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What does the term 'bioavailability' mean?
From what I've read,

Bioavailability is the degree to which food nutrients are available
  for absorption and utilization in the body.

How would you explain this with an example?

Bioavailability is a concept which applies to nutrients and drugs which pass through first-pass metabolism, i.e. orally (and to some extent nasally) consumed substances. Anything absorbed in the gut first passes through the liver before reaching the rest of the circulation, and both the gut and liver may metabolise it to some extent. The liver in specific has the powerful Cytochrome P450 system, a huge variety of enzymes to break down all sorts of substances, although in some cases it can actually produce more active or even toxic forms instead of breaking them down.
This can lead to drastic reductions in the amount available in the systemic circulation after oral administration. E.g. propanolol (a beta blocker) needs to be given in 100mg doses orally while intravenously (avoiding first-pass metabolism) only 5mg are needed.

Why is the bioavailability of drugs more important than the bioavailability of nutrients?

An unfortunate choice of words, you are right. I'll adjust that :)

Bioavailability is also used in plant biology with a similar meaning; the amount of a substance (nutrient) that can be absorbed by the plant. For example a soil can contain a lot of Phosporus, but only a small part is bioavailable.

IMPORTANT:  In addition first-pass metabolism, bioavailability also accounts for any hindrance of absorption through the gut wall due to limitations in solubility or permeability of drugs or nutrients (see BCS classification of oral drugs)


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What is the DNA/protein charge ratio?
To study DNA-protein interaction, I want to do a DNA retardation test by mixing the protein with DNA and afterwarts loading it on an agarose gel to see if the DNA migrates slower. I've found some articles where they do this and they state that they mix the DNA with protein in an 1:8 charge ratio, but I can't really figure out how to interpret this
Could anyone tell me how to calculate a DNA:protein charge ratio? If 1:8 is stated, how should I interpret this?

Could you please provide some more context, I'm having a hard time understanding what exactly you want to know.

I am guessing this refers to the isoelectric charge of protein molecules vs DNA molecules?

@Mad Scientist To study DNA-protein interaction, I want to do a DNA retardation test by mixing the protein with DNA and afterwarts loading it on an agarose gel to see if the DNA migrates slower. I've found some articles where they do this and they state that they mix the DNA with protein in an 1:8 charge ratio, but I can't really figure out how to interpret this

This is really sounds like a guideline, a starting place, not necessarily your best protocol.
In practice its hard to be more specific as MS says.  The pH of the buffer will affect the charge of the protein, and to a lesser extent the DNA.
Also the protein may have an ideal pH for binding which you could guess is in the range of 7.0-7.4, but might find that the strongest binding depends on unexpected pH and salt concentrations, or the addition of a small molecule.
The affinity of araC for instance is greatly increased by the presence of arabinose in sufficient concentration.
lac Repressor, in contrast releases itself from DNA in the presence of IPTG or  lactose.

source: Stack Exchange

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What is the relative power of GWAS studies in different species?
I would like to know of any publication studying the relative power of GWAS studies in different species. For example, I've seen reports that say genotyping and GWAS in dog breeds is much more powerful than in humans due to the extent of linkage disequilibrium and other population genetics considerations. Some claims say that many GWAS studies in dogs are 10-20x more powerful than many GWAS studies in humans. I have also heard from pigeons (pigeon-omics) to be a similar case. I would like to know if there are other comparisons for other species and the relative power of discovery for GWAS studies compared to human. For example, are there any numbers for yeast, Drosophila sp., C.elegans, zebrafish and then also for plants like maize, rice, etc.?

Part of the increase in power to detect a genetic association via GWAS-genotyping comes from long haplotypes. Many dog breeds went through selective breeding bottlenecks 100-200 years ago. Many lab model organisms, such as flies, worms and plants, have recombinant inbred lines that aid in GWAS discovery as well. The price one pays for this increased power, say for canine GWAS, is not being able to pinpoint the casual variant. The association SNP(s) found may be far, far away from the gene responsible for the phenotype, because of that long LD.
Another aspect not to neglect is the phenotype. In humans, there may be a 3-fold range in phenotype p, while in dog that value is just 35% (1.35x). That may mean that the phenotype is difficult to measure (accurately) and to assign to a given allele with statistical certainty.
A third aspect to consider is the effect size of the association, say on a per (risk) allele basis.
Thus, while I am not aware of any papers specifically taking such elements as haplotype length, phenotype range and effect size into an analysis of GWAS power across species, I feel that one versed in genetics of the organism of choice can readily accomplish this for the specific trait(s) of interest.

Does this mean that what one gains in increased power in canine GWAS is then partially lost in accuracy of fine mapping the causal SNP? See this piece I found: "The breed structure of dogs comes in particularly helpful here, as the very long haplotypes within breeds allowed the detection of the oncogene in a poodle-only dataset using only a 50,000 variant map, and the association could then be fine-mapped to a few tens of kilobases by looking at haplotypes across different susceptible breeds"

question looks like it's been dormant for a while, but i think there's some discussion to be had here-
I would argue that in many (most?) of the model organisms, power would be much greater than humans. Frequently (worms, mice, plants, yeast) you can work with basically isogenic inbred lines. I would argue this is much more important than long haplotypes:
a) less importantly, no heterozygosity.
b) more importantly, you can re-phenotype the same line repeatedly to directly estimate experimental/environmental variation, and get a very precise estimate of actual E(phenotype | genotype). this is opposed to humans, where you have the one individual, so you just have to pray that your experimental/environmental variation is low and your heritability is high in the sample population.
For example, for just 100 inbred lines of a plant, you get massive, beautiful GWAS peaks for many phenotypes: Atwell et al. 2010. Human GWAS sample sizes generally have to be in the 1000s before they are sufficiently powered (ref).
This subject is discussed a little further here.
In direct reference to the long haplotypes, note that power and mapping precision are different things. That is, your power to detect an association can be extremely high, but you might have a very broad chromosome interval that you will then have to go hunting in to find the causal locus. Note that this problem might actually be worse with large effects, which are probably under selection if they are interesting, and thus there is likely to be substantial linkage disequilibrium between the causal locus and surrounding regions. Of course, if the effect size is small (generally the case in humans though not in other orgs), this is less of an issue.

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Alternatives to fittest-win and Moran processes as simple mathematical models of selection
When modeling selective sweeps as a micro-building block in models of macroevolution (not to be confused with misuses of this in creationist arguments), I use the fittest-win model of selection as a first approximation, or Moran process model when I want a more reasonable approximation.
In the fittest win model the probability for a mutant of fitness r to invade a host population of fitness 1 is 100% if r > 1 and 0 otherwise. In the Moran process model, the mutant of fitness r invades with probability $\frac{1 - r^{-1}}{1 - r^{-n}}$ for a finite population. Alternative in the limit as n goes to infinite, a mutant with r > 1 invades with probability $1 - \frac{1}{r}$ and 0 otherwise.
In general I am interested in simple models of selection of a single (or small concentration of) mutant invading an asexual host population of fitness 1 (with fitness constant and independent of frequency). Are there other common mathematical models for selection of this type?

I may suggest to give a look to game theory based model and their generalization from homogenous spatial diatribution to network like model. An easy review can be found in Martin A. Nowak's Evolutionary Dynamics (Harvard press 2006).
In particular you can see the classical Moran process as an evolutionary graph game going on a complete graph with identical weights. Changing the topology of the graph can give different results, though it is not necessary (and there're results showing in which case a graph behave just as a Moran process).
Graph related behaviour are, i.e., suppressing or amplifier of selection...


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Online toolkit that provides functional similarity scores (in the form of a matrix) between two functional gene sets in the context of gene ontology
Where can I find an online toolkit that provides functional similarity scores (in the form of a matrix) between two functional gene sets in the context of gene ontology?
I have tried the following:

Batch tool for GSFS: PROBLEM: It says that my input yeast genes are not human genes (which probably means that the tool will work only with Human genes).
http://bioinformatics.clemson.edu/G-SESAME/Program/geneCompareTwo1.php : PROBLEM: provides score for every gene pair input. I have ~3600 genes. Impossible to do it for eveyr pair.
DAVID batch viewer gives a 1xN matrix (functional similarity score of one gene to a set of N genes, when I want all possible pairs of similarities which will give an NxN matrix)
GO funsimmat- I am unable to get this to work, so I'm not sure if it will give me the desied results.
GO FastSemSim- same as 4.

I think that you could try a similar approach to GSFS:

use transduction in proteins (if you don't know star code, then you must use 3 strings for each gene)
use a basic tool (a stand alone like UNIPROT tools) to identify the proteic domain type (chain alpha, ..)
divide the genes by proteic domain type (pdt): which contains which pdt and the pdt order frequencies

Now, you could use DAVID or similar (try wconsensus: it's old, basic but very custom) to compare similar sequence and obtain your scores.


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How do archaea relate to eukaryotes and bacteria?
I've read that they all share some genes, internal structure, and behaviour with each other, but with different degrees of overlap depending of what the function is. E.g., archaea have some eukaryotic and some bacterial function, and eukaryotes have bacterial function in the form of mitochondria and plastids.
However I'm finding the nitty-gritty of all this rather confusing. Could anyone please explain some of the detail for me as I can't seem to make any sense of this from reading Wikipedia, etc.

Heheh!  Wish I could upvote your username, "Luke".  :)

The relationship between the three is so overly complicated because of horizontal gene transfer, i.e. cells sharing parts of their genome with others instead of the normal passing-down to the next generation. This works between eukaryotes, archaea and bacteria and causes the mixing of the three.
An overview (originally proposed by Woese et al):

Bacteria are simplest considering cellular organisation. They have no nucleus or other internal membranes and no cytoskeleton. Their DNA is generally "junk-free"* (i.e. no introns), not bound by histones ("organising" proteins) and the organisation of regulatory sequences is relatively straightforward, typically with one 'operator' sequence before a gene.
Eukaryotes are complex cells in comparison. They have a nucleus and are full of internal membranes (ER, golgi, vesicles,...). Their complex cytoskeleton allows them to grow very large in comparison. Their DNA is usually full of more or less "junk"*, organised into tight bundles by histones and they tend to have a ridiculous amount of regulatory sequences way before, just at the start and even inside genes. Very importantly, they possess endosymbionts as you mentioned - mitochondria or plasmids, derived probably from some protobacterium.
Archaea at first appear to be a mixture between the two. A nice way to sum it up (though not very accurate) is "eukaryote in a bacterium's clothing". Their cells look a lot like prokaryotes because they are similar size, have no nucleus, endomembranes or cytoskeleton. However, some archaeas' DNA is bound by histones and they use similar machinery as eukaryotes for DNA replication, transcription and translation.

One possible explanation for this (theory by Margulis & Schwartz as explained by my tutor) is: From the last universal common ancestor, first prokaryotes and archaea diverged. After this branching, the differences in genetic machinery evolved. Archaea then branched, producing a protoeukaryote line which went on to endosymbiosis with some protobacteria. That would explain the similarities I outlined above: similar cell structure between archaea and prokaryotes but similar genetic machinery between archaea and eukaryotes.
It gets a bit more complicated though, because archaea and bacteria can exchange genetic material, and eukaryotes incorporated a lot of their endosymbionts' DNA in their own genome, so you end up with all of them having a huge mix of genes from the others.
Edit: Genetic machinery refers to the enzymes used for DNA replication and transcription (DNA and RNA polymerase and the transcription initiation factors) and translation (ribosomes and several other translation factors involved). For example: Prokaryotes only have one type of RNA polymerase which uses sigma factor to bind the initiaion site. Eukaryotes and archaea both have three types of RNA polymerase which use TATA-binding protein for initiation. Or: In Prokaryotes, the translation start codon codes for formyl-methionine while in eukaryotes and archaea it codes for "normal" methionine. (Source)
*) Unrelated to your question, but in my own defence: I am aware that the usage of the word "junk" is somewhat unaccepted nowadays, because it supposes that there is "useful" and "unuseful" genetic material. Also, some of what was thought to be junk has been identified to have regulatory function etc. However, it's also a fact that a lot has been identified to have no function to the cell whatsoever, most of it parasitic DNA which is dead or still happily replicating away (LINEs and SINEs). That is, "junk" to the cell.

Thank you for your reply, very interesting and certainly explains a lot! Could you please clarify a little further what you mean by genetic machinery though, and what are differences?

Made an edit :)

“just a theory” … aaaargh! Otherwise very nice summary, the only thing it’s missing is references. If I find time later today I’ll dredge them up, I have them somewhere …

Here's ref :) I could only find it on amazon though.

Isn't this the Margulis & Schwartz paper?

The link is the book my tutor gave as reference but that paper could have the same content.

Indeed the situation is a bit complicated and not totally well understood.  Archaea and bacteria are superficially very similar, they're both small, have circular chromosomes, and not a lot of internal complexity.  However, there are some very important differences, most notably they have very different cell membranes.
The origin of the eukaryotic cell is a very difficult subject, as it evolved over 2 billion years ago in organisms that don't fossilize well and there are no living descendants of intermediate forms.  (E.g. every known Eukaryote is descended from a eukaryote that already had mitochondria.)  My understanding is that the leading theory is that the eukaryotic cell was formed by endosymbiosis between an archaeon and two bacteria.  In that model the nucleus is descended from a methanogenic archaeon, the cell membrane is descended from a myxobacteria, and the mitochondria is descended from a proteobacteria.  But this is not fully understood, and there are several competing theories on the details.
One place to start reading about this (beyond wikipedia) is a nice article by Carl Zimmer in Science.


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Deletion errors with Phusion Polymerase?
I was wondering if anyone has ever seen large deletions (~40-50 bp) occur when using phusion polymerase to clone a gene.  I have recently tried using Circular Polymerase Extension cloning to clone a 200 bp insert into a 6.5kb plasmid and obtained two separate clones with 40bp+ deletions in the center of the insert.
Phusion has a 5'->3' exonuclease activity, but I didn't think it could cut in the center of a sequence.  While our inserts were created with oligo synthesis, it is my understanding that such large deletions are rare with oligo synthesis. If you have heard of this happening please let me know.

I don't think that it would be an exonuclease issue. Rather it may be an issue with hairpin formation during amplification. Are you sure you have the complete 200 bp insert?

I've just seen a 12 bp insertion in a cloned sequence amplified with Phusion polymerase.

In my own personal lab experience, I got some unexpected results using Phusion polymerase. However, I have not seen deletions, only insertions (ranging from single bases to 3 tandem copies of a primer sequence). This is not an answer to your deletion question, but it does suggest unusual things might happen.
I have seen deletions with T4 DNA polymerase during "blunting" reactions. According to the NEB website:
Q10: Is T4 DNA Polymerase active at room temperature?
A10: We suggest 12°C. The DNA ends "breathe" at higher temperatures allowing the exonuclease to remove nucleotides past blunt.


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Is there a consensus on whether or not race exists on a biological level?
The most recent survey I could find was from 1985 which said that 16% of biologist disagreed that "[t]here are biological races in the species Homo sapiens."
I was wondering if there's been a change in this position.

What, only 16%? That’s markedly different from the consensus that I’ve experienced so far, which is almost unanimously against a meaningful biological basis of races.

possible duplicate of Do humans have enough biological differences to be grouped into races or subspecies?

@GoodGravy Thanks for the link. Wasn't around when I asked.

This has been investigated extensively on skeptics.stackexchange.com.
Unfortunately, it’s not easy to determine a scientific consensus since nobody has cited a relevant survey. On the other hand, here are some salient quotes from scientific literature (stolen from the answers to the above-mentioned question) which I find worth repeating:

A subspecies (race) is a distinct evolutionary lineage within a species. This definition requires that a subspecies be genetically differentiated due to barriers to genetic exchange that have persisted for long periods of time; that is, the subspecies must have historical continuity in addition to current genetic differentiation. [Templeton, 1998], cited in [Long & Kittles, 2003]

Which speaks against the existence of races as a meaningful biological concept.
On the other hand, Jorde & Wooding (2004) contend that,

Genetic variation is geographically structured, as expected from the partial isolation of human populations during much of their history. Because traditional concepts of race are in turn correlated with geography, it is inaccurate to state that race is "biologically meaningless".

But they concede that

there is no scientific support for the concept that human populations are discrete, nonoverlapping entities.

Finally, it’s worth noting that in the universally agreed-on taxonomy, formalised in the International Code of Zoological Nomenclature there simply is no category for races, whether they would make sense or not. Whether or not this view enjoys a majority vote in biology, it’s the de facto consensus.

Jeffrey C. Long & Rick A. Kittles, Human Genetic Diversity and the Nonexistence of Biological Races, Human Biology 75 (4), pp. 449–471, Aug 2003
Lynn B. Jorde & Stephen P. Wooding, Genetic variation, classification and ‘race’, Nature Genetics 36, pp. 28–33, 2004

Anatomically modern humans are less than 200K years old, left Africa (or possibly Africa and Arabia) only 60K years ago, and migrate quite a lot (think of the Mongol invasion).  So you would not expect to have clear divisions into subspecies.  And indeed a quick search of google scholar pulls up no claims in the literature for human subspecies of anatomically modern humans (i.e. no subspecies of homo sapiens since Neanderthals and Denisovans).
On the other hand, it's certainly the case that you can work out a rough phylogenetic tree of humans.  Native americans are descended from certain northern and eastern asians, and so in the 1400s were more closely related to them then they were to other humans.  Similarly, Austronesians (of Indonesia and Polynesia, e.g.) are more closely related to Taiwanese aborigines than they are to Australian aborigines.  This tree is complicated by how much more migration there has been in the last 1000 years than there was previous to that, but it's still biologically meaningful.
But here's the striking thing: traditional notions of "race" do not match up well with this tree.  The deepest and most fundamental phylogenetic splits in the human tree are within Africans.  If you were going to try to "scientifically" come up with races, you'd end up with something vaguely like one for Khoisan, one for other Africans, and one for all non-Africans.  Even ignoring modern admixture, traditional races are not monophyletic.  Any clade including all "black" people includes all people, any clade including all "east asians" includes all native americans.  (Also note that traditional notions of "race" are not stable over time, remember that "Irish" used to be a "race" on the US census.)
Modern admixture even more clearly shows the non-genetic nature of traditional "races."  One genetic study of people who identify as African-American, found that African ancestry can be as low as 1% and as high as 99%, with the median African-American having 18.5% European ancestry (with 30% having European y-dna).  Furthermore, relatively ancient admixture (for example, in the Northern Africa, Northeastern Africa, Middle East region or in Madagascar) also complicates the situation significantly.
To summarize, although human genetic diversity is a real biological phenomenon which can be used to figure out the geographical history of people's ancestors, traditional notions of race do not match up well with the biologically meaningful concepts.

Sounds like the overlap is so great that such a description would have so many races that a couple of these answers use the word meaningful.

Its not known what the consensus is but there is definitely a decline in the race concept.
"The concept of biological race has declined significantly in frequency of use in physical anthropology in the United States during the 20th century. We present three kinds of evidence of this rejection of what was a core concept: (1) The frequency of articles using the race concept in the AJPA declined from 60 percent in 1918 to 4 percent in 2001 (r = -.89, p = .01). (2) Content analysis of university level textbooks of introductory physical anthropology for 1980-99 found only one textbook which supported the race concept. (3) A series of mailed questionnaires to members of the American Anthropological Association found that while 37 percent of responding physical anthropologists rejected the race concept in 1978, this rose to 69 percent in 1999.”
Section - Summary, paragraph 1
"The decline of race in American physical anthropology"


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Open protocol for Ligase Independent Cloning
Ligase Independent Cloning is a protocol that allow an insert to be integrated into a vector without ligation.  It uses T4 DNA polymerase with only ATP to first chew back from blunt ends to create long sticky ends and then a polymerase treatment with full dNTP compliments to fill in the vector.
While there are several nice articles and resources that describe the procedure, I really would like a protocol with concentrations, temperatures and timing, which I'm having problems finding.  OpenWetWare for instance has only stub pages with no details.  Can anyone point to a full step by step recipe to make this work, once you have designed the primers?

Here is the original article. I'm going to get working on that OWW article. http://www.ncbi.nlm.nih.gov/pubmed/2235490

You can look up Gibson Assembly or Circular Polymerase Extension cloning (CPEC).  For both of these the website for J5 has some good protocols.  Here is the one for CPEC:  http://j5.jbei.org/j5manual/pages/80.html
For CPEC you can look at the 2011 Quan paper: http://www.ncbi.nlm.nih.gov/pubmed/21293463
Hopefully that helps.

thanks for this @Justin, but the protocol link, while complete doesn't make clear to me how this works. Why does the Pfusion polymerase have all the dNTPs? I had thought that to chew back from a blunt end, the polymerase would need an incomplete set of NTPs? Also how is the vector cut?  Is there any decision to be made here or is it just any digestion cut at all?

I think i discovered that part of the answer to this question is that Gibson assembly is patent protected...


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Relative Property of Alleles
If there are three different alleles to a gene, is it possible that the first is dominant to the second, but recessive to the third?

Sure it is!
When we say that an allele is dominant on another what we really mean is that the phenotype obtained from that specific mutation of the gene somehow "masks" the phenotype of the other.
The easiest example would be that of pigment. A gene X could code for an enzyme which produces a red pigment. A mutation in X could result in a allelic variant x coding for a non-functional enzyme that does not produce pigment. In this case X will be dominant on x, as in the presence of both the pigment will still be produced (because you will have half functional and half non-functional enzyme molecules).
Things can, however be slightly complicated.
For instance, if the allele R codes gives a red pigment and r gives a white pigment Rr could give pink. This is called incomplete dominance.
On the other hand you could have co-dominance, where WW is white, ww is black and Ww is black and white.
The example you are asking for is called serial dominance and the "classical" example given is that of the rabbit coat color where you have for alleles with a dominance hierarchy like:
c+ > cch > ch > c
c+ gives a fully functional enzyme, called tyrosinase
c gives a non-functional enzyme, resulting in an albino phenotype
cch (chincilla phenotype) and ch (hymalayan phenotype) give partly functional enzyme (interestingly, the latter gives a temperature sensitive fur color).
In reality the rabbit coat genetics is even more complex, see this documents (PDF) for a more complete list of all the various loci and possible alleles involved.


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Could inhibition of progerin formation slow the rate at which a body ages?
According to wikipedia, progerin is activated in senescent cells. The protein itself is known to be the cause of a rare affliction 'progeria' - a disease marked by accelerated aging of the body. This disease is not accompanied by neurodegeneration.

Is progerin the key factor in the aging process?
If yes, could inhibition of progerin formation control the rate at which a body ages?

Progeria (and related) syndromes are essentially a collection of 'accelerated aging' phenotypes caused by single mutations; Progerin is a shortened version of the protein Lamin A, and is therefore not found in individuals without a loss-of-function mutation in the LMNA gene (the wiki page you reference). As far as we are aware these genes do not 'cause' aging in individuals without the mutations.
LMNA is a normal component of the nuclear lamina (a structure inherent to the nucleus). This review discusses the various diseases associated with mutations in this gene, some of which present 'accelerated aging' phenotypes. However, as far as I know, there is limited evidence to suggest that LMNA, or indeed any Lamina associated protein, is involved in 'normal aging'. A recent GWAS meta-analysis found a variant in LMNA that is associated with longevity in humans, however the association is relatively weak (OR=1.18, P=7(x10)-4), so even if this is a true association, it seems that (as usual in aging research) there are many other factors to consider, and it is not a single gene that is doing the aging.
So to stress the point: progerin has no function in 'normal' human aging - it is a defective protein caused by a germline (or novel) mutation in the LMNA gene.  Accelerated aging is the symptom of this genetic disorder, and is not completely analogous to normal aging (as you point out, there is no cognitive decline that is associated with normal human aging).

Could the LMNA be a catalyst, or a key element in the pathway though?

A catalyst to what, and what pathway? If you mean aging, there is no 'aging pathway'

Also note that although the symptoms of progeria resemble aging it is not true that aging results in the same cellular problems (for a start, progerin is not physiologically produced in old age)


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What is the timing of information assimilation within a human brain?
A little background: I'm an avid dreamer and have great dream recall, sometimes up to 5-7 per night.
In my experience, I can sometimes trace some elements of the dream to an event that occured within a 1-3 day window prior to the dream.
I've done similar experiments with the process of idea generation, where an idea that I have can be traced to experiences from the previous 1-3 days.
This makes me interested if there have been some kind of studies on how rapidly the brain absorbs and assimilates information from short term memory over to the long term memory. Has there been any studies on how long the brain keeps information before discarding or processing/assimilating it into dreams or new ideas?

I think this question is better suited for CogSci.SE where there are already questions similar to it

This question appears to be off-topic because it is belongs in  CogSci.SE

Try googling on "consciousness lag". I cannot cite any sources, but I have heard many times that working of consciousness happens in waves, and it is normal, when having some strong experience, for it to be experinced for some time, then come down, then rise again, say, in +1 minute, in +5 minutes, in +20 minutes, in +1 hour, in +1 day, in +3 days and so on... in some sense, the work of consciousness is similar to water surface with waves.. you can read much about that in eastern philosophy, and it plays well with electromagnetic nature of waves in the nervous system.


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What are tendons made of specifically
From what I read on wikipedia they are made of collagen. Collagen is just a protein. Right? How is this collagen structured (I imagine like fibers). Aren't there cells in this fibers as well?
From this picture:

Is the pink stuff the collagen? and the purple stuff the tenocytes?
If someone can expand on this with a picture preferably, it would be great.

As you correctly say, tendons are made up of collagen fibers. Collagen is one of the most important proteins (or, to be more specific, family of proteins, as there are many types of collagen) forming connective tissue in the body.
Collagen molecules have a particular structure that allows them to form long fibers, composed by three different strands that form a triple helix. This is a schema of a collagen helix (each ball represents one aminoacid):

(source: Wikipedia)
These helices can then be bound together to form a collagen fiber, through the action of an enzyme called lysyl oxidase which binds two lysine residues from two different helices together (lysine is one of the aminoacids that makes up collagen).
Here is a scanning electron microscope of a collagen fiber:

(source: Science photo library)
Collagen is secreted out of the cells that produce it so, although there may be cells around the collagen molecules, it is important to understand that it is part of what is called the extracellular matrix, the extracellular structure that supports the cells in our body.
As for the photo you linked, it is an hematoxylin and eosin (H&E) stain of a tendon. Hematoxylin colours cell nuclei in dark blue, so the dark spots are definitely cells.
The pink "waves" are indeed collagen fibers, the cells are probably the tenocytes, the specialized fibroblasts of the tendon, which produce the collagen.

Do these tenocytes move around the collagen fibers? Sort of like spiders in a web?

@user952: I don't really know. I would say no, but I may be wrong.

@user952 tenocytes can move: What causes tenocytes to migrate from intact regions of tendon into the wound site, and how do they move?

also Do tenocytes move around in a healthy tendon or do they stay at the same location?

{4} has a similar micrograph as yours but with some labels:

with the caption:

Figure 1.2: Tendon microstructure of healthy tendons: nuclei of tenocytes are darker in color and vascularization does not disrupt collagen arrays.  arrays
  http://www.onlineveterinaryanatomy.net/content/tendon-histology-labelled (mirror)

{5} presents both a longitudinal (a) and a transversal view (b):

Caption:

(a) A low power, longitudinal section through the limb tendon of a young calf in a section stained with Haematoxylin and Eosin (H & E). The tenocytes (TC) are typically arranged in longitudinal rows between parallel bundles of collagen fibres (CF) and are only recognizable in such routine sections by their darkly staining nuclei (i.e. the cytoplasm is not visible). Note the waviness (crimp) of the collagen. (b) A low power transverse section through the limb tendon of a young calf stained with H & E. Note that the collagen fibres are grouped into fascicles (FA) separated by endotenon (E). The tenocytes are recognizable within the fascicles by their nuclei (arrows).

Some illustrations showing the tendon structure:

(image source) (mirror)

(image source) (mirror)
Another illustration from {3}:

Regarding the cellular content of tendons, quote from {1}

The cellular content of tendons accounts for 20% of the overall tissue volume (Nordin et al., 2001). The main cell type present within tendons, which is responsible for the production and regulation of ECM, is the tenocyte (Maffulli et al., 2002). These are bipolar cells with elongated nuclei and spindle-shaped morphologies; they are regularly anchored in columns amongst the collagen bundles (Bernard-Beaubois et al., 1997). Other cells (though present in smaller numbers) include chondrocytes present at OTJ insertion sites, synovial cells composing the tendon sheath and vascular cells such as capillary endothelial and arteriole smooth muscle cells (Sharma and Maffulli, 2005).

Some more details from {2}:

The matrix is far more conspicuous than the cells. However, it is now widely recognised that the cellular elements hold the key to understanding development, repair and the ability of tendons and ligaments to respond to changing mechanical load. Tenocytes are mechanosensitive cells that are hardwired in a way that allows them to deploy a tensegrity architectural system to detect changes in mechanical load via deformation of their cell membrane and cytoskeleton (Wang, 2006). Strain in the extracellular matrix (ECM) tenses cytoskeletal fibres via integrin receptors in the cell membrane, and this in turn is relayed to the cell nucleus so that gene expression can be altered. An important principle of the tensegrity system is fibre continuity between the ECM and the cells. As Myers et al. (2007) point out, the implication is that the existence of a continuous network of fibres (i.e. collagen fibres in the ECM; cytoskeletal fibres in the cells) means that stress on one part of one cell can be dissipated throughout the entire tissue. Consequently, individual cells are protected from damage and a small mechanical stimulus can potentially affect many cells (Ingber, 1997; Myers et al., 2007). It is also worth noting that an under-stimulation of tenocytes that results from an altered cell–ECM interaction consequent upon tendinopathy could down-regulate cell activity (Arnoczky et al., 2007). Thus, the tendon becomes weakened and more vulnerable to damage from mechanical overload.
Although tenocytes and ligament fibroblasts are unremarkable cells in routine histological preparations and seemingly isolated within the ECM (Figs 14.2 and 14.3), they have a much more elaborate form when viewed by confocal microscopy (McNeilly et al., 1996). Each cell has numerous finger-like and sheet-like processes, extending around groups of collagen fibres and creating a 3D network of intercellular contacts throughout the tissue that fits well with the tensegrity model discussed above. The tenocytes are typically arranged in longitudinal rows, where the long axis is parallel to the tendon itself (Fig. 14.3). This reduces the risk of cell damage accompanying tendon or ligament loading. Adjacent cells communicate with each other via gap junctions – structures that allow ions and small molecules to be rapidly exchanged between individual cells. Two types of gap junctions are present in tendons – those expressing the protein connexin (cxn) 32 and those expressing cxn 43 (McNeilly et al., 1996; Ralphs et al., 1998). It is notable that the distribution of these two connexins is distinctive and implies they have independent functions. Connexin 32 is only present between cells within a longitudinal row, whereas cxn 43 also links cells in adjacent rows. Consequently, gap junctions containing cxn 32 are oriented along the line of tensile loading of a tendon, but cxn 43 junctions link cells in all directions. Waggett et al. (2006) have since shown that collagen synthesis is inhibited in avian tendon cells subject to cyclic mechanical loading in vitro, via cxn 43 and stimulated via cxn 32. Thus, it seems likely that the interplay between these junctions in response to load changes in tendons and ligament is critical in allowing them to adapt their ECM to changing mechanical load (Waggett et al., 2006). The integrity of the cell junctions in a compliant tendon seems to be ensured by the presence of longitudinally oriented, actin stress fibres within the tenocytes, which are associated with adherens junctions that link cells within the same longitudinal row (Ralphs et al., 2002).

For more details on tendon structure, see {5,6}.

References:

{1} L.A. Bosworth, in Electrospinning for Tissue Regeneration, 2011. https://www.sciencedirect.com/book/9781845697419/electrospinning-for-tissue-regeneration ; The quote I took came from https://www.sciencedirect.com/topics/engineering/tenocytes (mirror)
{2} M. Benjamin, in Regenerative Medicine and Biomaterials for the Repair of Connective Tissues, 2010. https://www.sciencedirect.com/book/9781845694173/regenerative-medicine-and-biomaterials-for-the-repair-of-connective-tissues ; The quote I took came from https://www.sciencedirect.com/topics/engineering/tenocytes (mirror)
{3} Docheva, Denitsa, Sebastian A. Mueller, Martin Majewski, and Christopher H. Evans. "Biologics for tendon repair." Advanced drug delivery reviews 84 (2015): 222-239. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Biologics+for+tendon+repair&btnG= ; https://doi.org/10.1016/j.addr.2014.11.015
{4} Mosca, Michael. "Re-evaluating tendon disease: an emerging role for inflammation and alarmins." Master Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:360eb093-9a3b-4271-a5b6-31314c7e1bbd ;  (Google Scholar) (mirror)
{5} Benjamin, M., E. Kaiser, and S. Milz. "Structure‐function relationships in tendons: a review." Journal of anatomy 212, no. 3 (2008): 211-228.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2408985/ ; https://dx.doi.org/10.1111%2Fj.1469-7580.2008.00864.x
{6} Lavagnino M, Wall ME, Little D, Banes AJ, Guilak F, Arnoczky SP. Tendon mechanobiology: Current knowledge and future research opportunities. J Orthop Res. 2015;33(6):813–822. doi:10.1002/jor.22871 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4524513/; https://dx.doi.org/10.1002%2Fjor.22871

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


text:
Do single crossovers occur in circular polynucleotides?
Single crossovers in circular pieces of DNA do not seem to be a big topic, because if they happened, they would lead to a kind of combined chromosome with two inner strands and one large outer strand. (A bit like an 8)
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But do these single crossovers actually not occur, for example because the crossover machinery is physically not able to do it, or do we just not observe them because they will inevitably lead to cell death and/or the chromosome somehow breaking?

this would be detected as DNA damage and normally be repaired I bet.  The RNA polymerase running around the cross over region would ruin the nifty figure 8 shape for sure.

Although crossover events can be observed in mitosis (mitotic recombination), they most frequently occur in prophase I of meiosis (crossing over in bivalents). Circular chromosomes are common in prokaryotes, but eukaryotes have linear chromosomes. Remember what meiosis accomplishes and that prokaryotes reproduce asexually. Prokaryotes don't have a need for -- or engage in -- meiotic division, so crossover events in circular chromosomes can really only be observed in instances of mitotic recombination, and I don't know the frequency of this in prokaryotes.
In prokaryote DNA replication, if any entangling of the two product circular chromosomes occurs, it is resolved by DNA topoisomerase. So perhaps a crossover would present a similar situation and the cell would resolve it by similar means.

thanks for your answer! valid thought, though crossover does occur in prokaryotes frequently - think of plasmids. the phenomenon I'm wondering about is that crossover from plasmids always seems to be doubled, exchanging a fragment between the chromosome and plasmid, and never single :)

good idea on topousomerase though! that might be

Changed the question to reflect this.

I'm accepting this answer because my understanding has improved in the meantime. As it is not possible to image recombination events as they happen (yet), it isn't possible to answer this conclusively.

Looking back at this question, I think this stems from a misconception in the first place. Crossovers are not events that affect single DNA strands but always both strands. The described double-ringed DNA molecule might exist as an intermediate in the process of a single crossover occurring.


text:
Genetic Models for Natural Selection?
My question is simple:
Given that evolution is described by random genetic mutations allowing certain members of a species to gain a reproductive advantage over others that coexist in the particular environment- I am curious- single genetic mutations do not seem to really explain complex morphic changes such as the length of a giraffes neck. Instead it appears it must be a compilation of many such mutations. So what are the statistics for mutations? How long does it really take for so many to favorably compile? How does this compare with the reproductive time of the species?

This is a good question but I’d remove / rephrase the last paragraph since it’s unnecessarily inflammatory and not actually accurate: most arguments for natural selection entirely take this into account (but it’s usually implied in mutation rates, rather than explicit).

just to clarify, evolution by natural selection is based on heritable variation that produces a reproductive advantage.  Evolution is simply a change in the allele frequency of a population over time and does not require natural selection.

The rate of mutation has been studied since the early 1900s, which is when your question was put to rest in a prescient paper by JBS Haldane (1949). Essentially the answer is that it varies a lot between organisms and environmental conditions, but for any given gene a mutation occurs once in about 50,000 sexual replications. That is equivalent to, in a human, several hundred new mutations in each person born. Impressively, Haldane's calculations have since been confirmed by a variety of other methods (e.g. Nachman & Crowell, 2000; Xue et al., 2009).
Faster rates of evolution have been recorded in other organisms, and there have been many, many studies looking at the rate of increase in sizes of the whole body or of particular organs of a wide variety of animals and plants.
For example, Azevedo et al. (2002) look at the rate of mutations affecting size (trying to select for decrease in body size) in C. elegans, and found mutations affecting size occured at a rate of ~0.0025 per haploid genome per generation.
In another example, with a result more definite regarding your question, Keightley (1998) investigated the rate of change in average body weight under conditions of selection for increased body size, over 50 generations in mice. They recorded an average increase of 0.23-0.57% body weight per generation from new mutations. That's pretty huge, and demonstrates how rapidly a complex trait can change by mutation under selection.
I wrote a small piece of python code to calculate the increase after x generations at the same rate (the formula is very simple)...
initial = 1
rate = 0.35
generations = 1000
result = initial * (1.0 + rate) ** generations
print result
>>>20.10655586861808

Thus if we assume that approximately the average rate found in the mouse study (0.35%) could be the rate at which giraffes' necks might increase under strong selection, after 1000 generations the mean neck length would be over 20 times the original length. A low estimate for wild giraffe longevity is around 20 years, thus for giraffe necks to increase around 20x might take 20,000 years. Of course this basic estimate is making a whole lot of assumptions, but the point is that rates of mutation are actually very high, easily enough to explain the diversity of traits we see in the world.
References

 Azevedo RBR, Keightley PD, Laurén-Määttä C, Vassilieva LL, Lynch M, Leroi AM. 2002. Spontaneous Mutational Variation for Body Size in Caenorhabditis Elegans. Genetics 162: 755–765.
 Haldane JBS. 1949. THE RATE OF MUTATION OF HUMAN GENES. Hereditas 35: 267–273.
 Keightley PD. 1998. Genetic Basis of Response to 50 Generations of Selection on Body Weight in Inbred Mice. Genetics 148: 1931–1939.
 Nachman MW, Crowell SL. 2000. Estimate of the Mutation Rate Per Nucleotide in Humans. Genetics 156: 297–304.
 Xue Y, Wang Q, Long Q, Ng BL, Swerdlow H, Burton J, Skuce C, Taylor R, Abdellah Z, Zhao Y, et al.. 2009. Human Y Chromosome Base-Substitution Mutation Rate Measured by Direct Sequencing in a Deep-Rooting Pedigree. Current Biology 19: 1453–1457.

wow- that's a really good answer. So these rates of mutation that are studied- in particular the Haldane paper- they represent mutations in the genome that are passed on to the offspring or just random mutations that occur in individual cells throughout the collective body?

okay i reread- nevamind the above..

Yes, they represent mutations that are passed on to the offspring.

You might have a look at the E. coli long-term evolution experiment lead by Lenski.  They've traced over 50 thousand generations of E. Coli and measured how they evolved when growing in a minimal growth medium.  Since these E. Coli reproduce asexually and do not trade genes via bacterial conjugations, the only genetic changes over time come from mutations.  Since they keep frozen samples of earlier generations, it's possible to test exactly what changed and when (and even to go back in time and rerun the experiment again).  The experimenters estimate that there were hundreds of millions of mutations during the first 20K generations.  Of those 20K, approximately 100 reached fixation (that is, where everything without those mutations died), and of those there were between 10 and 20 beneficial mutations.  During those 20K generations the fitness (measured by how quickly the population grew when introduced to a new media) grew by 70%.  Later studies have looked directly at the DNA and identified the precise mutations which lead to important increases in fitness.

Here's a paper on that experiment which includes a summary of the project and also a particularly stunning example of a trait that evolved due to a combination of more than one point mutation: http://www.pnas.org/content/105/23/7899.full

This is such a fantastic experiment. It must have been a hard slog for so many doctoral candidates endlessly curating E. coli cultures, reminiscent of Morgan's fly boys.


text:
Do any plants exhibit hormonal changes similar to puberty?
Just what the title states.
Are there any plants/trees that exhibit a growth spurt at a definite interval after the shoot appears?

In flowering plants (the angiosperms) there are several developmental transitions in the life of the plant. I won't list the plants, because the list includes pretty much all of them (although the magnitude in the change of developmental pace differs widely between taxa and environments).
First there is seed germination, which is controlled hormonally. Absence of germination is usually imposed by abscisic acid, whilst germination is caused at the appropriate time by gibberellic acid and ethylene (among other things; Holdsworth, Bentsink & Soppe, 2008).
Next, in many herbaceous species there is a transition between a spreading growth stage (e.g. rosette growth) and the flowering stage. The 'growth spurt' here is the differentiation and elongation of the flowering stem, and then subsequently the sudden flowering of buds. The transition is also controlled hormonally, by a variety of hormones including auxin (Zhao, 2010), gibberellic acid, ethylene (Schaller, 2012), and the long anticipated, recently confirmed florigen (Choi, 2012). Ethylene and abscisic acid then play important roles in the next developmental transition when seeds and fruits are produced and dehisced.
Small RNAs are also now being revealed to play a large role in controlling the timing of developmental, but they are upstream of the hormonal changes. In particular some key miRNAs are involved in auxin-based regulation of branching, and in embryogenesis (Nodine & Bartel, 2010), and RNA silencing is involved in the switch from rosette growth to flowering growth (reviewed in Poethig, 2009 and Baurle & Dean 2006).

 Bäurle I, Dean C. 2006. The Timing of Developmental Transitions in Plants. Cell 125: 655–664.
 Choi CQ. 2012. A Blossoming Field of Research: How Florigen Is Transported to Create Flowers. PLoS Biol 10: e1001311.
 Holdsworth MJ, Bentsink L, Soppe WJJ. 2008. Molecular networks regulating Arabidopsis seed maturation, after-ripening, dormancy and germination. New Phytologist 179: 33–54.
 Nodine MD, Bartel DP. 2010. MicroRNAs Prevent Precocious Gene Expression and Enable Pattern Formation During Plant Embryogenesis. Genes Dev 24: 2678–2692.
 Poethig RS. 2009. Small RNAs and developmental timing in plants. Curr Opin Genet Dev 19: 374–378.
 Schaller GE. 2012. Ethylene and the regulation of plant development. BMC Biology 10: 9.
 Zhao Y. 2010. Auxin Biosynthesis and Its Role in Plant Development.


text:
Features in individuals causing high population variation
As I understand it, a population with high variation is something sought after, since it makes the population better equipped to face a dynamic environment.
Then, I guess features in an individual which causes it's population's variation to be high, should be selected for (high mutation rate, other features.. ?).
If so, does this manifest itself partly as individuals preferring to mate with individuals from another population? (With genetic difference within reason, perhaps a norm for a proffered genetic difference between individuals)

I think you have an interesting question here but I think you are giving too much intent to evolutionary processes.  Unless the population is being managed (like in a preserve or zoo) there is no one to strive for high variation.  In a dynamic environment, a population with high variation is less likely to go extinct but this is not consciously anticipated or planned for by the members of that population in the anthropomorphic sense that you seem to imply.

Assuming a population lives in a highly dynamic environment and mutation is the only source introducing variation. Some in the population has genes that code for a slow mutation rate and the others have has genes that code for a high mutation rate. Shouldn't genes that code for a mutation rate appropriate to the environment be selected for? Perhaps a rate that is proportional to the environment's 'dynamicness' , in this case high.

The term "striving" and the phrase "the individual should strive" raise concerns like those in the comment by @DQdlM. I would suggest re-phrasing the question.

I believe there are evidences in both directions in terms of mechanisms to favor variation in a population: outbreeding and crossing within individuals that look alike. There is a fine line between the two. Outbreeding helps in keeping variation and mixing variants that appeared in different parts of the population, but too much outbreeding can generate inviable offspring. Too much inbreeding also reduces viability. Certain plants have features that are selected to favor outbreeding and make inbreeding incompatible by rejecting incompatible ("self") pollen (self-incompatibility mechanisms).

authors: Атанас Танев


text:
Is collagen supplementation useless?
When collagen is digested is it broken up into usable components that the body can use to produce its own collagen?
What evidence is there that supplementing with collagen type I & II etc.. can help connective tissue disorders?
What evidence is there that supplementing with collagen from animal products is not useful?

I don't see a reason why collagen should be digested differently from other proteins. It is broken down into amino acids. And of course they can be used to synthesise collagen if needed. I can't answer whether dietary supplements have been proven useful/less though.

Also note that the aminoacids that make up collagen are not special. They can be used by the body to make up any other protein.

We may want to put this on skeptics.se Let's see what response come here first.

Regarding the use of collagen supplements to help prevent or treat a tendinopathy:
A rather inconclusive quote from a 2016  systematic review {1}:

glucosamine and chondroitin sulphate, vitamin C, hydrolazed type 1 collagen, arginine alpha-keto-glutarate, bromelain, curcumin, boswellic acid, and methil-sulfonil-methane were considered […]. preclinical results are very encouraging, however they are not fully confirmed by clinical studies. There are few clinical papers on the use of nutraceuticals in tendon disorders, and their methodological quality is poor. Furthermore, in most of the studies more than one supplement was administered at the same time. This may bias the results, and the effect of each single component cannot be determined. Furthermore, the interactions between nutraceuticals and drugs, or other dietary supplements (especially at high doses) has not been evaluated, neither their effects on chronic diseases. For these reasons, it is not possible to draw any definitive recommendations on the use of nutraceutical supplementation in tendinopathies.

References:

{1} Federico Fusini, Salvatore Bisicchia, Carlo Bottegoni, Antonio Gigante,3 Fabio Zanchini, and Alberto Busilacchi. Nutraceutical supplement in the management of tendinopathies: a systematic review. Muscles Ligaments Tendons J. 2016 Jan-Mar; 6(1): 48–57. Published online 2016 May 19. doi:  [10.11138/mltj/2016.6.1.048] PMCID: PMC4915461. PMID: 27331031. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4915461/

This seems to be an interesting and ambiguous topic.
On one hand, the collagen as any other protein is cleaved into small-sized chunks (oligopeptides) and single aminoacids before absorption. The chunks of proteins which were not completely digested before absorption are broken up further in the body and cannot be selectively used for collagen re-building in the body. Therefore, there should be no difference between the collagen of different types and, basically, no difference between the supplements containing collagen and just a mixture of aminoacids. This also explains the fact why collagen supplement is in most cases taken in the lysate (pre-cleaved) form.
On the other hand, a quick search in PubMed and I found an interesting article on the topic (source), where the authors claim:

At 6 months, the proportion of clinical responders to the treatment,
  according to VAS scores, was significantly higher in the collagen
  hydrolysate (CH) group 51.6%, compared to the placebo group 36.5%
  (p<0.05).
...
This study suggests that collagen hydrolysate 1200 mg/day could
  increase the number of clinical responders (i.e. improvement of at
  least 20% on the VAS) compared to placebo. More studies are needed to
  confirm the clinical interest of this food supplement.

So, if the article is not a bogus (I failed to get the full version of it and the journal does not seem to belong to the top journal in the field of medicine), there could be some mechanisms yet to be discovered.

I guess it may be a result of the fact that CH has a very high % of Gly and Pro, more than what you would normally get from food. Wikipedia lists several studies that have given widely discordant results on the matter of whether it helps with joint diseases.


text:
DNA methylation and genome size
Is there any relationship between DNA methylation as a level of stability to epigenetic states and genome size? For example, it is claimed that DNA methylation is not required for epigenetic stability in Drosophila melanogaster and yeast, both genomes much smaller than mammalian or plant genomes. Could it be that DNA methylation is needed to help activate/repress certain genomic regions on top of other epigenomic marks when the genome is so vast that there is a need for an extra level of marking? Is there any evidence along those lines?

Is there any relationship between DNA methylation as a level of
  stability to epigenetic states and genome size?

I would say yes, because methylation is used to disable genes in differentiated cells. Disabled genes in differentiated cells generally need to stay disabled to maintain normal behavior for the cell type. Larger genomes usually encode more different types of cells.

it is claimed that DNA methylation is not required for epigenetic
  stability in Drosophila melanogaster and yeast, both genomes much
  smaller than mammalian or plant genomes.

According to my book (S377 molecular and cell biology, book 2, p140) Drosphila don't need methylation because they perform transcriptional regulation by persistent chromatin remodelling instead. Yeast being single celled would have less need for this type of control.

Could it be that DNA methylation is needed to help activate/repress certain genomic regions on top of other epigenomic marks when the genome is so vast that there is a need for an extra level of marking?

It is used as a repressor because it inhibits  hydrogen bonding of transcription factors and the like. I have not heard of it functioning as an activator.
There are also other uses for methylation, for example  newly synthesized DNA is hemimethylated - where the parent strand is methylated and the child one not. From this it can be determined which is the parent strand during DNA repair.


text:
Is extreme cladism a mainstream position in the species debate?
In the philosophy of biology it has been claimed many times that a popular position regarding the question of what species are, among biologists, is cladism. For my current purposes, the defining trait of cladism is captured in the following quote:

According to cladism, a species becomes extinct whenever it sends forth a new side species. (LaPorte 2004, 54)

So, for example, if Homo floresiensis is truly a species, and it derives, via a speciation event, from Homo sapiens, then, after the speciation, there is no Homo sapiens: there is Homo floresiensis and a new species, very similar to sapiens. In general, whenever there is speciation the mother species disappears.
I am under the impression that this description of the situation is not the one most mainstream biologists would endorse. I take it that a more common description would be one under which, if a number of Homo sapiens get isolated in an island and go on to form a new species, Homo sapiens exists both before and after this speciation event. I would like to know whether cladism, described as above, is really a popular position, or whether I am right about what most biologists would say about the relation between floresiensis and sapiens.
It might also be that biologists declare themselves cladists when explicitly theorizing about the nature of species, but fall back to a less extreme form of cladism in the actual practice. Evidence in favour of or against this possibility (coming from biology, not the philosophy of biology) would also be appreciated.
As Noah has pointed below, what I have called extreme cladism might be very far from cladism, as usually interpreted. This is precisely the kind of claim I would like to see substantiated.

LaPorte, Joseph. 2004. Natural Kinds and Conceptual Change. Cambridge University Press.

Sorry, the following comments got toasted in a testing catastrophe - my fault: "Depending on how strong the emphasis is on monophyletic concepts, it would have the consequence that has been pointed in the question: if the "mono" in "monophyletic" indicates a single, non-branching stretch in the evolutionary tree, a species cannot survive its "sending forth a new side species", as LaPorte puts it." & ...

"that seems to me to be very far from the defining characteristic of cladism. Instead I'd says cladism is characterized by emphasizing monophyletic concepts (archosaur or ray-finned fish) over polyphyletic ones (like reptile or fish) and emphasizing the arbitrariness of Linnaean ranks (calling everything a clade instead of phylum/class/etc.)." - many apologies :/

I've never heard of it, actually - though I can't speak for my professors or researchers I know, none have ever presented the Cladism argument as an argument for the delineation of species.
As far as I'm aware, the attempts to define a species fall along three lines:
The ability to produce fertile offspring in the wild.
Distinct physical characteristics.
An arbitrary amount of genetic divergence.


text:
What happens when cells in your body run out of telomeres?
In my biology book I read about an experiment where the genes encoding telomerase were 'knocked out', but they could still live a normal life and no adverse effects were noticed until the 6th generation of offspring (although it did not say what the effects were).
I have often often heard how longer telomeres indicate longer life potential, but what happens when you run out of them? Would rapidly proliferating cells be affected before others? Do the cells then just stop dividing or would they continue to divide? If they continue to divide what would the effects be?

do you have a link to the study that 'knocks out' the telomeres and finds the cells to not have any adverse affects? As I understood it the cells either enter a state of permanent cell-cycle arrest (senescence) or apoptose (programmed cell death) when they reach their Hayflick limit (i.e. when their telomeres run out).

A figure in the book taken from 6th generation telomerase deficient mice was taken from: Cell, Blasco, M. A., ‘Telomere shortening and tumor formation by mouse cells lacking telomerase RNA’, 91, pp. 25–34

I'm a student of Alevels n while preparing for my biology mcqs related to the chapter of cell division, came across an mcq..
"Chromosome telomeres promote DNA replication and are not completely replaced during mitosis.
A substance X is known that completely replaces telomeres during mitosis. What will be the effect of growing a cell culture with and without substance X?
Rhe answer was:The cells didvide continuosly with substance X and cell division eventually slows and stops without substance X.
But I don't really understand the answer..why is this the answer? Please help me out if you underst

@Taleah Please don't "hijack" questions to ask your own question, especially not if they are a year old. Your can ask this as an own question, tag it with "homework" and specify what you tried to answer the question.

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication.
Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in 'normal'/somatic cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (known as cellular senescence).

This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme, so they have unlimited replicative potential - a very important trait for stem cells.
So a rapidly proliferating cell would indeed 'use up' it's telomeres before a different cell type. The cell would then either enter a state of senscence (permenant cell-cycle arrest), or apoptose. There are a lot of factors governing which outcome is realized, but the senscent cell population increases with age, and is proposed to contribute to many aging phenotypes (there is a recent fascinating study published in Nature where the authors remove all the senscent cells from aging mice, and the mice actually get healthier! Can't wait for studies that relate to human aging and senescent cell clearance (ref.)).

I have elaborated on the function of telomeres in the context of organismal aging in my answer to this question.


text:
Do we get 1/4 of our genes from each grandparent?
I know that we get half of our genes from each parent, but does it necessarily mean we get 1/4 of our genes from each grandparent? Or is it possible that we might get say 30% from one grandparent, 20% from other, 15% from another, 35% from another?

possible duplicate of How many genes do we share with our mother?

If you know that you get half of your genes from each of your parents, would that make your parent's parents any different? -1

I have answered a similar question before: "How many genes do we share with our mother?".
It is not that you "get half your genes" from each parent, and thus a quarter from each grandparent, it is that you inherit the versions of the genes (we all have the 'same' genes).
The method that determines which traits are inherited from each parent by the offspring is known as homologous recombination, and this process is (essentially) random, and thus you end with ~50% of your traits (the alleles of the genes) from each parent, and ~25% from each grandparent, so you are right in this respect.
This is, however, a generalization; due to the chance nature of the recombination it is entirely plausible that you may inherit more traits from one grandparent in comparison to another, but this is unique to each individual (with the exception of course of genetically identical twins).

This comes down to the ever confusing use of gene to mean allele and loci. Just as in the "How many genes.." Q you answered before, the term gene is often used for both leading to the confused idea that we share 99% of our genes with chimpanzees yet we only share 25% with our grandparents.. Alleles are all the different variants (or versions as you called them) present at each loci (non-recombining region of DNA). We share 25% of our ALLELES with our grandparents (assuming no mutation and recombination) and 99% of LOCI with chimpanzees. Perhaps this can be added to both of your answers.

And we should wipe the word gene from the English language and just use Allele and Loci!

I agree with the person above. But it might be more correct to say we get 1/4 of our total DNA from each of our grandparents, because though the genes are really important to code for specific proteins, there are tons of non-coding DNA in between them. In fact, 98% of our genome is non-coding! Although we are discovering awesome novel functions for this DNA slowly but surely. But it is important to think of it as 1/4 of your DNA and not genes because it is in this non-coding DNA where a lot of mutations can occur, and these mutations are what we inherit and make things like DNA fingerprinting for forensic analysis possible, like in CSI.
I just wanted to add three more thoughts:
Though it is true that 1/4 of your DNA would come from each grandparent, that is only true for your autosomal genes, not your necessarily for your sex chromosomes. The X chromosome does recombine regularly in the mother, but in the father the X and the Y do not recombine. (Actually I think part of the Y can recombine, but for the most part, the sex-determining part of the Y and its associated genes stay completely intact). This means that if you are a male, your father, and his father, and his father all share the same Y chromosome.
Additionally for the women, because the woman makes the egg, and thus all the early embryonic organelles and RNA's, the woman donates the mitochondrial DNA, which has its own sets of genes that are really important and have been linked to many diseases. So every child of a woman, shares their mother's mitochondrial DNA, as she shares her mother's and her mother's mother, etc.
If ~1/4 of our DNA comes each grandparent, then 1/8 of your DNA comes from each great-grandparent. So then 1/16 of our DNA comes from each great-great grandparent, which are your grandparent's grandparents. And thus it continues exponentially upward. The result is that there comes a point where your ancestors have contributed so little to your actual DNA, that it becomes almost negligible. So if you are an American, who most likely has ancestors from all over the world, even if you have 1 great-great-great-great grandparent who was a French immigrant while the rest of your ancestors were all British, the French DNA is only 1/64 of your total DNA. So even if you are a complete mix, there comes a point where so many different people have contributed to you being you, that you can establish a cut-off and just say, 3/4 of my ancestors were born in America, I'm American!

Good point about the mitochondrial contribution from the maternal lineage.

Humans do not get an even 1/4 of DNA from each grandparent.
The main reason is that meiosis is not a precise 50/50 split. Parent cells undergo meiosis to recombine the grandparent chromosomes and produce a set of chromosomes to pass on to a child. This process is not a precise 50/50 split and produced chromosomes will have more of one grandparent DNA than the other.
The second reason is that different chromosomes have different DNA base pair lengths. So, while every human gets exactly 23 nuclear chromosomes from each parent, some of those chromosomes have more DNA base pairs than others, and children receive a different quantity of DNA base pair content from each parent.

Please put up references to prevent your post being flagged. Thank you.

Although you share 50% of your chromosomes with each parent, it is not necessarily the case that each of your four grandparents contributed 25% of your chromosomes. Ignoring the effects of recombination, the chromosomes in each gamete (think egg or sperm cell) are randomly either from one grandparent or the other. It is possible, for example, for the 23 chromosomes in a sperm cell to be (more or less) the exact same 23 chromosomes this male inherited from his father. There are 2^23, or about 8.3 million, different combinations of chromosomes possible for the gamete of a diploid organism with 23 chromosomes. It's possible that the gamete gets an even split close to 50:50, but it's also possible that the gamete got 100:0 making the offspring effectively not related to one of their grandparents. Unlikely, but it's not actually impossible.

The question asks for genes, not chromosomes.

Genes are located in chromosomes.

Although some of the previous answers also acknowledge it, this answer comes the closest to pointing out the surprising fact that we don't inherit equally from each Grandparent, and that it's possible that in the limit, we could inherit nothing from a grandparent.

There is a phenomenon known as genomic imprinting where the allele of the gene would only get expressed if it is passed on from the father (e.g. IGF2). This means that although the same genes get passed on from both your father and mother, only the copy from your father will get expressed. Thus, although you get 50% of your DNA from your parent (and probablistically speaking 25% from your grandparent), the same gene can be deferentially expressed depending who you get them from).


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What is an efficient way to spike 10-50 cells to a culture
I'm trying to add on the order of 10-50 mammalian cells to a mixture of other cells (order of 1e6 cells). What is the best way to do this?
(edit) I guess this wasn't clear. I would really like to emphasize how to sort 10-50 cells to give me an precise (not necessarily accurate but that would be nice too) method of getting a desired number of cells.

If you are you working with primary cell cultures or cell lines may be you could do this when cells are in suspension, after tripsinization, mix them well with a 5mL serologial pipete in a falcon 50mL tube and plate to a 100mm2 with a final volume of 7mL. And finaly draw an eight with the plate in the hood more than 3 times to mix them well.
Edit: For the addition of 10-50 cells, count these cells with trypan blue, and do a 1:100 dilution, for example if you have 1e6 cells in 10mL you could take 0.01 mL (10 microliters) to get 1, 000 cells

And then you add the 0.01mL into 1mL of cell media to get 1 cell per 1 microliter, and then if you wanna get 10 cells, take 10 microliters, and so on

So what about the getting the 50 cells part?

Check the edition of the answer

How do you avoid stochastic effects?

You can't avoid random effects in biology, because biological variability, do a power analysis to ensure you use the correct numer of samples or repeats in your experiment http://biology.stackexchange.com/questions/963/is-it-necessary-to-conduct-a-power-analysis-before-beginning-an-experiment. My answer is a standard method to work with cell cultures, you can also use cell sorting,  to be more precise on your cell count. And try bioforum (a community of methods), to get another solutions


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What is the purpose of the adrenal medulla?
The adrenal medulla is less of a 'real' endocrine organ like the others in the endocrine system and much more an extension of the sympathetic nervous system. In fact, its chromaffin cells are modified neurons by descent and secrete adrenalin and some noradrenalin upon stimulation by sympathetic preganglionic fibres, effectively turning the medulla into a sort of 'endocrine ganglion' with the whole cardiovascular system as its 'postganglionic fibres'.
Adrenalin in the circulation seems to have pretty much the same effect as all the adrenergic neurons of the sympathetic nervous system (which innervates all blood vessels, organs etc.): arteriole constriction, cardiac output increase, breath rate increase, pupil dilation, glucagon secretion and insulin inhibition, stimulation of glycolysis and glycogenolysis etc.
So what is the purpose of the adrenal medulla, if all of the effects which the endocrine adrenalin produces are essentially the same as those produced by the sympathetic mass response?

I have found the answer to the purpose of the adrenal medulla to be flexibility. Just like regulation for example of gene expression or metabolism occurs on many levels with different speeds and permanences of their effects, signalling needs to be available both quick and short-lived, and slower but with more long-lasting effects. The adrenal medulla provides exactly that.
Sympathetic adrenergic neurons are quick, but as quickly as they release their neurotransmitter, the effect is only of short duration and adrenalin is quickly cleared from the target area. Rather than giving off short bursts of adrenalin, the medulla maintains a constant systemic level of it and in response to stimulation raises or lowers that level. This response takes more time as blood circulates much slower than neurons respond, but its effects last longer.

I would argue that the adrenal medulla is a real endocrine tissue for the following reasons. First and foremost, it fits the definition of an endocrine tissue, which is to produce and secrete hormones in a regulated manner. You've already highlighted the physiological effects of those hormones, and I would ad dopamine as the other major secretory hormone/neurotransmitter. Chromaffin cells are dervived from neurons, but the presence of a regulated secretory pathway is a hallmark of endocrine tissues. @Armatus answer of plasticity is on the mark, although I think a term that more readily describes the system's ability react over a greater time scale would be impedence matching. Another differentiating characteristic is that the adrenal medulla is capable of sustained synthess and secretion in response to stimuli, whereas I don't think this is typical of most neurons which transmit a message only briefly.

I agree with you - of course it is an endocrine tissue, that's not the question here. The question is rather about its purpose when the wide-spread effect of adrenaline produced by it is also achieved by the sympathetic mass response :) I agree that plasticity was a bad choice of word. Your last point is correct and complements my answer. Such upregulation is possible for neurons too as far as my teaching has been (persistent firing), but it would be against the purpose of the sympathetic nervous system (quick response to stress) to use it in this kind of way.

I think we're agreed then: the adrenal medulla is a complementary organ to the mass response of the SNS. It is also more than that, acting as an endocrine tissue, which does take input from other endocrine tissues to modulate any sustained responses to stress.

I would also add the following distinctions: instead of releasing neurotransmitters, the cells in the adrenal medulla secrete hormones.
The adrenal medulla is where the main conversion of the amino acid Tyrosine into the catecholamines, epinephrine, and norepinephrine takes place.
The hormones are released quickly because the ANS, specifically, the sympathetic division, has direct control over the cells. Adrenaline is responsible for about 85% and noradrenaline for the remaining 15%.
Noradrenaline and adrenaline have a number of notable effects, including increased heart rate, blood pressure, blood vessel constriction in the skin and gastrointestinal tracts, smooth muscle (bronchiole, capillary), dilation, and an increased metabolism.


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How do you calculate or predict the charge of a protein at pH 7?
How do you calculate or predict the charge of a protein at pH 7 given a fasta sequence?
Any papers or online servers to do this is well appreciated.

Check this answer http://biology.stackexchange.com/questions/2459/are-bovine-serum-albumin-avidin-ficoll-70-and-dextran-70-positively-charged-or/2511#2511

ExPASy to the rescue! Although I didn't comb through all the tools, this nifty website provides quite the myriad of bioinformatics resources which most certainly contains the tool to calculate what you want.
Bear in mind though, most tools will tell you the isoelectric point of your protein. However, bearing in mind the relationship between pI and pH (i.e. if pI < pH, then protein is - charged, and vice versa), you can easily figure out the charge of a protein at pH 7.
http://expasy.org/tools/
*Update
Here's the exact tool to calculate isoelectric points: http://web.expasy.org/compute_pi/

Thanks for the info. Saw that though, so how would you calculate the charge - any hint on that?

Here's a tool that will give you charge: http://www.scripps.edu/~cdputnam/protcalc.html

Thanks! But wish it could in batch...

To calculate the charge at different pH:
At pH 3 K, R, H are + and D,E have no charge so add up all of the K,R,H in the sequence and that is your net charge at pH 3
At pH 6 K, R, H are + but now D,E are (-) so subtract one total from the other to figure if your net charge is + or -.
At pH 8 K and R are +, H has no charge and D,E are (-).
At pH 10 R is +, K, H have no charge and D,E are (-).
That can give you a general idea.  You can estimate the charge at pHs in between.


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Does every gland type have stem cells for regeneration?
Is there any gland in which there are no stem cells?
I know that:

sebaceous gland is maintained by unipotent stem cells
thyroid gland - some stem cells, apparently unipotent

Glands about which potency I am not sure

pancreas gland - contains probably many types stem cells, at least unipotent
pituitary gland - not sure if any exist

I cannot find any such gland that does not have stem cells.

Interesting question! You can add pituitary and pancreas to the mix.

Stem cells are not all 'unipotent' - they cannot necessarily differentiate into any type of cell. For instance, resident stem cells in tissues such as muscle - myo-satellite cells - are partially differentiated and during cell division one daughter differentiates further to become a myocyte (for example), and the other daughter the replacement myosatellite cell. As far as I'm aware, the majority of tissues have resident stem cells in varying degrees of differentiation (exceptions might include neurons and cardiac muscle, where cells are not replaced over the lifespan of the organism).
Here is some evidence for resident stem cells in glands;

The adult pituitary gland shows stem/progenitor cell activation in response to injury and is capable of regeneration (Fu et al, 2012),
The pancreas has been heavily studied from the perspective of diabetes research, with many studies looking to implant stem cells from elsewhere (Rezania et al, 2012). However there is some evidence for resident stem cells of the pancreas that may turn out to be more promising as treatment strategies in the future (Xu et al, 2004, Venkatesan et al, 2011),
Sebaceous glands are found throughout the skin, and secrete 'sebum' which keeps the skin waxy and waterproof. There is plenty of evidence for epidermal stem cells (Eckert et al, 2012),
There is also recent evidence for the existence of thyroid stem cells too (Fierabracci, 2012, Malaguarnera et al, 2012),
Saliva is mainly produced by the submandibular glands also contain resident stem cells, with this paper stating that stem cells have been isolted from salivary glands in humans (Okumura et al, 2012),

Given the limited (and very recent) evidence for the above (relatively well characterizd) glands, it seems likely that other glands will also have resident stem cells that remain to be identified.
Ageing: The so-called stem-cell pool gets depleted over a lifetime, so tissues lose the regenerative potential. However rejuvenation medicine is becoming a heavily invested in area of research (see www.SENS.org).


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Why is beta-mercaptoethanol often added to cell culture media
Many protocols suggest that beta-mercaptoethanol is necessary for growing cells. It is a reducing agent but what does it mechanistically do for your cells. When would one not add it.

2-me is a reducing agent necessary to be added to help keep free radical oxygen from affecting mouse cells.  It is generally not necessary for human cells.
Also from S Bannai and Ishii et al., 2-mercaptoethanol improves tumor cell uptake of cystine by creating a reducing environment.

BTW, the statement about human cells is not true. The addition of bME to primary immune cell cultures, especially B and T cell cultures, is common.

Common doesn't necessarily mean necessary.

I have never used it in human B and T cell culture. I'm switching to mouse work for my post doc and trying to figure out all the differences. Thanks for this post!


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Hoechst or DAPI for nuclear staining?
When is it best to use Hoechst vs. DAPI for nuclear staining? They seem to be very similar on paper. Are there situations where one is clearly preferable?

The Hoechst 33342 dye is similar to DAPI in that both are UV-excited, minor groove-binding, and emit signals proportional to total DNA content. Both are maximally excited around 355 nm and emit around 460 nm.  A UV light source is required, which may harm the cell. However, this is only a risk with Hoechst, as DAPI requires the cells to be fixed and/or permeabilized, which is incompatible with life. DAPI is more stable, but Hoechst is brighter. Both are subject to photo-bleaching after long exposure.
There is another newer DNA dye called DRAQ5 that makes up for all of the issues I mentioned earlier - it is bright, quite photo-stable, can be used in live cell imaging, and its excitation and emission wavelengths are in the far red end of the spectrum, meaning that no UV is needed. I found a good comparison chart at http://www.biostatus.com/product/draq5/live_cell_comparison_chart/ if you're interested. I have no connection to them, by the way, I've just used DRAQ5 a lot in the past.

Sorry, but this answer is wrong: Most microscopes have a dedicated DAPI channel and both DAPI and Hoechst can very well be used together with FITC-like dyes. Also, you are missing the main point here: Hoechst can stain live cells, while DAPI can't. This is the main reason why people choose one over another. -1 not for that, but for the advertisement. I don't think this belongs here.

-1: DAPI is absolutely compatible with GFP, FITC and Alexa 488.\

my bad, edited to reflect reality.

Use dapi for fixed cells, it's very bright, very specific, will let you know if you have mycoplasma contamination in your culture, has a good shelf life and is generally pretty inexpensive. If you have to do live cell imaging use hoechst and like @user1850479 stated there are multiple types, they are all generally less toxic. If you can't use a blue nuclear staine Draq works good, it's a little dim I've found but it is in far red range, it's relatively non/toxic, does not have as good a shelf life as the other I mentioned here, also it's really  expensive $$$$$$$!!!!

DAPI and Hoechst 33342 (there are different Hoechst dyes, 33342 is one of the most commonly used) have very similar spectral characteristics. The only point is that DAPI is much better excited at 405 nm than Hoechst. Some microscopes and flow cytometers nowadays have 405 nm lasers or LEDs instead of UV sources, so this can become relevant.
The main difference and the main reason to choose either is that Hoechst can be used to stain living cells as it can pass the cell membrane, whereas DAPI can't. DAPI requires fixed and permeabilized cells.

Does this imply that Hoechst stains are more hazardous to the researcher or the environment? If DAPI can't enter living cells but Hoechst can, are there concerns about mutagenicity (similar to e.g. ethidium bromide)?

Yes, indeed. But we treat Hoechst and DAPI the same way in our lab.

I realize this is an older topic, but I'd like to clarify some misconceptions:
1)  DAPI is usually referred to as a semi membrane-permanent dye because its penetration through viable cell membranes is concentration dependant.  At lower concentrations it is mostly excluded from viable cells, while at higher concentrations it stains live and dead cells about equally.
2)  Hoechst comes in both membrane permanent and impermanent varieties.  Make sure you order the correct one for your application!
3)  It is not necessarily true that Hoechst is preferred for viable cells.  Hoechst has very slow diffusion through thick tissue for instance, so for in vivo imaging applications (or in tissue sections), DAPI often stains viable cells much better than the (much heavier) 33342 because it is better able to diffuse through tissue.  For isolated cells however, Hoechst 33342 can much more rapidly stain viable nuclei (seconds vs. minutes for DAPI).


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Why Didn't Evolution Cause the Human Body to become Streamlined?
If streamlining makes movement/locomotion quicker and easier, why didn't the apes evolve into life-forms that had streamlined bodies (much like fish)?

No single advantage drives the evolution of body type.  The advantage of streamlining is much greater for aquatic animals as water has a much greateer influence on viability. On land other concerns, defense, physical strength and size are at least as important.  Most land animals don't even move quickly.

This question seems to be based on a fundamentally flawed premise, I don't think it is really answerable due to that.

I don't think the premise is flawed, as evidenced by @shigeta's comment. I vote to reopen.

I agree - @shigeta's comment does essentially answer the question. The reason we're not as streamlined as fish is that we don't need to be!

" 'cause we're lovers, not fighters!"

If streamlining makes movement/locomotion quicker and easier, why didn't the apes evolve into life-forms that had streamlined bodies (much like fish)?

As with everything in Evolutionary Biology, you must ask yourself: Gain vs. Cost?
In your specific case, the Gain is very little.  Air isn't nearly as dense as water, so a streamlined form won't show a major benefit unless the organism is traveling very, very quickly. This is why you see it in birds; raptors can travel over 100mph while diving, and at those speeds small changes in drag can mean the difference between dinner and starving. Smaller birds often make very quick turnabouts and changes in direction mid-flight where, again, small changes in efficiency can mean the difference between life and death. The cost was is worth it.
For apes and monkeys, moving very quickly isn't a case of living or dying. That's what we evolved opposable thumbs and prehensile feet(/tails) for. You don't need to run fast when you can climb a tree and simply get away from any predators on the ground. After we came down from the trees permanently, our larger brains allowed us to use tools to fend off predators - which, again, is much simpler than evolving an aerodynamic form that won't make a difference until you're running at the speed of a car.
So, in lieu of becoming a land-shark, we have hands that can use keyboards and minds that can invent the keyboard. Unfortunately, while the gains are many, the costs do include both a very long period of time where humans are helpless without parents, and an absolutely terrible form of locomotion with our upright stance on forward-pointing knees. Though you won't catch Cheetahs digging sewers anytime soon.

Who says we are not streamlined?
One could easily imagine body structures that would cause much greater drag in air and humans do not have them.


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Can the body of any organism on Earth live without impairment both in vacuum, and within Earth's atmosphere?
I know from reading that a human in vacuum needs a space-suit to survive.
Is the body of any organism on Earth capable of living equally in vacuum, and on/below Earth's surface within the atmosphere?

I think this is more of a physics question than biology.

Any body?  As in you're looking for an organism that is capable of surviving in a vacuum and with an atmosphere or you're looking for Chuck Norris?  Assuming not the latter , google suggests this but it's an unreferenced Wiki point :/

On what's surface?

Yeah, what do you mean by 'on its surface'?

Why the negative vote?

I didn't downvote, but people did because your question in its original formulation made no sense.

I'd like to add that most of the answers here have the organisms in hibernated forms.  I think there is a fungus that was growing in the space station, but I'm not sure anything on earth is functional in the vacuum of space, only hibernating... anyone?

Remarkably, Tardigrades are multi-cellular animals which can survive the vacuum of space.

I even think NASA sent a few of them up to space, brought them back to earth and awakened them...

"Tardigrades" are basically the answer to every biology question which begins with "can any animal...", aren't they?

And they're so cute too! http://cdn.zmescience.com/wp-content/uploads/2013/12/tardigrades-electronmiscroppe.jpg

Adding to Noah's answer, some lichens can survive the vacuum of space too. In an experiment led by Leopoldo Sancho from the Complutense University of Madrid, two species of lichen - Rhizocarpon geographicum and Xanthoria elegans - were sealed in a capsule and launched on a Russian Soyuz rocket on 31 May 2005. The lichens were in perfect condition when observed after the return to earth.