text:
intravenous (IV) in the tail vein of an anaesthetized mouse
I trained myself to do intravenous injection on live mice. However, on anaesthetized mice you don't see the flux of your product showing that your injection was successful. In the same way, on live mouse a slight back pressure can be used to pull blood into the syringe to confirm proper placement in the vessel before injecting. On anaesthetized mice, I really have difficulty to obtain blood. All my following experiments rely on this injection, so I really need to be sure that the injection was successful and I have no choice that to do the injection on an anaesthetized mouse. Of course I warm the animals before injection to dilate the veins but I don't know how much I can warm an anaestethized mouse.
I thought to put a catheter before anesthetization the mouse but I don't know if it will stay in place until the mouse is anaestetized.
Do you have any tips?

@Rory M: I am not so sure zoology really is the best tag, but definitely I am puzzled by the cardiology tag.

@nico zoology was a simple replace of animals as it didn't exist.  Cardiology is just going on the tag-wiki description - "The study of the physiology and pathology of the cardiovascular system".  I agree that they aren't fully right yet though, any suggestions? =S

@RoryM: ok for zoology, but here we are speaking of a technique for injecting an animal, I do not see it so related to cardiovascular system... maybe a "techniques" tag?

I'm definitely supportive of a techniques/procedure tag, I think it's a helpful classifier

Cleaning the tail with ethanol is of some help and also, as you said, warming the tail. We sometimes put one of those flexible lamps (such as this) to heat up only the tail.
When anesthesized (ketamine/xylazine or isoflurane) we keep our mice on a heated pad anyways.
Cannulation in the tail does not sound like a good idea to me, especially if you are going to have the animal wake up afterwards. If you're going to cannulate then go for the jugular, but be aware that doing it on a mouse requires quite a bit of experience and it's definitely way longer than a tail injection.
It really depends on your experiment


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What are the differences between white and brown adipose tissue?
What are the differences between white and brown adipose tissue? Here are some that I have come across:
Brown Adipose Tissue                        White Adipose Tissue

Thermogenic                                 Non-thermogenic
Multilocular                                Unilocular
Relatively many mitochondria                Relatively few mitochondria
Vascularised                                Relatively few capillaries
characterized by the presence of leptin     characterized by the presence of UCP-1

I think Shep had more of the right idea in his answer to your Meta question about this, I don't know how you can maneuver this to make it more constructive.  In its current form, it's still asking for a list.

but Kevin's answer on meta wasn't shot down, so I assumed it would be OK....

Well, see what everyone else thinks about it, but list questions are normally closed as "not constructive".  Is there anything in particular you are looking for in terms of the relationship between the two types?  That would make a much stronger question and would probably get a better answer, anyway.

My suggestion was to just ask the question. I didn't think you would answer it in the question.

Also, BAT is smaller than WAT having 20-40um,30-70um respectively.

Brown color of adipose tissue is due to cytochrome oxidase.... It's an extra point . I think it will help u in future.....punjab

there are a lot of differences between brown and white fat (and don't forget beige fat - that's a 'thing' now too) - anatomic differences, physiologic differences, biochemical differences, etc, etc...

Not sure what you are asking, except to add to the list?
Its worth mentioning that brown adipose tissue is the only organ in the human body whose primary purpose is to generate heat.  We are warm blooded, but the body temperature is regulated by other organs generating heat while they do work (like muscles or I suppose the stomach, kidney, etc).
Brown Tissue is supposed to not a juvenile attribute - doesn't show up in adults to the same extent (usually being limited to neck and upper chest.
Brown Tissue is thought to be present in only critical areas of the body - even in infants.  Its found in the inner body cavity around vital organs.
The color comes from the large number of mitochondria in the cells, which is where the heat is generated via uncoupling protein 1 (UCP1).
White adipose tissue is what we more commonly call fat tissue - its primary function is to store energy in the chemical form of long chain fats.  Fat tissue as it grows can inhibit the function of insulin in the body, increasing insulin resistance.
You could almost call them 'good fat' and 'bad fat'

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How Does Green Tea Increase Metabolic Rate?
According to the article "Green Tea Supplementation Affects Body Weight, Lipids, and Lipid Peroxidation in Obese Subjects with Metabolic Syndrome", Green tea increases metabolism and fat loss:

Green tea beverage consumption (4 cups/d) or extract supplementation
  (2 capsules/d) for 8 weeks significantly decreased body weight and
  BMI. Green tea beverage further lowered lipid peroxidation versus age-
  and gender-matched controls, suggesting the role of green tea
  flavonoids in improving features of metabolic syndrome in obese
  patients.

Is there any information available concerning the mechanism of that metabolic increase?

Caffeine maybe?

@Armatus, Caffeine was used as the negative control.

@Dale Your link is broken.

I updated the link, but the full article is behind a paywall.

Interesting question! Green tea increases metabolic rate of body because it contains antioxidants known as catechins1. Catechins are actually polyphenol flavonoids, and have been shown by Wang et al and team to affect body composition and decrease body fat in intra-abdominal area. Also, as per Khalesi et al, catechins improve blood pressure, especially when systolic pressure exceeds 130 mmHg, while some studies, such as Ellinger et al, have indicated that catechins may have effect on endothelium-dependent vasodilation which might lead to normal blood flow regulation. Another study, by Weinreb et al, shows that catechins can also reduce the risk of Parkinson's and Alzheimer's. However, their exact mode of action is unknown because of their extensive metabolism during digestion6.
Green tea also contains a little amount of caffeine. Now, as we all know, caffeine is known for its stimulating effects on the body. Caffeine, as stated by Nehlig et al, blocks the formation of adenosine in brain, thus increasing concentration of dopamine and norepinephrine in the brain which, in turn, allow quicker firing of neurons. Along with caffeine, another compound with similar effects is L-theanine, which increases the activity of GABA and leads to anti-anxiety effects, as reported by Nathan et al. Caffeine and L-theanine can together have synergistic effects on the brain and give much more pronounced effects together than individually.
A yet another, and probably less spoken of, effect of green tea, as concluded by Lee et al, is that it can even kill some bacteria and viruses (obviously, killing means preventing growth here) and thus reduces chances of bacterial and viral infections.
Obviously, there might be even more benefits of green tea than I've put here. To the precise point you were asking, we don't yet know how green tea helps in burning calories and fat oxidation. The proposed mechanisms of action are10:

catechins act on catechol-o-methyltransferase (COMT), an enzyme which degrades norepinephrine. Norepinephrine is known for regulating thermogenesis and fat oxidation. Thus inhibition of COMT by catechins may lead to prolonged effects of norepinephrine on fat metabolism.
caffeine can also affect thermogenesis, but by inhibiting phosphodiesterases & thus prolonging effects of cAMP in the cell. As a result, cAMP stimulates hormone - sensitive lipase and promote lipolysis.
catechins and caffeine can also work together and increase thermogenesis in body by 35-43% by increasing fat oxidation.

However, these are just the proposed mechanisms and more detailed studies are required to reach a conclusion.
References:
 1. Beneficial Effects of Green Tea—A Review; Carmen Cabrera, Reyes Artacho, and Rafael Giménez; Journal Of The American College Of Nutrition Vol. 25 , Iss. 2,2006
 2. Wang, H., Wen, Y., Du, Y., Yan, X., Guo, H., Rycroft, J. A., Boon, N., Kovacs, E. M.R. and Mela, D. J. (2010), Effects of Catechin Enriched Green Tea on Body Composition. Obesity, 18: 773–779. doi:10.1038/oby.2009.256
 3. Khalesi, S., Sun, J., Buys, N. et al. Eur J Nutr (2014) Green tea catechins and blood pressure: a systematic review and meta-analysis of randomised controlled trials, 53: 1299. doi:10.1007/s00394-014-0720-1
 4. Epicatechin ingested via cocoa products reduces blood pressure in humans: a nonlinear regression model with a Bayesian approach; Sabine Ellinger, Andreas Reusch, Peter Stehle, and Hans-Peter Helfrich
 5. Neurological mechanisms of green tea polyphenols in Alzheimer's and Parkinson's diseases; Orly Weinreb, Silvia Mandel, Tamar Amit, Moussa B.H. Youdim
 6. "Flavonoids". Linus Pauling Institute Micronutrient Information Center, Oregon State University
 7. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects.; Nehlig A, Daval JL, Debry G.
 8. Nathan PJ, Lu K, Gray M, Oliver C.. The neuropharmacology of L-theanine (N-ethyl-L-glutamine) a possible neuroprotective and cognitive enhancing agent. J Herb Pharmacother (2006) 6(2):21–30.10.1080/J157v06n02_02
 9. Lee H.J., Lee Y.N., Youn H.N., Lee D.H., Kwak J.H., Seong B.L., Lee J.B., Park S.Y., Choi I.S., Song C.S. Anti-influenza virus activity of green tea by-products in vitro and efficacy against influenza virus infection in chickens. Poult. Sci. 2012;91:66–73. doi: 10.3382/ps.2011-01645.
 10. Jówko E. Green Tea Catechins and Sport Performance. In: Lamprecht M, editor. Antioxidants in Sport Nutrition. Boca Raton (FL): CRC Press/Taylor & Francis; 2015. Chapter 8. Available from: https://www.ncbi.nlm.nih.gov/books/NBK299060/

May be because it contains xanthines that boosts Cyclic AMP and Subsequent Stimulation Of Oxidative Pathways .

References for both statements would be great =)

Green tea contains caffeine and catechin polyphenols. There are various proposed mechanism of these compounds
(1) These compounds have an effect on sympathetic nervous system (SNS). SNS is involved in flight and fight situations and controls thermogenesis and fat oxidation. In put in simpler words, the bioactives in green tea stimulate the part of nervous system which is involved in preparing body for emergency response by increasing the metabolism [1].
The catechins, inhibits Catechol-O-methyl transferase (COMT) that degrades norepinephrine resulting in prolonged shell life of norepinephrine in the synaptic cleft,
Caffeine inhibits phosphodiesterases which increases the life of cAMP, result in an increased effect of norepinephrine on thermogenesis.
(2) Catechins found in teas have shown potential to inhibit carbohydrate absorption in the intestines.
A very detailed review of literature can be found here [2]

[1] http://ajcn.nutrition.org/content/70/6/1040.long/-
[2]https://macsphere.mcmaster.ca/bitstream/11375/20419/2/Martin_Brian_J_Finalsubmission2016September_PhD.pdf

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Bicoid regulation of hunchback
I'm learning about development via the example of Drosophila embryogenesis. I understand that bicoid regulates hunchback, among other genes. My question whether the regulation is direct or indirect? In other words, does the level of bicoid directly govern the expression of hunchback, or are there steps in between?

These two papers[1] [2] argue that bcd is a direct activator of hb, although be aware that this does not rule out downstream events feeding back to further activate  hb. (In fact, given the complexity of the embryonic gene network, it is likely that both mechanisms have a role.)

Struhl G, Struhl K, Macdonald PM. 1989. The gradient morphogen bicoid is a concentration-dependent transcriptional activator. Cell, 57(7): 1259-1273, doi:10.1016/0092-8674(89)90062-7.
Driever W, Nüsslein-Volhard C. 1989. The bicoid protin is a positive regulator of hunchback transcription in the early Drosophila embryo. Nature, 337: 138-143.


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Is there a maximum amount of antibodies your body can keep?
I am wondering if you were theoretically able to get vaccinations or antibodies for any and every diseases and/or illness, would there be a limit to how many you can get and keep in your body at one time? If so, what is the limiting factor?
What would be the possible effects of this on the body and immune system? Thanks.

Everyone has an estimated number of around 10^12 (1 trillion) different antibodies, without counting any immune reaction to vaccines or other antigens (http://www.ncbi.nlm.nih.gov/books/NBK26860/).

Textbooks tend to quote different numbers whatever you read, our recommended one (http://www.garlandscience.com/product/isbn/9780815341468) comes up to 10^16 for example. But the number itself isn't useful anyway, the point is that it's a lot.

Antibodies are simply proteins and like any other protein have a relatively short "life", so after clearing out an infection, they are not retained for long (most of them anyway). What the body keeps is memory cells which can produce a much more rapid response if they come in contact with the same pathogen again.
You could see it as a selective process: the body produces immune cells, one or more specific cells for nearly every potential antigen that might exist in the world (there are more steps involved of course but they are of little relevance here). Only those which are used at some point mature into memory cells.
Unfortunately, I just realised that I can't explain why the immune system goes through this selective process; producing cells equivalent to memory cells in the first place would make the immune response much stronger. One explanation I can think of for why the body produces naive cells first is that either a) their production or b) their maintenance is less costly.
The other explanation I could think of is that even immune cells in the periphery which have undergone the proofing mechanisms of immune cell development already, may not be perfect and target body cells every now and then - in that case it would be devastating if they would go all-out like a memory cell.
From my three explanations, only alternative b) would mean there could be a limitation to how many vaccinations our immune system can bear (if memory cells take more effort to maintain than naive cells, having too many of them may overstrain whatever systems maintain them). Otherwise I don't see any limiting factor for how many memory cells you can retain; except if their numbers become so large that your lymph nodes swell and that causes problems.
Edit note: I'm not aware of any research about that question and couldn't find anything either.

I just realised that I can't explain why the immune system goes through this selective process; producing cells equivalent to memory cells in the first place would make the immune response much stronger. It would also mean making an essentially infinite number of cells, since there are an infinite number of potential antigens in the universe. Memory cells are only produced when they see a target, thus proving that their antibody sequence has potential utility.

@iayork My thought process came more from the fact that our bodies do maintain exactly that large number of naive cells specific for potentially useless antigens, so I don't see much sense in an argument based on maintaining a lower number of cells. If that was the case, it would be even more desirable to have naive cells being fully potent already. This argument to me only makes sense if naive cells die relatively quickly.

There is an extensive literature on this subject; if you are "not aware of any research about that question and couldn't find anything either", I suggest you delete your answer since it's simply your idle speculation based on mis-informed guesswork.

I wouldn't be surprised if the literature situation has changed in 6 years. It seems at the time, idle speculation based on misinformed guesswork was the best I could offer without spending disproportionate amounts of time on literature search. Particularly if it's so extensive, I suggest you post a better answer and then we can upvote it.

so I work in a B-cell and Antibody Memory lab and the answer to your question is no. First of all, your body does make a B-cell against every possible target conceivable and if they don't bind to their target, they will die within a few weeks. If they do bind to their target however, they turn into long-lived plasma cells, which are stored in the bone marrow and constantly pump out antibodies, and memory cells which are pretty much the same as B-cells except they're way more powerful in their response and they live forever. So, yeah, don't hold back on the vaccines (but careful of any autistic side effects)

Memory does have limits; it's been shown that adding new specificities eventually does start to crowd out old specificities. The point at which this happens is unclear and probably has complex determinants, and the vaccine schedule doesn't come close to touching it. Hopefully your "autistic side effects" comment is a joke, but given that a non-scientific audience reads this I hope you'll edit it out.

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Are the intestinal microbiota substantially different within a diverticulum of the colon?
From the Wikipedia page for the vermiform appendix:

This proposal is based on a new understanding of how the immune system supports the growth of beneficial intestinal bacteria, in combination with many well-known features of the appendix, including its architecture, its location just below the normal one-way flow of food and germs in the large intestine, and its association with copious amounts of immune tissue. Research...showed that individuals without an appendix were four times more likely to have a recurrence of Clostridium difficile.

This quote seems to be implying that the appendix can act as a breeding ground for certain gut flora that are slightly less common (like C. difficile) and not as ubiquitous as E. coli or Enterobacter sp. The appendix could be seen as an ideal spot for this growth of microbial populations in the gut.
Given that, to a first approximation, anatomically, the appendix and a common diverticulum of the colon are both outcroppings of the large intestine: to what extent would a diverticulum also be able to support less common or more diverse flora, and how likely is this to be due to a difference in extracellular environment (pH, ion concentration) and how likely is it simply due to shape?

This is a very interesting question given the rising importance of the gut microbiome, as well as the American Gut and British Gut microbiome sequencing projects

The appendix is a type of true diverticulum of the colon, although it is one that is present in everyone (unless a surgeon has removed it). There are bacteria in the gut from the mouth all the way down to the anus, and the numbers and types of bacteria change along the length of the intestinal tract. A recent review from J. Ridlon published in the Journal of Lipid Research (2006) is available online and has documented these observations from a number of investigators. In that paper the bacterial species are described as changing as well as the relative abundances of bacteria which increases along the length of the intestinal tract. Figure 1 from that paper which is open access available from the link above is below.

I think its interesting that the wiki page you're citing states that individuals without an appendix were more likely to develop a recurrent C. diff infection. One could interpret that as they did on that site that somehow the appendix is repopulating the colon and making that individual more resistant to a repeat or "Recurrent" infection. However, I don't know of any studies that have directly tested that hypothesis.
In terms of whether or not the gut flora - aka "gut microbiota" - are significantly different in the appendix is possible, but I don't think anyone has identified that just yet. One of the problems with this would be that we don't routinely remove appendices unless they are infected/inflamed which intrinsically would alter the microbiome locally.
So, is it possible that the microbiome could be significantly different in the appendix itself compared to the cecum just a few centimeters away? The answer would be - potentially, but no one has been able to address that question to date.

These may help: http://www.ncbi.nlm.nih.gov/pubmed/25588621 ,  http://www.ncbi.nlm.nih.gov/pubmed/24883147 , http://www.ncbi.nlm.nih.gov/pubmed/24039352 , Though it appears that you may have to decide whom to believe.

I thought the 5% colectomy with appendix versus 10% without was pretty telling, but there are just too many uncontrolled variables with humans or knowledge on the microbiome yet to say definitively what the exact cause of anything actually is. Maybe they all went swimming in Griswold Springs....

@AMR nice links, but all retrospective (and biased)... an interesting hypothesis though... I agree with you, numbers look convincing - but only 388 patients for a multivariate logistic model... definitely not enough power in that paper to be reproducible - that reeks of irreproducibility to me.


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How does laughing gas (N₂O) work?
Laughing gas (N2O), well, makes people laugh.
How does just a gas make us do that, there has to be some hormones at work...
So, I wanted to know how this works?  What is the mechanism?

This information is all strictly for Entonox - a brand of analgesic gas comprising 50% Oxygen (O2) and 50% Nitrous Oxide (N2O), Laughing Gas.  This mixture is known as 'Gas and Air' and is in very common use.
The active ingredient in Entonox is of course the nitrous oxide, so the discussion of the mechanism below refers solely to the N2O as you asked for.
Nitrous oxide enters the blood by diffusion from the alveoli whilst it is being inhaled, but does not bind with haemoglobin.  It is fat soluble so quickly moves into cells, including synapse ends in the brain.  Because of the stability of the compound, N2O is not metabolised by the body so has its effect as that molecule, then is eliminated by diffusion out of the lungs once inhalation has ceased (taking roughly 2 minutes for on and offset).
According to the material that BOC pharmaceuticals provide, the exact mechanism of the analgesia is not fully understood.  It is known, however, to induce "inconsistent changes in the basal levels of thalamic nuclei".
N2O inhibits NMDA receptors in the brain whilst simultaneously encouraging the stimulation of the parasympathetic GABA receptors.  This eventually produces an anaesthetic effect.  It is also understood that N2O promotes the release of endogenous opioid neurotransmitters ('natural painkillers' e.g. endorphins) that specifically activate descending pain pathways.  This inhibits the transmission of pain.  In this way the analgesia provided by nitrous oxide is antinociceptive (literally pain reducing) rather than a generalised limbic depressor.
However, nitrous oxide also positively effects potassium ion channels too [ref] - reducing the chance of an action potential being generated in affected neurons.  Research into this area of the effects of N2O is ongoing.
Euphoria is a common side effect of N2O usage, hence the name laughing gas.  This is as part of wider emotional changes that can occur when nitrous oxide is being administered.  For example, some people instead of laughing become scared or in other cases extremely aggressive towards those nearby. The emotional excitement may result in depressive or manic behaviour even to the point of psychosis and hallucinations especially in those who have a preexisting vulnerability to mental illness. The precise mechanism for these disinhibiting is again not fully understood.
Whilst it seems a lot of the answers are missing, the course I'm taking this information from is available online at Discover Entonox - modules 8-10 have relevance to this question.  It's free to register and view the materials, they're all nicely narrated with diagrams etc.

great answer ... but il just wait to see if others post something more

This answer lacks references. References to many of the facts stated are available.

@WYSIWYG this is very true, I'll try and go through it when I have a bit of time


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Cucumber on the eyes
In many spas and salons I have seen people place a cold cucumber on their eyes.
 I think this might be for coolness, but why a cucumber?
And Is it actually for coolness or for something else (like lightening of dark circles, etc.)?

Cucumbers have an anti-inflammatory effect that reduces puffiness. The
  vegetable not only has a high water content, it but it's often stored
  in the refrigerator and comes out cold. This means that the water
  hydrates your skin, and the cool temperature decreases the flow of
  blood to the space around your eyes. Together, additional hydration
  and reduced blood flow can sooth the skin around your eyes and
  alleviate swelling

Source
Also it has silica.

...What does the silica do? It'd also be appreciated if your answer wasn't entirely a direct quote from the article.

@Lance made it cw.

@Mahmud can u please provide some more info?


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Cause of short sightedness/ far sightedness
I recently had gone for an eye test. The doctor told that short sightedness/ far sightedness is caused due to shrinking or expanding of the eye.
One thing i forgot o ask him was what causes that shrinking/expanding.
Can anyone explain it to me?

This answer explains what's going on in more detail, but I'd be interested to know the causes for the change in size too =)

The physical shape of the eye and lens are as @RoryM points out, the reason we become near/farsighted.
The most common cause of farsightedness is pretty well known.  The lens of the eye allows us to focus as a ring of muscles pulls outward and flattens the lens, allowing it to focus on closer objects.  As we get older the lens of the eye becomes stiffer and inflexible, which means that the muscles that pull on the lens can't flatten it as easily and focusing on nearby objects becomes difficult or impossible.  This is why we need to get bifocals or reading glasses as we are older.
The reasons for nearsightedness are 'natural changes in the shape of the eye'.
Mentioned briefly in the WebMD link above is that close work (e.g. reading, web surfing, phone videos, reading and reading, etc) tends to cause nearsightedness.
25% of adults in the US and 40% of adults in Asia are myopic and it does look as if there is a strong genetic component to myopia.  If neither parents have myopia, the incidence is only about 7%.
I'm probably going to get ding-ed for this, but I am going to offer alternative explanation, which makes good scientific sense to me, so hear me out.
This seems like a poor adaptive phenotype for humans who are otherwise so optimized for survival.  Why would we naturally lose our ability so young (often before the fifth grade)?  So many people who have myopia are so impaired that they can't find their way around their own house (or legally drive) without glasses/contacts/corrective surgery.
This is supported by studies which show that non industrial societies have almost no natural myopia compared to industrialized ones.  This is just one example reference, not a survey of all evidence.
Physiologically the explanation for myopia is this: in the relaxed state, the eye is focused at the horizon (infinity).  If one habitually focuses on a book or screen within 1-2 feet from your face, the muscles might well adapt to a set point that is closer than infinity.  This would make myopia an adaptive response to modern life.
Eye exercises are proposed as a way to correct myopia.  This is a bit controversial - some say they help, others say they do not. I would not be surprised that myopia developed in youth (8-15 y.o.) when the eye and body are developing can't be overcome by eye exercises when you are 25-30, but the jury is still out.
There are enough free descriptions of eye exercises out there that you don't really need to pay for them.  Getting young students outside to look around once in a while doesn't sound like a bad idea either, given this.
If you are going to down vote or complain, I would appreciate it if you please cite counter reasoning other than 'this is not a popular explanation'.

Why is that not a popular explanation? What is the popular explanation?

@Armatus  The popular explanation is that this is a geneticly related condition, which happens as a natural course of events.  Its mentioned in the post, but beyond the genetic studies which assume myopia is genetic, I cannot find much supporting evidence except that this has been the assumed reason for treating children with prescription glasses for hundreds of years (glasses have been produced since the 15th century).  Sorry if this sounds paranoid, but there simply isn't much motivation to support preventive care research at least in the US.


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What is the contribution of viruses to the evolution of mankind?
I'm interested in horizontal gene transfer in bacteria, viruses, and organisms such as Bdelloid Rotifers. I've just read in Carl Zimmer's 'A Planet of Viruses' the following passage:

As a host cell manufactures new viruses, it sometimes accidentally adds some of its own genes to them. The new viruses carry the genes of their hosts as they swim through the ocean, and they insert them, along with their own, into the genomes of their new hosts. By one estimate, viruses transfer a trillion trillion genes between host genomes in the ocean every year.

It's interesting to consider the scale of DNA-swapping that has occurred given the frequency by which it happens and the evolutionary timescale.
Are there any examples of genes in the human genome that we know were deposited by viruses that would have given an evolving human a physical/mental advantage? Where did they come from? What benefit did they provide?
I'm interested in genetic additions from non-human-ancestor species, rather than the transfer of genes that occurred as mutations from other humans.

The number of candidates that help humans cognitively is hotter in comparing humans to other primates. Though it happens trillions of times a year, its much more common with bacteria and fungi than animals, so the catalog of human vertical transfers is small.

The processes that control the germline of metazoans (multicellular animals) are highly regulated compared to single cell bacteria and eukaryotes as well as plants.
At this point there are no clear stories of gene transfer into a complex animal, though there are some for plants:
"animals and fungi seem to be largely unaffected, with a few exceptions, while lateral gene transfer frequently occurs in protists with phagotrophic lifestyles, possibly with rates comparable to prokaryotic organisms."
Bacteria fungi and plants are more permissive and more susceptible to gene transfer and it probably is more important to their evolutionary path.
Its been estimated that as much as eight percent of the human genome has been affected by viral integration.  But viral genomes are highly selected against carrying non essential material - other genes rarely come along for the ride it seems.  What is probably more influential is that viral insertions could participate in rewiring the regulatory network of animal cells, not adding genes, but modifying the conditions under which they are active.

Human endogenous retroviruses (HERVs) have been an interesting (and expanding) topic of research in evolutionary biology and medicine. A retrovirus has an RNA genome in the virus particle, and integrates with the host cell's DNA upon infection to hijack the transcription/translation machinery and produce copies of itself. For this reason, it is not possible to "cure" a cell of a retroviral infection; instead all of the infected cells must be destroyed or commit suicide through apoptosis, also known as programmed cell death. Common examples of retroviruses include HIV (causative agent of AIDS), HTLV (human T-cell leukemia virus), and the Hepatitis B virus.
Viral infections are most common in somatic cells, where any change in the DNA sequence is not passed along to the next generation. However, any retroviral infection in germ cells (eggs, sperm, and the progenitor cells that make them) could be passed on to the next generation, and over time spread throughout a population. Some HERV fragments are apparently completely inactive (at least as far as we are able to tell currently), and are a possible source for some of the so-called "junk" or non-coding non-regulatory DNA that makes up a significant part of our genome - one estimate claims that 8% of our genetic material is of retroviral origin. Other HERVs have been implicated in various pathological conditions, including multiple sclerosis.
I'm not sure that any human genes have been found that were picked up by a virus, stayed with it for a time (and potentially mutated), then was reinserted back into the human genome, if that's what you're asking. There are certainly many cases of genes and gene fragments (coding regions, promotors, enhancers, etc.) being moved around as a result of viral integration/splicing. http://en.wikipedia.org/wiki/Endogenous_retrovirus#Genome_Evolution is a large, rather well-written section with numerous links to the primary literature showing how our genome has been altered over the years by HERVs.


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What animals stop other members of their species from mating and why?
(In particular primates)
I know chimps do. Powerful alpha males chimp would beat up omega males that they caught mating.
I know gorillas do. Powerful alpha males gorillas would beat up omega males that they caught mating.
I know humans do. Politically powerful alpha males would jail or stone weaker omega "peasant" humans that they caught mating.
I know bonobo doesn't.
What about other primates/animals?
So what's the difference and why?
Reference:

The alpha animals are given preference to be the first to eat and the
  first to mate; among some species they are the only animals in the
  pack allowed to mate. Other animals in the community are usually
  killed or ousted if they violate this rule.

http://en.wikipedia.org/wiki/Alpha_%28ethology%29
How do preventing and punishing others from mate improve ones' own gene pool survival? Are there similarity between primates (including humans) in this regard?

You want list of animals that do this? if yes, then this is off topic.

@Ashu "So what's the difference and why?"

@RoryM as far as i know "list" questions are considered off topic on SE

Do you mean those that are caught mating with a desirable female are beaten up, or just in general?  As always, references would be great for these assertions.

I'd take issue with "just like humans."

You mean we're different? Very well, I remove just like humans phrase.
let me come up with references. Basically chimps would beat up weaker chimps. Basically chimps and gorillas cannot mate unless "allowed" by the ruling class.

@Ashu yep, they'd be considered Non-Constructive rather than off-topic but still closed, however this question is asking for the reasons behind the difference as shown in the quote I took out :-)

what does non-constructive mean anyway?

Possibly it could happen in mice through the Bruce effect, although its real advantage is quite debated.

@JimThio pretty much everything in this section of the FAQ =D

Thanks. I am just really puzzled. All those acts that are claimed to be unselfish are definitely selfish, but how?

As the comments suggest, I think a little basic reading so you understand the definitions involved here might be appropriate.  The questions are a bit anthocentric, and I think that's why folks with a bit more biological culture might be concerned about the answers.
Alpha type structures can be found in all sorts of animals.  Sperm competition, where many males simply mate with the female and let the sperm work it out are also v common from snakes to mice to primates.
Its hard to say without you asking a more specific question, but the essential question is whether the competition occurs between the animals themselves or between the intermixed sperm of the males inside the female.  If that sounds gross, that's a typical reaction if you are not a monkey, snake, duck or mouse to name a few.  Different species choose different social roles in mating and for reasons that may be difficult to divine.
For animals in an alpha troop modality, the alpha male will eventually get older or weaker and the younger ones will have their chance to mate.  There is always tomorrow.  That's my very brief answer.
It might be worthwhile to take some time to read some about this - a page of response to your questions is not going to really answer your questions.  (I say this having answered several of them :).  I would recommend "The woman that never evolved" by Sarah Hrdy.  As a feminist in the 70s Hrdy decided to do a survey of primate male/female roles in mating, to try understand how human men and women became who they are (and who has not wondered this?).  This book will give you an idea of how so many different animals have come to different roles and possibly why.
Since I have a little time today, I'm adding a couple of tangential references:  Mice sperm have responded to sperm competition so much by evolving hooks on their heads and chain up together and swim together which enhances the chances of paternity.  Ducks are quite different.  they have a lot of forced copulation, but female choice of mate is still quite influential.  Duck vaginas are very complicated, with corkscrews and dead ends to make it difficult to copulate without 'consent'.

@JimThio ...just a thought.   Feel free to contact me directly if you wish to chat about any reading.

Thanks Shigeta. So bonobo do not kill each other because their sperms fight (bravely) and humans and chimps kill, stone, and seize each others' car in civil forfeiture because their balls are much smaller and they, rather the sperms have to fight for more mates. That makes a lot of sense. Why are people concerned about the answers. Shouldn't they be exited to understand humans better? Don't we want to understand our species as well as we understand chimps.

@JimThio I'm sure it goes deeper than this, but its an okay short answer.  A common pattern for primates to live with nonexclusive mating, and just let it all come out in the wash so to speak.

@JimThio  Biology's such a sensitive issue as there are so many social ramifications.  I think the commenters just want to make sure that this is all kept on a scientific level.  Of course the only answer is for everyone to learn as much as they can about how biology really works.  Its very easy to personify these answers, but no worries really as far as I'm concerned.


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Why animals can move and plants cannot in general?
To clarify, I think the answer should be able to explain:

What are animals?
What are plants?
What's the difference between animals and plants (How do biologists differentiate them, if they differentiate them by moving ability of course it's simple, but we know they don't)?
How do those differences affect their evolutionary paths so that most animals can move around and most plants cannot? I know there are exceptions, but that's just the exceptions that show the rule.

Animals and plants are both classified as Eukaryotes, and as such can form large, complex, multi-cellular organisms. There are several major differences at the cellular level that distinguish the 2 Kingdoms (Animalia and Plantae). Without getting technical, the most crucial difference in relation to your question is that plants contain chlorophyll, and as such can generate their own food using sunlight.
This is very important when you consider that plants (by definition, those Eukaryotes that contain chlorophyll) have therefore evolved to be very efficient at converting sunlight to 'energy', whereas animals have evolved without this option and have to eat what food they need. So they have instead evolved mechanisms that allow them to forage, or even to hunt, for their food.
At some point, a unicellular organism incorporated chlorophyll, leading to multicellular plants in the course of evolution. The ancestor of animals evolved independently from the last common ancestor of plants and animals. Therefore, plants and animals are quite diverged, e.g. in mating 'rituals' (in plants this involves flowers and seeds - whereas in animals there are mating and gestation periods), and systemic changes, such as the immune system and the circulatory system (these are generally much more complex in animals than plants). All of which has stemmed from the difference in evolutionary pressures applied by the choice of food-source.
As you have pointed out, there are exceptions to all rules, so not all plants have chlorophyll, but as a rule it is the case! (Wikipedia: "Some plants are parasitic and may not produce normal amounts of chlorophyll or photosynthesize.").

Also, plants get their nutrients via their roots, so it is quite handy for them to stay in the ground! :)

Awesome answer. Not all plants have chlorophyll? I guess I'll look at wikipedia then.

So what's exactly biologist use to differentiate plants and animals? Chlorophyll?

@Jim Thio: think of red algae for instance

@nico the rhodophyta (red algae) all have chlorophyll, they are red because they also have red accessory pigments. An example of a plant lacking chlorophyll is the parasitic Hydnora africana

@Richard Smith: I was pretty sure there were deep sea red algae without chlorophyll, but maybe I just remember wrongly

@JimThio generally plants and animals look sufficiently different that biologists don't need to find "the one trait" that differentiates them - there are usually many differences, different cell structures, different molecules (like cellulose, chitin, glycogen...)... But nowadays there is a very simple way of differentiating animals from plants on the off-chance it isn't obvious from their appearance: DNA. The plant and animal kingdoms have diverged long enough ago that they have very different DNA. It would also help recognize freakish combinations or previously-undiscovered kingdoms.

Plants are multicellular organisms that utilize diffuse inorganic molecules (CO2, NO3, etc...) for energy and growth and thus they have evolved anatomical features that maximize the efficient concentration of these molecules (i. e., the root - shoot).
Animals are multicellular organisms that utilize concentrations of organic molecules for energy and growth (i.e., food) and thus they have evolved anatomical features that maximize the efficient harvest of these molecules.  Note that not all animals move.  There are many sessile filter feeders.


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Are there other mechanisms for mutation besides imperfect DNA replication?
I was reading http://www.askamathematician.com/2012/05/q-is-quantum-randomness-ever-large-enough-to-be-noticed/ and saw:

[...] the evolution of entire species can be changed by a single
  mistake in the replication of a strand of DNA (this is one mechanism
  for mutation).

... implying other mechanisms for mutation exist. Do they?

Absolutely. Ionizing (X-rays, neutrons, electrons, heavy ions) and non-ionizing radiation (UV), chemicals, etc. are able to induce DNA Damage, which is then imperfectly repaired. So it's not an issue of imperfect replication, but also of imperfect damage repair.

DNA methylation over CpG doublets can cause mutation since 5mC can undergo spontaneous deamination and covert to a thymine.


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How do susceptible organisms prevent parasites from overcoming resistance?
Bt corn is genetically modified to kill borers, but "regulations require farmers to plant conventional varieties as well, which is intended to stop the borers becoming resistant."
-Source
How do susceptible organisms prevent parasites from overcoming host resistance?

In an environment where all plants are resistant to certain parasites, a rare breed which has a mechanism against this resistance has free play - lots of food and no competition. However, in plants which do not have the resistance, this rare parasite breed may be at a disadvantage compared to parasites who do not have the mechanism against that resistance (even if only because they do not waste energy on a defensive mechanism they don't need).
By mixing resistant and unresistant plants, it is probably possible to maintain high enough a competition of parasites without that defensive mechanism to prevent the ones with the mechanism from developing. It's natural selection at work :)


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Do somatic cells alter their own nucleotide sequence?
I seem to remember reading that embryonic cells will frequently replicate the section of their genome containing rDNA by splicing in duplicate genes. The cells use this to produce ribosomes at a rate which would be impossible with the DNA present in cells from full-grown organisms. Is this real? Are there other examples of cells altering their their own nucleotide sequence?

Would you consider transposons as a cell altering 'its own DNA'?

@Armatus: that would be a good example I would say. An answer explaining Barbara McClintock experiments would be great for instance!

@Armatus How often does this happen though? Transposons are usually silenced. In fact, it’s a problem if they aren’t.

@Konrad Rudolph: happens quite often in maize...

Cells have many tandem repeats of the rDNA genes (in part to produce many transcripts simultaneously), but I believe the number of copies is generally set by inheritance, although because they are tandem repeats they are subject to copy number variation that occasionally occurs in such an arrangement.

One case where human cells alter their DNA occurs in the immune system.  In the early stages of the continuing production of B-cells and T-cells, the developing cell recombines (shuffles) genes in a particular DNA region which codes for what are called Variable, Diverse, and Joining gene segments.  This shuffling is called somatic recombination or V(D)J recombination.  This rearrangement gives the cell a genetic template for a random instance out of a enormous set of possible antigen-recognition proteins used by the immune system to recognize foreign molecules (in order to fight infection).

yes that's an important one!

I'm assuming you mean, physically changing the DNA polymer.
The answer is yes.  And how they do this depends upon which cells they are and what they are supposed to do.   A partial list:
In multicellular animals, cells DNA 'ages' where the telomeres, sequences at the ends of the chromosomes, will be degrade and shorten.  This relates to how many times the cells have divided and acts as a sort of clock for development and probably also ageing.  Telomere degradation does not happen in all cells - the germline cells are not modified of course.  This is one of the probable reasons that cloning animals sometimes doesn't make perfect copies.
Cells will also add Methyl groups to the DNA nucleotides.  Methylation is triggered when environmental or developmental conditions.  The textbook example for methylation is the markers on the DNA of children whose parents have experienced starvation conditions.  Methylation can disappear in subsequent generations.  It also happens to cells in the brain which mark different stages in their brain development.
Meiosis, When sexual mating happens, the cells that make the sperm and eggs shuffle the pairs of chromosomes, editing so that about half of the resulting single set of chromosomes contain half of each parent's chromosomes.
Then, there is DNA repair. When radiation or chemicals breaks the chromosome, there are enzymes that repair them. Usually they read the opposite strand of the DNA to see how the repair happens. Sometimes the DNA is not reparable from the strand, and the result is not the same as the DNA the cell started with.
Short repeat DNA seem to show up in chromosomes - segments of short repeats can change length (AGGAGGAGGAGGAGT -> AGGAGGAGGAGGAGGAGGAGTAGGAGG etc). I'm not sure how this happens, but its different between identical twins.  It also probably happens to cells in different parts of your body.
What else have I forgotten everyone?
There are also enzymes that coil the DNA up onto nucleosomes, but don't really make any changes, but we won't count that.

He's referring to some sort of selective multiplication of rDNA - have you heard of anything like that? Apart from viruses (and DNA fragments what probably originally were viruses) I haven't heard of such gene-specific replication.

there are segmental duplications too.  I know of no bias to rDNA, but that isn't my forte. There are many more copies of LINEs and SINEs and viruses in the human genome than rDNA.

This answer has shown that my question wasn't precise enough. I've fixed it now. I'm asking about cells altering their own nucleotide sequence, not so much turning on / off genes. Telomeres are a good example of this, though.

There aren't too many examples of this happening.  By nature cells tend to avoid editing their DNA.  Germline editing is almost never done. Meiosis is the largest DNA edit imaginable.  two sets of chromosomes go in, only one comes out.


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What happens to colloidal particles in a liquid medium? And how to stabilize it?

Definition

Colloid is a dispresion of small particles of one material in another.

Definition 2 (Wikipedia)

A colloidal system consists of two separate phases: a dispersed phase (or internal phase) and a continuous phase (or dispersion medium) in which the colloid is dispersed. A colloidal system may be solid, liquid, or gas.

I am trying to answer problem 2:

Question
"Colloidal particles: What are colloidal systems, give an example, what happens to colloidal particles in a liquid medium. How to stabilize colloidal systems in a liquid medium."

My lecture slides mention this about gel: "a continuous network extending throughout the sample formed by association of colloidal particles or molecules in a liquid", "formed in concentrated polymer solutions" and "formed by association of sol-gel particles". Next lecture slides is about "liquid crystals", now I am confused -- not sure whether gel or "liquid crystals" is something to look here.

...I think I solved this but I feel it can be useful for future random walkers and do not hesitate to comment whether I have misunderstood something or there is something to add about my trial, is it right?

"Colloidal particles: What are colloidal systems, give an example,--"

Milk, bear foam, paste, blood, ---

"what happens to colloidal particles in a liquid medium."

I understand the q as solid in liquid so a gel. Examples about gel are "agar, gelatin, jelly and opal" according to my lecture slides. The electrostatic forces are in some sort of middle phase: not enough to repulse into liquid form but not strong enough to form liquid either.

"How to stabilize colloidal systems in a liquid medium."

Wikipedia about stability (here)

"The stability of a colloidal system is the capability of the system
    to remain as it is. Stability is hindered by aggregation and by
    sedimentation phenomena, that determine phase separation."

Now different things to consider are:

Electrostatic stabilization

"In a stable colloid, mass of a dispersed phase is so low that its buoyancy or kinetic energy is too weak to overcome the electrostatic
    repulsion between charged layers of the dispersing phase."

steric stabilization

"particles in polymers which prevents the particle to get close in the range of attractive forces."


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How to manufacture different sized micelles in nano -scale?
I am trying to answer q5:

"How can you manufacture micelles in A) nanometerer -scale B) and in ten nanometer -scale?"
My Thinking

Observations and some thinking

Oil in water forms a micelle here, not making it soluble.
Whey protein in Water forms a micelle or is this due to other reason? Protein folding with hydrophopic-tailed-and-hydrophilic-headed-particels? Is this micelle or not?

Required Vocabulary about one answer

what is IVC?
PLoS?
"[E]xtrusion step" = some sort of burst?
PCR=Polymerase chain reaction here.
monodisperse = A collection of objects that "have the same size, shape, or mass." (source
    here).

On your other question, you have listed your attempt at the answer.  Please expand the information you have started to collect here within the question to show what you have tried.

Seems to me that "formation" is a more appropriate term.

...I wish I could read the biology articles also at home, irritating...have to try some sort "ssh -XY" -thing to get those articles there, everything payware stuff.

A key factor that determines the radii of a micelle is the critical micelle concentration. The other is the the hydrophobicity of the micelles which can be measured using the contact angle. A lipid nanoparticle has a minimum size on the order of 50 nm due to the surface tension of the lipid bilayer. However, micelles can be much smaller.
As for the creation of uniform nanoparticles, I am going to claim that what I say next can be in no way a reasonable answer to a HW problem. Why? Because the information is hidden in some obscure PLoS paper (Stapleton and Swartz) with 7 citations using IVC. Typically, micelles created for emulsion-PCR are created by vigorous mixing and followed by an extrusion step. However, this creates a polydisperse droplets. Alternatively, if you were to use a microfluidic device, then more monodispersed droplets can be formed. The control of droplet size can be achieved by varying the flow rates of the aqueous phase and the oil phase as well as changing the surfactant.

...I cannot understand the pictures. Could you somehow explain what is happening there? I added some open issues to the q to decipher this.


text:
Gametes of two different species
I always wondered why gametes from two different species dont fuse together to form an offspring. eg a donkey (sperm) and a female dog (egg)
I know this is not possible but I'm just curious.

Circular reasoning warning: because that’s how species are defined (i.e. two individuals belong to different species if they cannot produce viable, fertile offspring). Now, this definition breaks down in some cases but it’s still the common definition.

As an exception to this rule, you may want to read about the amazon molly or the fire ants. You'll find more info about these species and references in this answer

Daniel's answer excellently explains the issue in an understandable fashion, though you may have been looking for a more cell biological approach.
According to Immunological aspects of sperm receptors on the zona pellucida of mammalian eggs, 1976, Dunbar & Shivers, the egg cell has a receptor construction which is necessary for the sperm to attach. If the receptor is too different from what the sperm is built for (which will be the case in different species), it will not be able to attach and fertilise the egg.

+1 Indeed, I may have overlooked the point of the question, if indeed fusion was the keyword. Excellent answer in any case.

The biological environment in every cell and tissue of your body is an extremely complex, tightly controlled system. There are tens of thousands of genes in a typical eukaryotic genome, and depending on tissue types and environmental conditions, these genes are turned on and off in a very controlled manner. There is regulation at every point in the flow of genetic information: nucleosome disruption to expose DNA; RNA transcription from the DNA; protein translation from the RNA; and in some cases, additional modifications of proteins or intermediate mRNAs. At early stages in development, regulation of RNA and protein levels is even more crucial than, say, when an organism is fully developed and healthy.
All living organisms share some basic building blocks--DNA, RNA, and proteins work pretty much the same in all of life (there are a few rare variations of the genetic code but the basic premise is identical). However, the way that specific genes, transcripts, and proteins work together to sustain life varies widely between different organisms.
For a very rough analogy, imagine you want to bake a batch of cookies. Then consider the three following scenarios.

You look at two different recipes for chocolate chip cookies. They will have some slight differences, but they will share a lot in common. If you put the ingredients for both recipes in one bowl, it's likely you can still come up with some pretty good chocolate chip cookies in the end.
You look at two different recipes: one for chocolate chip cookies, and one for chocolate muffins. There will be some big differences in these recipes, but combining all the ingredients and baking, you still might be able to come up with something edible (and maybe even tasty).
You look at two different recipes: one for chocolate chip cookies, and one for French onion soup. If you combine the ingredients from these recipes and try to cook or bake them, there is no way you will come up with something that anyone would want to eat.

The first example we can relate to two individuals of the same species mating. Of course there is natural variation in the population, but this doesn't typically lead to lethality during development. The second example we can relate to individuals of two related species (such as a horse and a donkey). Sometimes these matings can produce viable offspring, although these offspring are often sterile. The third example we can relate to individuals of two very divergent species (such as donkey and dog in your original question). The biological systems inside donkeys are just so different from those inside dogs that this mating cannot produce a viable offspring.
Admittedly this is a rough analogy, but hopefully is sheds some light on the issue.

+1 because i found it quiet informative but i found Armatus' answer better answering the question. Thanks

No worries, I spoke very generally and he spoke very specifically. He deserves it!

Often, they do fuse together but the chromosome pairing is not precise enough to guarantee faithful cell division without loss of genetic material. Consider for example a simple inversion of one large part of a chromosome. In a closely related species that does not have this inversion, either the inverted part pairs or the non-inverted ends pair, but never the whole chromosome. That leads to strand-breaks and loss of large amounts of genetic material. That's an easy event for speciation, since it does not disrupt much. Only the ends where the inverted piece joins has two disruption. So, maximally two genes might be broken, but the chromosomes modified in this way won't pair.

I can answer this for mammals.  The mammalian oocyte (egg) is surrounded by a layer called the zona pellucida. There are three well-characterized proteins in this layer, called ZP1, ZP2 and ZP3 (not very imaginative, I know).  I don't know much about ZP1 but ZP2 and ZP3 are involved in fertilization.  The sperm's outer surface has receptors for ZP2 and ZP3.  Part of the 'zona reaction') to prevent fertilization by more than one sperm) involves destruction of these sperm receptors.  The ZP proteins are species-specific, meaning that ZP receptors on, say, human sperm, would not recognize ZP2, ZP3 on the zona of hamster eggs.
There is a test that was used in fertility assessments of human sperm, checking their ability to fertilize an egg.  Human eggs are kind of difficult to come by, so they developed a test based on the ability of a human patient's sperm to fertilize a hamster egg.  For that to work, they had to first remove the zona from the hamster egg, so sperm had direct access to the egg membrane.
This might not be freely available, but here is a link to an article:
https://humrep.oxfordjournals.org/content/13/3/624.full.pdf
There is also a brief wikipedia page about this test.


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What factors are known to affect evolution?
My understanding is that the possible mechanisms of evolution are:

Environmental changes
Cultural/mating preferences
Population Immigration
Genetic Mutation

Am I missing anything? I've heard that population shifts within a existing populaces will effect evolution, but imagining the most simplicity scenario, it's hard to see why the would make a difference.

It's not really clear what 'factors of evolution' you are referring to... there are many factors that play a role in evolution - availability of nutrients, availability of reproductive partners, space,... Could you clarify a bit what kind of factors you mean?

@Armatus: "availability of nutrients" would be an environmental change. I'm not sure about "availability of reproductive partners", though I believe that if the availability partners was stable, it would not be a factor, and I already stated in the question that it is unclear to me if "population shifts" beyond population immigration play any significant role.

@Armatus: My list is based on this video, the "Five Fingers of Evolution" - though I've edited it's meaning to make more sense to me; for example, "Environmental changes" I believe are called adaption, which to me is less clear the saying the changes are a result of the environment changing. If it's still not clear what I mean, please attempt to be more description on were exactly things are clear, and unclear. Thanks!

I'll have an attempt at an answer in a moment :)

If I understand right, it may be good to change your question to "What mechanisms can cause evolution" and also quote that definition - that evolution is merely any change in the gene pool. On the other hand, you are answering your own question - it's all in that clip which you linked. Maybe you could include that in the question and more specifically ask something you don't understand in the video?

+1 @Armatus: Yes, mechanisms is more clear, I've updated the question. Also, I agree that evolution is genetic change, though currently genetic change unless previously tied to a known trait is meaningless.

@Armatus: As for the video, I found the use of 'mating' to mean non-genetic bias, not genetic, which to mean upon reflection seems a likely mechanism, and would be it's own; meaning there's a delay in the genetic mating bias generational stabilization of a genetic mating bias. Population shift role in evolution appear unimportant if selection within the shift is random; non-random shifts would another mechanism.

I've changed the question title slightly from active to passive phrasing. The reason being is that not all of these directly affect changes in the gene pool (ie, environmental factors). Furthermore, evolution can be semantically argued to have differing definitions.

+1 @leonardo: Thanks, so are you saying environmental changes are not the mechanisms of change when the only change done within lab setting is within the environmental factors, and a minority genetic trait within the genome of a populous shifts due to the change? If so, then what is the mechanism in those circumstances? As for the meaning of evolution, "Evolution is any change across successive generations in the inherited characteristics of biological populations."

@blunders - I would put that definition in your question so that we have a standard definition (it can be mis-used in popular speech). I'm saying that generally, environmental factors are not physically causing a change to the genetic material (except for mutagens, carcinogens, teratogens) and the organism's adaptation to this change is what is causing heritable changes to its genetic material. Environmental factors change dynamically and passively, but it is the organism that is dynamically reacting. You wouldn't say that weather or food edited your genome. A small point of semantics.

@leonardo: Thanks, I've updated the question attempt to pull content from the comments into the body of the question. So, yes, in fact I would say that environmental factors "edited" the genome of our species, and most species for that matter. Species don't make up genes to adapt to change, genetic traits either becomes more or less used. Just because environmental change dynamically and passively, does not mean environmental changes are not the one to the mechanisms of change in my opinion.

The first version of the question was vastly superior. In the current form, it’s much too long, needlessly detailed, contains errors, and no longer is a question. I’d suggest reverting to something much closer to the original form.

@blunders - You're sort of right. Let's take climate as an example. The organism certainly senses the climate. Among the population, there are genetic variations that make up the collective gene pool. The error in your logic is assuming that there exists a gene and that provides adaptation to the climate, but that it is currently "switched off", and when a specific climate is sensed, turns the gene "on". This is incorrect because it is impossible for the gene pool to hold potentially adaptive genes for all scenarios of climate.

The climate is a possible stimulus, to which invidual species, with their individual genetic differences, stand a better or worse chance to exist in that weather. The better suited organisms (better adapted) survive and bias the gene pool with their offspring. These changes build until new features or traits are acquired. The important thing here is that climate is independent of the organism, and is independent of the gene pool, but it provides a stimulus to which the organism can respond.

why would you find out more here than on wikipedia, which has 1000 lines on it, with all references.

Evolution is defined as a change in the allele frequency of population through time.  The Hardy-Weinberg model predicts that the allele frequency of a population will not change (i.e., evolution will not occur) if the following conditions are met:

no natural or sexual selection
no gene flow (immigration or emigration from the population)
no mutatation
no genetic drift (changes in allele frequency due to random events)

So we can conclude that if any of the above conditions are not met then there is a change in allele frequency and thus evolution, and thus that factor is the cause of evolution.

+1 @DQdlM: Awesome! Knowing now that Hardy-Weinberg appears to be the source of the logic was a huge help, and you're answers was within my range of plain-English. Taking a step back from "bio-lingo", would it be correct to say that the "inputs" for natural selection are only mutation(s) and/or statistically significant changes in the way the organism interacts with the environment? Also, assuming mating was completely random, why would emigration affect evolution? Meaning it would appear that other conditional changes would be the source of the evolutionary change, not emigration. Thanks!

@blunders natural selection requires heritable variation and a survival or reproductive advantage based on that variation.  The ultimate source of all variation is mutation but note that the thing that evolves is a population, so you can change the allele frequency by having individuals enter or leave a population.  This would be an evolutionary event unto itself but would also potentially add more heritable variation that natural selection could act upon.

The answer is actually partially wrong. I agree that under all of the above conditions, no change in allele frequency can occur. However, this is true even if you drop the last condition (random mating). In absence of random mating (and in presence of the other conditions), genotype frequencies may change through time (and differ from Hardy-Weinberg's predictions) but allele frequencies would still remain constant.

@Remi.b thanks for your comments. I agree with your feedback so I have edited the answer in response.   Thanks.

You have to leave random mating. First, releasing random mating will change genotype frequencies SO it is evolution. eg : aa = blue Aa=green AA=brown, if not random mating, this biological feature will change its frequency, so population evolved. Moreover, you think human/mammals but many species also reproduce using clonality (so no "mating") which change again the evolution of both genotype and allele frequency. By the way, "random mating" includes 2 factors of evolution: reproduction modes (clonal vs sexual) and mating mode (selfing, inbreeding, panmixia, outcrossing).

Please, delete your edit and reintegrate "random mating" as it is the major factor to explain evolution (eg  http://ebd10.ebd.csic.es/pdfs/Duminil_etal_2007_AmerNat.pdf  ; Charlesworth (2003, p.  1052):  “The  mating  system  is  probably  among  the factors  with  major  effects  on  variability,  clear  enough  to be discernible even in the presence of other factors.”

I downvoted for the removal of random mating. As sol noted, it is critical to the understanding of evolutionary change in a population.

@Bugmo I already had "no sexual selection" in the answer so the whole random mating issue is covered.  Nonetheless, it does appear to have caused confusion so, I agree it is best removed.

In the real world this boils down to does it have heritable characteristics and does it reproduce? If yes to both it will evolve. good answer though

@KennyPeanuts You might want to add something like If one were to use another definition of evolution (see [How to define “evolution”?](https://biology.stackexchange.com/questions/11400/how-to-define-evolution) for a discussion), of course the below list of mechanisms that are driving evolution would be different. to deal with users that are bothered by the quite standard definition you're using. +1

What is evolution?
The first step is to remind ourself of the definition of the term "evolution". Evolution is most often defined as "any change in allele frequency in a population". I will assume that you are willing to use this standard definition.
If one were to use another definition of evolution (see How to define “evolution”? for a discussion), of course the below list of mechanisms that are driving evolution would be different.
Forces that drive evolution
Categorizing the processes that affect allele frequencies might be subject to issues of semantics. Without going into the details, we generally recognize 4 forces that drives evolution

Natural selection

Natural selection refers to the deterministic change in allele frequency due to a differential in fitness among different genotypes. Sexual selection and artificial selection are typically considered as part of natural selection (although that may vary from author to author)

Genetic Drift

Genetic Drift refers to the stochastic sampling process of individuals

Mutations

A mutation refers to any spontaneous change (substitution, indel, chromosome duplication, etc...) in an individual's genotype.

Gene flow  (aka. migration)

Gene flow refers to the transfer (migration) of DNA sequences among populations.

KennyPeanuts's answer, random mating and hardy-weinberg equilibrium
In his answer, @KennyPeanuts also talk about random mating. Random mating refers to the condition where the probability of two individuals to mate depends only on their respective fitness. Many people phrase random mating as absence of mate choice but it actually refers to the absence of variation for mate choice in the population.
Hardy-Weinberg states that under the above four conditions and random mating, then the frequency of the genotype that has the allele $i$ derived from the mother and the allele $j$ derived from the father, where $x_i$ and $x_j$ are the frequency of these alleles is $\cdot x_i \cdot x_j$. This means that for a bi-allelic locus, the allele frequency of the genotypes AA, AB, BA and BB are $x^2$, $x(1-x)$, $x(1-x)$ and $(1-x)^2$, respectively where $x$ is the frequency of the allele A. For the heterozygotes (AB and BA), we often care little which of the two allele is inherited by the mother and which is inherited by the father (assuming there are genders) and we therefore call AB both AB and BA genotypes (which can eventually be confusing). As such, the frequency of the AB genotype is $2 x(1-x)$.
The condition of random mating ensure that there is no deviation of genotype frequencies from the Hardy-Weinberg's expectations and it ensure that there is no change in genotype frequencies from the first to the second generation considered (after one generation, the equilibrium genotype frequency is immediately reached). Random mating is therefore not a condition for evolution to not occur.

Evolution: change in the frequency, not of "allele frequency" but of heritable biological feature,

The usual so called "population genetics definition" of evolution refer to change in allele frequency. It is a very standard definition. You might want to put emphasis on the phenotypic trait that which variance is at least caused by genetic variance but the detail definition gets a little trickier.

"Science sans conscience n’est que ruine de l’âme" Rabelais (Pantagruel) and “The enemy is the gramophone mind, whether or not one agrees with the record that is being played at the moment.” Orwell (Essays)...So, you might have one locus, two alleles A & B, let's say f(A)=0.5, f(B)=0.5, if at generation t, you have all diploid (but works with polyploid also) individuals [AA] and [BB], the next generation t+1, all individuals are all [AB], you HAVE evolution while "allele frequencies" have not changed. You get it? In popgen, mass thinks in alleles but as Ewens 2004 tells, genotypes only matter

...and that's one of the multiple point you miss by saying "Evolution = change in ALLELE frequencies", so replace by "change in heritable trait (can be genotype, phenotype) frequencies". Pop gen comes from information sciences. This definition includes also heritable but non mendelian traits, which changes in frequencies are also evolution.

I am repeating a very standard definition. I am well aware of its limitations. A definition is completely arbitrary and it may or may not fit the intuition. You are free to use the definition you want. In no way am I claiming that this definition is the only, pure and perfect definition. It is just a simple and very standard one and I think that when someone asks what causes X everyone would expect the person answering to use the standard definition of X. Your citations of Rabelais and Orwell are really off-topic btw.

Note that your definition is slightly unclear as many of the considered traits take continuous values and therefore, one cannot consider a frequency without making arbitrary grouping of those values. Also, your definition depends upon the concept of heritability and the heritability of trait themselves vary through time, among environments and among populations. Also, the (sometimes arbitrary) grouping of individuals into populations will affect heritability of traits.

Your definition will likely run into problems when considering things like reaction norm (and reaction norm of the slope of the reaction norm), developmental noise, niche construction too. So do not think you found the holly grail with your definition!

Don't be gripped in the vice of an excessively rigid definition which ultimately will make the concept open to challenge. Repeating a definition because it is "standard" is not scientific but dogmatic. Moreover, a parsimony approach tells us that there is no need for this term added: "allele" to this definition, if not to enclose the thought. Finally, where did you see that this definition is standard? I quote you a reference book in gen pop that says the opposite, what are your sources? Dear Black knighnt, read more books and original articles before throwing Holy Hand-Grenade of Antioch.

Let's not extend this discussion too much. I have justified the use of this definition, not because it matches better the intuition than other definitions but for the fact that it is what people usually mean. I have also highlighted why your definition was in no way better. I don't think there is much interest to keep arguing on it, esp. if you start calling me "black knight" or naively accuse me of not reading many original articles in the field.

If you want to discuss the definition of evolution you should have a look at the post How to define “evolution”?. I will likely not answer to further comments of the kind here.


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Is the eukaryotic nucleus composed of a single or double membrane?
I know that it is usually considered a double membrane like those surrounding mitochondria and chloroplasts, but I read a review that stated "according to topological details it is actually a single lipid bilayer; this distinction is important"1.
Could anyone please explain how this is true and why the distinction is important? And why this topological analysis wouldn't apply to other membranous structures in the cell?

The nucleus is topologically single membrane but functionally, and as visualized, double membrane.  Naturally, this is a bit confusing.
First consider the mitochondria and plastids.  One of these organelles has two entirely separate lipid bilayers, one of which is nested inside the other.  If you start inside the organelle and draw a line to an external point, the line will pass through two lipid bilayers (assume there are no membrane folds to be encountered), first through the nested one and then through the entirely separate outer bilayer.
The nucleus at a gross level appears to be structured similarly.  A line from the interior to the exterior will usually pass through two lipid bilayers, one that is the inner wall of the nucleus, then through the outer wall.  This may seem like the inner wall is separate from, and nested inside, the outer wall, but it is not.  As nicely illustrated in your reference (Martin 2005), the two walls are continuous with each other and not nested.  Because of this, a line from nuclear interior to exterior may in fact not pass through any lipid bilayers; it may pass though a nuclear pore.  Topologically (mathematically) speaking, the two walls are one surface, and the "inside" of the nucleus is on the same side of the surface as the outside.  (The topological interior is perinuclear space and the interior of the endoplasmic reticulum.)  Functionally though, the structure acts as a double membrane since it physically constrains its contents.
The distinction is not very important for most biological contexts, but for a few purposes needs to be considered.  The main reason to pay attention to the distinction is that it probably is related to the evolutionary history of the nucleus: it is likely to have evolved from a single bilayer somehow.  In contrast, the mitochondria and plastids, with nested bilayers, evolved from two bilayers, one from a separate cell and one from an enveloping piece of a host cell.  This is why the distinction is important in the cited paper, which concerns the evolution of the nucleus.


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Epilepsy explained by computational neuroscience
A few years ago, on my maths masters, I did a module in theoretical neuroscience. I was shown that the mathematical framework the course developed for neurons, with a small adjustment in the parameters, would produce spike trains similar to those observed during epileptic kindling. These parametric tweaks could be attributed to mutations in ion channel/receptor structures. This was one of the highlights of the course, and when I came to apply for a math/bio interdisciplinary doctoral program, I cited it as such in my personal statement.
Now the interview is fast approaching, and I'm pretty sure it's going to come up, but for the life of me I can't track down a reference. After four years out of the game, my memory is hazy at best.
As I recall, this had something to do with short term plasticity. Normal neurons' response to unrelentingly high frequency spike trains decayes over time, while pathological neurons' does not. This may however be entirely wrong.
What is a reference for the model I describe above? An introductory/educational treatement is prefered, but the original paper is fine.

To meet the standards of SE please consider concentrating on asking a well-pointed question (not on personal story, urgency, ...).

I echo Piotr's sentiment, but is this the article?  Lopes Da Silva is a leader in the field.

@PiotrMigdal I don't think there is an inherent problem with adding a person flavour to a question, as long as the question is still clear. In this case it is a reference-request for a very specific result.

@ArtemKaznatcheev Yes, as long as one does not need to read one's life story before the actual question. Personally I am irritated by 'questions' in which I need to search for the actual question.

Unfortunately, epileptic spiking can occur very easily in many neural modeling studies, and therefore one should be very careful in asserting the possibility of certain aspects of model as a cause for epileptic activity. One possibility, as you mentioned, is the lack of short-term depression which prevents long sustained firing. But again, a simple increase in the global excitatory coupling can also exhibit similar dynamics.
Good luck on your interview.


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What is the healing process of mouth wounds?
When we have an external wound, blood generally tends to clot there, forming a layer of solid scab.
Yesterday, while brushing my teeth, I somehow hurt my gums and it got all bloody. However, it did not clot, neither did it hurt just after the incident.
After maybe like 12 or 15 hrs I had trouble opening my lips and when I looked at the spot in the mirror the gum tissue around and on the wound had colored white/yellowish.
Our mouths are supposed to be the among the most contaminated parts of the human body, so why do mouth wounds heal in just about a week and don't get infected?
What is the healing mechanism found in the mouth tissue, because I figure it is completely different from the processes in wounds occurring in the external skin.

To build on the answers from @Armatus and @S-Sunil
The healing mechanism involves the inflammatory process, which is the same in almost the entire body. In particular in both skin and mucosa (both referred to as "epithelial" tissues), when there is a break, platelets and clotting factors clot off any bleeding vessels, white blood cells (neutrophils and macrophages in particular) collect and destroy any bacteria, dead cells and muck, and then the process of regeneration occurs (with ongoing inflammation), where stem cells in the surrounding tissue regrow cells, new blood vessels may be formed and scar tissue is laid down to give extra strength. Eventually after these stages of healing, there is "remodelling" where the structure basically gets better.

As to why oral wounds heal quickly and don't get infected that much? There are a bunch of reasons. One is that the head and neck has an excellent blood supply- just think of scalp wounds where you bleed like crazy but then they heal very well. Another is that mucous membranes have immune functions that stop invading microbes. Generally speaking we divide this into "innate" immunity which is a general response, and "adaptive" immunity which is tailored towards specific bugs. The mucosa has both. There are neutrophils and macrophages (innate) which live in that area, there are lymphoid patches (like lymph nodes, and adaptive), there are immunoglobulins specific to mucosa (IgA) which is adaptive in nature, and the epithelial lining cells themselves will signal to the rest of the immune system if there is damage or an infection. Plus, saliva itself has chemicals and enzymes which break down oral bugs.

Most of the oral bacteria themselves are not particularly invasive. Just think, every time you brush your teeth, you cause multiple abrasions in your mouth. In fact, measurable amounts of bacteria from the mouth end up in your bloodstream every time  you brush your teeth! And yet, we don't end up with bloodstream infections as a result. This is partially because the rest of our immune system (and the structure of our heart and vessels) is intact, and partially because oral bacteria are not very invasive or pathogenic. They kind of have a sweet deal living in your mouth minding their own business and not killing their host, and even causing infection in an oral wound would make their continued survival less likely.
In addition I should probably point out that skin has a great deal of bacteria on it as well, and yet we rarely get infections from them (unless colonised by an invasive species), for the same reasons.

@UV-D Cheers! NP!

The mucosa ("slimey" skin) of course has different properties from your epidermis (outer skin) but the wound healing process is pretty much the same; the blood clotting process might be different though. About this I'm not entirely sure, but my best guess is that the "scab" is washed away by mucus and only the clots inside vessels remain, making them invisible from outside.
The white/yellowish colour is the underlying layer of fatty tissue. Chances are your wound does get infected but your immune system is able to clear it away easily. If infection is a bit heavier, it can strain the immune cells a bit more and some of them may die - you can then see them as pus (which is mostly white blood cells).

The mechanism of oral wound healing is similar to that elsewhere in the body. Depending on the type/ extend of wound, it may be primary or secondary.The clot and the encrustations are the part of the healing process.


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Does becoming martyr have an evolutionary advantage?
This is related to
How does "be altruist to those who are similar to you" evolve?
Altruism that is

Not reciprocal
Not familiar

has little explanation. One possible explanation is that the trait itself may correlate well with genetics. One great answer there is that often the cost of altruism is small anyway. It can explain why people vote. Here the expense is small anyway.
Still there seems to be some factors that are even bigger.
Let's take a look at people that die for their ideology. Christian martyrs, Muslim suicide bombers, or Communist guerilla fighters. They seem to get so little and well, die.
And that's pretty common. It seems pretty easy for a leader or pedagogue to rouse men to be soldiers. Of course, becoming a soldier is a pretty shitty job, yet most men don't mind.
These people make a huge sacrifice for the sake of their country, ideology, or people that are not even genetically related to them.
Why?

If it does not pay on genetic level (as they die, perhaps without offsprings), it may be beneficial on memetic level - i.e. spread (or defend) the idea of country, religion, ideology etc. I does not even need to give any (genetical) advantage to others.

Traits do not have to give an advantage, they can simply not bear significant enough of a disadvantage in survival of a common gene (/genetic group).

Or maybe they're just removing themselves from the gene pool...

@Armatus A trait that removes you from the gene pool has a huge disadvantage though. In fact, a decisive, win-every-argument one (not accounting for memetics here, nor for the fact that martyrs might first bear offsprings, which doesn’t seem to be the case usually).

+1 for Piotr Migdal, and that memetic may help genetic. That's I think how it works. For example, by dying for socialism, you may benefit fellow socialists. But that would require SIGNIFICANT non genetic based non reciprocal altruism which is strange. Or perhaps memetic, like genes, have a life of it's own? Now Budha's question of "Who am I?" start getting more and more reasonable.

Martyrdom is not an evolutionary stable strategy. Although there are a lot of people who believe in suicide bombing, each generation, only a small fraction of them actually meet the conditions that make them want to suicide bomb making the willingness to do so get very slowly weeded out. Not even 2,000 years have passed since Islam started which means not enough time has gone by to weed it out.

Perhaps suicide bombing hurt others more than it hurt them? Does it make sense that people choose a strategy because it hurt others more than it hurt them out of despise?

Your question is quite broad and asks for explanations for various behaviours which can lead to self-sacrifice.
Religious reasons: The genetic influence here may be a predisposition to let others influence you. This is what gives rise to culture in the first place, in other words: the predisposition to at some point maybe sacrifice yourself because you are taught to do so can only die out if the basic behaviour which gives rise to culture dies out. Cultures which lead their members to die may decimate their own numbers, but they will not wipe out culture itself because in the bigger scale, those with culture do better than those without. (Plus, those who sacrifice themselves may have children as well, so any genetic influence on their behaviour can be carried on.) This also goes far into the field of memetic evolution, which is disputed but may be interesting to read about.
Political reasons: As in, dying for one's nation or country rather than because of teachings. This probably has a defensive behaviour towards one's own group as the genetic influence. Also, reputation plays a big role: see shigeta's excellent answer.
You also mention willingness to subordinate oneself which is a very common pattern not only in humans. Richard Dawkins touches on this in The Selfish Gene, but there are probably papers more focussed on this particular topic out there as well.
I think it is far-fetched to assume a genetic inheritance of in general "willingness to die for something" (which would be required for genetic evolution to work on it). Each thing that some people may be willing to die for can have completely different reasons. I think in these terms the willingness to die is usually an exaggeration of a behaviour which evolved for different reasons.

I like the predisposition to let others influence you theory. That make sense. Like telomere for example. Death it self doesn't help, but telomere does. The same way dying for ideologies doesn't help, but predisposition to let others influence you might. Thanks Armatus.

There isn an effect called "Indirect reciprocity" where individuals just give to everyone they meet without direct requirement of reciprocity.
This sort of benefit to others is common - hospitality to strangers, general politeness, good customer service all fall along these lines.  You hope they will come back and benefit you again, but maybe they will tell someone else who will know you are a good community member.
It is only sustainable in a system where the cost/benefit ratio is less than the reputation benefit of the act.  It sounds as if this is only good for public acts but if the benefit is transferred to a social entity that outlasts the individual (like your children, a relative's children, a religion or a corporation say), the result could still hold.
If you think about typical morality/ethics really it still makes sense to think that what we call altruism must still have a net positive benefit.  If there is no benefit long term or to anyone, it really isn't useful or even good, its random.  What we usually call altruism is usually some sort of reciprocal cooperation.
A soldier who dies in combat or someone who dies for their beliefs but everyone knows about it as a public statement benefits from their act indirectly.  I don't think its altruism in the pure sense of the word. Defending the nation, ones' beliefs or whatever is, in its sense its own reward.  Veterans come back from a war are hopefully respected for their work.  Having a purple heart can be a good thing to show people.  I'm not saying these people are adequately compensated for what they have been through, but just trying to draw a distinction between pure biological altruism and 'indirect reciprocity'.
Examples of Indirect reciprocity might be the use of tax money to build highways and build power and water infrastructure.  Its important - its the glue that holds a nation or a group together.  If you got punished for doing these things we wouldn't be hanging as a nation very long!
A martyr with no family at all who would benefit would still count as an altruism I think, but most acts of public piety and sacrifice do benefit the individual by reputation. Something to think about.

I don’t see the connection. The individuals certainly have no benefit from dying. There is no reciprocity in such an action towards the individual (there may still be towards alleles, if those are shared between the martyr and those (s)he died for) – the cost/benefit ratio is infinite. None of the benefits you list apply to martyrs, only to people who stop one step short of martyrdom.

Actually it does. Say a member of Thio family dies for his country. Perhaps Thio families get respected more. But that's far fetch. That's still reciprocal.

@Jim On the allele level, yes. But this answer makes it sound as if the individual had an advantage, and that’s patently not the case.

@JimThio Its an extension of reciprocal altruism - i think you have to stretch biological theories to cover some human behavior, but as long as the offspring or relatives benefit it still makes sense. I do think i mentioned this.

I would say a better question would be, "Why would anyone die for a cause?". People benefiting from a cause may not be genetically related. The cost is significant. The cause tend to benefit those who are similar, but because similarity doesn't mean genetically related, how come genes that say, "die for a cause" evolve?

I think you incorrectly describe 'indirect reciprocity'. Indirect reciprocity just means that there is some sort of reputation-like effect that allows you to receive reciprocity not directly from the person you cooperated with but from others who see your good reputation (which you maintain by cooperating). The classic paper on this is Nowak & Sigmund (1998). For a general intro, I mention this and other mechanisms for cooperation in a TEDx talk & blog post


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Productive turnover and generations in the fruit fly
I was reading about the Lenski experiments on the evolution of E. coli bacterium and Dr. Elders's experiments on the evolution of the guppy.
These two experiments absolutely fascinated me, and seemed to happen relatively quickly by evolutionary standards. It was mentioned in the book that the fruit fly's productive turnover time is especially short.
I am extremely interested and would very much like to conduct an experiment into the evolution of the fruit fly, in much the same way as the Lenski and Elder experiments when I'm older.
Just so I can get a good idea, as I can find nothing on the internet, how long would it take for the fruit fly to get through, say, 10 generations?
Also, what would be the best way to go about beginning an experiment like this? Would there be certain people to contact? Would you need certain qualifications?

I love the subject of experimental evolution! Give me some time and I'll write more about it.

It is one of the most amazing things

What do you mean by you couldn't find anything on the internet? Drosophila generation time is explained here?
Your other question is a bit off-topic here but I'll give all advice I have heard myself:
You can leave out a banana skin and catch some fruit flies, then do the experiment in your kitchen :) Joke aside, unless you perform the experiment independently it will probably take a long time and it's well possible that you won't be able to do it at all (unless you become some famous scientist). I'm not familiar with the experiments you mention, but if you require equipment and/or funding, you will need a qualification and/or a good explanation why people should give you money or let you use their equipment for this experiment.
I don't know what stage of education you are at, but it sounds like you are still at school ("when I'm older")? Most countries have some schemes where students (below uni) can apply for young researcher kind of things, so you could try and google that. Apart from that, the best bet is probably to try and get into a uni with good facilities and research programmes for their students. What you study shouldn't matter so much as long as it's science.
In response to Marta's commment: if you understand the experiment and you think you can gather everything they used at home, nothing speaks against just doing it on your own. Just make sure you don't let those flies swarm your house ;)

Quite discouraging. As far as I know one don't need very expensive equipment to experiment with natural selection (especially among fruit fly!). Creativity and a lot of patience would be much more needed.

I'm not aware of what experiment they carried out there so I wrote my answer trying to stay on the safe side, assuming that it was a full-out scientific project :) Of course, experimenting is well possible on a small scale especially with these little ones.

Yes I'm still at school, I'm 16. I'm well aware of the length of time it would take and why would you need to be a famous scientist? Also, if Elder and Lenski gave reasons for wanting invested money (if they did at all), I'm sure I could give the same reasons. But yes, overall, rather discouraging

You would need a good explanation why you want to repeat the same experiment. And being famous has the advantage that people tend to give you access to things more willingly - and may not ask for as many explanations if you ask for things :)

@Armatus but one have to do something to become famous. It's not something that just come to you when you get older :)

Yup, and there's an excellent video on ted about that :) http://www.ted.com/talks/lang/en/richard_st_john_s_8_secrets_of_success.html