text:
Why is most tissue cellular?
Most tissue is comprised of cells.  Why? It would seem inefficient to have so many individual nucleus, membranes, etc.?
Specifically: Not all tissue is cellular.  Much tissue is extracellular matrix.  Since the body can use noncellular tissue, what is the role of cells in cellular tissue?
Another way to ask my question: Do the cellular organelles directly contribute to the tissue and organ's function? Or are they just there to maintain the cell itself?
My hypothesis is:

In some cases, the cellular organelles directly provide the tissue's function.  Eg endocrine system - synthesized at the cellular level.
In other cases, individual cells function discretely in the tissue.  Eg, nervous or muscular tissue.
In other cases, the cell doesn't directly support the tissue's function.  But it's needed to grow and preserve the tissue.  Eg connective tissue.
And finally, in cases where preserving and growing the tissue is a small enough task, a small number of cells simply extracellular tissue.  Eg bone tissue.

The above is my hypothesis.  Is it correct? Fix, revise, or replace it with something better!

I am not sure I get your premise. Would you think that one gigantic cell would be more efficient then?

Why "one gigantic cell"? Why cell at all? Why have zillions of small parts (nucleous, membranes) which don't directly contribute to tissue function? As a note, very few artificial machines work that way (though perhaps integrated circuits could be argued to).

membranes are extremely important for things like compartimentalization and signalling. For instance, neurons could not work without membranes, as they are required to generate electrochemical gradients. One very important signalling pathways is that of DAG/IP3, one of the components of the membrane. Membranes allow for storage of calcium ions in high concentrations. And I could go on listing other millions of functions.

Also, the comparison of a cell to a machine is not really a good one. A cell is more like a factory, where you have the CEO's office (the nucleus), an assembly line (the ER) with workers (ribosomes), a packaging department (Golgi), power plants (mitochondria) and so on (blatantly copied from this PDF)

Also, I wouldn't trust anything artificial longer than 100 years, from experience. Eventually something gives, and then where is the repairman if it cannot repair itself like a cell that simply divides to survive?

Since cells are the origin of every life, any tissue must at least be based on cells. Some tissue matter is outside the cells (plant cell walls), some apparently non-cellular tissue is really a bloated organelle. Both happens. As to your theses,

yes, an example are oil reservoirs in plants
no, these are just big cells. A striking example is spinal cord nerves that can be very long; irreparable if injured, because you can't repair single cells
connective tissue is cartilage, bone, adipose tissue, blood, hematopoietic tissue and lymphatic tissue. These together fit in both the organelle and extracellular substance slots, so you would have to differentiate
bone belongs to connective tissue

So, yes, you can differentiate between functions belonging to whole cells, cell organelles, or extracellular material. And there is no reason to narrow this question to humans.

Thanks - can you clarify: Does the cellular nature directly contribute to tissue function? Do organelles directly contribute to tissue function? Why are cells the origin of every life? Has this question been explored ever?

Yes and yes, by their physical and chemical properties and those of their content, respectively. Because evolution started with cells and it proved the best solution over the years. And there is even enough evidence to see why it all starts with cells: because lipids will form spheres by themselves in water, with or without content. It's just the physical optimum.

Please give an example of the "bloated organelle" you refer to.

Biological tissue by definition is tied to cellularity. To start this post, it might be useful to include important definitions:
A definition from wikipedia:

Tissue is a cellular organizational level intermediate between cells
  and a complete organism. A tissue is an ensemble of similar cells and
  from the same origin, that together carry out a specific function

The ECM or extracellular matrix, as the name suggest is a matrix.

WP: In biology, matrix (plural: matrices) is the material (or tissue)
  between animal or plant cells, in which more specialized structures
  are embedded, and a specific part of the mitochondrion that is the
  site of oxidation of organic molecules. The internal structure of
  connective tissues is an extracellular matrix.

Lastly,in chemistry, matrix generally refers to any chemical species which is not of direct immediate regard to the context of the observer (e.g. a chemist), but may or may not have significant effect on the chemistry or chemical environment in question.

Do the cellular organelles directly contribute to the tissue and organ's function?
No, they do not directly contribute to the tissue and organ's function but organelles contribute indirectly:

There is a hierarchy of structure: Everything is composed of smaller
  things and is a part of something larger. The character of structures with different
  scale changes according to the interplay of various physical forces. Quantum
  phenomena control the small scales, while gravity dominates on large
  scales, and both come into play at the beginning of the universe.

(Source: The Little Book of the Big Bang: A Cosmic Primer, pg 6 By Craig J. Hogan).
Mathematically the matter of hierarchies in science is tractable through renormalization. That isn't directly relatable to (structural) biology, but theoretical scientists have applied it.
Or are they just there to maintain the cell itself?
Out of necessity, the cell's organelles take part in the function of the cell, yes. The reason is that the organelles are enclosed by the cell and as such all prerequisites for sourcing energy are "enclosed by one additional level" as well. That being said, the organelles must maintain themselves, structurally (referred to as turnover) and information-wise. Information may not always be as accessible as through a designated external information carrier molecule, but may be a molecules properties or even another's  molecules properties, serving for instance as a "nucleation template".
Thus, the word just in your question is not applicable.
Lastly, I would like to give you a few pointers related to cellularity and the question of "why" in a context of evolution.
Cellularity may be a universal restriction that follows from the laws of thermodynamics. These laws are by consensus equally valid anywhere in the physically tractable universe. To do any work you need to have a gradient of a physical property, which is relatable to an interconvertable form of energy. To do work in an open environment in a sustainable manner over a long-term period, it is good to have insulation.
On this planet, inhabited by carbon-based lifeforms with evolution being confined to immediate (geo)chemistry**, that meant the use of lipids. Conveniently, lipids form micelles through intermolecular self-organization, in order to allow the system to reach a mimimum free energy state.
Chemical systems with say ions too spontanously assemble given favorable energetic conditions,- all you have to do is let table-salt water evaporate, yielding you little salt-cubes which even shed a bit of insight into the underlying makeup of the crystal's unit cell. But the energies of bonds that make up the insulation layer must be in a reasonable vicinity of the local thermal energy (k*T), where k is the Boltzmann constant, and T the temperature in Kelvin.
Thus, chemical species where the weak London forces outweigh any other intermolecular forces, is ideal for self-assembly of an insulation layer in a biological context. It is not the only solution that evolved. But the insulation layer crucially determines your abilities and interactions as an unicellular or multicellular organism in the tempo-spatial regime. (How large can you get? How fast can you hunt? How fast can you bud something off or engulf? How flexible are you towards shifts in your environment? Those things...)

(Dileptus - a predatory protozoan - hunting, hiding, and playing around)
Self-organization can be observed across many hierarchies, serving the minimization (or optimization) of one or several properties.
A lipid membrane is ideal on a planet whose surface is covered by an extremely polar molecule. Insulation-wise lipids are impermeable to ions to allow the formation of an membrane potential. As electrical insulators lipids are excellent thermal insulators, locally confining electrons, and finally at providing mechanical insulation. Additionally lipids can serve as fuel, nutrients, signalling molecules, and many other tasks - which really just follows from or less local molecular evolution.
Evolution:
Speaking of evolution. Just like biology doesn't make sense without the context of evolution, evolution doesn't make sense without the context of energy.  For science, evolution starts at the earliest physically tractable point and transitions across many hierarchies. Matter itself is just another form of energy, and as poorly defined as space: as "anything that has mass and takes up space".
Concluding:
No-one can conclusively tell you what any given organelle is for (yet).
But science has furnished a comprehensive picture, by looking at the molecules that make up the organelle and tracing it back to genes to let scientists marvel at an organelles function from a bioinformatical perspective. What greatly helps the exploration of organelle function are many high-resolving imaging techniques, with a plethora of labeling techniques. This array of labeling methods was amassed over the course of a century. Recently imaging equipment has seen a rapid increase of better resolutions in the time domain, which is very important as each level of hierarchy has its own sort of "time-signature" - which is of course strongly influence by the masses (or inertial forces) involved.
The entire picture of organelle function is however subject to a major revision-cycle with the ongoing efforts to map out entire cells at an atomic level, with large scale preparations already underway.
This post isn't thoroughly sourced, and much of it is only a layman's perspective. Consider this only as a starting point.
Disclaimer: universe-review.ca has been around for almost a decade, despite an unclear author backing this project- for obvious copyright reasons of the textbook contents. it is scientifically sound.
***Immediate [geo]chemistry* would exclude anything from say Alpha Centauri, but not for instance Kiuper belt objects that may have had a significant role in the composition of earth's geochemistry. This subject is so far outside my field, I cannot give you any better information.


text:
Does DNA contain information beyond protein synthesis?
It's well known that genetic information is stored in DNA.  As far as I know, DNA only has information at the protein level.  What about higher levels, such as organelles, cells, tissue, organs? Is there any known carrier of information at that level? If not, what guides those levels of structure?
Hypothesis: Above the protein level, there is no real genotype/phenotype.  Instead, it's all done through cell division.  So, there is no split between information and embodiment.  Instead, it's through a prototype-duplication model: cells grow and split, creating more cells.  As for differentation into different types of cells, and organization into tissue and organs: the information and control systems for that are currently unknown.

Excellent question. Welcome to Biology.SE!

What a timely question.

Does DNA contain information beyond protein synthesis?

Yes. In fact, protein-coding genes only constitute a tiny part – less than 2% – of the whole DNA. There are of course many other genes which aren’t protein coding: there are genes for ribosomal RNA and we find more and more genes which code for small RNAs, such as tRNA. But even if we count all those genes we won’t come above maybe 10% of the total DNA.
Most of the DNA is instead devoted to the regulation of gene expression, most importantly via the binding of transcription factors (but the picture is much more complex than that). With the conclusion of the ENCODE project, a whole slew of papers were published which show that in fact most of the DNA is actively implicated in the binding of various factors (although it’s not known how much of that actually contributed to the cell’s fitness).
But I’ve hijacked your question a bit here. So let’s come back to what you’re actually interested in:

What about higher levels, such as organelles, cells, tissue, organs?

There is no known mechanism (beyond the already mentioned regulation) which would encode such information in the DNA. Excluding its existence categorically may be hard but given that we haven’t found any machinery which would be necessary to read such information, we can be pretty confident that it doesn’t exist.

If not, what guides those levels of structure?

The higher levels of organisation are to all appearances emergent. That is, they are a consequence of the lower level organisation. For instance, take the cytoskeleton which carries much of the cell’s physical structure. It is composed of different protein complexes which form spontaneously through assembly of globular proteins (such as actin). The are several ways in which the process can be guided but strikingly it’s largely stochastic – i.e. mostly unguided, and it still succeeds in building a stable skeleton, simply by virtue of molecular properties encoded in the proteins.
I think this is a common theme of cell organisation: the elementary building blocks are encoded by the DNA, and their abundance is tightly regulated. Everything else, i.e. higher-level organisation – follows from that: abundance and localisation of the right proteins.

As for differentation into different types of cells, and organization into tissue and organs: the information and control systems for that are currently unknown.

In fact, much is known here, and it goes back to regulation on the level of DNA: we know that genes are differentially expressed depending on the cell type and stage of development (and the stage in the cell cycle). This regulation is highly complex and decoding it is a slow process. Nevertheless, the factors involved here are decoded one by one. This is the domain of developmental biology.

Thanks! Very helpful.  What about my hypothesis that not all biological information is split between genotype/information carrier and phenotype/embodiment, but some actually is closer to prototype + copier? Specifically, organelles and cells are never created ex nihlo from any type of information but always split from a preexisting one?

@S.RobertJames I don’t know. I would guess that most (though obviously not all, e.g. mitochondria / chloroplasts) organelles could also form de novo since their constituents are once again coded for in the nuclear genome and their assembly might again be either spontaneous or aided by other proteins. In fact, a friend just reminded me of things like centrioles which require a helper protein for assembly.

It really isn't correct to interpret the ENCODE data as showing that most of the DNA in the human genome is "actively implicated in the binding of various factors". According to ENCODE scientist Ewan Birney only 8% of the DNA functions in binding factors. Almost 60% of the DNA is intronic, classed by ENCODE as functional simply because it is transcribed.
http://genomeinformatician.blogspot.co.uk/2012/09/encode-my-own-thoughts.html

@Alan It absolutely is. The interaction is shown in vivo. The debate over whether this binding performs a function (and the definition thereof). Whether functional or not, it is, at some point or other, bound to – either by transcription factors or transcription machinery (i.e. transcribed). Ewan says exactly that in the blog post you linked, and he even qualifies his use of the word “functional”.

@Konrad This is a direct quotation: "using very strict, classical definitions of “functional” like bound motifs and DNaseI footprints; places where we are very confident that there is a specific DNA:protein contact, such as a transcription factor binding site to the actual bases – we see a cumulative occupation of 8% of the genome." I interpret this to mean that just 8% is "actively implicated in the biding of various factors".

@AlanBoyd No. Both I and Ewan would disagree. Ewan makes a clear distinction between the definition of “functional” which his detractors use, which would be under positive selection (and which would yield the 8% estimate, still way above classical estimates), and the one he uses, which yield 80% actively implicated in the binding of  factors (but which doesn’t necessarily contribute to the cell’s fitness, and which therefore maybe isn’t under selective pressure).

@AlanBoyd where did you see Ewan claiming that 60% is intronic? Don't you men intergenic but transcribed? Also, konrad, sorry to be a pedant but genes in the human genome are around ~5% of human DNA, protein coding exons are ~2%.

Ewan Birney: "...60% of the genome with the new detailed manually reviewed (GenCode) annotation is either exonic or intronic..."
As Konrad says, the generally quoted figure for coding (=exonic) DNA is "less than 2%" Therefore 58% of the genome is intronic: this is "almost 60%".

@AlanBoyd I see, sorry, I thought you meant protein coding genes.

source: Stack Exchange

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

sort: votes


text:
How are antibodies designed?
Antibodies have the ability of recognising highly specific peptide sequences and bind it at their antigen-binding site.
This ability is harnessed as a tool in research to purify target structures in the cell (e.g. in chromatin immunoprecipitation, ChIP).
Now let’s say that I’ve identified an interesting target structure (such as a particular transcription factor) and I want to design an antibody to use in ChIP against said target. How would I go about producing such an antibody, taking into account that it should be both highly sensitive and specific?

Don't know enough about synthetic antibody design to give a complete answer, but this could be a good start: http://www.nature.com/nbt/journal/v25/n10/abs/nbt1336.html

Do you really mean "synthetic"? The mammalian immune system is pretty good at generating antibodies that are highly sensitive and specific - how about going the traditional route and making monoclonal antibodies? I note that the paper cited by nico describes the improvement in vitro of an existing antibody, not one designed de novo.

@Alan I didn’t. Nico added that word. I was actually interested in in vivo route. I think nico also meant the same (I wasn’t even aware that there was another route) and simply wanted to stress that they are designed.

Oh, sorry for the confusion @Konrad, I thought you were talking about completely synthetic antibodies (i.e. designed in silico) rather than the traditional "inject an animal with the antigen and then purify" way. I guess the design word tricked me into that.

@Konrad, I'm still not sure what level you are coming into this at. At risk of insulting you: here at the Pierce website [ http://www.pierce-antibodies.com/custom-antibodies/monoclonal-antibody-development.cfm ] is a good summary of the approaches that are usually taken. I have no connection to this company, they are just one of many  who offer a custom service. If you wanted to improve the antibody in vitro it would be necessary to clone the gene from the hybridoma cell line.

If you Google this doi [10.1093/protein/gzs024] you will get to a very recent review on Computer-aided antibody design in the journal Protein Engineering, Design & Selection.

@Alan I was actually talking about the monoclonal antibody design described in your previous link. The description there is quite good (mind writing up an answer?) although I’d wish for more detail in steps 1 & 2 … (there’s also a nice Wikipedia article but it’s less concise and not as well suited for an answer here, I think).

I worked for a long time at a leading high-quality antibody company, so I'll try and share some of my experiences with you. The process of making a highly specific antibody (I'll focus on monoclonals) has three important parts - antigen design and immunization, cloning and subcloning, and screening/validation. Each part is crucial on its own, and the better one is performed, the higher your chances of success downstream become.
In order for an antibody to work, it needs to bind specifically to its target. I won't get into all the specifics here, as there is a good open literature on antigen design, but basically you need something that will promote a strong immune response in the host, give you a variety of clones to choose from, and be specific - it shouldn't bind other targets besides your protein of interest. There are lots of factors to consider, including antigenicity, solubility, ease of production (for immunizing and screening), steric considerations (does another protein or nucleic acid obscure the target site in vivo?), and others. Antigens can be roughly divided into two types - peptides (typically less than 20 or 30 amino acids) and proteins or protein fragments. You will most likely want to try several antigens to maximize your probability of success. After the antigen is synthesized and purified, you need to come up with an immunization schedule for priming and boosting the animal(s), then determine when and how to test them (screening), and at what time and how to harvest it for the monoclonal process.
The cloning process then comes next. Clones can be generated by a variety of methods, some widely available, such as the various hybridoma methods, and some proprietary to individual companies. My former company employed a mix of both, depending on the species of animal, using some really cool in-house tech that was constantly being improved and expanded upon. These processes are very dependent on the quality of materials being used and the expertise of the cloners. The input B cells (which make the antibodies) need to have been harvested, treated, and stored according to a set of precise steps to allow for the highest number of viable clones. Once the immortalized cells have been obtained (after fusion with the myeloma partner cells in the hybridoma process, for example) they are diluted to a pre-determined cell count and plated in 96-well plates and allowed to recover and grow for a time, during which they are secreting antibodies into the medium. This media is then tested quickly (before the cells overgrow the well), and positive wells are diluted out to (hopefully) single-cell suspensions and subcloned, or frozen down for later. The first testing is frequently by ELISA using the immunizing antigen, although depending on your application of interest it may be by high-throughput screening via flow cytometry, immunohistochemistry, or immunofluorescence. After the initial testing, subsequent steps of subcloning and re-testing can occur at a more measured pace, as the cells can be frozen indefinitely after generating sufficient quantities of antibodies in the supernatant.
This is where the quality of your screening program comes in. Your assays need to be well-designed, robust, well-documented and performed, and have appropriate positive and negative controls so that you can truly tell whether a certain clone is of interest, or performs better than an existing product. This means controlled conditions, standardized reagents and protocols, and a high degree of repeatability from assay to assay. Also, the appropriateness of your controls cannot be emphasized enough. Do you have a knockout or non-expressing sample for comparison, or a way of looking at baseline vs. induced or inhibited activity? For ChIP, unless you have a good control antibody and primer pair for your gene of interest, how will you know if the assay works? You may get a great result doing a straight immunoprecipitation-Western blot, but still not pull down DNA-bound protein. If your ChIP method doesn't produce clean DNA, you may never get binding. And if you don't have appropriate data analysis protocols in place with multiple replicate wells, you may waste time chasing noise instead of specific signal. Additionally, along with testing all your clones, you also need to titrate them to determine the optimal working concentration. I've seen a lot of antibodies that look like crap when you first test the supe, but diluted 100 or 1000X they are clean, specific, and still strong. Be patient, testing is a lot of work and requires a ton of repetition to confirm your results, but it'll be well worth it in the end.
Finally, after all this is done, you hopefully have a great clone that does what you want it to do, and better than anything else out there. You now need to decide what you're going to do with it, because if you're an academic lab and publish with it, the world will come knocking at your door. Don't slack off at the end and decide 100 ml of supernatant will be enough to last forever - save the clones and put them in a cell bank, or try to get a commercialization deal with a manufacturing company so you don't have to do all the work!
I hope this helps, please let me know if you have any additional questions or concerns.

Very nice. However, where I’m still lacking understanding is the very first step, before the cloning process: how do you synthesise an antibody that binds to a target antigen?

Konrad - are you asking about how the immune system makes a specific antibody to a certain antigen, or how you could design a de novo antibody by computer?

@MattDMo I know how the immune system does it. I was unclear of how you get from your choice antigen to a tailored antibody. KT8’s answer covers that (i.e. you do it by exposing an animal to your antigen and let its immune system do the work for you).

@Konrad, that is the most straightforward way to go. However, there is now technology available that allows you to design very specific antibodies using libraries of antibody sequences. When the animal has started producing an immune response to the antigen, each activated mature B cell only makes one particular "clone." Using http://en.wikipedia.org/wiki/Next-generation_sequencing#Next-generation_methods you can harvest B cells and sequence the binding region of the antibody. These can then be recombined in silico and new recombinant monoclonal antibodies produced and tested.

Do you need the entire animal for step one?

@TheEnvironmentalist sorry, just saw your comment. The B cells are harvested from the spleen, but because the spleen is an essential organ, you need to euthanize the host animal. Depending on your process, you may save frozen splenocytes to do multiple rounds of immortalization and cloning.

Answering Konrad's comment, you produce the peptide or protein of interest using bacteria or chemically synthesize them (chemical synthesis generally only work for short peptide chains. After which, you get a lot of side products). This peptide or protein of your interest serves as your antigen. You inject this antigen into mouse or rabbit. The animal's immune system will naturally mount an immune response to produce antibodies against it. The B cells which are responsible for producing those antibodies can then be harvested. After which, you basically follow the protocol Matt stated.
You could, of course, also choose to just directly isolate the serum of the animal and purify it. However, this leads to the production of polyclonal antibodies which can be less specific than a monoclonal antibody.

Where in the organism are the B cells harvested from?

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


text:
What reasons allow for women to outlive men?
It is a well-known fact that women tend to outlive men.
I often hear people unscientifically stating that men generally generally die younger because of the higher stress encountered in their work lives. I would personally immediately rule this out, as who's to say that that women's (past) home lives just weren't as stressful? Also, shouldn't we see a narrowing of difference in age with the recent gender equality issues? Since the trend in question still occurs in virtually all countries of the world, I think it's safe to assume that the phenomenon is purely physiological.
I am curious as to the most sound scientific theories or known reasons for why women typically outlive men. Finally, I understand that aging in itself is not a process that's completely understood, and thus am not expecting a "complete list" of factors.

In a study on longevity in 121 countries, women tended to outlive men by about 5 years [1]. The suggested causes for this are numerous, some of which are temporally, geographically, or culturally specific.
On the terminology, sex tends to refer to the absolute biological differences, whereas gender relates more to differences in perception/lifestyle (for instance, socio-economic differences).
Evidence
In a study on Greek centenarians the authors found that women outnumbered men (1.68:1), with men having a higher likelihood of smoking, and thus are more at risk of smoking-related illness and mortality (historically this was more true than today) [2]. This is also true for alcohol consumption. The authors also report that having a first degree relative who was also a centenarian is associated with longevity (highlighting the importance of genetic factors in lifespan determination).
There is also evidence that the rate of telomere shortening (number of cell-divisions until cell-cycle arrest) is sex-specific [3].
rwst cites an interesting paper, that presents evidence that suggests male hormones may decrease lifespan [4]. This may be due to differential onset of atherosclerosis and cardiovascular disease, caused by exposure to different sex hormones [5].
In a review on the brain/behaviour specific aspects of differential ageing between the sexes, the authors discuss differences in brain anatomy and cognitive (and emotional) functionality between the sexes [6].
Remarks
This is by no means an exhaustive list of the reasons for differences in lifespan between the sexes in humans. There are likely to be many other causes, such as men tending to have more 'risky' behaviours, and possibly other unknown genetic effects, such as having 2 X chromosomes, vs. XY.
References

Møller, A. P., et al (2009). Why men have shorter lives than women: effects of resource availability, infectious disease, and senescence. American journal of human biology : the official journal of the Human Biology Council, 21(3), 357-64. doi:10.1002/ajhb.20879
Tigani, X., et al (2011). Gender differences in Greek centenarians. A cross-sectional nation-wide study, examining multiple socio-demographic and personality factors and health locus of control. BMC geriatrics, 11, 87. doi:10.1186/1471-2318-11-87
Barrett, E. L. B., & Richardson, D. S. (2011). Sex differences in telomeres and lifespan. Aging cell, 10(6), 913-21. doi:10.1111/j.1474-9726.2011.00741.x
Min, K.-J., et al (2012). The lifespan of Korean eunuchs. Current Biology, *22(18), R792-R793. doi:10.1016/j.cub.2012.06.036
Pérez-López, F. R., et al (2010). Gender differences in cardiovascular disease: hormonal and biochemical influences. Reproductive sciences (Thousand Oaks, Calif.), 17(6), 511-31. doi:10.1177/1933719110367829
Kryspin-Exner, I., et al (2011). Geropsychology: the gender gap in human aging--a mini-review. Gerontology, 57(6), 539-48. doi:10.1159/000323154

Update
Just been reading this interesting paper by Maklakov, et al (2013, BioEssays) titled "Evolution of sex differences in lifespan and aging: Causes and constraints", which presents a more evolutionary/genetic argument for the differences.
Abstract
Why do the two sexes have different lifespans and rates of aging? Two hypotheses based on asymmetric inheritance of sex chromosomes (“unguarded X”) or mitochondrial genomes (“mother's curse”) explain sex differences in lifespan as sex-specific maladaptation leading to increased mortality in the shorter-lived sex. While asymmetric inheritance hypotheses equate long life with high fitness, considerable empirical evidence suggests that sexes resolve the fundamental tradeoff between reproduction and survival differently resulting in sex-specific optima for lifespan. However, selection for sex-specific values in life-history traits is constrained by intersexual genetic correlations resulting in intra-locus sexual conflict over optimal lifespan. The available data suggest that the evolution of sexual dimorphism only partially resolves these conflicts. Sexual conflict over optimal trait values, which has been demonstrated in model organisms and in humans, is likely to play a key role in shaping the evolution of lifespan, as well as in maintaining genetic variation for sex-specific diseases.

@LanceLafontaine just been reading this article which is very interesting

Although many studies have shown that there are trade-offs between
  longevity and reproduction, whether such trade-offs exist in humans
  has been a matter of debate [1,2]. In many species, including humans,
  males live shorter than females, which could be due to the action of
  male sex hormones. Castration, which removes the source of male sex
  hormones, prolongs male lifespan in many animals, but this issue has
  been debated in humans [3]. To examine the effects of castration on
  longevity, we analyzed the lifespan of historical Korean eunuchs.
  Korean eunuchs preserved their lineage by adopting castrated boys. We
  studied the genealogy records of Korean eunuchs and determined the
  lifespan of 81 eunuchs. The average lifespan of eunuchs was 70.0 ±
  1.76 years, which was 14.4–19.1 years longer than the lifespan of
  non-castrated men of similar socio-economic status. Our study supports
  the idea that male sex hormones decrease the lifespan of men.

Brand new article!
Kyung-Jin Min, Cheol-Koo Lee, and Han-Nam Park: The lifespan of Korean eunuchs. In: Current Biology, Volume 22, Issue 18, R792-R793, 25 September 2012

Are they really saying that the lifespan of their control samples (i.e. men with testes) was only 51-56 years? That is worryingly low - I suspect that something else may be going on there .. ?

Very interesting though!

They are talking partly about mediaeval times, the Chosun dynasty from 1392 to 1910. http://en.wikipedia.org/wiki/Joseon

Ahh! That makes sense then :-) Even so, it would be interesting to know if they accounted for things like syphilis which might make sense in the context of this study. OK, I should read the paper ...

I'd also add that differences in the lifestyles of eunuchs compared to non-castrated men may influence these findings. Eunuchs likely had a special, maybe even pampered, role in society. The other men likely were engaged in dangerous work. Recall that industrial and work-related accidents was one of the top 120 killers (in the USA) well into the 20th century.

But they compared with "men of similar socio-economic status", as quoted. If you think they did this wrong, you must first cite how the details of the comparison.

The testosterone effect mentioned by @rwst is an exciting new discovery, but there may be a deeper answer which is an evolutionary adaptation.  There is a theory called the grandmother effect that tries to guess why women live often quite a long time after menopause.
Longevity in women doesn't make a great deal of sense from the standpoint of selection, since a lifespan past popping out the little ones wouldn't really increase fecundity.
As you might guess, having a parent around for a long time after a human child is born might increase the number of offspring that reach the age.  The grandmother effect surmises that females have a stronger, more direct relationship with offspring and can contribute directly to the viability of her offspring even after she stops having children herself.  Grandfather's probably don't enjoy this benefit as much because they are thought to contribute less to the offspring.  You have to remember that over the length of human history men's tendency has been to be a little more distant because of the difference in parental certainty.  while it can be very low for fathers, it is pretty much zero for mothers.
There are other adaptive arguments for human gender biases in longevity.  Men are going to try to contribute to their older age fertility by producing offspring later in life too.  Still, women do tend to live longer than men.
It would be surprising if the grandmother effect were the only reason women live longer then men, but it sounds like a stronger selective effect to me and men can probably evolve longer lives by taking an interest in their offspring longer.  This would have to be on an adaptive scale - over the entire population though.
Individual variations in longevity can of course be more important than these effects, but these theories try to explain the bias.


text:
What specifically allows alpha-complementation in beta-galactosidase?
I'm familiar with the use of alpha-complementation of beta-galactosidase with the pUC alpha-peptide and the M15 lacZ gene product, and would like to hypothetically apply alpha-complementation in other settings with different enzymes. I do have a few questions, but hopefully they are similar enough to all be answered here.

What specifically allows for the non-covalent association between both truncated protein products to form a functional beta-galactosidase? How is beta-galactosidase unique in that separating it into two portions still yields a functional enzyme (in other words, why wouldn't other enzymes remain functional if I split them)?
What other proteins, if any, have been engineered to perform similar alpha-complementation? What steps were taken to accomplish this?

Maybe this review is a good start: http://www.ncbi.nlm.nih.gov/pubmed/22070901

Two other (free) papers on beta-gal complementation and other split reporter systems: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835542/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137764/


text:
Is there a relationship between Melatonin, Norepinephrine and depression in humans?
I'm reading a booklet on melatonin published in 1996, titled "Melatonin and the Biological Clock". This particular paragraph caught my attention and I would like to better understand what it means:

The requirement of intact beta-receptor function for melatonin
  synthesis, and the stimulatory effect of norepinephrine on melatonin
  synthesis and release, point up a theoretic relationship of melatonin
  to depression.

I've been looking at the biosynthesis of norepinephrine  and tryptophan metabolism and do not see how the two cycles are connected. Is there a connection between the norepinephrine system and the melatonin synthesis in humans?

You might like to read papers which are more recent, as studies from 1996 do not include many recent findings on the interactions between NE and MEL. For example, a recent study finds there is an interaction between NE and MEL in the sleep-wake cycle. http://www.sciencedaily.com/releases/2012/06/120619225725.htm Although this doesn't directly describe a link between depresssion NE and MEL, it gives an interesting hint, since many depressive disorders include sleep problems.

This answer addresses your question about a link between norepinephrine and melatonin, but I have nothing to say about depression.
In vertebrates, the link between norepinephrine (NE) and melatonin lies in the regulation of the melatonin biosynthetic pathway.
Arylalkamine N-acetyltransferase (AANAT) is an enzyme in the biosynthetic pathway for melatonin, and controls the diurnal rhythm of melatonin production in the pineal gland. NE is released as a neurotransmitter by neurons innervating the pineal gland, and which themselves are regulated by the circadian pacemaker of the hypothalamus. One of the effects of NE on the pineal gland is to elevate the transcription of the AANAT gene via adrenoreceptors and cAMP levels.
The paper cited below describes this, and other relevant diurnal rhythms in the viscacha, a rodent of the chinchilla family. This animal was chosen because it has an interesting diurnal behaviour pattern with two apparent peaks in melatonin biosynthesis. It's a good starting point for further research into the literature on this topic.

Calderon,C et al. (2008) Daily rhythms of norepinephrine, β1-adrenoceptor mRNA, serotonin, arylalkylamine N-acetyltransferase mRNA, arylalkylamine N-acetyltransferase and hydroxyindol-O-methyltransferase activities, and melatonin in the pineal gland of viscacha. Biological Rhythm Research 39: 93-107

Thank you Alan! As far as I understand, there are two transferases, first AANAT and then HIOMT that are involved in Melatonin production from Serotonin. NE elevates the AANAT levels, influencing transormation of Serotonin to N-Acetyl-5-HT


text:
Creating a cell, not from another cell. Will it be possible?
If some time in the future, we can know exactly what a cell (for example simple prokaryote bacteria) contains, (I mean, exactly which molecules, the shape of them, the density of each, everything), Then can we create a new cell (not from another cell)?
I mean, if we have such technology, then create a soup just like what that cell contains, and a DNA exactly same as that bacteria cell, and then put some of it inside a Cell membrane, will it start living?

This has -at least partly- been done by Craig Venter's group: http://www.sciencemag.org/content/329/5987/52.abstract However, they did not recreate the entire cell, "just" the genome which they reimplanted in a recipient cell. Recreating a whole cell would be much much much much [...] much more complicated.

@nico But will it be possible in the future?

I should check in my crystal sphere... :D Jokes aside, I think 10 years ago Creig Venter's experiment would have raised a lots of eyebrows and would have been said to be impossible. I think we cannot do it right now, but possibly in the future we will have the technology to do it. Synthetic biology is a brand new branch of biological sciences so we should not expect too much too soon! My knowledge on the topic is quite anecdotal however, I will leave the answer to someone more knowledgeable than me!

So, is it believable that some day, we may can create Two primary cells of a human so we can create a complete person?!

Again, we are extremely far away from creating a whole bacterium, a yeast cell already will be WAY more complex, let alone a human cell. Ethics aside, right now we are not even able to clone a human using preexisting cells.

Science advances incredibly fast :D Maybe we can do that in the next 50 years! Can you post your comments as an answer?

There is the more recent work by Szostak on artificial protocells. The IVC world all aims to achieve this to some degree.

@bobthejoe Can you explain some more?

I think it could feasible to assemble complete synthetic cells in future. One of the first successes will probably be a simple bacteria. The synthetic genome is already on the road, so here, I'm pointing to other technologies that can be helpful. Feel free to add/edit/complete.
Inorganic chemistry. Self-replicating inorganic cells can be already obtained from polymer emulsions: optimistically, one may try in future to work with organic macromolecules.
3D printing technology may also evolve to the point that it will be possible to assemble cells by printing microscopic 'ink' molecules with the correct cellular organization. 3D printing works by serially printing one layer on the top of the other: to prevent molecular layers to mix, a technology to serially froze the printed layer will help in obtain a frozen synthetic cell.

Many of the parts of a cell, which perform its basic functions, such as transcription, translation, DNA replication, etc. have been already isolated and successfully recreated in a test tube. So if we obtain a complete list of all the parts we need and know how to make those parts and mix them together, we can make a cell from scratch.
However, this will probably be very time-consuming and costly and will serve no other purpose than showing that it can be done. It is much more time- and cost-efficient to create a genome only, transplant it into an existing cell, and wait for the cell to replicate and synthesize new molecules until it changes in a way that completely fits the new genome.


text:
Survival of E. coli on agar plate at -20 degree C without glycerol stock
If I kept E. coli transformed with plasmid at -20˚C without making glycerol stock, will it survive? Actually I have kept it this way for 18 hours. What will happen with it? Will it grow in fresh media?

My guess is that you may be able to rescue something at this stage, but this is definitely not recommended for long-term storage. If you can't recover any living cells you should still be able to recover some plasmid from the cells for retransformation.

e coli are tough bugs.  they will last in the freezer for a while, but good experimentalists don't leave things like this to chance.  They live fine in a regular refrigerator for a week or more - no need to freeze.  replate and then transfer to glycerol asap.

Over time I suspect that ice crystals will form in the colonies from defrost cycles in the freezer and the moisture in the agar.  This will cause rupture of the bacteria membranes and over time may destroy the bulk of the bacteria cells.  The plates will also desiccate over time as well from the defrosting cycles of the freezer.  You may be able to leave them in the freezer for a while but I can't foresee them surviving indefinitely.
If the strains are really important I recommend just sucking it up and spending the small amount of time necessary to make the glycerol stock.  Glycerol is used in bacteria stocks as a cryoprotectant to prevent the crystallization of the stock.

Trehalose[1],[2] is the cryoprotectant used by bacteria to keep things going when all else freezes (or dries up), and they grow in it, too!

Trehalose accumulates dramatically in microorganisms during heat shock
  and osmotic stress and helps protect cells against thermal injury and
  oxygen radicals. Here we demonstrate an important role of this sugar
  in cold-adaptation of bacteria.

Kandror O, DeLeon A, Goldberg AL. 2002. Trehalose synthesis is induced upon exposure of Escherichia coli to cold and is essential for viability at low temperatures. Proceedings of the National Academy of Sciences USA, 99(15): 9727-9732, doi:10.1073/pnas.142314099
http://en.wikipedia.org/wiki/Trehalose


text:
How are long time periods measured in biological systems?
Biological systems are pretty good at measuring fairly long times, for example, menstrual cycles (month), or puberty (years). Counting days or years seems to be implausible, and chemical concentration also seems implausible. What are the physiological processes that are involved in keeping track of such long periods? Is it just a long sequence of finite state changes?
I understand there are environmental correlates such as seasonal changes and relative position of celestial objects to measure the relative time, but regardless of these external cues, I suspect that a pretty good internal clock for longer time scale could exist. For example, the time to menopause can actually be thought of as a counting mechanism of a shorter clock which is the menstrual cycle. But, how does the body know when to stop growing? I cannot think of biological processes with such long time constants that is stable.

So your question relates to successful and timely development and maturation of an organism? And how is this regulated?

The short answer is: we do not know exactly, although we do have some insights.
I will take the example of puberty.
Although a clear definition of puberty is lacking, it is quite clear that it corresponds to a period where gonadal function starts.
This, in turn, is derived from the activation of the gonadotropin system, which consists of two main cell types:

a small number of neurons located in the preoptic area of the hypothalamus (a nucleus at the base of the brain) called the GnRH neurons. GnRH is the Gonadotropin-releasing hormone, a small peptide that stimulates the production of gonadotropins from the pituitary.
the gonadotrophs, a specialised group of cells in the pituitary (a gland located underneath the brain) which produce two hormones, called luteinizing hormone (LH) and follicle-stimulating hormone (FSH) which stimulate the gonads to produce various hormones, such as estrogen.

In mammals, the secretion of GnRH, and thus LH/FSH varies during the course of the menstrual/estral cycle. This cyclicity lasts several days (4-5 days in rodents, ~1 month in humans) and entrains the cyclical secretion of estradiol (E2) from the gonads.
Note that this is a sort of self-sustaining cycle, as cyclic levels of E2 will then allow for cyclic GnRH secretion and so on.
But, back to your question: how does the GnRH/LH/E2 system "wake up" at puberty?
The exact mechanism is still unknown, but recent work has found an important mediator, called kisspeptin, that is produced from two population of neurons in the hypothalamus, called the kisspeptin neurons.
Kisspeptin has been shown to be a very potent activator of GnRH neurons and work in the mouse has shown that these neurons appear at the time of puberty, their number increasing dramatically between 25 and 31 days (puberty is at around 30 days in mice).
Postnatal Development of Kisspeptin Neurons in Mouse Hypothalamus; Sexual Dimorphism and Projections to Gonadotropin-Releasing Hormone Neurons  - Clarkson and Herbison - Endocrinology, 2006
Similar work exist in the monkey:
Increased hypothalamic GPR54 signaling: A potential mechanism for initiation of puberty in primates - Shahab et al. - PNAS, 2005
In humans mutations in either kisspeptin, or its cognate receptor GPR54 results in disturbances of pubertal maturation because of underactivation of the system (hypogonadotropic hypogonadism) or hyperactivation (precocious puberty).
So, now the question is shifted: why do kisspeptin neurons show up only at puberty? We don't know for sure, but it looks like increased levels of E2 could be important for this.
Again, we get into a self-sustaining cycle. Growth of the body generates an increase in E2 production (possibly due to increased volume of the gonads?), which, when over a certain level permits the development of kisspeptin neurons, which will then stimulate the GnRH neurons, resulting in increased LH and E2. We then have more E2 and this makes kisspeptin neuron grow even more etc etc.

From: Postnatal development of an estradiol-kisspeptin positive feedback mechanism implicated in puberty onset. - Clarkson et al. - Endocrinology, 2009

Though chemical concentration seems implausible, at the deepest level it is the cause.
On a smaller scale - how does a eukaryotic cell know when it is ready to divide? By the concentration of different cyclins and CDKs. They are produced all the time, in amounts dependent on the general availability of nutrients, but they are used at different times. Some are used during DNA synthesis, so that if they are present, the cell "knows" that there is not enough DNA to divide itself; others are used during cell division, so a freshly divided cell "knows" that there is a long period before next division. How do our hairs grow at seemingly same intervals? Because their location was decided on the basis of concentrations of certain proteins or small molecules when skin was just being formed (I don't have Developmental Biology right here, so no protein names, sorry).
The menstrual cycle is regulated by the concentration of the hormones and ovulation triggers changes leading to menstruation. That's why menstruation happens 14 days after ovulation and not just 28 days after the previous one - if a woman has a 30 day-long cycle, her ovulation will be on 16th day of the cycle. Menopause generally happens when the supply of eggs ends and they stop providing cues about the proper time for menstruation.
The cues about puberty and aging may be more subtle. One well-known cause of aging is the shrinking of the telomeres, the ends of the chromosomes. Cells with short telomeres can't divide. Too low of a "concentration" of these telomeres "tells" the cell that it is old.
Another well known fact - malnourished girls don't go through puberty and malnourished women stop ovulating. Low food "concentration" is a sign of a bad time to burden your body with nourishing and feeding a baby.
Detailed mechanisms behind those processes are often different, but the general rule is the same: each process has threshold(s) for certain chemicals; if they are exceeded, the organism reacts.

I think you sort of have 2 answers here - chemical concentration and chemical modification.  there are only 2 copies of the DNA in most metazoan cells - that's not really concentration.  Epigenetic effects like this more akin to computer memory.  If one or two copies of a gene are marked, it will behave differently.

What I meant was that in G1 there is just one copy of the whole genome, so not enough to divide between two daughter cells. During S phase the second copy is produced (and some cytokines and CDKs used), so that during G2, when cytokines and CDKs necessary for cell division are accumulated, all the time there are two copies of the genome - enough to perform a cell division. Sorry about the misleading description, I found this place only today and haven't been using my Molecular Biology Explaining Skills in 2 or 3 years. I'll be better :)

no worries - just trying to draw out a distinction...

There has been some recent advancement answering this question, especially in terms of puberty. Here are some quotes from the news article about it.

The timing of puberty onset is highly variable and ultimately mysterious.

So, our understanding is pretty limited.

Contrary to popular belief, however, puberty is not a simple developmental progression of maturation of the reproductive axis, as this system is fully mature long before puberty and, in fact, must be suppressed during a period called the juvenile hiatus. The key component of the axis is the gonadotropin-releasing hormone (GnRH) neuron.

But, how is GnRH controlled temporally?

The authors have thus established that epigenetic repression of at least Kiss1, and probably other genes, mediated indirectly through the PcG family of transcriptional repressors, is the brake on the hypothalamic-pituitary-gonadal axis that must be released for puberty to proceed. More importantly, an epigenetic regulator provides the perfect interface for coordinating the genetic and environmental influences that are known to buffet this process.

This is just one piece of the puzzle as the title of the news article says, and there are still a lot of gaps in our understanding.

Lomniczi, A. et al. Epigenetic control of female puberty. Nat Neurosci 16, 281–289 (2013). http://www.nature.com/neuro/journal/v16/n3/full/nn.3319.html
Margaret M McCarthy. A piece in the puzzle of puberty. Nature Neuroscience 16,
251–253 (2013) doi:10.1038/nn.3339 http://www.nature.com/neuro/journal/v16/n3/full/nn.3339.html

I have heard of a case where a 5 year old got pregnant. It was in a search for world's youngest pregnancy. She probably didn't have menstruation but she obviously was ovulating. Maybe that it a case where the reproductive system wasn't completely suppressed as in menstruation suppressed, ovulation not suppressed.


text:
Why do vaccines cause your arm to hurt?
When you get a shot for a vaccine (for example, the annual flu vaccine), the nurse frequently indicates that your arm will ache for a day or two, maybe more. This ache is typically not just a pain from having your skin punctured, but is actually an ache of the entire arm.
What mechanism causes the entire arm to ache from a vaccine? Why doesn't that ache extend to other parts of the body, like the hands or the shoulders? Why do non-vaccine arm punctures (such as drawing blood, injecting drugs) not cause the ache?

My guess would be local inflammation, but it's just a guess

I would also say local inflammation. Since vaccines are designed to trigger an immune response, and inflammation is one of the initial mechanisms of the Innate response, it would make sense.

Vaccines contain adjuvants. They are designed to enhance the immune response, which means creating something like an inflammatory response.

i think it may partially be "just in our heads"

@tryingToGetProgrammingStraight No, it's an aching arm, not a headache. ;-)

The goal of the vaccine is to provoke an immune response, therefore some degree of inflammation is expected in order for the vaccine to work. As swbarnes2 says, vaccines contain adjuvants, pro-inflammatory molecules that produces local inflammation and recruits immune cells to the site of the inoculation.
Since you get the shot intramuscularily, intradermally or subcutaneously, it is local, and the inflammation does not spread. The reason why your whole arm seems to hurt (rather than the place where the vaccine was deposited) is, I think, that where you got your shot, you have not many pain receptors, and your brain is not able to determine the pain source very exactly.


text:
Salvaging a plasmid from a cell culture stored at the incorrect temperature
I have E. coli with transformed plasmid on agar in a vial.  It has been stored at -20 degree C without glycerol stock for 18 hours.
This is a continuation of: Survival of E. coli on agar plate at -20 degree C without glycerol stock
I have transfered this vial from -20 degrees to 4 degrees after 18 hours when I determined that I had made a mistake. Since this is a very important vial and I don't have another one, what should I do in this stage?
What is the procedure for saving the plasmid if I am unable to save the whole cell?

I would rinse the cells off the agar using a small volume of LB or similar rich medium. Then use a small aliquot (10 μl) to inoculate a 5 ml culture under selection to see if anything will grow. Meanwhile the remainder of the cell suspension from the vial can be used as input for your favourite miniprep procedure.
If necessary, the DNA that you recover should then be used to transform a suitable E. coli strain. Don't bother trying to analyse the rescued DNA first since polysaccharide contaminants from the agar will probably inhibit any restriction enzyme that you might use.
Good luck!


text:
Help with designing the analysis of radio telemetry study
I was wondering if there are any spatial ecologists out there who can provide some insight on the trouble I'm having with my Masters research.
I am looking at the association a bat species to high density aggregations of a flowering plant. The bats were tracked throughout the night with a point taken at approximately 10 minute intervals. The bats were tracked over consecutive nights until an asymptote in their space use was reached. So now I have point patterns for each bat that pretty much covers the entirety of their space use at that period.
When the data is displayed visually there is a clear pattern of the bats that were tracked during the flowering period moving into the aggregations of the plant however they also spend a lot of time foraging around their roost sites.
I have simulated the point pattern of each bat 999 times by randomly shifting and rotating the points within the study window (the internal structure of the observed pattern was maintained in the simulations to account for autocorrelation). I then did randomisation tests to see if the average distance to the nearest plant aggregation for the observed data is within the lower 5% of the distribution of the averages for the simulated point patterns. However because the majority of the points collected are highly associated with the roosts the average distance is primarily effected by the position of the roost in relation to any of the plant aggregations.
I've been thinking of ways to disentangle the association with roosts and the association with the plant.
First I was thought about putting a buffer around the roosts and removing the points falling within these buffers from the analysis. The problem is deciding on a buffer. In the other areas I have been using a buffer equal to the circular error probable of the radio tracking error but placing this around the roost will only incorporate the points where the bat was actually inside the roost not foraging around it. All the bats have different foraging patterns around their roosts and I can't see how to assign a buffer distance that is not completely arbitrary.
The second method we have been looking into is taking out the points that are more closely associated (closer in distance) with the roost than the nearest plant aggregation and then running the randomisation to look at the association of the remaining points to the plant. I want to get an idea of whether or not removing the association with the roosts in this way will potentially bias the analysis.
Any thoughts or further suggestions?!
Thanks in advance!

Very interesting question. However, I would suggest to migrate this to CrossValidated, as probably the folks there will give more appropriate answers.

Yes, but I think the idea of comparing the data without plants with data that include plants is the right idea. Have you only measurements where plants are in the vicinity? Then only a realistic simulation of movement in the absence of plants can be a good model for comparison. But maybe someone else has already created a good simulation?

@ rwst Unfortunately there has been very little spatial work done on these bats. We tracked four bats before the plant came into flower an four during. That's probably not a large enough sample size to make any serious conclusions with so that's why I went down the road of simulating the bat locations but I'll look into it thanks!

@Georgia: I think the moderators can do that directly. I will flag for their attention.

@Georgia has already posted this herself to CrossValidated so I'll close it here


text:
What is the biological basis for the perception of time?
How is the "time axis" of memories encoded in the brain? I guess the time of the event could be "stored" with each event, but how is this translated into neurons etc.?

I'm no expert on the topic, but was about to find the following;
In mammals, the hippocampus region of the brain is one of only 2 regions with the capacity for lifelong neurogenesis (the creation of new neurons). This happens continuously with the creation of new memories and experiences (neurons are even created just to mark time passing - even if no memories are stored alongside - so that a perception of 10mins and 10secs is possible, even if nothing memorable happens). As new clusters of neurons are generated, they gradually differentiate and mature to become fully functional, and in this way time and memory are interlinked, and experiences are clustered together [1].
In a human study where individuals were asked to recall whether news events occurred within 1 week of each other (some related, some not), same-week and separation judgements were more far more accurate for related events. Unrelated events were essentially guesses, whereas deductions could be made about related events. [2]. This lends weight to the above argument that memories are clustered in the brain with temporal information embedded within.
The hippocampus is also involved in imaging the future. (Inconsistent) findings suggest that activation of the hippocampus allows mammals to conceive a scenario constructed from previous memories and experiences, and to store these for later use [3].
Refs

Aimone, J. B., Wiles, J., & Gage, F. H. (2006). Potential role for adult neurogenesis in the encoding of time in new memories. Nature neuroscience, 9(6), 723-7. doi:10.1038/nn1707
Friedman, W. J., & Janssen, S. M. J. (2010). Do people remember the temporal proximity of unrelated events? Memory & cognition, 38(8), 1122-36. doi:10.3758/MC.38.8.1122
Addis, D. R., & Schacter, D. L. (2011). The hippocampus and imagining the future: where do we stand? Frontiers in human neuroscience, 5, 173. doi:10.3389/fnhum.2011.00173


text:
What light intensity determines the start/end of a photoperiod in humans?
I'm reading this article, which discusses the influence of Long Photoperiod (LP) and Short Photoperiod (SP) on melatonin production:
HIOMT drives the photoperiodic changes in the amplitude of the melatonin peak of the Siberian hamster[1].
I'm interested in knowing what light intensity is interpreted as the onset and end of a light-dark photoperiod.
The referenced article indicates that animals were kept in cages, with a pre-set photoperiod duration, this sounds to me like it was done indoors. If it has been done indoors, then artificial lighting was involved, and I would guess it was an on-off affair, rather than gradual change or jumps in intensity.
The reason why I'm asking is that I'm trying to understand the implications of this article for humans, who may wake up before dawn, and spend some time under artificial lighting of various intensity before sunrise, and continue to function after sunset. For example a person may be looking at a TV or a monitor, and I would like to get an idea if this "presence of light" is enough to trigger photoperiod-related changes in the brain. Is there some "critical" density (or density at a specific wavelength) of light that signals the start/end of a photoperiod?

Ribelayga C, Pévet O, Simonneaux V. 2000. HIOMT drives the photoperiodic changes in the amplitude of the melatonin peak of the Siberian hamster. Regulatory, Integrative, and Comparative Physiology, 278(5), R1339-R1345.

The effects upon sleep of blue light exposure from screens is quite a current topic. Have a look at this blog post which points to a couple of recent studies:  http://www.marksdailyapple.com/how-light-affects-our-sleep/#axzz26uyWBa1R

Thank you! That article mentioned melanopsin as a pigment responsible for blue light detection in the eye. Since human eyes differ from hamster eyes, I would expect that the density of melanopsin in the eyes differs.  It would help to know what intensity of blue light triggers sleep-wake related changes in the brain.

It isn't really a specific light intensity that an organism will interpret as the start of a photoperiod. Maynard Johnson reported in 1939 that intensity of light used had an effect on the rate at which mice would shift their circadian rhythms. So, brighter light has a stronger effect, but there isn't a cutoff point that I'm aware of. Johnson was using illumination as low as 2.5 foot candles, which is pretty dim. Aschoff and Pittendrigh did some more work on light intensity in the 50s and 60s, but I don't think anyone ever found anything resembling a cutoff point, only the degree to which intensity had an effect.
Computer monitors are pretty bright. Luminance rating is typically 250-350 cd/m2, which, for comparison with Maynard's experiment, is eqivalent to 23-32 foot-candles. http://computer.howstuffworks.com/monitor6.htm
Johnson, Maynard S. "Effect of continuous light on periodic spontaneous activity of white‐footed mice (Peromyscus)." Journal of Experimental Zoology 82.2 (1939): 315-328.


text:
Are some non-coding RNA spliced?
Are some non-coding RNA spliced like mRNA? I tried to find some information but I don't find anything...

yes yes - many of them are spliced out of mRNA too

You should check out Howald C, et al[1].  This is one of the many recent papers tied to the ENCODE data. They've used RT-PCR to amplify exon-exon junctions and then sequenced the results. Supplemental table 2 shows 3076 validated exon-exon junctions in putative processed transcripts which, in the main body of the paper may be sub-classified as:

Non-coding, 3prime_overlapping_ncrna, Ambiguous_orf, Antisense,
  LincRNA, ncRNA_host, Retained_intron, Sense_intronic,
  Sense_overlapping, Processed transcript.

Howald C, Tanzer A, Chrast J, Kokocinski F, Derrien T, Walters N, Gonzalez JM, Frankish A, Aken BL, Hourlier T, Vogel JH, White S, Searle S, Harrow J, Hubbard TJ, Guigó R, Reymond A. 2012. Combining RT-PCR-seq and RNA-seq to catalog all genic elements encoded in the human genome. Genome Research, 22: 1698–1710, doi:10.1101/gr.134478.111.

Do you call ribosomal RNA non-coding? rRNA is spliced both in prokaryotes and eukaryotes.

can you give some reference, please?

Sure. Some general information on pre-tRNA and pre-rRNA processing from Molecular Cell Biology: http://www.ncbi.nlm.nih.gov/books/NBK21729/

And of course rRNA is non-coding. Coding refers  specifically to sequences coding for protein.

One of my teachers considered all "functional" RNA coding.

Yes, check out HOTAIR (in human), as well as cyrano and megamind in zebrafish -- they are all spliced.


text:
Are there yearly variations in HIOMT (HydroxyIndole-O-MethylTransferase) availability?
I'm reading a booklet on melatonin published in 1996, titled "Melatonin and the Biological Clock". And see the following statement:

HIOMT (HydroxyIndole-O-MethylTransferase), one of enzymes of melatonin
  synthesis, rises and falls in an annual rhythm, with troughs in March
  and October and peaks in January and July.

Seeing how HIOMT is the last methyltransferase involved in Melatonin synthesis in humans, I'm interested in learning if there's indeed a yearly variation in this MT production in humans, and if it is regulated by genetics or photoperiod duration.
Thank you for your input!

usually the author of a book gives references for all quoted statements.

This isn't really a complete answer but I can't fit it into a comment.
I've found that there is a large body of literature on seasonality of melatonin levels in various vertebrates, particularly livestock, because of its interaction with breeding patterns. Similar studies in humans are however, difficult to find, but the review paper cited below looks at a link between seasonal variations in melatonin levels and seasonal variations in immune system functions. It cites a few references that might be worth following up.

Srinivasan, V. et al. (2008) Immunomodulation by melatonin: Its significance for seasonally occurring diseases. Neuroimmunomodulation 15: 93-101 DOI: 10.1159/000148191
Abstract
Melatonin is not only synthesized by the pineal gland but also in many other organs and tissues of the body, particularly by lymphoid organs such as the bone marrow, thymus and lymphocytes. Melatonin participates in various functions of the body, among which its immunomodulatory role has assumed considerable significance in recent years. Melatonin has been shown to be involved in the regulation of both cellular and humoral immunity. Melatonin not only stimulates the production of natural killer cells, monocytes and leukocytes, but also alters the balance of T helper (Th)-1 and Th-2 cells mainly towards Th-1 responses and increas- es the production of relevant cytokines such as interleukin (IL)-2, IL-6, IL-12 and interferon-γ. The regulatory function of melatonin on immune mechanisms is seasonally dependent. This fact may in part account for the cyclic pattern of symptom expression shown by certain infectious diseases, which become more pronounced at particular times of the year. Moreover, melatonin-induced seasonal changes in immune function have also been implicated in the pathogenesis of seasonal affective disorder and rheumatoid arthritis. The clinical significance of the seasonally changing immunomodulatory role of melatonin is discussed in this review.


text:
Transcript(omics) terminology: cDNAs, ESTs, RNA-seq, etc
I've worked pretty frequently with genome and transcriptome data for several years now, but I'm still not 100% sure I understand the proper usage for certain terminology related to transcripts and transcriptomics. Let me give it my best shot.

cDNA: in general, this term corresponds to any DNA that is derived from an RNA template via reverse transcription (complementary DNA); however, it is often used to refer to full length cDNAs, DNA sequences that correspond to complete mRNA molecules
EST: expressed sequence tags correspond to cDNA (sub)sequences obtained from a single read of a cDNA sequencing experiment
RNA-seq: this refers to the use of high-throughput sequencing technologies to characterize entire transcriptomes, such as by transcript assembly or expression analysis

Here's my concern: I've seen ESTs described as "one-shot" or "single-pass" sequences, which I interpret to mean a single sequence read. However, they are also typically described as being hundreds of base pairs in length (Wikipedia claims about 500-800bp in length max), which (currently) limits this definition to reads derived from Sanger-style sequencing.
Does this mean that a short read derived from a high-throughput sequencing platform is not an EST? Is this distinction based on read length? platform? throughput?
Due to technical limitations, short reads are often assembled before they are used for other downstream analysis. I have sometimes heard the contigs belonging to these assemblies as ESTs, but this doesn't seem to be consistent with the previous definitions.
Is our terminology becoming inconsistent due to the rapid improvements in sequencing technology, or am I missing or misinterpreting something?

Although for historical reasons an EST is usually a longish sequence (ESTs were defined in 1991 when only Sanger sequencing was available so reads would naturally be several hundred bases in length), operationally it really only needs to be long enough to tag an expressed sequence, i.e. to provide evidence for the existence of an mRNA from a specific region of a genome.

The quick answer is that you are misinterpreting ESTs. EST stands for Expressed Sequence Tag. They are obtained by collecting and sequencing any mature (i.e. poly-A) mRNAs found in a living cell. Well, it was living until the experiment was performed at any rate :).
The term EST is not applicable to sequences derived from genomic data. It only applies to expressed sequences. You do have ESTs that are derived from cDNA libraries but these are expressed cDNAs. Short reads are not ESTs because we have no information on whether that sequence is actually expressed in a living cell.
You could apply the term to RNAseq reads (depending on the experimental procedure involved) but that is not what most people would understand by the term.
In summary, the operative term of EST is "expressed". You cannot call anything an EST if you do not have evidence that it is actively expressed in a living cell.

When I said "short reads", I was referring in that case to RNAseq reads. Of course, in general short reads can be genomic (if you're sequencing the genome) or transcriptomic (if you're doing RNAseq analysis or something similar).

Still, RNAseq can also pick up non-poly A RNAs. Personally, I would only use "ESTs" to describe sequences derived from "naturally occurring" mRNAs. Given the recent findings of the ENCODE project, most of the genome seems to be actively transcribed. Such transfrags do not, again in my personal opinion, qualify as ESTS.

@terdon: I must be missing some subtlety when you qualify ESTs as having been "found in a living cell" ... RNA-seq libraries are constructed from "living cells" as well, so what's the difference here? Capturing these reads are evidence enough that they are expressed (noise control required, obviously) Also: I suspect "mature mRNAs" are captured for "EST-ifying" much the same way they are captured for constructing a highthroughput sequencing library (via oligo-dTs to prime the polyA tail ... or even "cap trapping" if you're doing some *CAGE experiment). Can you clarify those two points a bit?

@SteveLianoglou, I was differentiating more between cDNA libraries made from DNA templates and ESTs. Yes RNAseq reads come from living cells. In my answer I just say that "most people" would not call the ESTs. Not that they are not indicative of expression. I quite agree that technically you could call RNAseq reads ESTs, its just that the term is more commonly used for the older EST type data.

My 2 cents:
To answer your main question:

Is our terminology becoming inconsistent due to the rapid improvements in sequencing technology, or am I missing or misinterpreting something?

I think what you are witnessing (being subject to(?)) is, as you say, an inconsistency of terms due to the rapid improvements in the field.
I put the caveat in that you are being subjected to this because I suspect the people referring to the "things" that a second-generation-sequencing protocol generates as "ESTs" are using a familiar word to describe something that might be unfamiliar to them.

Does this mean that a short read derived from a high-throughput sequencing platform is not an EST? Is this distinction based on read length? platform? throughput?

I guess it's (i) construction; (ii) platform; (iii) throughput; and (iv) relative "quantitativeness".

Due to technical limitations, short reads are often assembled before they are used for other downstream analysis.

You lost me here with the word "often" -- are you talking about RNAseq now or is this an EST. If you have a reference genome, I think assembling RNAseq reads before downstream analysis (alignment(?)) is an exception instead of a rule ... which is why I'm lost.

Ok, perhaps my use of "often" is biased by my own experience. I am working on genome annotation, and both the Maker annotation pipeline and some of our in-house workflows require RNA-seq data to be assembled before they can be used as evidence when predicting gene models. I understand of course when mapping short reads to a genome or quantifying gene expression, assembly is not a prerequisite.

I think RNA-Seq assembly prior to alignment is common in non-model species, where you need to first describe the features you align the reads to.


text:
laboratory mice, nutrition, and humans
It seems that many nutrition experiments [directed at human diet] are carried on laboratory mice. Is there any justification that nutrition that is good or bad for laboratory mice will also be same way applicable to humans ?
I wonder because mice and humans, although both being mammals, are separated probably by tens millions years of separate evolution.  By the "mammals" logic, dolphins, cows, wolves, and goats, all being mammals, shall have same diet as mice ?
Sometimes one man's food is another man's poison (lactose differences for example, due to genetic differences). That's man to man, same species. On what is "transfer of nutritional information" from species to species based ?
2) Was it ever established, or the opposite, that all humans have same best diet. Other than known lactose metabolism difference.

This is an important question I think. The commonality of genes among eukaryotes does not necessarily mean they share the same metabolism etc.

Whether using quantitative models, or "animal models", I think this is a useful quote to keep in mind:

A model is a lie that helps you see the truth.
-- Howard Skipper

As for evidence that using mice models for human nutrition is justified -- I believe there has been a good deal of research that has provided useful insight on the influence of genetics on the susceptibility to diabetes in humans using mouse models, so ... yes?

My impression is that the use of mice as human models for anything is primarily the result of historical precedent. A lot of work has been done to breed different lines of mice for particular purposes, and a lot of related methodology has therefore been established. Similarly, a lot of comparative genetic/genomic work has been done to characterize similarities between the mouse and human genomes. Developing similar methods and resources for another species could potentially require a huge investment of time and resources.
Additional reasons are purely technical and practical. Non-human primates are demonstrably more closely related to humans than mice, but breeding, storing, and working with these animals is a much more complicated issue.
And, as @SteveLianoglou mentions, any model has to be taken with a healthy level of skepticism. I prefer the quote from G.E.P. Box:

Essentially, all models are wrong, but some are useful.

No model of human nutrition is going to be perfect, whether it was modeled in mice, primates, or even other humans (as you suggested). This does not mean, however, that we cannot gain insight from the models just because they are not perfect.

+1 for the mention of practical reasons. Also, another extremely important point is that mice are pretty much the only mammal where you have the availability of an enormous amount of transgenic lines, which allow to dissect the system much more in detail. As much as I would like to work on transgenic wolves we are not quite there yet! :P

Human life span is too long and not suitable for such studies, so mice are used pretty much because their life span is much shorter and because they're already used for pretty much everything.
Mice and men as mammals have the same heritage and a metabolism which is very, very similar, almost identical - compared to the metabolism of insects, for example.
However, the millions of years of separate evolution made us the most capable omnivores on the planet, who learned to cook, became monogamous, evolved intelligence and grand-paternal care etc. We even evolved to drink milk as adults and eat gluten. So you can't possibly come up with conclusions about such complex species by looking at a simple creature that is an evolutionary dead end.
If you're using mice for your study, you can find out how something affects a mammalian species in general, e.g. radiation, but not how nutrition affects humans - because human nutrition is unique. The scientists basically don't know much about nutrition to begin with, and I suppose they're trying to figure out the basics for now, some general rules which apply to all mammals, and that's why they're using mice. A less complex organism.
But you'll get nowhere if you're researching traits unique to the human race by looking at another species which doesn't have those traits.


text:
How are melatonin levels measured in humans?
I'm wondering how it is possible to measure diurnal variations of melatonin levels in humans. I keep reading that there should be a large difference in amplitude between melatonin levels measured at night and in the middle of the day.
Have there been any studies of melatonin levels in humans where I can take a look at the methods they used for this kind of testing and/or see sample results?

On the analytics of melatonin I have here a german language text by the RKI with references. Translated quote:

Assay of melatonin is done by serum or sputum using RIA or ELISA.
  Alternatively, to infer the nightly amount of melatonin secretion it
  is possible to look for the melatonin catabolic metabolite 6-hydroxy
  melatonin sulfate (6-OHMS) in urine.[1,2] ... standardized
  conditions of sample taking are a must to get good results.[3,4]

Ref.:

P. Levallois, M. Dumont et al: Effects of electric and magnetic fields from high-power lines on female urinary excretion of 6-sulfatoxymelatonin. In: American journal of epidemiology. 154, 7, October 2001, 601–609. PMID 11581093
D. H. Pfluger, C. E. Minder: Effects of exposure to 16.7 Hz magnetic fields on urinary 6-hydroxymelatonin sulfate excretion of Swiss railway workers. In: Journal of pineal research. 21, 2, September 1996, 91–100. PMID 8912234
E. Gilad, N. Zisapel: High-affinity binding of melatonin to hemoglobin. In: Biochemical and molecular medicine. 56, 2, December 1995, 115–120. PMID 8825074
D. K. Lahiri, D. Davis et al: Factors that influence radioimmunoassay of human plasma melatonin: a modified column procedure to eliminate interference. In: Biochemical medicine and metabolic biology. 49, 1, February 1993, 36–50. PMID 8439449


text:
What is the life-span of the various organs in the human body?
It is possible for a person to donate the harvestable organs (kidneys, eyes, and such) posthumously. Let's assume for a moment that the technology exists to kill rejection, and maintain the organ in excellent shape after it is harvested.
Could the organ/s ( e.g. Eye ) (assuming a decent life-style) travel for centuries from one donor to yet another donee? What is the typical life-span of the various organs in the human body assuming a healthy, and low stress life?
p.s. It's a curiosity question; my eyes even millenia after my death would continue to see.

Perhaps you can infer relative lifespan from the age at which organs start declining in someone of average health.
Skin, muscles, bones, eyes, and ears start to visibly decline around age 40.
Kidneys become smaller and their ability to filter blood starts to decline around age 30.
Brain function begins to decline around 70, even in the absence of neurodegenerative diseases such as Alzheimers.
I don't think any organs can be passed through people for centuries, since decline of virtually every organ is observed even in individuals in perfect health. There may be two exceptions: The digestive tract and liver seem to be the most long-lived and are very little affected in healthy elders, probably because they regenerate their cells.
Reference


text:
How to build S16 rRNAs phylogenetic trees?
Here is what I know so far:

Multiple copies are present in prokaryotes, but according to a paper by Lukjancenko el al.[1] it is enough to select the most similar ones.
There are stem regions in the S16 which I suspect are much less variable than the loops.

And here are my questions:
About 1., it is this the usual procedure?
About 2., do people use the loops or the stems to construct a phylogenetic tree? It they use stems, do they consider the coupling between stem bases? And, if they do so, where can I get a "map" of this coupling (preferably in a parseable form, not an image)?
In the other hand, is it correct to use a simpler nucleotide substitution model? which one?
Thanks in advance for any hints.

Lukjancenko O, Wassenaar TM, Ussery DW. 2010. Comparison of 61 Sequenced Escherichia coli Genomes. Microbial Ecology, 60:708-720, doi:10.1007/s00248-010-9717-3.

OK, first of all do not use CLustalX to align the sequences. It is a very old algorithm and is outperformed by just about any modern aligner (including its descendent, clustal omega, and t-coffee, mafft, kalign etc etc).
As for 1) that depends on what you want to do, there is no perfect solution. What question are you trying to answer? If you want a tree with species-level resolution, use all sequences. If you don't need that high a resolution, choose a representative sequence from each order or genus or whatever. In all cases, remember to use a significantly different sequence as an outlier.
As a general rule, I would use the entire sequence to build a tree, both the stems and the loops. To include structural information in your alignment you may want to check out r-coffee from the t-coffee suite.
Finally, you don't really want to use a nucleotide substitution model. Most such models assume that the sequence codes for protein and are not suitable for non coding RNAs.


text:
Does culling badgers restrict the spread of bovine tuberculosis?
The British government has announced that it plans a large-scale badger cull which they argue are implicated in the spread of Mycobacterium bovis - so-called bovine tuberculosis. Any cattle that contract this disease need to be slaughtered under EU regulations.
However, the link between badgers and cattle doesn't seem that clear to me. What is the evidence that badgers spread tuberculosis to cattle? Also, what is the evidence that badger culling will have a significant effect on the spread of the disease to cattle?

I have added the second part of my question which I left out - apologies.

This is apparently a debate since decades in the UK. As to the pathology:

Eurasian badgers (Meles meles) are an important wildlife reservoir of
  tuberculosis (Mycobacterium bovis) infection in Ireland and the United
  Kingdom. As part of national programmes to control tuberculosis in
  livestock, considerable effort has been devoted to studying the
  disease in badgers and this has lead to a rapid increase in our
  knowledge of tuberculosis in this host.

L. A. Corner, D. Murphy, E. Gormley: Mycobacterium bovis infection in the Eurasian badger (Meles meles): the disease, pathogenesis, epidemiology and control.'' In: ''Journal of comparative pathology. 144, 1, January 2011, 1–24. doi:10.1016/j.jcpa.2010.10.003. PMID 21131004. (Review).
A summary of the pre-1997 debates is here:
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/tb/publications/krebs.htm
The up-to-date DEFRA informations are at:
http://www.defra.gov.uk/animal-diseases/a-z/bovine-tb/
For an alternative approach see:
http://www.ncbi.nlm.nih.gov/pubmed/19846226 (in short: educate them not to piss everywhere)
I have been asked to give also a summary. Tuberculosis is probably one of the nastiest bacterial infections in existence. It is a prototype of those diseases which are called latent: you can be infected for decades without symptoms, but when your immune system falters (or you have to take immune suppressants) it breaks out and kills you. One third of the human population has such a latent infection with Mycobacterium tuberculosis, and the HIV wave plus the high mycobacterial mutation rate with following extreme resistances make for interesting epidemiology. But this is also a result of our lifestyle, depending on huge cattle herds, as cattle can be cross-infected with human TB. In the west we have succeded to cut human infections by controlling cattle infection with human TB. Still, cattle can get bovine TB, and this may be economically disastrous. One of the pools of the infection is the badger population which can get bovine TB too and spread bacteria with their urine. It is unclear if protozoa may be an even more important pool. It is likewise unclear if culling of badgers would be successful for cattle TB control; the government bases its decision on a long-term study of regions where culling has happened. Alternative approaches include vaccination (which only affects uninfected animals), different cattle grazing regimes, habitat manipulations and badger latrine management. Physical exclusion of badgers from farm buildings is suggested as the simplest, and potentially most effective, method of reducing contact and opportunities for disease transmission between badgers and cattle. The government expert opinion clearly concluded that without such additional measures, culling won't be successful in reducing cattle TB.

This doesn't answer the question...

Much better :) +1 For an even better answer you could summarise the main points?


text:
What is the effect of garlic on intestinal flora?
Now that we can compare whole microbiomes, has there been investigations on the effect of garlic (or diallyl disulfide, its main ingredient) on intestinal flora? From the proven antimicrobial activity, it should work like antibiotics. But does it leave "good bacteria" counts untouched?

From studies,

lactic acid bacteria were found to be more resistant to GP (garlic
  powder) compared to the clostridial members of the gut microbiota.
  While for most bacteria the antimicrobial effect was transient, the
  lactobacilli showed a degree of resistance to garlic, indicating that
  its consumption may favour the growth of these beneficial bacterial
  species in the gut. Once the strains of other bacteria (eg:
  Bacteroides ovatus, Bifidobacterium longum DSMZ 20090 and Clostridium
  nexile A2-232) became resistant, they retained their resistant
  phenotype upon sub-culturing. Garlic intake has the potential to
  temporarily modulate the gut microbiota (reference).

Overall garlic can prove to be beneficial, because it seems to have more of an effect on detrimental bacteria like Helicobacter pylori (H. pylori), even when its strains were resistant to antibiotics. Overall garlic was found to be more detrimental to pathological bacteria when compared to normal gut flora (reference). Garlic’s diallyl disulfide has also been found to effectively cause cell death in Candida albicans which is a fungus in our gut which if not kept in check can cause health problems (reference).
Inulin and fructooligosaccharides present in garlic can also serve as nutrients for the probiotics colonizing your body (reference).


text:
In the vacuum of space would death be instantaneous?
I was arguing with my colleague about this matter (I'm not going to mention which side I fall on).
Would death be immediate in the vacuum of space? For example, if I was suddenly teleported into the vacuum of space would I die straight away? Or would I experience a suffocating sensation?

Sounds like a perfect candidate for http://what-if.xkcd.com/! :)

Please see skeptics for an answer: http://skeptics.stackexchange.com/questions/8521/would-a-humans-blood-suddenly-boil-or-eyes-body-explode-in-a-vacuum

Nope, you wouldn't die instantly. While explosive decompression has never been tested on humans (for obvious reasons), the dangers of a vacuum have mostly to do with the pressure differential between your body and the now pressure-less void around you. The most fragile parts of the biological system would be the lungs and ears, and the instantaneous transportation would cause a severe case of the Bends if you were rescued quickly enough. You would pass out within a few seconds stated by NASA when an experiment went awry, and death might be from lack of oxygen to the brain, although after a few minutes everything bad starts to happen so nobody really knows what you would die of:

At NASA's Manned Spacecraft Center (now renamed Johnson Space Center) we had a test subject accidentally exposed to a near vacuum (less than 1 psi) in an incident involving a leaking space suit in a vacuum chamber back in '65. He remained conscious for about 14 seconds, which is about the time it takes for O2 deprived blood to go from the lungs to the brain. The suit probably did not reach a hard vacuum, and we began repressurizing the chamber within 15 seconds. The subject regained consciousness at around 15,000 feet equivalent altitude. The subject later reported that he could feel and hear the air leaking out, and his last conscious memory was of the water on his tongue beginning to boil.

"While explosive decompression has never been tested on humans..." Love it!

not until somebody does the test with a chimp first

Not tested under controlled conditions, but there was the Byford Dolphin diving bell accident - 9 atm to 1 in under a second, four souls lost.

Didn't the Nazis test low-pressure on humans, if not outright explosive decompression? It's one of the atrocities we discuss at ethics classes in college.

Also worth commenting that exposure to the vacuum of space isn't the same as exposure to an artifical vacuum generated here on Earth. Spatial vacuum is full of radiation. If an astronaut were blown out into space at Earth orbit, sunlight would probably damage his skin considerably in the absence of a protective ozone layer, which would not occur down here. Additionally his body would eventually collide with micrometeorites, if not with larger bodies.

If an astronaut were teleported into space without her spacesuit/helmet, she would feel a suffocation feeling, likely making breathing motions even though there is no air to breathe.  She would also feel her sweat, saliva, tears, mucous, and any other water on her body boil off, though her body would maintain blood pressure, at least until her heart stopped. She would be unconscious within 15-20 seconds and dead within 90-120 seconds.

Please provide some references to support your answer.

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


text:
How can GMO contaminate biologic plants?
Let consider two use cases :

I am the only farmer within a 200km radius. I first grow GMO plants. A few cycles later I decide to grow bio plants, so I uproot all of the GMO plants and plant fresh new bio plants.
I am surrounded with GMO plantations and I decide to grow bio plants.

In both cases, can we consider the plantation as bio or was it contaminated and how?

First let me say this: I am no gardener. Every plant that enters my home or yard dies a slow death of neglect. I do have some experience trying to remove weeds from other non-weeds, and there is a practical aspect of "uproot every GMO plant" that I think may be impossible, but this is speculation. Let's get into a literature review.
A frequently cited paper is Dröge, M., Pühler, A. & Selbitschka, W. Horizontal gene transfer as a biosafety issue: A natural phenomenon of public concern. Journal of Biotechnology 64, 75–90 (1998). Table 3 contains the most relevant information about horizontal gene transfer between plants.
In situation number 1, consider that the rhizosphere (the area of soil around the root of a plant) is constantly populated with bacteria. These bacteria are shown to sometimes transfer genetic material to and from the plant, through the roots. Unless you somehow sterilize the soil after uprooting your previous crop, consider everything you plant in that field possibly contaminated.
Situation 2 is less clear, but Monsanto does sue farmers found to be using their seeds without a contract, and many farmers say this is because of cross-pollination. I think you should assume that your field will soon be contaminated.

Unless you somehow sterilize the soil after uprooting your previous crop, which is not very smart if you want to grow something else afterwards!