. Probably a naive question - so is there any evidence that this has occurred? From my lay perspective this is what attempts at genetic engineering use, so it's possible nature already did this?
It's always seemed to me that natural selection and point mutations, and the chance meeting of two people with the same mutation would be too slow and viruses would be a more efficient method to evolve a large population at the same time. Things like punctuated evolution might support this? not really sure.

Why would two people with the same mutation have to meet unless the allele was recessive?

There is plenty of evidence of integrated viral genomes (eg, retroviral genomes) within the human genome. I don't think we currently understand the role the left over genetic material plays in human evolution, but we are certainly "stamped" with viral interactions.

those viral elements are still being evolved and altered into useful things by point mutations why would it e less effective? viral segments don't come into the genome useful they have ot mutate into something useful afterwards.

There is some nice work from Pardis Sabeti in this broad area (not just viruses but pathogens in general). Her colleagues have found polymorphisms in SLC40A1, encoding an iron transport protein, that influence susceptibility to tuberculosis. She's also looked at human genetic variation and susceptibility to Lassa fever. And this paper talks about CD36 and malaria in sub-Saharan African populations (no association). Look at her work from 2009 onward, as there is a lot there. They're also looking at variation in the pathogen because it is a two-way interaction.

The simplest example, that I can recall are the flu pandemics. The 1918 pandemic is the first to be described because of its severity, but quite possibly not the first in human history (see for example the Black Death - Yersinia pestis is a bacterium, but in the 15th century in just a few years it covered almost all of Europe, sometimes killing up to 40% of population in a given area).
Influenza pandemics appeared quite regularly during the 20th century, usually every 20 years and killed suspiciously many people compared to yearly influenza strains. Additionally, a person who survived one pandemic, was unaffected or only mildly affected by the next pandemic.
All this suggests, that the pandemics "clear" the population from susceptible individuals, and regularity of pandemics (notice, that 20 years is more or less the time of one human generation!) assures that the new generations also go through this kind of selection. The surviving individuals are more resistant to all strains of influenza then those, who never suffered from a pandemic. Maybe the influenza didn't mutate our DNA, but it could be a major force of natural selection.
And one more note: did you notice the great noise in media every time a new potentially pandemic strain is discovered? Actually, it's not just hyperboly of the danger. Last pandemic was in the '70s, so it's high time for a new one. And, since the last one was  almost 40 years ago, the new one (when it happens) will probably be very severe.

indeed, but the selection there is can this virus/bacteria kill me. You could argue that certain personality traits/intelligence etc was a byproduct of this - e.g. a fear of rats from the plague, and perhaps an intelligent person would be more inclined to notice patterns and adjust their behaviour to avoid infection. I was wondering if there was a more direct result - fragments of dna inserted into genomes that altered organisms, certainly possible I'd imagine - was wondering if it ever actually happened - that anyone knows about anyway.

I think it did, but right now this is just a vague memory of an Evolutionary Genetics lecture. I'll find more time tomorrow, and try to locate my notes and the actual data.

"[...] the new one (when it happens) will probably be very severe.". You were right about that.


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How useful are vitamin and trace element additions in E. coli culture medium?
In protocols for minimal media for growing bacteria I often see that a vitamin mix or a mix of various trace metals is added. But at least for E. coli I know that those are not strictly necessary, they also grow in minimal medium without any of this.
Does it make sense to add vitamins or trace elements when growing common E. coli for protein expression like BL21 (DE3) in minimal medium? Is there some literature data on how this can affect the growth of the bacteria?

Not sure that I have ever come across trace metals in recipes (I assume that you aren't referring to the Ca/Mg salts component of M9), but it is certainly the case that many K12 strains (e.g. C600, DH5α) require thiamine because they are thi mutants. This doesn't apply to BL21 since it is from a different lineage (it is a B strain). In a lab where several strains are being used it will always make sense to standardise on a universal recipe so that the medium available will suit all strains in use.
There is a useful list of E.coli genotypes here.

Adding trace elements (Fe, Co) and vitamins will increase the growth rate of E coli quite significantly.
However in the context of protein expression, more is sometimes not better. The proteins produced under high yield conditions may be miss-folded and non functional. The only way to know is to test it out.


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What triggers creative thought in humans?
Creativity, innovation and ideation. Is there something in the brain that makes the brain think that way, as opposed to "normal baseline". What triggers creative thought in humans?

Define idea, please. I have no idea what you mean with the term.

I mean the positive effect on cognition that allows a person to be innovative, think of new things, and in general be more creative.

I'm quite sure that, if there is such a system, evolution will select against it. Most people live quite well without being innovative or running after any new idea they come up with. I really think you're overly optimistic about the idea. Einstein also said genius is 5% inspiration and 95% transpiration.

Being overly optimistic about the idea supports my point :) This is exactly what I'm interested in - what are the systems involved in this and how long does it take for the system to reach homeostasis, where a person is no longer excited about the idea.

But don't you see? Being overly (!) optimistic about anything is a source of illusion that can, in the extreme, get you killed and certainly shortens your lifespan if applied constantly. That's why I said, evolution will select against it.

@rwst, I guess you a re a plant guy :). In animals, it is perspiration and not transpiration.

So you mean creativity?

Cretivity, innovation or ideation. What makes the brain think creative thoughts?

@rwst, innovative people would have been more likely to live longer than those who couldn't invent things.  Tribes that could invent tools and weapons would surely outlive tribes that could only use their bare hands to catch food.

This is a part answer to your question.
The three-factor anatomical model of human idea generation and creative drive presented in "frontotemporal and dopaminergic control of idea generation and creative drive" (Flaherty, 2005) focus on interactions in and between the temporal lobes, frontal lobes, and the limbic system.
Increase in the quantity of idea generation, at times at the expense of quality is associated with changes in the temporal lobe.  Conversely, frontal lobe deficits may decrease the quantity of ideas generated, largely due to judgements of an idea's worth.  The authors assert that interaction between the two mainly affects verbal and some non-verbal creativity
.
Further,

Mesolimbic dopamine influences novelty seeking and creative drive. Dopamine agonists and
  antagonists have opposite effects on goal-directed behavior and hallucinations.

The authors emphasise that creative drive is not the same as skill, and that the 3-factor model is an alternative to the left and right brain hemisphere skills based model.


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Is better healthcare a bane to the long-term survival of the human race?
The theory of natural selection has it that individuals with better genes tend to survive and reproduce, passing their genes to their offspring. This gradual process results in a population more adapted at survival. However, due to the advancement in medical science, humans with poorer genes tend to survive and reproduce just as well.
For example, in the past, many people, excluding those with natural immunity due to some genetic mutations, would have succumbed to illnesses such as malaria and typhoid. But with better hygiene and medical treatment, these patients tend to survive.
Now, imagine a future where all illnesses including cancer can be treated. How would it impact the survival of the human race? Would we become more and more vulnerable such that our survival hinges heavily on medical technology, analogous to how an astronaut's survival is dependent on his spacesuit?

First, healthcare after reproductive age should not affect the survival of the humans as species. Second, if healthcare is here to stay, not just some temporary episode, then even healthcare for those under reproductive age shall not harm survival of humans, no more than knives and fire would harm survival. Think of healthcare as another tool like fire and knives and there should be no reason it would harm the survival.

Gene frequencies (frequencies of each allele at a given loci) in populations are affected by many things divided in to systematic and dispersive processes. Systematic process (migration, mutation, selection) affect gene frequencies in an often quite predictable manner and strength. Dispersive process (Random drift, differentiation between sub-populations, uniformity within sub-populations, increased homozygosity) are random in their direction and only predictable in their amount. Your question focusses on the systematic process called selection.
In a large population (if we ignore dispersive processes for the time being) the gene frequencies will reach an equilibrium called Hardy-Weinberg equilibrium. This means, with constant rates of the systematic processes, each locus will reach a point of stable equilibrium. Mutation and migration bringing more variation, and selection reduces it (over simplified - sometimes selection maintains variation, see my answer about why variation exists here). The frequency of each allele at equilibrium will be where these effects balance out. If selection becomes weaker against one allele it will become more frequent in the population.
By using medicine etc. to cure diseases we reduce the selection acting on a deleterious mutation thereby putting the gene frequencies in to a state of flux during which they move to new equilibrium points. So in short the answer is yes, modern medicine is decreasing our genetic fitness by allowing deleterious mutations to become more common.
I raise the question, will we ever be able to cure all genetically caused disease? In my reckoning, no, at least certainly not in our lifetimes.
It only represents a real risk if we suddenly are unable to cure diseases. This would increase selection against that allele and the gene frequencies would move back towards the equilibrium point which existed before the selection was reduced. What this means for the population is the loss (death) of those with the low fitness genotype.
The best reading you can do on this is the opening chapters of Falconer and Mackay's Introduction to Quantitative Genetics. Also read about Hardy-Weinberg equations.
HTH

I have to read a few times to understand. But this is certainly a great answer!

I know how you feel, I have read the chapters in that book many times and they are not easy! condensing it down was hard!

"It only represents a real risk if we suddenly are unable to cure diseases." True that. -- Late to the party but have you considered that one possibility is the degradation of our ability to think well? The only realistic (and hopefully astronomically unlikely) scenario in this regard is where humanity is dependent on technology and the tech fails for some reason. -- Biological warfare seems orders of magnitude more likely to cause us serious permanent harm .

The theory of natural selection has it that individuals with better genes tend to survive and reproduce, passing their genes to their offspring.

Yes, under selective pressure, that is. The stronger the selective pressure, the more the population will change. Without a selective pressure, there isn't an impetus to change.

However, due to the advancement in medical science, humans with poorer genes tend to survive and reproduce just as well.

You're making a mistake. "Poor" and "Good" are purely contextual. You might say that Sickle Cell Anemia is a poor lot to be stuck with... Unless, of course, you're in an area ravaged by Malaria. Then it's a boon.
What would be more accurate is that there aren't any strong forces acting upon humans that causes selective pressure and the proceeding adaptation. Of course, we are the result of such evolution, so by a basic standard all modern humans who reproduce are fit in a Biological sense.

For example, in the past, many people, excluding those with natural immunity due to some genetic mutations, would have succumbed to illnesses such as malaria and typhoid. But with better hygiene and medical treatment, these patients tend to survive.

The brain is the one of the finest products of evolution. Because we're no longer dying en masse at the whims of bacteria or virii (usually) does not mean we haven't adapted. Our ability to build advanced tools and perform science is an adaptation. One for which we pay heavily; we're practically helpless until our teens.

Now, imagine a future where all illnesses including cancer can be treated. How would it impact the survival of the human race?

We'd live longer, and assuming the rate of reproduction stays the same, there'd be a lot more of us.

Would we become more and more vulnerable such that our survival hinges heavily on medical technology, analogous to how an astronaut's survival is dependent on his spacesuit?

Well... Vulnerable to what? To disease? Probably not. Current Immunizations and treatments often utilize the body's own immune system; basically getting sick and all the benefits of encountering the disease without the side-effects of significant death.
To genetic diseases? No. The human population has exploded in the last hundred or so years, and our genetic diversity has been greater than at any point in the last 40,000 years when a major bottlenecking event occurred. For a genetic disease to deal significant damage on a species, it would have to be suffuse throughout the population. That's not happening.
To a post-apocalyptic world where technology breaks down and suddenly we're facing off against parasites and predators? Well, if the event ever occurs, then a lot of us won't be ready, that's for sure. The stress such a life put on us in the past limited our lifespan to nearly half what it is now, but unless there's a complete lack of knowledge many basic safety habits should persist. Cooking, boiling water, dressing wounds, how illnesses spread - these are all things which dramatically increase quality of life when utilized correctly.
Will we ever reach a point where we, quite literally, cannot live without technological intervention? No idea. Humans have very, very strong reactions to things which aren't human but appear human (The Uncanny Valley is a great example). It's just as possible that those instincts will prevent us from such a fate as the possibility that we'll be completely fine with becoming cyborgs. Nobody can even begin to give you a time-frame, though. As-is, there's no reason to become cyborgs (no Selective Pressure), and won't be for the foreseeable future.


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Modern reference for Kropotkin's lazy bees
I have been reading through Peter Kropotkin's Mutual Aid: A Factor of Evolution and he mentions a curious fact about bees (bolding by me for emphasis):

predatory instincts and laziness continue to exist among the bees as well, and reappear each. time that their growth is favoured by some circumstances. It is well known that there always are a number of bees which prefer a life of robbery to the laborious life of a worker; and that both periods of scarcity and periods of an unusually rich
  supply of food lead to an increase of the robbing class. When our crops are in and there remains but little to gather in our meadows and fields, robbing bees become of more frequent occurrence; while, on the other side, about the sugar plantations of the West Indies and the sugar refineries of Europe, robbery, laziness, and very often drunkenness become quite usual with the bees. We thus see that anti-social instincts continue to exist amidst the bees as well;

He does not provide a citation for this (and even if he did, it would be something from the late 1800s). Is there a good modern reference for the above behavior?
I would in particular be interested in something like a graph of %-robber-bees vs. plentiness-of-food (in some abstract measure of the latter) so that I could intuitively see the increase in lazy/robber bees as the environment is low on food, or as it is overly abundant and compare it to 'typical levels'.
Theories that explain this behavior are of interest, as well, but I am primarily after experimental measures/observations to support and quantify the above quote.

Can you define what you think he means by Robbery? Is it robbing from the plant or raiding other colonies?

@niallhaslam that is his full treatment of the subject. He says nothing more on it in terms of defining things.

@niallhaslam I think we can assume that he's referring to what we would call today "cheat" or "selfish" individuals, rather than nectar robbers.

The quote refers to 'robber' bees, but in today's terminology, there are actually three separate phenomena. "Cheating" in bees and other social animals refers to the exploitation of a social contract for one's own benefit. Example: bee workers lay their own eggs rather than tending those of the queen. "Laziness" or "inactivity" of bee or other social insect workers is incredibly widespread, but it is not clear that it is selfish: it may be a side-effect of imperfect task allocation, or those individuals may be a reserve work force. "Robbing" in bees usually refers to removal of nectar or pollen from flowers without pollinating them.
"Cheating" associated with illicit reproduction is widespread in social insects, including in bees, and there's a broad literature on it (search terms "anarchist" "queenright", "policing") but it sounds like your question concerns differential effort and environmental resources specifically.
Differential effort in labor ("laziness vs. busynesss") has been seen in many social animals. The way you frame the question seems to be in terms of:

"how many lazy individuals can a society tolerate given environmental
  conditions?"

Most observational/experimental studies seem to have approached the question in terms of:

"how can what appears to be cheating actually be adaptive?"

For instance, Kukuk et al. suggest that in Halictine bees, lazy bees who avoid the high-mortality-risk foraging tasks are actually acting as caretakers and orphan-rearers for the brood of the foraging busy bees. It's also been proposed that apparently lazy insects act as a "defensive reserve" for the nest, although at least in Bombus impatiens, experiments show no evidence that lazy bees defend any more than busy bees (Jandt et al.)
Lazy individuals could also be acting a labor reserve ("substitute helpers"), in case of food or colony depletion. To me, this scenario is the closest to what you mention – the idea that lazy individuals become busier, either voluntarily or through coercion, in time of need. Baglione et al. show that this is the case for carrion crows, and quantify it to some degree along the terms you suggest. On the other hand, Cartar (cited in Jandt and Dornhaus) shows that for a number of bumblebee species, it was more likely that busy bees would work harder or switch tasks than it was that the lazy bees would become busy!
In sum, what you/Kropotkin suggest exists in all social insects, although the mechanisms of sociality and of laziness are diverse and various among species.

 Baglione V, Canestrari D, Chiarati E, Vera R, Marcos JM. 2010. Lazy group members are substitute helpers in carrion crows. Proc Biol Sci 277: 3275–3282. (free)
Cartar RV. 1992. Adjustment of foraging effort and task switching in energy-manipulated wild bumblebee colonies. Animal Behaviour. (full text not online?)
Jandt JM, Robins NS, Moore RE, Dornhaus A. 2012. Individual bumblebees vary in response to disturbance: a test of the defensive reserve hypothesis. Insectes sociaux. (behind paywall, buy Jandt kindly has uploaded for free on her site)
 Jandt, Dornhaus. 2009. Spatial organization and division of labour in the bumblebee Bombus impatiens. Animal Behaviour 77: 11–11. (behind paywall, but also free on Jandt's site)
Kukuk PF, Ward SA, Jozwiak A. 1998. Mutualistic benefits generate an unequal distribution of risky activities among unrelated group members. Naturwissenschaften. (Behind paywall, but this free article by Forbes et al. reports similar information)

Also see:
Jandt JM, Dornhaus A 2011 ‘Competition and cooperation: bumblebee spatial organization and division of labor may affect worker reproduction late in life’, Behavioral Ecology and Sociobiology 65: 2341-2349.
- shows that selfishness/cheating may actually play a role
Dornhaus A, Holley J-A, Pook VG, Worswick G, Franks NR 2008 'Why do not all workers work? Colony size and workload during emigrations in the ant Temnothorax albipennis' Behavioral Ecology and Sociobiology 63: 43-51
- this paper reviews other literature about how many bees/ants in a colony are lazy; up to 75% or even more at a time!