text:
How do Proteins migrate in MES vs. MOPS
My gels look significantly different in MES (2-(N-morpholino)ethanesulfonic acid) and MOPS (3-(N-morpholino)propanesulfonic acid). That is to be expected. What I don't understand is why the simple presence of the counter-ion significantly changes the velocity of certain proteins.
Is this due to the different pH (MES is usually run at pH 8.0, MOPS is usually run at pH 7.0) or is the charge distribution on the counter-ion responsible for everything?

I'm pretty sure the net effect is caused by the charge distribution of the counter-ion. This will have the most immediate effect on the net electric field and therefore directly effect the electrophoretic velocity of the proteins. The pH of the buffer indirectly affects this because it will determine the net ion balance based on the pKa values of MES/MOPS, so you will get different results using the same buffers but at different pH values.

@leonardo. I feel that you're correct. Now that I'm looking at the chemical structure, I'm surprised that the single carbon difference creates that much difference in the pKa. However, if one is running a gel at the suggested pH for the buffers, the charge ratio should be the same.

these are non denaturing protein gels (No SDS)?

Well, to rationalize everyone's comments, I think @leonardo is right.
This is a denaturing SDA PAGE gel.  The migration of the SDS Micelles which are negatively charged, depends upon the shielding of the solution around it.  The difference in mobility is because the SDS micelles will experience a slightly different field at pH ~6.2 (MES) vs 7.2 (MOPS).
The thought that these have the same charge would be right at exactly the pH corresponding to the pKa.  For these two ions the proportions will not be the same when running 0.8 pH units from their respective pKas. the ion concentration goes as +/- log ([BH]/[B-]) and the charge environment of the buffer should not be the same.  I think that the higher pH for MOPS running will tend to create more negative charge in the solution from MOPS- but also OH- in solution, slowing the mobility of the micelles and favoring the resolution of the larger proteins with MOPS.
This is all given even if the buffering ion concentration is the same.
I'm sure the gory details are buried in the musty tomes of some physical biochemistry journals deep in the library, but this is how it sounds to me.

Congrats, you get my reputation. @Leonardo gets props for showing us the way.

I'm glad you could do the leg work to construct an answer for us. :)


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When collecting cell lysates for a Western blot, how do I induce di-sulfide bonds?
I would like to conduct a simple dimerization experiment for some protein I'm collecting from a cultured cells. My thought is, that if I'm running a non-reducing, denaturing PAGE gel, then removing beta-mercaptoethanol/DTT from the sample buffer should be enough to allow di-sulfide bonds to form.
I have seen several authors incubate the cells first with a drug called BSS that diffuses across membranes and creates protein cross-links. I may be wrong, but the use of this drug seems more appropriate when trying to follow up with an immunoprecipitation or a pull-down assay.
If anyone has any experience with this, could you please enlighten me?

For the introduction of new cystine bonds, you will probably need to maintain an appropriate redox potential when dialyzing your cell-lysate to allow your cystine bonds to reform. To break the current di-sulfide bonds, we have been adding in Disulfide Bond Isomerases (DsBC to be precise) which will allow your lysate to get to an appropriate equilibrium.
As for examining for disulfide bond formation that has already occured between proteins in your lysate, removing reducing equivalents like DTT and beta-mercaptoethanol should do the trick. You can even denature your proteins by incubating them in LDS or Laemmli buffer at 90C as those components will not reduce your cystine bonds. In our experience the bands typically run at the expected molecular weight on a SDS-PAGE.

source: Stack Exchange

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

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Glomerular Filtration Rate
In practice, when you have vasoconstriction of the glomerular capillaries and subsequently an increase in blood pressure, glomerular filtration rate increases. However, this seems counterintuitive to Bernoulli's principle.
During vasoconstriction, because the radii of the capillaries are getting smaller, we should expect an increase in flow rate and blood velocity. According to Bernoulli's principle, the outward hydrostatic pressure should drop.
How does this lead to an increase in filtration rate?

The previous answer isn't quite correct, because, well, blood flow is complicated and the body has autoregulatory mechanisms. As Alex mentioned, vasoconstriction doesn't occur in capillaries because they lack a muscle layer. It does occur in the small arterioles before and after the glomerulus (the afferent and efferent arterioles, respectively).
Bernoulli's principle mainly applies to larger arteries and arterioles, and not capillaries. Capillaries are so tiny that the red blood cell is a significant portion of the diameter, so the assumption of no viscosity is no longer valid. See this discussion for an explanation.
To address your question, here's a basic picture of the glomerulus, from Gray's Anatomy.

The afferent arteriole is in red, and the efferent arteriole in blue. The glomerular filtration rate (GFR) depends on the pressure difference between the two, which affects the hydrostatic pressure at the glomerulus. Also, note that vasodilation has the opposite effect of vasoconstriction on GFR.  (For a nice image and explanation, look at Figure 6 here) So:

Constriction of the afferent arteriole decreases the blood flow into the glomerulus and thus the glomerular hydrostatic pressure, which leads to a decrease in GFR.
In contrast, constriction of the efferent arteriole decreases blood flow out of the glomerulus, and this increases the glomerular hydrostatic pressure and leads to an increase in GFR.

Both the afferent and efferent arterioles are regulated through hormones (and drugs that inhibit the hormones). Prostaglandins dilate the afferent arterioles, and NSAIDs inhibit this action. Angiotensin II preferentially constricts the efferent arteriole, and this action is restricted by an ACE inhibitor. (Source: First Aid for the USMLE Step 1)

It's worth noting that the afferent arterioles are significantly larger than the efferent arterioles, which creates the high-pressure environment required for filtration in the first place.

To my knowledge, capillaries in general and the renal capillaries in glomeruli in particular do not have muscle cells to constrict. The latters have only a basal layer with podocytes lying directly on it (link to the open textbook).
Therefore, the vasoconstriction takes place only in arterioles before the glomeruli, and this vasoconstriction leads to the increased hydrostatic pressure which propagates to the glomerular cappilaries. The blood flow rate and velocity do not change, therefore the increased hydrostatic pressure works against the constant pressure of Bowman's capsule and osmotic pressure of the colloid medium, leading to the increased net filtration pressure (NFP). Filtration rate and filtration pressure are directly connected, so that the rate increases either.
For more details, please, refer to the textbook I provided the link to above.

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


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What temperature should mammalian B-Cells be stored at outside of the incubator?
I'm working with murine B-cells. The general protocol is to keep cells on ice to keep them from dying but I've noticed that it makes these cells aggregate and precipitate out. I've heard suggestions that these cells should just be kept at room temperature. How would I be able to determine which conditions at which I should be keeping my cells?
I was trying to collect cells to prepare them for cell binding studies to antibodies and then assess the cells on a filterplate. Typically, you keep them on ice to pause the metabolic state as well as to prevent endocytosis of the bound molecules. However, that shift seems to cause settling. How do you troubleshoot the appropriate temperature to process cells and what are the usual scientific justification for making such decisions.

I know I'm not supposed to ask for clarification here, but I think it's completely necessary in order to provide an appropriate answer. Could you please clarify what you're doing with your cells? i.e. do you need to keep them physiologically active? How long are they out of the incubator? If cells are just going to FACS, ice is fine, just pulse the pellet prior to reading, a little EDTA can also help keeping them from clumping. In general, I would recommend ice or 37 degrees most of the time.

@Rhill45, really?  would say that part of the answer does involve "how long can you keep cell on ice". For instance, if you're going to FACS, what processing steps can you do before running them through the machine, what is the rate of aggregration, etc

Also, why are people collapsing questions from 2 years ago?

For the settling there's little you can do except agitation and using a taller thinner tube and larger suspending volume.
For the clumping however if the analysis permits it, adding serum to a [final] of 5% will help slow the clumping (in the short term). You can also filter out initial clumps by pushing the cells through a nylon mesh filter (they make these especially for flow-commonly used with fixed cells). I've analyzed cells on ice in dark probably as long as 6 hours after harvesting with little change in viability, however this is of course bad practice.


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How long does it take to stain cells?
I'm never going to run these type of experiments but I do need to have a good idea of their timescale. After I fix my cells, if I stained my cells with histology stains like DAPI, Fluorescein, and various labeled antibodies, how long do I have to wait before I can examine my cells with microscopy?

For fluorescence immunocytochemistry, there are 3 main incubations that determine duration of the procedure. Generally it takes 2 days to stain your cells before you can visualize them. Once cells or tissue are fixed onto glass, you first incubate with a primary antibody to directly target a specific antigen(s), usually overnight. After primary labelling, a secondary antibody is applied to target the primary antibody, which usually takes a few hours. These secondary antibodies come conjugated to some fluorescent dye (Cy5, TRITC, FITC, AlexaFluors, etc). A nuclear counterstain is really quick, only 5 minutes. After all the labelling and nuclear stain, you can mount the coverslip with mounting media and once it cures you can visualize them.
Abcam has one of many quick reference guides.

The temperature plays an important role, too: incubating at 4°C or at RT makes a big difference.

Certainly. I also left out blocking which is arguably most critical to the process, but on the time scale of the whole procedure, is relatively quick (30-60 minutes). @bobthejoe was simply asking for an idea of total time.

And another factor is what you are staining: times are shorter for cells in culture compared to tissue slices (i.e.: ICC vs IHC), as the antibody will need time to deeply penetrate in the tissue.


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Why do eukaryotic organisms have introns in their DNA?
We touched on introns and exons in my bio class, but unfortunately we didn't really talk about why Eukaryotes have introns. It would seem they would have to have some purpose since prokaryotes do not have them and they evolved first chronologically, but I could easily be wrong. Did the junk sections of DNA just evolve there by some sort of randomness or necessity as opposed to an actual evolutionary advantage? Why hasn't evolution stopped us from having introns since they seem to be a 'waste' of time and DNA? Why do prokaryotes not have introns?

Not everything needs a function to exist in biology.  One way to answer this question is to look to see what kind of selection pressure is acting on introns.  Do they evolve neutrally?

I guess a better response to your question is: Why not have introns?  Take a look at the neutral theory: https://en.wikipedia.org/wiki/Neutral_theory_of_molecular_evolution

There is still a lot to be learned about the roles introns play in biological processes, but there are a couple of things that have been pretty well established.

Introns enable alternative splicing, which enables a single gene to encode multiple proteins that perform different functions under different conditions. For example, a signal the cell receives could cause an exon that is normally included to be skipped, or an intron that is normally spliced out to be left in for translation (the Wikipedia article on the subject has a basic overview of the possibilities). This would not be possible, or at least would be much more difficult, without the presence of introns.
In recent years, we have discovered that RNA molecules (especially small RNAs such as siRNAs and miRNAs) are much more involved in regulating gene expression than previously thought. Often the small regulatory RNAs are derived from spliced introns.

There is probably more, but essentially introns enable a finer level of regulatory control. Biological complexity is often not the result of having a larger complement of genes, but of having additional layers of regulation to turn genes on and off at the right times. Prokaryotic genes are often organized into operons, and a single polycistronic mRNA will often encode multiple proteins from multiple adjacent genes. Since the biological processes required to sustain microbial life are much less complicated than those required to sustain eukaryotic life, they can get away with much less regulatory control.

I would add that there is a general assumption that this is a reason that eukaryotes might have the ability to adapt to roles higher on the food chain than prokaryotes, like form multicellular organisms (there are a few exceptions, but really very few and they are pretty simple like - cyanobacteria which form chains of cells).

While this is a good "how" answer that resumes what we know now, is not by any means a "why" answer. For example, what's the limitation of prokariotic regulation that introns solve? Why do nature needs to squeeze more proteins in a single gene and then have 93% of garbage in the rest of the genome? I think that  the answer by @apoz it is a better fit.

I was under the impression that a lot of our introns were just from retroviruses that got into our genome at some point in our evolutionary past. Since the competitive disadvantage incurred by carrying some non-expressed junk DNA is very low, there's not selection pressure to get them back out.

Evolution - Douglas J. Futuyma, Chapter 19, p. 461

Michael Lynch and John Conery (2003) have pointed out that a variety
  of genomic features that appear to have little fitness advantage for
  organisms-introns, transposable elements, large tracts of noncoding
  DNA-may be more prevalent in species with small effective population
  sizes. They have suggested that viruses and bacteria have extremely
  large population sizes that facilitate the sweep of advantageous
  mutations that enable genomic streamlining. By contrast, eukaryotes
  have smaller population sizes that facilitate the fixation of
  nonadaptive traits. This is the best hypothesis advanced
  so far that would explain the diversity of genome sizes and
  structures.

I was explaining it to my girlfriend: imagine you have two rooms in your two-and-a-kitchen house full of cartridges of adhesive tape... you really don't need it, but have no way of getting rid of it. Now, the hose of the vacuum cleaner gets broken, and you take a small amount of adhesive tape (you have so much) and patch it...  nobody would seriously believe that you were storing all that much adhesive tape for that sake, and you rather should have ordered a new hose. But you did the best of your circumstances. That much is going on in eukariotic genetics: easy and dirty patches everywhere.

I think the Lynch and Conery paper is so far the most reasonable explanation on the origin of introns, and combined with the other answer (http://biology.stackexchange.com/a/1725/658), it gives a complete explanation about the origin and the current fitness advantage of having introns in certain organisms, but not in others.

Hi apoz - this answer is considered useful by the community but still needs to consist of more than direct quotes.

@149781-32509185: the Lynch & Conery paper does not explain introns by saying they have a fitness advantage.  A small population size that they refer to means that genetic drift is creating the fixation of the introns.

Prokaryotes can't have introns, because they have transcription coupled to translation. They don't have time/space for that, since intron splicing will stop the coupling. Eukaryotes evolved the nucleus, where splicing can be done. The ancestor of eukaryotes that developed the nucleus could afford more variability (because of introns) than species without it, so they had a greater fitness.
Bacteria can't afford high complexity compartmentalization, a process that requires a lot of available energy per gene, a eukaryotic cell can have tens, hundreds or even thousands of mitochondria that have similar energy output to a bacterial cell, while having a genome about 100-500 times smaller (16 kb of a human mitochondria compared to 4.000 kb for a E. coli cell).
I hope that clarifies your doubts, and you can see that this is a debatable answer.
Sorry for my bad English.
Sources:
Lane & Martin 2010.
Martin 2011

This is a good answer.  Comparing the lack of introns between prokaryotes with eukaryotes that do have introns does not mean that introns exist in eukaryotes because it infers an evolutionary advantage to have them.  A more likely reason is that introns are highly deleterious in prokaryotes due to genome size limits but not deleterious in eukaryotes.  See the C-value problem.

But prokaryotes do have introns - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC177115/ - although on nowhere near the scale that Eukaryotes do.

Many archaea (which are prokaryotes) also have introns.

There are several good answers here already.  Daniel Standage points out the value of alternate splicing.  For a compelling example of the role in regulation of gene expression, read one of the reviews of sex determination in Drosophila melanogaster (sex-lethal, transformer, doublesex).
None mentions the idea of exons as "cassettes" of reusable function that can be introduced into an existing gene during evolution.
The bounding introns represent regions where inexact "grafting" can occur without destroying the already functioning reading frame of the newly introduced xeno-exon (I just made up that neologism) or of the recipient gene.
In other words, introns provide regions which allow for sloppy transposition of functional subunits while reducing the likelihood of wholesale chaos at the transcription/translation level.
Evolution shows over and over that it is capable of promoting mechanisms that promote evolution.  How else can you explain meiosis?

You need to read how to write a good answer for SE. You refer to the Drosophila sex determination system but do not provide any explanation or reference. How do you expect anyone to understand this? And if you talk about exons as "cassettes of reusable functions", you should provide an example. Do you know of any? And your language, even when you are not inventing new terms is incomprehensible gobbldey gook — "sloppy transposition of functional subunits...". Sloppy ideas and sloppy writing, more like.


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What does the 34/70 in Saccharomyces pastorianus Weihenstephan 34/70 stand for?
I've searched everywhere.
No Wikipedia page.
No information on NCBI.
I searched all occurrences of 34/70 in some primary research articles!
The best I've found is this brewery forum where someone asked the same question.
And the user rockfish42  answered:

No idea why they use that number, but it's the catalog number at
  Weihenstephan's hefebank.

I went to the Yeastbank website at Weihenstephan for some info. The keyword here is "Stamm," which is German for stem, clade, clan, or strain. So, I would take this to mean that the 34/70 is an isolate (#70) of strain 34. Two of 34/70's strengths, according to the link above are it makes clean beer and gives a pleasant taste profile due to its low yeast-like aroma in the finished beer. I can attest to that firsthand, having had on numerous occasions the pleasure of partaking of Weihenstephaner beer in its home city of Freising.

That seems like a reasonable explanation. It reminds me of a lot of mammalian cell lines that go by common names (PC-12, Ins-1, Min-6, P19) that get a name based on the isolate number they came from in the original experiment.

I am not sure why you say there is no information... a quick Google search returned a few interesting pages...
In this paper:
Progress in Metabolic Engineering of Saccharomyces cerevisiae - Nevoigt, Microbiol Mol Biol Rev. 2008
the author says:

The identification of the entire genomic sequence of a commonly used lager brewer's yeast strain, i.e., Weihenstephan Nr. 34 (34/70), represents a breakthrough in the molecular analysis of lager brewer's yeast.

So, it would look like 34/70 is just a catalogue number, with no specific meaning.
Curiously, according to the Wikipedia page on Saccharomyces pastorianus:

S. pastorianus never grows above 34 °C (93 °F)

So, I cannot exclude the hypothesis that 34 could come from there although, well, I personally propend for the catalogue number.
Other interesting links:
The paper about the S. pastorianus genome sequencing:
Genome sequence of the lager brewing yeast, an interspecies hybrid. - Nakao et al., DNA Res. 2009
An article comparing two different strains of S. pastorianus, 34/70 and 34/78 (again, catalog number hypothesis seems to be the most obvious explanation)
Molecular species of phosphatidylethanolamine from continuous cultures of Saccharomyces pastorianus syn. carlsbergensis strains. - Tosch, Yeast. 2006
The NCBI taxonomy page (entry #520522)

That was a lot of effort for an answer that contained no new information. The question already said that 34/70 is the catalog number. The question was what the 34/70 means.
And no it is not the temperature at which it starts to grow, that would mean Stamm W 195 starts to grow at 195°C !! Larry_Parnell's answer is much better.

No, the yeast stops growing at 34, so that's most probably just a coincidence, as I said. As for the new information... your question does not contain any of this and you said there was no Wikipedia or NCBI page, so I pointed out that there are in fact such pages, that's all. If the other answer is better accept that, I surely won't be offended.

Yes my question said that it was the catalog number. See the quote. There's no wiki page for Saccharomyces pastorianus Weihenstephan 34/70, and I didn't say there's no NCBI page, just that the NCBI page didn't have any information about the 34/70. Sorry that I misread it as 'starts growing' rather than 'stops growing' , but the argument still stands the same =)

It seems like @nico was trying to help identify what was known from these public sources (NCBI, Wikipedia) for others that read the question as well. He was able to come up with the same informaation you seem to have found, and though he did not find a definitive answer as to the history of the name, it is relevant information. :)


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How does a cell sense its size?
Cells come in all sorts of sizes. How do they regulate their cell size to the point where similar cell types have a fairly mono-disperse size distribution?
Reasked from http://www.quora.com/How-Does-a-Cell-Know-Its-Size

Of particular interest to this question might be the latest issue of Curr Biol that has a special section devoted to this topic: Curr Biol, Vol 22 Issue 9 (http://www.cell.com/current-biology/issue?pii=S0960-9822%2812%29X0009-5)

This is a question that has been the focus of study for the last century (e.g., Amodel of cell size regulation - Ycas et al, J. Theoret. Biol. (1965) 9, 444-470). Cell size regulation may be in part determined by ribosomal activity (through mTor regulation) and is a critical checkpoint in cell division.
How the cell senses its size, however, is not understood. In 2009, two reports suggested that protein gradients could be responsible for the sensing of cell size. You can read a commentary about those articles in Cell size control: governed by a spatial gradient. - Almeyda and Tyers, Dev. Cell. (2009) 17(1), 3-4:

The phenomenon of cell size homeostasis, whereby cells coordinate
  growth and division to maintain a uniform cell size, has been an
  outstanding issue in cell biology for many decades. Two recent studies
  in Nature in fission yeast demonstrate that a gradient of the polarity
  factor Pom1 is a sensor of cell length that determines the onset of
  Cdc2 activation and mitosis.

These articles demonstrate one way in which cells may sense their size, but most probably several other mechanisms are also in place.

Rebecca Heald and her group at Berkeley do very interesting work looking at how organelle sizes are controlled by comparing two Xenopus species, very much related to the question here. Check out Nuclear size is regulated by importin alpha and NTF2 in Xenopus


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Which factors besides the thermodynamic stability are important for the hairpin in intrinsic transcription termination?
Intrinsic termination (rho-independent) relies on a stable hairpin with a subsequent uridine repeat. The common explanation on how these sequences cause the termination of the transcription are based on the thermodynamic stability of the sequence. The GC-rich stable hairpin together with the destabilizing U-repeat supposedly destabilize the binding of the polymerase enough to cause it to disassociate from the template.
What I'm looking for are specific requirements on the termination sequences that are not based on thermodynamics.

Are there any specific requirements on the hairpin sequence beyond a certain thermodynamic stability.
Are there any loop variants that are known to reduce the termination efficiency?
Does the shape of the hairpin, e.g. any kinks or bulges in it, have an influence on termination efficiency?

The typical requirements I read are 5-14bp and GC-rich, and I'd like to know if there are any more specific requirements, especially ones related to the structure and not the stability of the hairpin.

I'm going to suggest this for now and write it up later: http://nar.oxfordjournals.org/content/37/14/4736.abstract

The RNA hairpin transcription terminator in prokaryotes is terminated by the GC rich hairpin followed by 4+ uracil bases as you describe it.
The original reference describing the hairpin, described the sequence requirements as being for the thermodynamic stability of the hairpin, but the protein nusA has also been found to stimulate termination.
You might think that there would be some protein that would precisely bind this motif and mediate the termination, but at least as far as I can find, it appears that the hairpin clogs up the polymerase itself, causing termination.  This review linked here has some nice pictures of the RNAP bindig pocket model.


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Origin, or source, of rhesus negative in human blood
This is my first post here, so please be gentle. I recently learned that I have Rh- blood (I'm A-), and was idly looking into blood types on Wikipedia. I was surprised to find that relatively few (~15% of all) humans have it, and most of those seem to be European. Looking just a little further, I found a bunch of crackpot-looking sites that try to explain how people got Rh- blood, and what weird abilities they possess as a result.
I managed to find one site that seemed at least less laughable, which suggested that interbreeding with Homo neanderthalensis (or possibly Homo sapiens neanderthalensis, since the site seemed to indicate that there was some question about how different H. s. sapiens were from H. neanderthalensis) might have accounted for the introduction of the condition.
It seems that from more reputable (medical) sources, the only difference between Rh+ and Rh- is that complications can arise during pregnancy if the mother is Rh- and the fetus is Rh+. Indeed, most sites (e.g., WebMD) seem to explicitly state that there are no other differences of note.
I am not a biologist, or an anthropologist, or a life-science kind of guy at all. However, as a computer scientist, I like to think that I have both an open mind but one which demands scientific and/or logico-mathematical evidence for claims. Lots of the pseudo-scientific, paranormal, etc. theories on the web I basically dismiss out of hand, as explanations which are almost certainly fantasies, but most definitely baseless and untestable.
My question:

What, if any, is the current scientific understanding of the origin, or source, of rhesus negative blood in human beings? Do individuals with Rh- blood have any common (in a statistically significant sense) characteristics or health issues, aside from the issue with pregnancy and tending to be more European than not? Is there anything to continuing to look into this?

For context, I got started down this rabbit hole while looking into different dieting strategies, and found the "blood type diet". Just as an aside, I don't think there's a lot of merit to that diet... sounds like a fad thing. Any sources or information or help on this subject are appreciated.
EDIT:
I have been looking a little more, and I stumbled across a paper entitled, "The influence of RhD phenotype on toxoplasmosis and age-associated changes in personality profile of blood donors" which looks at the effect of the Rh- trait on personality changes caused by toxoplasmosis (if you Google the title, you should be able to download). Using Cloninger's and Cattel's personality factors, they seem to show a variety of things, including (a) personality differences between Rh+ and Rh- individuals not affected by toxoplasmosis, and (b) different reactions to prolonged toxoplasmosis affection in Rh+ and Rh- individuals.
I didn't even know that parasites could affect your behavior; that seems frightening on the one hand, but on the other, it's fascinating if it's for real, especially since the incidence of toxoplasmosis is not insignificant in most people. Anybody who knows anything about this or who reads the paper and can help me understand what it's saying would be doing me a great favor to answer/comment/chat. Thanks!

The blood type diet is a bunch of junk. There is no scientific merit to its claims. Genetic differences could be matched to a diet, but those differences should map to genes relevant to metabolic diseases such as cardiovascular disease, type 2 diabetes and the like. A genetic variant in phenylalanine hydroxylase (PAH) can lead to phenylketonuria (PKU) and specific diets can, usually are, prescribed to alleviate (risk of) symptoms. See http://omim.org/entry/261600.

@Larry_Parnell Yeah, that was my impression as well... blood type should have little to nothing to do with diet, and certainly the guy's reasoning seems to be pure fantasy. It seems like most named diets are fads, and that the best way to live healthy is to eat a varied diet of appropriate quantities of fresh, healthful foods, stay hydrated, and to get some exercise... common sense stuff. Still, I'm interested in the origin of Rh- (interbreeding? mutation?) and what other traits have been observed to be correlated to (not necessarily caused by) it.

For the blood type diet see this question on our sister site Skeptics.SE.

You may wish to also see our question: Is there any advantage to one blood type over another?

Your question has many questions in it.
As for the evolution of Rh factor, Blancher and Apoil (2000) attribute the high level of sequence similarity (92%) of the two RH locus genes, RHD and RHCE to a gene duplication event in the common ancestor of human, chimps, and gorillas. Their analysis of the cDNA from these genes revealed "complex recombination events" after the lineages split.
Basically the most recent common ancestor of apes had the "human" RH genes, which then differentiated after the lineages diverged. Duplicate and differentiate is a common theme in evolution.
As for why it's called rhesus antigen, that's just as experimental artifact:

The term "Rhesus antigen" was introduced by Landsteiner and Wiener,
  who found that rabbits (and later, guinea pigs) immunized with red
  blood cells (RBCs) from a rhesus monkey produced antibodies which
  agglutinated 85% of Caucasian blood samples (Landsteiner and Wiener
  1940, 1941).

They probably weren't even correct about the antibodies being rhesus:

In conclusion, if the term "Rh" was coined by Landsteiner and Wiener
  because of the source of antigens (the rhesus monkey) they used to
  obtain anti-Rh in rabbits, it is highly probable that, in fact, they
  produced anti-LW antibodies.

http://www.frozenevolution.com/origin-rh-blood-group-polymorphism

The high proportion of Rh-negative persons in the European population
  could be connected with the fact that, until recently, big cats (the
  definitive host of Toxoplasma gondii) were practically not present
  here and thus toxoplasmosis was rare (and Rh-negative persons were at
  an advantage compared to the rest of the population). The low
  percentage of Rh-negative persons in Africa (less than 1%) could be
  related to the high prevalence of toxoplasmosis there, which often
  approaches 100%.

http://www.sott.net/article/228188-Toxoplasma-gondii-Cat-parasite-may-affect-cultural-traits-in-human-populations

Lafferty suggested that because climate affects the persistence of
  infectious states of Toxoplasma in the environment, it helps drive the
  geographic variation in the parasite's prevalence by increasing
  exposure risk. The parasite's eggs can live longer in humid,
  low-altitude regions, especially at mid latitudes that have infrequent
  freezing and thawing. Cultural practices of food preparation such as
  rare or undercooked meats, or poor hygiene, can increase exposure to
  infection, as can having cats as pets. Lafferty added, "Toxoplasmosis
  is one of many factors that may influence personality and culture,
  which may also include the effects of other infectious diseases,
  genetics, environment and history. Efforts to control this infectious
  pathogen could bring about cultural changes."   / this is why I feel
  rh- is a newer blood grouping due to the last ice age conditions.
  these were the conditions in nw Europe back then and the rh- trait has
  persisted in that area. it just all makes sense . you may also search
  out " congenital toxoplasmosis infection " and I believe you will find
  when a pregnant woman gets toxo infection the baby comes out with the
  same symptom ology as erythroblastosis fetalis, rhesus disease.this is
  why all pregnant women are cautioned to avoid cat feces and stay away
  from cat boxes where they defecate.

OPINION ? i'll have you know i'm 61 y old retired medical worker who has studied biology and etc my whole life . this opinion is not just anyone's .  btw i'm o- myself  /

http://www.ncbi.nlm.nih.gov/pubmed/18766148

RESULTS:
RhD-positive subjects have been confirmed to be less sensitive to the influence of latent toxoplasmosis on reaction times than Rh-negative subjects. While a protective role of RhD positivity has been demonstrated previously in four populations of men, the present study has shown a similar effect in 226 female students. Our results have also shown that the concentration of testosterone in saliva strongly influences (reduces) reaction times (especially in men) and therefore, this factor should be controlled in future reaction times studies.
CONCLUSIONS:
The observed effects of RhD phenotype could provide not only a clue to the long-standing evolutionary enigma of the origin of RhD polymorphism in humans (the effect of balancing selection), differences in the RhD+ allele frequencies in geographically distinct populations (resulting from geographic variation in the prevalence of Toxoplasma gondii), but might also be the missing piece in the puzzle of the physiological function of the RhD molecule.

Welcome to the site. You answers take heavily from quotes, which should be marked as such. Rather than three separate posts, why not try to combine them into a single post with some additional analysis or insights?

It's my opinion the rh antigen developed from toxoplasmosis infection. I only recently learned that this protozoan can actually insert its genes into a host's genome. Once it's in the genes, it can be passed in the germline. Toxoplasmosis can infect all primates, human and otherwise. Monkeys get it, and so do humans living in toxoplasmosis endemic places. The life cycle of toxoplasmosis is connected with mice and cats as an evolved survival strategy for the toxoplasmosis protozoan. There never were cats in northwest Europe, and that would explain why the people with ancestry from that area were never exposed to toxoplasmosis. I look for the rational biological explaination. One great clue to my thinking is I found a term used in some research writings, the text read "RH strain of toxoplasmosis". Yes they seemed to be doing experiments with the toxoplasmosis found in rhesus monkey.

Can you provide citations to back up your hypothesis? Opinion doesn't go very far.

I am pretty sure there were wildcats in northwest Europe.


text:
Why does Penicillin only affect bacterial cell walls
I was quite fascinated by the feature Should Science Pull the Trigger on Antiviral Drugs—That Can Blast the Common Cold? in this month's Wired magazine.
They explain that Penicillin is effective at killing bacteria because it interferes with the growth of bacterial cell walls.
How does Penicillin do that exactly? And why does it not dissolve human cells as well?

The simple answer is that human cells don't have cell walls.

The reason why penicillin affects only bacteria and not Eukaryota cells has already been explain. It is true that Penicillin can also kill Gram-negative bacteria. One study I conducted, several Gram-negative bacteria have been removed from my cultures using Penicillin G Sodium Salt. I presume it is because the outer-membrane that protects Gram-negative bacteria is weak or thin. But maybe GWW can provide some references as I don't have them.

Bacteria have a mesh-like structure surrounding their plasma membrane called a cell wall.  The cell wall is made up of peptidoglycan polymers that form a rigid crystalline structure that helps protect the osmotic pressure of the bacterial cytoplasm.
Penicillin and other β-lactams work by inhibiting the final step of peptidoglycan synthesis, which prevents transpeptidation (crosslinking) of the peptidoglycan molecules. This leads to the death of the bacterium by osmotic pressure due to the loss of the cell wall.
This drug doesn't affect human cells because they lack a cell wall surrounding their plasma membrane.

n.b. penicillin only affects gram positive bacteria.

@RoryM: That is not totally correct, penicillin does affect some gram negative bacteria but it is not very effective.  There are other ß-lactams that do affect gram-negative bacteria such as Carbenicillin.

I don't think that this is necessarily correct. The beta-lactams doesn't inhibit the synthesis but rather the reorganization of the peptidoglycans. The rigidity of the now static wall then prevents cell division.

@bobthejoe:  I updated my answer to better explain it. Thanks.


text:
To which distinctions does the term "hymenoptera" refer?
Hymenoptera is an order of insects that includes bees, ants, and wasps. A quick search gives the following etymological analysis of the term hymenoptera.

hymen (membrane) + pteron (wing)

Does the term hymenoptera have a firm basis in biology and physiology? In other words, what is different about membranes or wings (or membranous wings) in species of hymenoptera as opposed to species of other orders of insects?

I don't have a definitive answer, but I suspect Hymenoptera is "just a name," albeit a name that has lasted through the phylogenetic nomenclature revolution.
Hymenoptera was erected by Linnaeus in the 10th edition of Systema Naturae (1758). The description of Hymenoptera (membrane wing; p. 553 [hope your Latin is better than mine]) follows that of Lepidoptera (scale wing) and Neuroptera (net wing) and precedes Diptera (two wing).
Classical taxonomy, which Linnaeus was more or less inventing at the time, was based on shared similarities. Those insects which Linnaeus thought more similar to each other than to other insects (e.g., ants, wasps, bees) all shared the characteristic of having a membrane based wing. The scaly wings of moths and butterflies made them more similar to each other.
He needed names for these groups, so he chose logical ones based on outward appearance of the wings: scaly, netted, membranous, or paired. That fact that these major groupings have more or less stood the test of time suggests that Linnaeus picked a good characteristic on which to name his classification of the major groups of insects.

For the most part most of biology is History..

@shigeta: Arguably, most of everything is history :). But this is particularly true for taxonomy, for sure.


text:
What is the difference between "dikaryotic" and "heterokaryotic" states in the sexual lifecyles of fungi?
Many fungi undergo a reproductive phase in which more than one genetically distinct nuclei (from 2 separate mating types) is present within the same cytoplasm. In the Ascomycota and Basidiomycota, this phase is termed "dikaryotic", whereas in other fungal phyla the phase is "heterokaryotic." What is the difference here? Is it purely number of nuclei per cell, or does the difference depend on how many genetically distinct nuclei are present (2 or >2)?

A heterokaryon is a fungal cell which has two or more genetically-distinct but allelically-compatible nuclei, as suggested by this resource, as well as this Wikipedia article.
A dikaryon is a fungal cell which has precisely two genetically-distinct but allelically-compatible nuclei, as shown here and here.
In this sense,  a heterokaryon is a general term, whereas a dikaryon is a specific term. A dikaryon and a trikaryon (although not often seen in literature) are both heterokaryons.

So heterokaryon is the general case, and dikaryon is a specific case?

Good answer, thanks - one other thing I found is that a dikaryon may then divide, with each nucleus being replicated once per division, to form  dikaryotic hyphae. In Basidiomycota, the entire basidiocarp (mushroom) is formed from these dikaryotic hyphae.

dikaryotic does - by definition - mean that there are exactly two nuclei in the cells, it does not say that the two nuclei are genetically distinct!
heterokaryotic does also mean only one thing: the nuclei (the number is not important) are genetically distinct.
that's the reason why, for example webster, writes "heterokaryotic dikaryon".
in fact the nuclei are distinct in almost all cases, that's why some only write "dikaryon"

A dikaryotic fungi contains only 2 genetically different nuclei but a heterokaryotic fungi may contains more than 2 nuclei

can you add some references to back up your answer?

Heterokaryotic = contains two or more nuclei
Dikaryotic = one cell contains two separate nuclei that are not fused; usually indicated as n+n

Welcome to Biology.SE! It isn't clear that this is adding anything to the already existing answers.  In addition, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!

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


text:
What is the distance between the 3' 18s rRNA (the Kozak consensus sequence) and the A-site of eukaryotic ribosomes during protein translation?
Reposted from Quora
The Kozak sequence is shown to be important in translation initiation, and the A-site is the anti-codon recognition site. If the distance is not known, how could I find out what it is? Is the crystal structure of the whole mRNA-rRNA-tRNA complex determined? If so, what modeling program would be best for establishing intermolecular distances?

Kozak consensus sequence (KCS) is present near or overlapping with the start codon. I am not sure what you mean by distance between that and A-site. Start codon is localaized at P-site at the time of translation initiation. Distance between start codon/KCS and A-site at initiation is same as distance between P- and A- sites (I guess ~20Å). A-site keeps moving during translation and hence the distance keeps increasing. Crystal study is available; See here.
See this figure from the abovementioned study for the relative positions of start-codon, P-site (exit) and A-site (entry).


text:
Does the MS2 RNA binding protein have any translational repression effects?
Reposted from Quora: http://www.quora.com/Does-the-MS2-RNA-binding-protein-have-any-translational-repression-effects
I'm thinking of the MS2 protein binding to its RNA hairpin target. Would the interaction of the MS2 protein to the hairpin placed upstream of a ORF cause any translational repression?

Why don't you place the MS2L downstream of the ORF? What exactly is the experiment you want to do?

I assume you are talking about the mTAG visualization technique for mRNAs (1). You are probably familiar with it, but the OFR of interest is tagged with MS2L sequence downstream of it and upstream of the 3'UTR. There is also a modified version, in which you can visualize both the mRNA of interest, and the protein that is translated, see the figure below (2). Haim and colleagues found that yeast expressing mCherry and MS2L tagged ATP2 grew on glycerol-containing media, which would require efficient translation of ATP2.

So I would assume that there is no translational repression if you tag the mRNA downstream of the ORF. Unless you have a very good reason to tag the ORF of interest with MS2 upstream of the start codon, I wouldn't do it, because these stem-loop structures would most probably stall translation, as mRNA secondary structure has been implicated in translation initiation efficiency.

The idea would actually be to repress translation via the mecahnism that you suggest. Hence, the rationale of putting the MS2 hairpin upstream of the ORF.

Oh I see now... Interesting idea. Worth exploring. Why don't you use Cas9?

Probably because I asked this question back in 2012 and was more of a curiosity question rather than an actual experimental question. More specifically, I'm concerned more about generating a tuneable analog type of repression system where you can generate a range of repress rather than perform a complete knockdown using CRISPR.


text:
How to clone and sequence a gene transcript of unknown sequence?
How might I go about amplifying a gene transcript (mRNA) from animal tissue of which little is known about the genome? In some applications, I have used reverse transcriptase PCR to amplify all mRNA transcripts from cultured cells, but this required that I knew the sequence to PCR amplify.
How do I go about this without knowledge of the gene or transcipt?

Do you know the function of the gene? What is the purpose of your experiment?

I know it's an endocrine hormone, and I can draw parallels from human endocrinology, but beyond that I don't know much about it (and there doesn't seem to be much in the literature either). The purpose really is just to see how conserved the mammalian orthologs are compared to lizards.

Having the hormone sequence does help a bit. While not entirely unbiased, you could try to enrich your sequence by amplifying from a conserved region.

Ya, bobthejoe is right: just search in google 'homology-based cloning'

@bobthejoe - thanks, I will look up homology-based cloning. I suspect there's a fair amount (50%) of conservation between humans and lizards so I'll see if this pathway can yield a meaningful result.

Perhaps you can draw inspiration from classic paper on lambda cloning:  Maniatis T, Hardison RC, Lacy E, Lauer J, O’Connell C, Quon D, Sim GK, Efstratiadis A. 1978. The isolation of structural genes from libraries of eucaryotic DNA. Cell 15: 687–701.
Try selecting tissues from the animal which you think is "enriched" (i.e. highly expressed) for the specific gene you're looking for. This might take a little bit of guessing. For example, if gene A is very highly expressed in tissue B, then you can "assume" most of the mRNA transcripts will be for that of gene A. Do a RNA purification, RT-PCR, and clone the cDNA into lambda vectors and pick plaques. With a little bit of luck, you'll be able to identify the gene by cloning, hybridisation, and subsequent chromosome "walking" to determine it's structural origin.
This was done back in the day to identify novel genes way before genomics, sequencing, or even PCR!

That's pretty cool. Thanks for the reference and explanation jp89.


text:
On which date did the official name change of Lactobacillus sanfranciscensis change?
When did the change of official name from Lactobacillus sanfrancisco to Lactobacillus sanfranciscensis happen? An answer ((to the exact day OR within a few days) AND the name of the conference at which it happened) would be appreciated.

Most rule of nomenclature that I am aware of require that changes be made formally print and not at conferences.

Lactobacillus sanfranciscensis first shows up in pubmed in Gänzle et al. (1998). They reference Trüper and De'Clari (1997) for the name Lactobacillus sanfranciscensis. The latter say:

As none of them makes sense in the nominative apposition construction,
  we hereby correct these names to forms that are in agreement with Rule
  12c as follows.
...
Lactobacillus sanfrancisco ("the city San Francisco") is corrected to Lactobacillus sanfranciscensis (adjective: "from San Francisco").

That issue of Int J Syst Bacteriol was published 1 July 1997, so I guess that's your date.
References
Gänzle M G, M Ehmann, and W P Hammes. 1998. Modeling of growth of Lactobacillus sanfranciscensis and Candida milleri in response to process parameters of sourdough fermentation. Appl Environ Microbiol 64(7):2616–2623.
Trüper H G, De'Clari L. 1997. Taxonomic note: necessary correction of specific epithets formed as substantives (nouns) "in apposition." Int J Syst Bacteriol 47:908–909.


text:
What are all possible vectors for unicellular human parasites?
I got the given question. They want the following pieces of information about protozoological human parasites:

disease - parasite - vector.

There are 10 proteogenic diseases at the Wikipedia. I added the corresponding parasite and the vector next to them:

Malaria - Plasmodium - Apicomplexa
Amoebiasis - Entamoeba histolytica - sarcomastigophora
Giardiasis - Giardia lamblia - no vector
Toxoplasmosis - Toxoplasma gondii - no vector
Cryptosporidiosis - Cryptosporidium - Apicomplexa
Trichomoniasis - Trichomonas vaginalis - no vector
Chagas disease - Trypanosoma cruci - insect
Leismaniasis - Leishmania donovani - sand fly vector
Sleeping sickness - Trypanosoma brucei gambiense - tsetse fly vector
Dysentery - Entamoeba histolytica - sarcomastigophora

I am unsure what I should answer to the question since it is asking "all" possible vectors for unicellular human parasites.
There are many possible diseases, much more than the given ten in my opinion.
It seems also that there are many possible ways of getting the infection for each disease.
I hope that I am wrong in my statements.
It is my first course in Parasitology.
What would you answer to the given question?

This is a good question, because the term "vector" is not used consistently in the literature. This probably is because the context of the discussion is often limited to a subset of parasites. The term is sometimes used to refer to blood-sucking insects. However, animals (including humans) can also be vectors. More generally, anything with mass could be a vector (e.g. biological warfare might use a missile or a blanket as a vector).

Note that if you can answer broader to the question I will accept your answer. It is very difficult for me to accept my own answer so please answer to the question such that your answer is outside of the standard textbooks.

I think the textbook answer is good here, and in line with epidemiological terminology. There are always exceptions, and this topic is outside of my area of expertise. Perhaps you could ask your professor for some more details on the use of the term "vector" - maybe print out this discussion and ask for details that you could use to improve your post.

Based on my course material, I managed to get the following list:

Malaria - Plasmodium falciparum, p. malariae, p. vivax, p. ovale - female anopheline mosquito
Babesiosis - Babesia devergens, babesia microti - tick ixodes ricinus
Balantidiasis - Balantidium coli - waterborne
Coccidiosis & toxoplasmosis - Eimeria species - waterborne
Toxoplasmosis - Toxoplasma gondii - waterborne
Amoebic dysentery - Entamoeba histolytica - waterborne
Periodentitis - Entamoeba gingivalis - oral-oral contact
PAM - Naegleria fowleri - waterborne
GAM - Acanthamoeba species - waterborne
BAE - Balamuthia mandrillaris - waterborne
Trichomoniasis - Trichomonas vaginalis - sexual contact
Trypanosomiasis - Trypanosoma brucei gambiense, trypanosoma brucei rhodesiense - bite of a tsetse fly
Leukopenia - Leishmaniasis specieses - different genera of sandflies: Plebotonus & Lutzomyia

Waterborne means that the parasite is transmitted to the host through contaminated food, water or hands, or by swimming in warm pools or mud pools, for instance.


text:
Why is the 3'UTR region highly methylated in most of the human genes?
Most of the human genes are found to be highly methylated in their 3'UTR region (0.8-0.9%). I was wondering if there is any specific reason for this?

any reference? would be interested to see it...

According to Choi et al. Genome Biology 2009, 10:R89, DNA methylation at both coding boundaries may regulate transcription elongation and stabilize splicing by reducing the occurrences of exon skipping.
From the abstract:

Here we report a genome-wide observation of distinct peaks of
  nucleosomes and methylation at both ends of a protein coding unit.
  Elongating polymerases tend to pause near both coding ends immediately
  upstream of the epigenetic peaks, causing a significant reduction in
  elongation efficiency. Conserved features in underlying protein coding
  sequences seem to dictate their evolutionary conservation across
  multiple species. The nucleosomal and methylation marks are commonly
  associated with high sequence-encoded DNA-bending propensity but
  differentially with CpG density. As the gene grows longer, the
  epigenetic codes seem to be shifted from variable inner sequences
  toward boundary regions, rendering the peaks more prominent in higher
  organisms.

Their data (figures 1 and S2), however, do not support a generalized increase in the 3' UTR regions in either human T cells, mouse liver, yeast or flies.

Thank you so much. This paper looks very interesting. I will read it and see if I have more to discuss.


text:
Where do the bacteria within the vagina originate from?
I understand that it's feasible the bacteria within the gastrointestinal tract originate from the food we eat and air we breath, but where does this population of microbes originate from?

Actually, the bacteria in the human gut originate from the birth canal. There are vast differences in the gut microbiome between kids born vaginally and those born by C-section, and these differences can have health consequences later in life.

That's an interesting difference you point out, but ultimately, from where did the bacteria from the birth canal? Is it even known, or just a symbiosis that has existed before homo sapiens evolved?

@Larry_Parnell do you have any reference? It seems really interesting!

One of the Potential and major cause of vaginal infections and micro-flora is due to the hygienic habits are not followed during cleaning ass after defecation. There are certain important rules to clean the region appropriately.

@VAR121 Can you provide citations for this?

Most of the initial colonisation is said to be coincidental ('happenstance' as the textbook puts it!) exposure.
It's then fairly predictable depending on:

type of delivery (as Larry commented);
feeding; and
receipt of antibiotics.

In terms of feeding, there are differences in flora between babies fed human milk and those that are given cow's milk.
There's a section called 'Establishment and Composition of Normal Flora' in chapter 187 of Principles and Practice of Pediatric Infectious Diseases (3rd ed) by Long which discusses the above.
It's also said that hormones may influence indigenous flora. For example, premenarcheal and postmenopausal vaginal flora are very different to those present during the childbearing period.[1].

Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 7th ed. 2009. Churchill Livingstone.

There is some interesting information here from the Human Microbiome Project, but no details regarding the source of vaginal microflora. I would say that the sources would be gut and skin.
Ethical issues of manipulating a baby's microbiome are brought to light here.


text:
Why are goosebumps so ineffective at keeping us warm?
If the purpose of "goosebumps" is to keep us warm, why is it so ineffective? Or are the changes subtle, but important?

When your brain, the hypothalamic temperature centers in particular, detects that the temperature is too warm or cold, it initiates a number of controls to try and correct this.
Goosebumps appear due to piloerection. This is one of the reactions that occur when the temperature is too low.
This causes hairs to stand on end as a result of contractions in muscles attached to hair follicles called arrector pili.
This particular reflex is not actually important in human beings. However, in animals, this mechanism allows entrapment of a layer of air allowing insulation. This way, the heat loss is greatly reduced.
The other mechanisms are very adept at maintaining temperature in the human body. These include sweating, dilation (vasodilation) and constriction (vasoconstriction) of skin blood vessels and increasing and decreasing the body's heat production.
For example, when it's too hot, dilation of the skin blood vessels can increase heat transfer by up to eight times.
Source: Guyton and Hall. Medical Physiology. 11th ed. Elsevier Saunders.

Cutis anserina (goosebumps) are caused when the sympathetic nervous system induces the arrectores pilorum muscles at the base of each hair cell to contract and raise up the hair.  Zoidberg has posted an answer describing the mechanism as I was writing mine, so I'll move directly onto effectiveness.
The reason that, as you say, the mechanism is not particularly effective in humans is our relatively small amount of body hair.  As mentioned the purpose of the erector muscles causing the hairs to stand up is to allow for air to be trapped at the surface of the skin rather than absorbing heat from the body then taking it quickly away.  Mammals with denser fur/hair are likely to have a much better insulating effect from goosebumps.
Some animals have adapted to use the mechanism for another purpose, however; the porcupine being a prime example.  When threatened, the porcupine uses its arrectores pilorum muscles to elevate all its quills, making it appear larger and more threatening or to actively repel an attacker.  The extra rigidity that they gain from doing this1 also helps to contribute towards making their spines a very effective defence:

Goosebumps have also been reported in humans during periods of stress, anxiety and even sexual arousal.  This is related to the stimulatory effect that adrenaline has on the sympathetic nervous system which, as mentioned above, is responsible for the stimulation of the erector muscles.

1Mechanical design of hedgehog spines and porcupine quills. Journal of Zoology
Volume 210, Issue 1, pages 55–75, September 1986


text:
Is the 'fluttering feeling' when under stress neurological or physical?
I'm sure that everyone is familiar with the sensation commonly known as "butterflies in the stomach".  It is commonly experienced during periods of anxiety or stress (e.g. before high stakes job interviews or roller coaster rides) and apparently (after my web research) often felt in new romances without an obvious cause of tension.
However, whilst my googling did turn up an inordinate amount of rubbish regarding love-sicknesnes, I have been unable to find even a suggestion as to a mechanism as to the physiology behind this feeling.  Is it a sensation of physical change in the stomach (some sites vaguely mentioned the restriction of blood flow to critical organs but it was entirely unsupported) or is it neurological in nature?

apparently (after my web research) often felt in new romances without an obvious cause of tension. +1 sympathy vote.

@Poshpaws lol what can I say - I'm obviously just too smooth to get nervous ;-)

If you want to find out about the the relationship of this response to romance in particular, there's a pretty comprehensive research paper called Love is more than just a kiss: a neurobiological perspective on love and affection[1] which reviews a lot of the work done in this area. This is pretty good as it discusses all the different stages including breakup.
Essentially, there seems to be a lot factors at play which elicits various responses through different stages of love.
In terms of anxiety and stress, initially, there's a large increase in levels of cortisol[2] and a marked drop in serotonin. Depletion of serotonin is found in many psychiatric conditions such as depression, anxiety and panic disorder. There's even been evidence that these levels at early stages of love are similar to those suffering with OCD. Obviously, the 'symptoms' of early love are quite similar to these conditions so it's hypothesised that this, at least in part contributes to those feelings.[1]. It was found that these levels are back to normal in 12-24 months.
The elevated levels of cortisol contribute to the feelings of stress but this hormone has also been shown to promote attachment.[2].
There are also changes in activity of the amygdala. Responsible for regulating a lot of emotions such as fear and sexual drive, the amygdala can activate autonomic nervous system responses through the mechanisms which Kevin described.
There are a bunch of other things at play here including dopamine, oxytocin, vasopressin, nerve growth factor (NGF), testosterone, increased activity in the hypothalamic-pituitary-axis (HPA) and variations in activity in other areas of the brain.
Again, that first reference gives a pretty comprehensive overview of the mechanisms involved.
To answer the actual question about the fluttering feeling, as Kevin mentioned, it's hypothesised that this is caused by reduced peristalsis in the intestines as a result of sympathetic stimulation. I don't have an academic reference for this but there are plenty of non-academic sources that talk about it (a quick Google of butterflies in stomach and physiology will probably show them).
A lot of the mechanisms noted above can contribute to, sensitise for or cause sympathetic activation. For example, panic attacks and anxiety, mentioned earlier with the serotonin relationship, can cause the same feeling.

Boer, et al. Love is more than just a kiss: a neurobiological perspective on love and affection. Neuroscience. 2012. 201:114-124.
Marazziti, et al. Hormonal changes when falling in love.
Psychoneuroendocrinology. 2004. 29(7):931-936.
Guyton and Hall. Medical Physiology. 11th ed. Elsevier Saunders.

The review was really very interesting, but unfortunately didn't answer my main question :)

Oh, sorry! Do you mean the 'fluttering feeling'? I edited the post and added some more info. Does that help at all?

Hope it's useful!

Nervousness or excitement should cause an increase in activity in the sympathetic nervous system (the so-called "fight or flight" side of the autonomic system). Increased sympathetic activity will be associated with decreased parasympathetic activity (primarily digestion, but also crying and other "emittive" glandular activity).
I don't have a citation, but I suspect that the "butterflies" feeling is associated with the cessation of peristaltic activity in the gut, which puts the digestive and nervous systems in conflict. If you have just eaten, then there is a difference between what your gut wants to do (digest) and what your brain wants it to do (not digest) -- thus the frequently accompanying nausea.


text:
How can I pare down a PDB file in Python to only include specific residues?
I'm trying to make a script that will take a MTZ file (reflections), convert it into a CCP4 map, then pare that map down to only encompass a desired area to cut down on the size of my PyMol session files so they're email-able (a.k.a. not 200 MB) and ease the burden on my POS computer.
I currently have a Python script that can fft (CCP4) to create the map and mapmask to fix unit cell tiling issues.  What I want to add now is something that can take a PDB file and strip out most of it except, for example, residues within 10 Å of #123.
I've been looking at ProDy, but not quite sure where to start.  I would also be open to using something in the CCP4 toolkit.

I'm curious in the PDB format as well. If you already have a PDB file output, you could try removing all information other than the ATOM lines, and further, remove all the ATOM lines that list atoms from residues outside the range of a subset of your structure. If you could view it in PyMol then perhaps that's good enough?

@leonardo some sort of manual hack like that may work (as mapmask seems to expand a little anyway), but doesn't seem that optimal.  I'll beat on this for a while and let you know what I come up with.

Is it possible to use a PDB viewing program to select a subregion of a single chain and save a new PDB? If so, you might want to compare the source file to the subregion file and see if it is indeed this simple and then hack yourself a solution.

Pymol has a selection operator that matches everthing in a specific distance around an atom, is should be possible to use that for this purpose.

@MadScientist from within a script running outside of PyMol?

I was thinking manually inside the program, but if you have to automate it, I believe you can use the pymol library from any python script.

Better fit for scicomp.se?

@David unfamiliar with that site, if you think it's better there, feel free to flag a mod down.

ProDy works quite well, especially from within an existing Python script.
The following code takes an existing PDB file, performs some selection query on it, then saves it to another file.
import prody

def pdbsubset(inpdb, outpdb, selection):
    with open(inpdb) as protf:
        prot = prody.parsePDBStream(protf)
    atoms = prot.select(selection)
    prody.writePDB(outpdb, atoms)

An example selection query builder

residues is a list e.g. ['A12', 'A39'] with each element in the form <chain><residue number>.  They were captured from the command line using argparse with
    parser.add_argument('-i', '--residues', nargs='+')

so you would specify -i A12 A39 or whatever.

pdb and outpdb are file paths
radius is the distance in angstroms to expand the selection by.

reslist = ["(chid {0} and resid {1})".format(res[0], res[1:]) for res in residues]
selector = 'within {0} of ({1})'.format(radius, ' or '.join(reslist))

# and running it:
pdbsubset(pdb, outpdb, selector)

The documentation on ProDy selection queries is not the most straightforward, but fairly analogous to PyMol, so doable.

With the program RasMol, you can select, as Mad Scientist explained it for PyMol, everything in a specific distance around an atom. RasMol can be run from command line, using a script (with the -script option under UNIX).


text:
Is Aspergillus clavatus an unicellular organism?
I could not find the piece of information form Burton Human Parasitology -book and not by Google.
Yeast is divided to two phylums: one of them is Ascomycota.
Aspergillus clavatus belong to the given phylum.
Yeast is unicellular.
So it is possible that Aspergillus clavatus is unicellular.
Can you tell whether the Aspergillus clavatus is an unicellular orgarism or not from the following picture?

I need to find unicellular parasites that cause damage of brain. The fungus causes patulin so hemorrhaging of brain, but should still be unicellular to meet the criteria.

You're right in saying that yeast is single celled.
However, moulds are described to be filamentous fungi that are multicellular. The filaments of the mould give colonies "a woolly, fluffy, or velvety appearance, sometimes punctuated with a granular or powdery aspect that is produced by the formation of asexual reproductive structures"(1).
Aspergillus is such a species. The filaments are called hyphae. In Aspergillus, hyphae have divisions or walls which separate it into multiple cells. This is called septate hyphae.

McPherson, et al. Henry's Clinical Diagnosis and Management by Laboratory Methods. 22nd ed. 2011. Saunders.


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What is a inhibitory tone when talking about neurons?
In this SE answer: Could an "overactive" brain increase the chances of Alzheimer's Disease?
user @nico used the word inhibitory tone What does that mean?
More examples of it used:
http://www.ncbi.nlm.nih.gov/pubmed/18234887
http://www.cell.com/neuron/abstract/S0896-6273(11)00479-X

Neurons communicate electrochemically. That is, when a signal arrives to a neuron it fires a series of electrical signals, called action potentials.
Action potentials are depolarization events that propagate along the neuronal membrane, down to the neuronal terminal.
The terminal of a neuron is (with some exceptions) in contact with another neuron, via a structure called synapse.
When the depolarization arrives at the terminal, it allows the entry of calcium, which then mediates the release of a chemical substance, a neurotransmitter into the synaptic space. Finally, neurotransmitters act on the postsynaptic neuron, by binding to specific receptors on its cell membrane and can either stimulate it, in which case the postsynaptic neuron will fire more and release more of its neurotransmitter or inhibit it, in which case the opposite happens.
The textbook example of a stimulatory neurotransmitter is glutamate, and the inhibitory one is GABA1.
In various areas of the brain certain neurons are constantly receiving inputs from GABAergic afferents. This means that those neurons are constantly receiving a GABA stimulus that inhibits them, and are thus under a constant inhibitory tone. This will prevent their firing until a sufficiently potent stimulatory stimulus arrives or until the inhibitory tone is somehow released (for instance if the inhibitory GABAergic afferents are themselves inhibited by some of their own afferents).

1note that this is not always true: GABA can also be stimulatory in various situations


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Why is SOC medium recommended for transformations?
In pretty much every transformation protocol I've seen SOC medium is used to grow the bacteria for a short while after the tranformation and before plating.
I've usually substituted LB medium for this step for easy retransformations, but I gather that the SOC medium is supposed to make some difference in efficiency, or else the simpler LB medium would be recommended in the protocols.
Why is SOC medium used for transformations? What difference does substituting with LB medium cause for the transformation efficiency?

To summarize from Hanahan's paper (see below for reference), he carried out a systematic review of conditions necessary to improve transfection efficiency. Among the conditions tested were the presence of various cations (Ca2+, Cs+, Mn2+, K+, Mg2+), DMSO, and growth temperatures (and a few other conditions not so commonly used these days). He worked with a strain that he subsequently isolated a derivative of, called DH1, which is now available commercially as DH1-alpha and other strain derivatives.
He defined transformation efficiency to be the number of transformed colonies on a plate, a measurement still used today. He found when the transforming media contained: certain cations, specifcally Mn2+, Ca2+, Rb+; as well as DTT, hexamine cobalt (III) and DMSO; greatly improved the transfection efficiency compared to the standard Ca2+ treatment. He also found that sucrose and K+ were useful, though not strictly necessary for his experimental strain. It was stated in this paper, though not explained, that sucrose acted as a stabilizer, possibly to guard against his initial use of 0°C incubation and/or freeze/thaw cycling. For the rest of his work, he did not use sucrose.
Among his conclusions, he states that DTT is necessary, as well as di-valent and mono-valent cations, but that they seem to be nonspecific. In other words, there is no strict requirement for having Ca2+, since Mg2+ and Mn2+ perform equally well, nor is there a requirement for K+, though it's admittedly easier to use than Rb+.
There are today a number of "rich" media broths that are available: SOB, SOC (SOB + MgCl2 and sucrose), 2xYT, NZY+, TB, etc. All of these are superior to LB for transformation purposes because of the refined salt balance and in particular the inclusion of these di-valent and mono-valent cations. Sucrose seems to be included for the ease of metabolism and stability of the heat shock process (though I can't find a paper explicitly explaining why it is used, other than tradition).
The two most common ways to transform bacteria are to have them chemically compentent (E. coli already in a rich media broth) or to electrically transform them (electroporation). The purpose of both of these is to induce holes into to cell membrane of the E. coli (chemical transformation relies on the heat shock process for this). Once these holes are made, DNA is free to enter into the bacteria. Naturally, this process is very traumatizing to the E. coli, especially since chemical transformation has the added insult of temperature shock (0°C to 42°C then back down to 0°C).
Substituting LB for any rich broth, such as SOC, will greatly improve transformation yield. If a protocol calls for SOC media, and you don't have any, you may substitute for another rich media. I have used 2xYT for SOC many times quite successfully, and as I stated earlier, only the valence number for the various ions seems to matter, so just make sure they are present.
It was my understanding that sucrose/glucose was added as an additional nutrient source for E. coli to expedite their recovery from the transformation protocol. I speculate that this is the case. Hanahan refers to sucrose as a stabilizer but does not define what it is stabilizing. I speculate that it acts as a cryopreservation aid and prevents ice crystal formation when undergoing cooling on ice in the heat shock method. Given the earlier bio.SE question about shifting E. coli feedstocks, it seems unlikely that sucrose will be used as a nutrient source in the one hour growth period immediately after transformation because that article quotes 4-12 hours as the common time range to shift metabolism from amino acids to carbohydrates.
Sources:

Hanahan D. Studies on transformation of Escherichia coli with plasmids. J Mol Biol 1983 166(4):557-80.

(Super Optimal broth with Catabolite Repression) SOC media contains glucose whereas Luria Broth (LB) doesn't. SOB also has a more delicate salt balance.
Naturally the glucose will help the cells recover and grow faster after the heat shock. Your transformation efficiency should improve since less cells will die.
On the other hand, the reason why SOC media isn't always used is because of the detrimental effects of having too much glucose. The glucose will be consumed in the Krebs cycle and produces a lot of acetate which can be pretty harsh on cells.

Do you have any literature source on that glucose helps the cells to recover?

bobthejoe and @Mad Scientist - I've addressed this in my answer below. I thought the same as you.


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What causes a 'stuffy' or 'runny' nose when you have a cold?
When humans get the common cold, a common symptom is a stuffy or runny nose. Is that the body's immune response or is that the virus's doing?

I don't have a reference for this, but I believe it's because of the viral shedding that occurs in the sinuses.

Interesting. I haven't heard that before. A similar but unrelated question is: http://biology.stackexchange.com/q/445/238

There are different causes and mechanisms behind runny and stuffy nose.
I cover them separately below.
Runny nose
My professor of pathoanatomy and pathophysiology says that the correct answer here is serous inflammation to the runny nose.
Serous inflammation

Marked exudation by relatively thin fluid
Cold is caused by Acute respiratory viral infections

Acute viral respiratory infection

Exudate is very watery and clear - serous inflammation.
At 3rd day, whitish mucose excretion - catarrhal inflammation.
At 5th day, greenish colour - a lot of neutrophils and mucose.

The other answers mostly discusses about the mechanisms (secondary), but not the cause itself.
The most upvoted answer describes factors affecting the inflammation but not explicitly mention serous inflammation and its factors.
Stuffy nose
Congestion in nose is a passive and local process resulting from reduced outflow of blood from a nasal tissue.
The nasal epithelium is very thin which makes it vulnerable to flu and cold.
The viral particle passes through the membrane (often because of scarring) and causes the change in the vascular permeability of the surrounding big vein.
Mechanisms of stuffy nose are covered partially by Ram and Aleadam:

local edema
because of changed vascular permeability of large veins surrounding the nose
bradykinin
histamine (cetiritzin)
counteracted by epinephrine

which respond against viral particles and cause

atrophy
dryness of nose.

Stuffy nose is about the reduced outflow of blood from a nasal tissue i.e. isolated venous obstruction.
Even small obstruction (scarring) can lead to it.
I know no safe systemic medication that can prevent the change of vascular permeability of the nasal big vein.
Local steroids like Nasonex improve the recovery time by reducing the congestion when taken during long term - however, it cannot prevent the vascular permeability change of the large vein.
I have an intuition that the the nasal venous congestion can be relieved by the systemic lymphatic drainage massage by special movements involving

abdomen (attention to deep breathing with abdomen and exhale too)
supraclaviculus
under medial occipitalis
under auricles

which help to drain the accumulated fluid from the nasal tissues.
I know no substitute or medication to replace the stimulation of lymphatic drainage.
Prophylactics for the symptoms
You can oil your membranes but to oil them all even at the back side is difficult - even more difficult if have to have them oiled continuously.
So there remains some membranes unoiled.
I think it takes rather much time for the venous side to recover.
Therefore, you feel stuffy nose long time after the runny nose has ended.
Local oiling is not enough during cold and allergic times for many patients.
Some medicines for Prophylactics

Xylometazoline (Olynth) - cause atrophy and dryness, but good for stuffy nose
Quixx - sea water
Eucalyptus and vitamin E (Coldises spray for instance)

It's mainly caused by swelling of large veins and by an increase in vascular permeability that leads to an accumulation of fluids in the nasal mucosa. These effects are mediated, at least in part, by bradykinin and histamine, and can be counteracted by epinephrine. These mediators are part of the immune response to the viral particles.
You can read more about it here:

http://www.cardiff.ac.uk/biosi/subsites/cold/commoncold.html
Chernick-Mellins basic mechanisms of pediatric respiratory disease
By Gabriel G. Haddad, Steven H. Abman, Victor Chernick (page 520)

The stuffiness is due to edema or swelling of the mucous membrane covering the nasal cavity. The swelling is caused by vasodialatation or dialatation of the capillaries and leaky vessels which accumulate fluid within the mucous membrane.
The runny nose is mainly due to hyperactivity of the mucous cells of the lining which causes vastly more secretion than normal, triggered by the inflammatory reaction to the infection.


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Why are trichomes important for both the roots and shoots of plants?
In what ways are trichomes vital to the plant?
Why have them on the plant shoots as well?

This question would be better with more context. Trichome is a generic term for diverse, often microscopic, structures with a wide variety of functions. The question "but how does that work" should be addressed separately.

Ok let me fix it.

Plant leaf hairs, or trichomes are vital for many reasons.
Interestingly in 1975 researchers were correct when they stated:

"It can be argued that essentially the same genetic system should be required for both root hairs and trichomes." [1](Pay-wall)

For example:

C. salvifolius, there are more adaxial trichomes present to avoid UV light from injuring the abaxial surface.[2](Pay-wall)
Increased transpiration [3](Pay-wall)
Protecting against insect herbivores [4](Pay-wall)
Increasing tolerance to freezing [5](Pay-wall)


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Do men have more extreme variations than women?
This question was considered unsuitable for Skeptics and I think it is more suited to BIology than Cognitive Sciences
I was reading this article which I found interesting. It is not supported with references but was an invited address for the American Psychological Association.
It makes the claim that men go to more extremes than women.
People can point to plenty of data that the average IQ of adult men is about the same as the average for women. So to suggest that men are smarter than women is wrong. No wonder some women were offended.

There are more males than females with really low IQs. Indeed, the
  pattern with mental retardation is the same as with genius, namely
  that as you go from mild to medium to extreme, the preponderance of
  males gets bigger.

[...]

Almost certainly, it is something biological and genetic. And my guess
  is that the greater proportion of men at both extremes of the IQ
  distribution is part of the same pattern.

[...]

Nature rolls the dice with men more than women. Men go to extremes
  more than women. It’s true not just with IQ but also with other
  things, even height: The male distribution of height is flatter, with
  more really tall and really short men.

Another notable example of a similar claim was Lawrence Summer's speech regarding the possible reasons for dearth of women in tenured positions in science and engineering at top schools.
Summers outlined 3 possible reasons, with a major kerfuffle erupting - resulting in his firing from the job as a Harvard University President - over his presented second reason [ quotes from Wiki ]:

The second hypothesis, different availability of aptitude at the high end, caused the most controversy. In his discussion of this hypothesis, Summers said that "even small differences in the standard deviation [between genders] will translate into very large differences in the available pool substantially out [from the mean]
Summers referenced research that implied differences between the standard deviations of males and females in the top 5% of twelfth graders under various tests. He then went on to argue that, if this research were to be accepted, then "whatever the set of attributes... that are precisely defined to correlate with being an aeronautical engineer at MIT or being a chemist at Berkeley... are probably different in their standard deviations as well".

QUESTION: Are there any studies or evidence to support the claim that men have more extreme variations than women (in other words, that the trait's distribution in males have fatter tails) in a variety of traits?
Possible areas of research can be:

Intelligence (general IQ or specific linguistic or spacial abilities)
Physical attributes (strength, height, weight)
personality traits

for lack of anything better, let's take the FFM's Five:
openness
conscientiousness
extroversion
agreeableness
neuroticism

In order for the answer to be "yes", the research needs to show fat tails in at least 5-6 traits from all 3 of the buckets above (intelligence, physical, and personality), although precise trait mix may be arbitrary and not necessarily limited to my examples, as long as 5-6 somewhat independent traits fit.
In order for the answer to be "no", at least 8 of the 11 traits above should have no fatter tails in men.
Anything else means "inconclusive".

The first article referenced has been taken down (possibly due to controversy). The latest available snapshot can be found at https://web.archive.org/web/20131002194704/http://www.psy.fsu.edu/~baumeistertice/goodaboutmen.htm

Having a less oppressive environment increases variance in many phenotypes. The IQ variance of (less-oppressed) whites is greater than (more-oppressed)  blacks despite less genetic diversity. Since women are on average more oppressed (i.e. outcasted more for a given deviance from the norms and given norms that take more effort to conform to) their traits would be narrower.

keep in mind even in the studies showing the largest difference the effect is incredibly minor (1.5% max) and cannot be shown to be independent of cultural factors. The wiki actually has a decent review and set of references, this question pops up over and over in my class. https://en.wikipedia.org/wiki/Sex_differences_in_intelligence#Researchers_in_favor_of_males_in_g_factor

First of all for the first 22 chromosomes (and the mitochondrial chromsome) are the same between women and men. The X and the Y together are something like 1.5% of the total DNA in the human cell.  The X chromosome is also in common, so it has the same chromosomal (genetic) variations the same as women and men.
While I am not sure about the differences you point out, its for sure there are lots of differences between the biology of men and women!  The reason that women's traits might have different variances than men comes from the fact that in women there are 2 X chromosomes and in men there is only one, as well as the additional Y chromosome.
If there are any singular defects in the X chromosome a man carries, it will not be balanced out in the human male.  (other organisms have different sex chromosome schemes).  For instance because there is a cluster of genes that help the eye see in color, women's sense of color (i.e. from their cone cells) is sometimes better than men.  With 2 X chromosomes there is even the possibility of a woman who has four different color receptors in their cones.
On the other hand, why men see better in the dark (i.e. greater sensitivity in the rod cells), is possibly due to an extra Blue Rod pigment gene that remains on the Y chromosome (see above reference).  This is both an accident of genetics, but also an adaptive 'choice' that men would have different visual acuities than women.
Its also known that woman and men may have different epigenetic patterns, with some epigenetic modifications coming from the mother and others from the father.  This is adaptive and also not the direct result of the XY chromosomes.
Interestingly, it turns out that for the most part women's 2 X chromosomes are mosaic.  That is, in each cell only one of the randomly selected X chromosomes are active.  Recessive/dominant X genes are often not the case.
This could result in a greater observed genetic variance for women because when you have two chromosomes, often one of the genes is completely silenced.  Women display all of the alleles of their X chromsomes, whereas men have only one X chromosome entirely, the Y chromosome being much smaller.
So in other words, I would say that while men and women actually have the same variation in their DNA sequences, there are different patterns in the X and Y Chromosomes that might create more variance in terms of what we see in women's displayed genetic traits.

My question is not about the difference between the sexes, but the degree of variance.

The biggest problem with this question, (not just here, but for everyone who asks it,) is drawing on our culturally constructed definition of maleness to look for mechanisms of genetic inheritance of what are considered "male" traits.  We could measure frequency distributions of height, but we don't have a way to accurately probe any of the other qualities you listed on a genetic level.  Since we can't make these mechanistic connections, any conclusions we draw would be confounded by the nature vs nurture debate.
That said, I don't know of any studies to this effect.  So this isn't much of an answer to your question.
EDIT: I've been thinking about this question all day.
The sources of heritable variation within genders that could be attributed to gender differences are (1) X and Y chromosome mutations and expression profiles, and (2) heritable epigenetic gender differences.
(2) might be more difficult to argue, since the currently known mechanism for epigenetic inheritance is the same in men and women.
One way to make this problem tractable is to look at transcriptome analysis -- it's an indirect approach to this question that gets from genome to phenotype quickly.
A cursory pubmed search led me to a study in Drosophila that takes a different approach to this question.  They sought out previously undetected levels of gender difference.  Most current studies (and there are a lot of them, including for humans) look to quantify differences in expression between genders for specific tissues. This is a prerequisite for estimating this within-genders variation, standardized against the number of genes expressed.

+1 because I agree that there are too many confounding factors due to the environment/society for the specific phenotypes considered.

-1 It's more a comment rather than answer.

@MartaCz-C: I think it is a good answer, as it points out why the question cannot have a correct answer for the specific characteristics listed (things like oppenness, or extroversion, are too ill-defined to link them to a specific genetic mechanism).

@nico And that would make it a great comment. Still it's not the answer. I'm quite irritate about amount of answers like "I don't know the answer but still I want to say something" on this site.

@Marta, I had put this as a comment, but I switched it to an answer because if I had left it as a comment, it would really be saying that I'm interested in moving to close the question as off-topic.  I think it's not enough off topic to close. Besides, if the questioner doesn't know enough to know that the scope of their question is too narrow, a strict interpretation of the rules forcee all feasible answers into the comments section. I am reasonably certain that, as asked, this question has no good answer.

This isn't an issue of  a culturally constructed definition. It is about differences between biological sexes. The cultural fluff on top is irrelivant to my question. Dealing only with hard data, do males tend to have a greater range of variance in most areas when compared to females?

At least for physical data (heigth, weight etc) you can have a look of the DINED Anthropometric database http://dined.io.tudelft.nl/dined/.  Here you can find mean and standard deviation data for Dutch population studies on numerous anthropometric measures, and you can stratify the results by sex.

that would make a great comment but not much of an answer.

So far as we can tell any difference in variability (standard deviation) in humans is cultural not genetic and thus not consistent across the species.
You are talking about something called the Variability Hypothesis, which is most often referred to in intelligence. Variability hypothesis has long been criticised for being unsupported by evidence, or in the rare cases it has been supported, it is likely to be entirely cultural since it changes drastically with culture.  It also quickly runs into the problem of defining intelligence, since different skills show different distributions with large influence by culture.
There have been no studies showing a difference in variability in any physical characteristics in humans across gender that I am aware of although males and females often have different means (height for instance). Keep in mind if men have a higher average height then their variability will appear to be higher just due to boundary effects (IE you cannot have negative heights)
In biology there is the Bateman's hypothesis that males will often show more variability than females, but this is unproven and largely untested. This study also shows numerous flaws in the original work. Don't get me wrong their are species where males show much higher variability in some characters but there are also plenty where females show higher variability, meaning this is likely a situational outcome and not a general principle.
source 1
source 2
Source 3
Source 4


text:
Synthetic biology using existing cells
I was watching the video at this link:
http://www.bbc.co.uk/news/science-environment-17436365
The speaker says that a cell is taken and its original DNA content is stripped out and replaced with synthetic DNA.
Does this mean scientists are not able to create a synthetic cell yet? Is this why they use existing cells, stripping them out and replacing the DNA?

Related question?  http://biology.stackexchange.com/questions/406/can-scientists-create-totally-synthetic-life/407#407

The J. Craig Venter Institute recently has indeed created a synthetic, self-replicating cell (see the press release). So it's definitely not impossible to create completely synthetic cells for use in synthetic biology, but that doesn't mean it makes much sense to do so. E. coli in particular have been used as bench tools for decades: lots of protocols exist for using them in the lab, their genome has been extensively sequenced and is well studied, and they're cheap. I'm not a bench biologist anymore, but I'm guessing these are the reasons they stripped living bacteria and replaced their DNA rather than trying to build a completely synthetic microbe from scratch.

From the article: "The complete synthetic M. mycoides genome was isolated from the yeast cell and transplanted into Mycoplasma capricolum recipient cells that have had the genes for its restriction enzyme removed." It seems to me that a fully synthetic cell (synthetically made lipids, proteins, etc) are still a long way off, but it it is still impressive to reprogram a cell by a complete substitution of one genome for another.

@leonardo Good point. I guess there is some room for debate as to how truly synthetic the JCVI microbes are.

It's true. It strikes me as a compelling engineering challenge to have to synthesize all of the other components that come along with a cell. The transplant and donor species would have to be very close evolutionary relatives when only swapping nuclear genomes. If they weren't, then everything from structural protein interactions and lipid profiles of membranes would be completely off and the cell would fail to function.

May also find V.natriegens interesting. It's not as well documented as E.coli but makes for a good teaching subject because of its rapid growth (Td ~ 10min).

There is this guy, Martin Hanczyc, working on protocells to better understand how the beginning of life occurred. He makes synthetic protocells. They don't have any DNA in them but they are pretty cool and maybe the beginnings to making synthetic cells. Perhaps once science has figured out how cells began and their very minimal needs they can create completely synthetic cells.
http://www.ted.com/talks/martin_hanczyc_the_line_between_life_and_not_life.html
Also, just thinking, what would we consider completely synthetic cells? If we took synthetic protocells and they eventually evolved into a cell with DNA would that still be synthetic?


text:
Difference between biological control and introducing species for conservation?
I have a biology assignment and we have to explain various methods and strategies for conservation, two of which are:

Biological control
  Introduced Species

What is the difference between these? I was under the impression that they are essentially the same thing – biological control being the introduction of species to predate pests (eg. the abysmal failure of the cane toad).
Any clarification would be great.

After talking to my teacher, he said that biological control is the introduction of species to control another species, however species may be introduced for other reasons (the "Introduced Species" method), such as to "assist an ecosystem cope, flourish or re-establish itself."
The example he gave was the introduction of South African veldt grass to Western Australia in order to stabilise sand dunes, so that they can later be built upon further (eg. plants which may not perform well in sandy, unstable soil can then be planted).
Hopefully this helps anyone else with the same problem.

Biological control does not have to be with an introduced species.  It can also be accomplished by either artificially inflating the number of existing predators.
E.g.  Spruce bud worm has a natural predator in the form of a tiny wasp.  But budworm can spread through a stand faster than the wasp can.  By moving popluatins of the wasp to the forefront of the budworm advance, you get most of the 2nd generation budworms.  The trees have a bad needle year but aren't killed.
It can also be done with habitat modification.  If you create conditions that favour the existing predator, then there are more predators in place.  E.g.  create places for ladybug overwintering to reduce aphid populations. (I have no idea if this would work.)
Anohter example -- although ecological controll may be better than biological -- I had a significant mosquito problem.  Lots of small puddles in spring.  I created a permanent pond.  This has resulted in much smaller mosquito population.

The pond is a local year round water supply for insectivorous birds.
The pond is by far the largest water body around, so tends to get most of the mosquito eggs.
The pond now has a permanent population of boreal and chorus frogs.  Tadpoles of these make it tough to be a mosquito larvae.

Is this species introduction?  Only if you consider immigrant species from neighborin populations to be introduction.