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How does Humira work when injected into patients with rheumatoid arthritis?
OK, I have rheumatoid arthritis and I've been injecting Humira 2 times a month for the last 8 months.
As far as I know rheumatoid arthritis is simply an immune system disorder which makes the immune system produce more proteins called Tumor Necrosis Factor alpha which regulate body disorders.
When I inject Humira I actually import a protein called Adalimumab which is a TNFα inhibitor.
So far so good but my question is
Does my body throw this protein away after some time? How is this protein removed from my body?
What about the way Adalimumab inhibits TNF, does it bind to TNF?
Also the details of how rheumatoid arthritis appears are not well known but the main reason is because of the patients DNA isn't it?

Adalimumab is an antibody that binds to tumor necrosis factor alpha (TNF-alpha). Antibodies have high-affinity binding sites for their antigens, and for a small antigen such as TNF-alpha, would bind to it and prevent it from binding to its target receptors. Antibodies, like all proteins, degrade over time and are then removed from circulation, and since the body does not produce more of this antibody, it must be re-administered every few weeks.
The mechanism is somewhat ironic in that the chief role of antibodies is binding to (and thus neutralization of) foreign antigens, but this antibody binds and neutralizes a part of the immune system itself. This part is TNF-alpha (a cytokine) whose function is to promote inflammation at a site, which draws white blood cells to it and activates them. TNF-alpha also induces fever, and suppresses tumor formation and viral replication by activating programmed cell death pathways.
Aggressive immune responses always cause collateral damage to surrounding tissue, but in autoimmune diseases such as rheumatoid arthritis the damage is compounded by the fact that the target of the immune response is an element of the body itself. The immune system should be tolerant to self; sometimes tolerance fails and while it is known that genetics is part of it, the process is not yet well-understood.

Prufrock +1 for the answer ! It would be helpful if you could include a source for this.

i still dont know how exactly this antibodies degrade after a certain period of time . As far as i know things in our world dont just disapear they just transform to other things.

Recall that antibodies are proteins, and proteins are composed of smaller molecules known as amino acids. Proteins are extraordinarily elaborate entities, but as all things become damaged over time and no longer function. The antibodies eventually break in a literal sense, and the cells of the blood decompose them back into amino acids to be made into new proteins. The matter in the body is not static but is constantly being reorganized.

@biogirl - Although not a great general source, Wikipedia gives most of this information regarding Adalimumab. One of the original pharmacokenetic studies of this drug is described by Weisman et al. in the journal Clin Ther. 2003 Jun;25(6):1700-21. In PubMed there is also a review by Bang and Keating in BioDrugs. 2004;18(2):121-39, but I do not believe it is freely available. It is likely there are other reviews of Adalimumab that are freely available.

Here's a nice image that can help visualize how Humira and other similar drugs bind TNF-alpha and prevent it from participating in the signal cascade that causes abnormal immunologic activity.

@Don_S Your "image" link seems not to work.

Afaik. RA and psoriasis are probably caused by a malfunction of genes which regulate IL-23 production. IL-23 is required for Th17 cells to survive. Th17 cells produce a lot of things which result in inflammation and since TNF-α is a key mediator in inflammation and break down of joints, reducing the amount of available TNF-α reduces the inflammation.
(Th17 cells produce IL-17, IL-21, IL-22, IL-6 and TNF-α. Th17 cells are playing against Treg cells, which try to protect self cells. IL-17 promote osteoclastogenesis, and osteoclasts break down bone. According to several Wikipedia articles IL-17 induces the production of other cytokines such as IL-6, IL-1β, TNF-α. IL-21 is required for sustained CD8+ T cell effector activity. IL-22 is a mediator of cellular inflammatory responses. IL-6 modulates the resistance of T cells against apoptosis, induces activation of T helper cells and promotes osteoclastogenesis. TNF-α is an endogenous pyrogen which is able to induce fever, apoptotic cell death, cachexia, inflammation and inhibits tumorigenesis and viral replication. IL-1β is a mediator of the inflammatory response, and it is involved in the regulation of apoptosis as well.)
Adalimumab is an immunoglobulin, which binds to TNF-α, and so it prevents it from binding to TNF-α receptors and causing inflammation. After it is bound to its target you cannot reuse it, that's why you need daily doses of it. It is degraded by liver and kidney cells, and probably by phagocytes.
There are other TNF-α blocking pharmaceuticals. There are IL-23 inhibitors, one of which is ustekinumab. It is an immunoglobulin too and it is used for treating psoriasis. For, RA it is currently under clinical trial, but I guess it will work for RA as well. There is an IL-23 inhibitor which is not an immunoglobulin and can be taken orally, called apilimod. Sadly it failed the clinical trials; it had only a mild effect. It probably does not reach the inflammation in sufficient amounts. Maybe one day there will be an effective delivery method and thus a drug which can be taken orally.
There are alternative natural therapies: TNF-α inhibitors which you can take orally, for example γ-linolenic acid, ω−3 fatty acids, chondroitin sulfate, etc... These can be useful for mild cases of RA. Probably fever therapy works for mild cases as well. Afaik. cryotherapy has nice results in treating RA and its positive effect lasts much longer than the effects of any drugs, so if you aren't afraid of cold, that is a nice alternative therapy as well.

2013 - The interleukin-23/interleukin-17 axis and the role of Treg/Th17 cells in rheumatoid arthritis and joint destruction
2010 - IL-23 in the pathogenesis of rheumatoid arthritis.
2003 - Dihomo-γ-linolenic acid inhibits tumour necrosis factor-α production by human leucocytes independently of cyclooxygenase activity
2011 - Omega-3 supplementation lowers inflammation and anxiety in medical students: A randomized controlled trial
2006 - Discovery of a TNF-α Antagonist Using Chondroitin Sulfate Microarrays
A Study of the Effectiveness and Safety of Ustekinumab (STELARA) and CNTO 1959 Administered Under the Skin of Patients With Active Rheumatoid Arthritis, Despite Existing Methotrexate Therapy
2014 - Cryotherapy in inflammatory rheumatic diseases: a systematic review
2012 - A Phase IIa, Randomized, Double-Blind, Placebo-Controlled Trial of
Apilimod Mesylate, an Interleukin-12/Interleukin-23 Inhibitor, in Patients With
Rheumatoid Arthritis

Fever therapy for rheumatoid arthritis is not written about much, it seems. The little I could find seems to deprecate it, except for infectious arthritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2242205/pdf/tacca00014-0256.pdf .As for cryotherapy there's a lot about it on the internet but Wikipedia mildly deprecates cryotherapy, it seems. As for whole body cryotherapy : ttps://www.fda.gov/consumers/consumer-updates/whole-body-cryotherapy-wbc-cool-trend-lacks-evidence-poses-risks

@MatthewChristopherBartsh I would try them out if I had RA. You lose only a little money with them. If it is urgent, then Humira works pretty well.

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How does extracellular potassium ion concentration and calcium ion concentration affect the excitability of a cell?
When extracellular $K^+$ concentration increase by a certain amount, excitability of cells is higher because the resting potential shifts toward a higher equilibrium potential of $K^+$, therefore causing depolarization. However, when there concentration of extracellular $Ca^{2+}$ increases, excitability of cells decreases. If $Ca^{2+}$ and $K^+$ are both positively charged ions, what is the cause behind their opposite physiological effects?
I'm not a biology student, so detailed answers would be kindly appreciated. Thank you!

Hyperkalaemia (high potassium levels) actually paradoxically decreases the excitability of cells due to increased channel inactivation

Rory M - that's not always true about decreasing excitability. Case and point: > 25 mM K+ is a standard depolarizing agent in cell culture that triggers action potential firing. Also, a high K+ gradient across the membrane still leaks some K+ into the cell. Strictly speaking, this depends on the complement of voltage-gated and voltage-insensitive ion channels expressed on the cell surface.

If extracellular $Ca^{2+}$ concentration increased, it makes the extracellular membrane more positive then it used to be, then it would take the membrane potential to lower level then the excitability of the cells will be decreased
if extracellular $K^+$ increased more than the concentration inside the cell than it will make the $K^+$ on extracellular space move inside the call down the concentration gradient, it would take the potential membrane to higher state make it easier to reach the threshold (easier to be excitable)

Well, the answer which explains the difference between calcium and potassium is quite simple. Do we agree that charge separation (between the two sides of the membrane) is the thing which creates the potential? meaning, if the charge concentrations at the two sides were the same, then the membrane potential was zero. right?
So here is the thing. You have much more Ca outside the cell than inside and you have much more potassium inside than outside. So now, if you add Ca outside, you increase the difference between the two sides (the separation of Calcium ions) so that Ca will be in a greater state of unrest, the system will be less stable and the potential will be higher. On the other hand, when you add K outside, you narrow the gap between its two concentrations on the two sides (decrease its gradient), so now it'll experience less tension, less unrest, hence contribute less potential to the membrane.
Remember that in our cells, the ion pumps are the ones which serve as the battery that keeps the potential fixed. When do you think the pumps will have to work harder and to do more work (voltage times charge is work), when you add more K outside, or when it's the Ca which is being added?

Welcome to Biology SE! Can you add more sources to this answer.

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How far into a pregnancy is it before visible signs of it is apparent and risk of physical trauma increases
I'm doing research for a series I'm writing. in it the main character is pregnant however goes off to fight a criminal organization who have been killing her friends and i want her appearance to show that she may not be pregnant however she fights and defends as if she is mindful of heavy impacts could cause a miscarriage
I am wondering how far into a pregnancy is it before visible signs of it is apparent and risk of physical trauma causing miscarriage increases, if there is also a point during the pregnancy where the fetus could mutate via outside interference then that would be good to know too however I can go without that information.
NOTE: I want to know this information so that even though the world in this series I'm writing is totally fictional, one can begin to question how fictional it really is when some parts are based off actual science and logic of real life.

You should consider cutting down the largely irrelevant background for your specific application, and go directly to the biologically interesting question. Many will ignore your question simply because of the long introduction. Remeber that Stackexchange sites are not general chat forums.

@fileunderwater i'll cut it down given no other option, i included it so that people don't think this question is about trying to hide pregnancy

Around the second trimester.  That's an article from WedMD, which says quite a few things.  To summarize, by the end of the first trimester:

You may be noticing some of the first physical signs of pregnancy: breasts that are sore or tingle at the slightest touch, skin that's drier or oilier than usual, and "morning sickness" -- which may or may not restrict itself to the morning hours. As many as 70% to 80% of pregnant women have it, but not feeling morning sickness doesn't mean there's anything wrong with the baby.

In the second trimester:

Most pregnant women begin to "show" during the second trimester. You likely gained less than 5 pounds during your first trimester, but now the number on the scale is edging relentlessly upward. As your second trimester proceeds, you'll gain an average of 1 to 2 pounds per week.

The exact time and rate of "showing" can vary, including whether or not this is your first pregnancy.  By the third trimester, the infant is rapidly becoming more and more capable of surviving on its own.

As far as "mutations" go, I think the term you're looking for is teratogenesis. Birth defects are most likely to form early in the pregnancy, but different toxins can have different windows. As an embryo develops, different tissues are growing and differentiating. If it is exposed to the right toxin at that time, that tissue may be damaged and not develop properly. If the tissue gets past that stage, exposure to the same toxin might have no affect at all.
Wikipedia may be a decent starting point: http://en.wikipedia.org/wiki/Teratogen
Studying birth defects is hard because it's tissue specific, toxin specific, and time specific. For some reason pregnant women just don't like to volunteer for studies on potentially dangerous chemicals.

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Is fat distributed proportionally around the body?
One guide I have been using to tell me if I really am gaining a lot of weight is a ring around my 2nd last finger on my right hand, if I can slip it on and off without any resistance then I'm fine, however I've been basing this from the notion that if I gain weight it's proportionally distributed around my body, as such, if I get fatter so do my fingers
So I am wondering, is fat distributed proportionally around the body (ie. if your waist gets bigger then your fingers will get bigger along with it)?

What about simply using scales to track your weight? However, this is of course separate from the fat distribution question (to which I suspect the answer is no), but it would save you some trouble.

@fileunderwater's suggestion to use a scale is probably the best answer you could get, but looking at this broadly, the answer is no.  The oft-referenced apple and pear shapes are indeed very real and have medical consequences.  One of the issues is that there are sex differences in fat distribution.  There is no evidence I can find that finger fat is a good correlate of overall body fat, although admittedly yours could be.  It is also likely a function of how much overweight you were when you began the "experiment" i.e. the relationship probably isn't linear.
That being said, in men the ratio of the length of the second and fourth digits are otherwise meaningful.


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In Japan, the official average body temperature is 36.0 °C. Why so different from that of Europe?
The Japanese Wikipedia states that the average human body temperature is 36.0 °C (here,"ヒト").
The statement references the data from the Japanese government.
Actually all of my Japanese friends think the same.
A body temperature of 37.5 °C is considered a serious illness in Japan, justifying absence from work.
Most other countries' sources cite 37.0 °C as an average.
Is there a biological explanation for this apparent discrepancy?

Here is a somehow related article you might want to read. http://www.health.harvard.edu/press_releases/normal_body_temperature

Hi Remi.b: Interesting, feel free to propose it as answer! I see two points: 1) Well-accepted means are erroneous 2) Mean depends on the group's age and potentially other parameters.

I won't pre-empt @Remi.b but the English Wikipedia's got a good breakdown of the variations.

36.0 °C is what I was taught when very young, but then it got to 36.8 °C. Actually, my own normal temperature is more like 36.1 °C and I am not japanese. As I literally only had a real fever once in my life, 37.5 °C would be a pretty serious condition for me. For my cousin, who gets a fever with every light cold, it would be kind of normal. So, there is a lot of variation even between related people.

already been answered on http://skeptics.stackexchange.com/questions/10309/do-japanese-people-have-a-lower-body-temperature-than-caucasians

Related: http://health.stackexchange.com/questions/9981/fever-lower-limit-99-0-f-37-2-c-at-armpit-is-it-universal and http://biology.stackexchange.com/questions/54127/do-human-populations-differ-in-core-body-temperature

Put every subject(both male & female) in the same environment/conditions, and take multiple temperature readings via oral, rectal, by ear, and under the arm routes. Make comparisons by sex, route of measurement, age, race. As well, the use of different thermometer types, ranging from the old "gold standard" glass mercury rectal thermometer/oral thermometer, thru the digital, ear type and electronic probe types such as FILAC and IVAC with respective oral/anal probes should be considered as there are always questions as to which is the best to use.

Factors that can lower body temperature:

low environment temperature
low metabolic rate
hypothyroidism

I couldn't find any relevant study addressing the Japanese people situation, but:

There is significant variation in metabolic rate in humans, independent of differences in body size, body composition, age, and gender. Although it has been generally held that the normal human "set-point" body temperature is 37 degrees C, these interindividual variations in metabolic rate also suggest possible variations in body temperature [1].

And here's a factor that increases body temperature:

The present experiment investigated the effects of skin pressure by foundation garments (girdle and brassiere) on the circadian rhythms of core temperature and salivary melatonin. [...] The results suggest that skin pressure by clothing could markedly suppress the nocturnal elevation of salivary melatonin, resulting in an increase of rectal temperature [2].

Whether there are differences between Japanese and other people in metabolic rate and /or clothing behavior remains unclear.

References:

Rising R, Keys A, Ravussin E, Bogardus C. Concomitant interindividual variation in body temperature and metabolic rate. Am. J. Physiol. 1992 Oct;263(4 Pt 1):E730-4. PubMed PMID: 1415692.
Lee YA, Hyun KJ, Tokura H. The effects of skin pressure by clothing on circadian rhythms of core temperature and salivary melatonin. Chronobiol. Int. 2000 Nov;17(6):783-93. PubMed PMID: 11128295.

Kinda surprised this answer got the bounty and is the most upvoted. While it describes factors related to human body temperature, it completely lacks any connection between these factors and Japanese people. It simply does not answer the question.

This entire post is taken from odd thinking:
https://skeptics.stackexchange.com/questions/10309/do-japanese-people-have-a-lower-body-temperature-than-caucasians
There may be a difference, depending on whether you are talking about internal or skin temperatures.
This study compared 9 Japanese men to the results of a similar study done in Ohio with Caucasian men:

Thermoregulatory responses to heat and exercise in Japanese and Caucasians
K. Ohara, N. Okuda and S. Takaba, International Journal of Biometeorology, Volume 19, Number 2 (1975), 99-107, DOI: 10.1007/BF01463865

The subjects were made to walk on a treadmill for 2 hours, in carefully controlled conditions.
There were a  number of differences in the amount and composition of their sweat.
Internally, they maintained the same body temperature:

There were no differences in rectal temperature or heart rate, both at the period of equilibrium rectal temperature and at the end of the walk.

However, there were differences in the skin temperature - perhaps not in the direction you were expecting:

Mean skin temperature during the walk was significantly higher in Japanese than in Caucasians.

They concluded that:

the Japanese group was better heat acclimatized than Caucasians, though the two groups were considered to have been naturally heat exposed by season to the same extent.

While this result is suggestive, I don't find it to be definitive, as the caucasians were tested at a different time in a different facility, making them a poor control. Also the sample sizes were small, in an area which may vary by age and other factors.

Joo-Young Lee, Hitoshi Wakabayashi, Titis Wijayanto, Nobuko Hashiguchi, Mohamed Saat and Yutaka Tochihara Ethnic differences in thermoregulatory responses during resting, passive and active heating: application of Werner’s adaptation model European Journal of Applied Physiology, Volume 111, Number 12 (2011), 2895-2905, DOI: 10.1007/s00421-011-1912-5

This study didn't involve Caucasians, but compared Malaysians ("tropical natives") and Japanese males.
They put them under a number of different scenarios, such as soaking their feet in a warm bath, but also at resting.

The results saw that: tropical natives had a higher resting rectal temperature and lower hand and foot temperatures at rest [...]

ok... I put forth the link and you copied and pasted the answer.. What exactly is your contribution?

meta.stackexchange.com/questions/172307/duplicate-questions-on-other-se-sites @TheLastWord

While the CC licence allows copying the entire post, you still have to make clear which parts of the post are copied. You also have to mention the user that made the original post explicitly in addition to linking to the post.

The discrepancy can be partly explained by where the temperature was measured from since the human body temperature ranges from 36.5 and 37.5 °C. For example it is 36.8 ± 0.4 °C when measured under the tongue (http://en.wikipedia.org/wiki/Human_body_temperature). Additionally The body temperature of a healthy person varies during the day by about 0.5 °C (0.9 °F) with lower temperatures in the morning and higher temperatures in the late afternoon and evening, as the body's needs and activities change.

Do you have any references for that (temperature in various parts of the body and methods of measuring in different countries)? It would be quite important to cite them in this case...

@daniel Where did you read that?

I was thinking "front" is a part of a head above an eyes: http://en.wikipedia.org/wiki/Forehead Sorry I am not native English.

Oh! Your English is very good. That's why it didn't occur to me. Cognates are tricky. No problem.

This study states a 0.35 degrees difference between a japanese and a malaysian, 36.95 and 37.3, it's alot.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3929238/
The following study states states a 0.15 degree difference measured with similar precision,
https://www.ncbi.nlm.nih.gov/pubmed/20824480
This graph shows that the human body temperature is 36.2 at rest in the morning/at night and 37.5 in the middle of the day. : http://millar.bio.ed.ac.uk/andrewM/WE%20book99/Part2-examples.html#tth_sEc8.3.4.2
That may account for the 1 degrees difference in Japanese studies, they measure first thing in the morning/ after 4 hours of fasting and rest/at night, and japanese body temperature of 0.15-0.35 lower that some other ethnic groups.


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External tissues, connected to the body?
Some cancer tumors suppress themselves from spreading. When such tumors are removed by surgery, the metastasis process is accelerated.
Isn't it possible to put such tumors into external device like hemodialysis device and slow metastasis process this way?
Are there any experiments or clinical usages of own body tissues in such a devices? Not for cancer, but probably for some other reasons, in humans and animals?
Some sort of grafting for animals.
Such a tissue can interact with main body by blood and cause some effects.

I've actually wondered this myself from time to time, without ever bothering to look it up.  Well, it's actually happening.  That WSJ article says the following, which just blows my mind:

Researchers at the Rogosin Institute are taking tumor cells from mice, encapsulating them in beads made from a seaweed-derived sugar called agarose, and implanting them in the abdomen of cancer patients. There, cells in the beads secrete proteins researchers believe could signal a patient's cancer to stop growing, shrink or even die.
So far, at least 30 patients have been treated with the cancer beads in an initial human study, and a phase two or intermediate-stage trial has been launched—with the approval of the U.S. Food and Drug Administration—to test the technique in patients with advanced colon, pancreatic and prostate cancers.

You can find the info on the Phase II trial here; they are currently at the "recruiting participants" point.

[The treatment] consists of small beads that contain mouse cancer cells from a mouse kidney cancer cell line. The cells in the beads produce substances that have been shown to slow or stop the growth of tumors in experimental animals, veterinary patients, and 23 humans with different types of cancers in a Phase 1 safety trial.


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How do trees lift water higher than 10 meters?
The atmosphere pressure is 10 meters of water (approx). This means that it is impossible to lift water higher than 10 meters with vacuum or сapillary action (on Earth, under normal conditions).
There are trees higher than 10 meters.
How do they lift water to their tops?
UPDATE
In other words: how cohesion-tension theory can be true if it apparently contradicts the laws of physics?
UPDATE 2
Atmospheric pressure helps to rise the water, not resists rising. What is resisting is water weight. When water column is 10 meters high, then atmospheric pressure can't help anymore.
Any adhesion/cohesion mechanism can't help here too, because it acts only in thin molecular layer. To transfer action force further the pressure is required, which is insufficient at 10 meters.
UPDATE 3
If we had capillary small enough to rise water to 10 meters and then we will build smaller capillary which we expect will rise water higher, we will fail. Water column will break and does not climb higher than 10 meters.

Menisci acts like small piston and can't help rising water higher than 10 meters.
UPDATE 4
Common pressure distribution in capillary is follows:

$P_0$ is atmospheric pressure. As you see, right under menisci, the pressure is lowered by $2 \sigma / R$ where $R$ is the radius of menisci and $\sigma$ is surface tension. The entire term is called "Laplace pressure". As you see, it can't supersede atmospheric pressure, because water continuity will be broken in the case.
I.e. no any menisci can rise water higher than 10 meters.
The existence of higher trees PROVES that there are some other significant mechanisms, not adhesion/cohesion, not capillary.
UPDATE 5
Current version, as I understood it, is based on a declaration, that a water, if put into thin capillary, can behave like a solid body. Particularly, it can resist tension up to minus 15 atmospheres.
This is a tensile strength of concrete, so I don't believe that without additional proofs.
I think it is just not hard to make thin tube, put water into it and check, how high it can climb.
Was it done ever?

It is not the atmospheric pressure alone that pushes the water up to the tops. Have a look at Cohesion-tension-Transpiration pull theory https://www.boundless.com/biology/water-and-solute-management-in-plants/transpiration/the-cohesion-tension-hypothesis-for-pulling-of-xylem-sap/

Possible duplicate of How does water move throughout plants?

@SatwikPasani so this is wrong theory then. "Negative pressure" can't rise water higher than 10 meters. This is more basic law -- physics.

@Amory this is not a duplicate, the linked question is answered by capillary action, this one is asking how that works specifically at great heights.

It seems like you are mixing up three different mechanisms/forces for moving water: 1) pressure, 2) capillary action and 3) cohesion-tension. The 10 m rule is referring specifically to pumping water using vacuum/atmospheric pressure.

Maybe this discussion provides a better explanation of current thinking.

@terdon It boils down to the same thing, really.  The comment there answers this well enough.  I think the underlying problem here is really about physics.

@Amory I hadn't seen the comment, OK, fair enough.

@fileunderwater see my update2

@AlanBoyd point 4 on your link is just completely wrong: no any small menisci can rise water column higher than 10 meters. To rise water on 100 meters, we need to live on Jupiter.

@SuzanCioc The thing is that you do not seem very open to appreciate the complexity of water transport in a plant. There are several forces in play, and we are not talking about a single water column being sucked up 50m. As have been mentioned, capillary forces, cohesion-tension, osmosis and horizontal movement between cells in xylem are all hypothesized to contribute.

@SuzanCioc Also, the first update in your question could just as well be rephrased as: How can the laws of physics be true, since they are obviously contradicted by living trees?. Either your understanding of the physical laws relevant for this case are mistaken, or some very fundamental laws must be revised. That trees are transporting water to their crowns is a fact.

@SuzanCioc I believe Update 3 in your question is wrong. Water can rise over 10m by capillary action though that is not the only thing pulling up water in a plant. The "10m law" is very specific only to a confined column of liquid and is no way related to the physical processes pulling up water in a tree.

@fileunderwater I am open to any answer, including "we don't know". But I can't accept capillary forces and cohesion-tension because they would violate Pascal's law.

@fileunderwater I don't thinks trees contradict physics. I think biologists do, if they think that capillary forces can rise water to 100 meters.

@SuzanCioc Those processes not only do not violate pascal's law but aren't related to them in a way you think are related to them. And I suggest you provide here a quantitative (mathematical) proof to validate your argument about capillary forces and cohesion not being valid for ascent of sap according to physics,

@SatwikPasani suggest any other force that can rise water, this is the question. Menisci can't. If it can, then pumps would not required to water supply buildings. We would use just thin capillary.

My last contribution - try this.. There is a whole literature on this topic out there, and I suggest that you explore it.

@AlanBoyd I explored it, but found no answer; may be I missed it, then, if you didn't, please, answer the question.

@SuzanCioc Really?  "The air–water interfaces in the cell walls of the leaves, where the matrix of cellulose microfibrils is highly wettable and the spacing between them results in effective pore diameters of something like 5 to 10 nm. A wettable capillary with a diameter of 2.91μm pulls on water just strongly enough to balance the 0.1 MPa atmospheric pressure, so the pressure in the water is zero. For smaller diameters, the capillary force is capable of lifting water higher than 10.33m. For example, the maximum height of a water column with a capillary diameter of 10 nm is nearly 3 km."

@Amory capillary with 10nm diameter can't lift the water to 3 km, I already said that. If somebody states this, he or she is just wrong. Of course, I can be wrong too, but I have an explanation of my point (see above), while others just use Jurine's law blindly.

Disclaimer: This is not my field of research.

First, this is not a complete answer to our question. A nice explanation of the current hypothesis of water transport in trees (Dixon-Joly cohesion-tension theory, originally proposed 1894) can be found at The Amazing Physics of Water in Trees but also in Tyree (1997). The key points are that the stoma (leaf surface pores) are so small that the menisci can withstand huge water columns, that water has strong cohesive forces, and that water is transported using the negative pressure that is created by transpiration. The webpage linked above contains a beautiful visualization of how multitudes of stomata and menisci create strong negative pressures:

Second, much of the current discussion in the comments (an indication that the question might be a poor fit for Bio-SE?) revolves around the plausibility of the cohesion-tension theory, and specifically on whether water can sustain strong negative pressures. Caupin & Herbert (2006) review metastability and cavitation in water (in a physics journal), and contains experimental results on negative pressures in water. The paper references a large number of experiments under various experimental setups (I cannot fairly judge these). In their conclusion they state that:

Among the countless cavitation experiments, only the ones with special care about water purity can reach large negative pressures; with a variety of techniques, they all obtain Pcav around −25 MPa at room temperature (see Fig. 3 (b)), which falls far away from the theoretical value (from −120 to −140 MPa). There is a notable exception: experiments with mineral inclusions achieve −140 MPa. The large gap between these data requires special attention.

So basically, the theoretical estimates lie at -130MPa and empirical results at -25MPa (-250 atmospheres), and water can clearly achieve large negative pressures. This would also mean that the current estimates are much larger than what is needed for the cohesion-tension theory to work (atmospheric pressure= 0.1MPa, negative pressure in water column at 50m ~ -0.5MPa).
They also have a section specifically discussing trees:

7.1. Water in nature
  The law of hydrostatics teaches us that the pressure drop in a water column of 10.2 m is 0.1 MPa. This points out that negative pressures can be reached in the ascending sap of tall trees. In fact additional effects (viscous flow, drought) make the pressure in the sap negative even at smaller heights. The cohesion-tension theory, first proposed by Dixon and Jolly [56], explains that the sap column is held at the top by the meniscus in the pore of the leaves: by Laplace’s law, the meniscus curvature allows a pressure jump between the outside air pressure and the negative pressure in the sap. The trees thus contain large amounts of metastable liquids. Cavitation may sometimes occur, disrupting the liquid column and stopping the flow (xylem emboly). The complex hydraulic architecture of trees limits the damage, and strategies exist to refill the embolied xylem channels. Much work has been devoted to this topic, and is reviewed in Refs. [110,111].

There is also evidence that the risk of xylem embolism increases with tree height, and this creates a trade-off between water transport efficiency and structural adaptations to deal with embolism (Domec et al. 2008). This is for instance facilitated by the pit aperture diameter of tracheids, with apertures decreasing with height along a tree, causing increased resistance to embolism but at the same time lower water conductance. This will clearly limit the height of trees, and the paper indicates that the tallest Douglas firs are at the edge of what they can achieve.
Another recently published paper that should be relevant is 'Methods for measuring plant vulnerability to cavitation: a critical review' by Cochard et al. (2013), but I haven't had time to look closely at this. See abstract below:

Abstract:
  Xylem cavitation resistance has profound implications for plant physiology and ecology. This process is characterized by a ‘vulnerability curve’ (VC) showing the variation of the percentage of cavitation as a function of xylem pressure potential. The shape of this VC varies from ‘sigmoidal’ to ‘exponential’. This review provides a panorama of the techniques that have been used to generate such a curve. The techniques differ by (i) the way cavitation is induced (e.g. bench dehydration, centrifugation, or air injection), and (ii) the way cavitation is measured (e.g. percentage loss of conductivity (PLC) or acoustic emission), and a nomenclature is proposed based on these two methods. A survey of the literature of more than 1200 VCs was used to draw statistics on the usage of these methods and on their reliability and validity. Four methods accounted for more than 96% of all curves produced so far: bench dehydration–PLC, centrifugation–PLC, pressure sleeve-PLC, and Cavitron. How the shape of VCs varies across techniques and species xylem anatomy was also analysed. Strikingly, it was found that the vast majority of curves obtained with the reference bench dehydration-PLC method are ‘sigmoidal’. ‘Exponential’ curves were more typical of the three other methods and were remarkably frequent for species having large xylem conduits (ring-porous), leading to a substantial overestimation of the vulnerability of cavitation for this functional group. We suspect that ‘exponential’ curves may reflect an open-vessel artefact and call for more precautions with the usage of the pressure sleeve and centrifugation techniques.

Everybody get plus, but I still can't accept minus 15 atmospheres in trees. Of course I agree that metastable states can exist in principle. Will explore all this...

@SuzanCioc I agree that it is both hard to believe and really cool at the same time. However, with -15atmos you are talking about the tallest trees around. There is also a lot of evidence that at these heights trees are really on the edge of what they can achieve - see e.g. Maximum height in a conifer is associated with conflicting requirements for xylem design.

@SuzanCioc Also, my answer was mainly inspired by your update 5 that questioned if "...water, if put into thin capillary ... can resist tension up to minus 15 atmospheres".

Another disclaimer: this is not my field and I am not competent to judge the content of the paper that I am bringing to your attention.
I said above that I wouldn't make another contribution, but I found something else worth sharing in this context and which complements the answer from @fileunderwater
Wang Z et al. (2012) Capillary Rise in a Microchannel of Arbitrary Shape and Wettability: Hysteresis Loop. Langmuir 28: 16917-16926
This paper includes modelling, free energy calculations and experimentation on this problem. The maths is far beyond me, but they do come to a very interesting conclusion, namely that although a tree cannot start from a position of no liquid in the xylem and then fill up to the top it can start very small and grow beyond the height that can be maintained by simple capillary action and up to 100 m as long as the water column is never broken.
The paper is behind a paywall, but I reproduce below what is essentially the discussion section. Although this gives a flavour of the work, I must emphasise that it presents a very turgid theoretical treatment of the problem and is well worth a look.

V. IMPLICATION FOR WATER TRANSPORT TO THE TOPS OF TALL TREES
  Most plant physiologists accept the “cohesion-tension theory” as the explanation for the ascent of sap.26 In this qualitative theory, the move of water depends upon three important physical-chemical properties of water, which actually corre- spond to capillary rise (cohesion), cavitation (tension), and the hydrated wall (low contact angle), respectively. In this section, we focus only on the implication of the general force balance and loop hysteresis in the capillary rise of a tall tree. The height to which water in a tree rises is dependent on the size of the transport conduits. If one cuts down a tree and looks inside, the capillary dimensions of the relatively large conduits (the xylem tube) are on the order of 100 μm.27 As a result, the capillary rise is about 0.1 m. If capillary pressure alone were to explain the water rise to the treetop of a 100 m tall tree, such as the coastal redwoods of California, a capillary radius of about 100 nm is required. It was suggested that the relevant capillary dimension is the air−water interfaces in the cell walls of the uppermost leaves. The matrix of cellulose microfibrils is highly wettable, and the spacing among them yields effective pore diameters of about 10 nm. It has been pointed out that it is not necessary for the capillary to have a small bore throughout its length. Only the bore at the meniscus (i.e., in the uppermost leaf) is relevant.27 This consequence has been proved in our general expression of force balance, eq 4. Note that a microchannel containing corners or cusps on its cross section is not considered in the derivation of eq 4. Liquid filaments extend to infinity in the corners or cusps.28 Nonetheless, the elevation of the liquid column is still inversely proportional to the characteristic dimension of the cross section of the tube. For the solutions satisfying the force balance, nevertheless, there exists the issue of physical stability.
  A small bore at the uppermost leaf connected to a larger xylem conduit reveals the presence of a convergent micro- channel. As a consequence, multiple stable heights are possible, as described in the aforementioned analyses. However, the final state depends on the initial condition. The liquid will rise to a stable height corresponding to the larger xylem conduit if the microchannel is initially empty. In other words, the liquid will not rise of its own accord to the stable height near the top of the convergent channel because it will not be able to traverse the larger conduit of the channel. This situation is, nonetheless, stable if the liquid is sucked up to the top and then the suction is removed. How does a tall tree acquire such large negative (suction) pressures from above? As demonstrated in our experiments, the gradual rise of an initially immersed cone is able to maintain the stability of the meniscus on the top of the truncated cone as long as the force balance is satisfied. Note that the contact angle in the vicinity of the small pore mouth can be tuned up to fulfill the force balance when the microchannel is not high enough. The slow growth of the tree can be regarded as a gradual rise of the convergent channel. As long as water transport to the pores on the uppermost leaves is not interrupted throughout the entire course of the tree’s growth to 100 m, this stable height can be achieved without resorting to suction.

Now that's an interesting one. What an approach.

Here's Veritasium on youtube has one explanation which is same as @AlanBoyd's comment.

 Meta-stable liquid can have negative pressure.

if your are capable of translating that video into an answer, please do so.  That would get my vote. @suzancioc My understanding before, re-enforced by that video, is that trees are in the amazing field of nano-hydraulics.

So, the point of this video is that water can behave as solid body and express tension up to minus 15 atmospheres if put into small capillary. Can this point be proved by direct experiment? I don't believe it as is. Also I think, that if that would be true, it would have some subsequences. For example, if tree cut at a hight level, we should hear shot sound like taut string cut...

Please see my update. Ability to resist negative pressure is called "tensile strength". And ability to resist minus 15 atmospheres equals to tensile strength of concrete. Do you yourself believe that trees turn water into concrete?

@AtlLED I don't exclude nano hydraulics, but wish to have justified answer.

Thanks for the comments. Since @fileunderwater did a great job, so I won't bother updating my answer. :)

The following paper surveyed work on exploring water at negative pressure, from the first attempt a hundred years ago, when the largest tension reached was -3.4 MPa @ 24 degC, till the most recent measurement of water at room temperature down to -26 MPa:
http://hal.archives-ouvertes.fr/docs/00/72/64/37/PDF/Caupin-JPCondensedMatter-2012.pdf
Therefore trees can lift water higher than 10 meters because water is pulled up by negative pressure at the top (Cohesion-tension theory CTT). The tension needed to lift water to the tallest trees is -1.2MPa, which is very plausible, since it is less than the value measured a hundred years ago.

The same text has also been published in Journal of Physics: Condensed matter.

Good summary, thank you.


text:
Criteria for the numbering of human chromosomes
What were the criteria devised for the numbering convention employed in human chromosomes? When was it fixed?
Correct me if I am wrong; it appears that chromosome pairs 1 to 22 were originally ordered in terms of perceived structural size, which ended up fitting neatly with the quantity of base pairs (but not with the quantity of genes).
The sex chromosomes in turn were arbitrarily assigned as "pair 23".
Is this sound?
Thanks in advance.

Why do you think it was "fixed?"  Here's a nice review of the history of human cytogenetics, which included not only the original image from 1956 but points out a report which comments on the standardization of chromosome number.  The autosomes were indeed numbered by length, and the sex chromosomes are traditionally put at the end as they are "numbered" 23 but clearly function quite differently.  Gene content was decades away from being known at the time, and honestly isn't even known now.  It's also just as arbitrary; simple size is easy enough and makes for rather nice pictures.


text:
Family tree for edible plants?
I am looking for a family tree for plants, particularly veg / herbs / fruit.
Something similar to:
If it could be slightly less technical than all the Latin names too :). The aim is to easily find out what plants are related such as Cabbage, Broccoli, sprouts, Cauliflower (all Brassicaceae). Currently having to look them all up on Wikipedia which is quite painful.
Another example, but a plant version.

By a Family tree, do you mean a phylogenetic tree (http://en.wikipedia.org/wiki/Phylogenetic_tree) or a "classification" tree?

I very much doubt that you will find any sort of family tree for edible plants, because a plant that is edible may be closely related to another that is poisonous.  The common example is the Solonaceae family https://en.wikipedia.org/wiki/Solanaceae which contains familiar foods such as potatos, tomatos, and peppers,  along with datura, mandrake, and deadly nightshade.  Indeed, some parts of plants may be edible while others are poisonous, as with potatos and the aboveground parts of the plant.

A tree of edible and non-edible would be the complete tree. Remove some elements and you have a partial tree, of edible plants. The accepted answer has already covered this, but thanks all the same!

Basically just search "thing you want" and "phylogeny" and you'll find a million results on Google.  For you, I might recommend the Botanist in the Kitchen blog, which has a whole page on the subject and has assembled this phylogeny, including many, many others.  It's pretty impressive!

Yes, it is definetely the best solution. For detailed information concerning the phylogeny of any taxon, the best website to my knowledge is http://tolweb.org/tree/ but it will not be good looking like any picture you wil find with a simple google search. There is also this site http://www.onezoom.org/ but I am not sure it is complete.

I hadn't heard of http://onezoom.org before, that's pretty neat.

+1 for bringing my attention to Botanist in the Kitchen – what a great site!

Thanks, I think this is pretty much what I am looking for. Botanist in the kitchen is great too. onezoom.org seems good but have not found a plant section as yet.

Beware that tolweb is not very accurate: from what I understood, they lack the funding necessary to update it. So it doesn't reflect the state of the art in terms of phylogeny.

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


text:
Evolutionary Cell Structuring
I'm a total novice when it comes to biology, and I'm really just looking for an answer to a question that has been posed to me by people who deny evolution fervently.
Evolution dictates that we've gone from simple, single cell organisms to complex, multicellular organisms. If we consider the hand, for example, the hand is made up of various cells. Those cells are created according to DNA, which acts like a cell-level instruction manual.
Where are the "instructions" for where those cells go? I.e Where are the instructions that state that various cells have to line up in a thin, long, appendage structure to form a finger, or hand.
This isn't a particularly difficult question, I imagine. If it's been asked before, apologies. I don't know any of the technical terminology; this is just something that I would like to learn about.

I am afraid you would expect a simple answer but the subject is actually very broad. It is called Developmental biology or Ontogeny. This wikipedia article might give an introduction into this subject. Or maybe one wants to smake a summary this field. Or do you want specific details on the regulatory genes, signaling cascade, transcription factors, gradient of signaling molecule, mechanism of apoptosis and other things allowing to develop a hand?

Well, and I know this might be wildly ignorant, I was hoping for some sort of biological governing principle that will explain how cells behave in this way. If you could give me an answer to my question (even if it's complex, I'm pretty good at understanding stuff) that would be cool. I'm kind of just looking for an explanation of what happens to produce this effect (in this case, the hand).

Ok, I am not able to make this precise answer for the hand, but I'm sure someone will ;) I just wanted to give you the wikipedia links and to let you realize how this field is called and how big it is.

@ChrisCooney I would recommend the book "Endless forms most beautiful" by Sean B Carrol. I think it will give the best answer to your question in a simple, non technical language.

The main governing principle is very simple and one of the most elegant mechanisms in biology. It is based on concentration gradients.
Briefly, certain cells secrete signaling molecules (called morphogens) that are detected by other cells. These molecules then activate the transcription of genes in the target cells. Since the molecules in question are produced by a subset of cells, their concentration varies according to the distance between the receiving cell and the producing cells. Different concentrations of the signalling molecules have different effects and this allows the formation of really quite complex patterns.
This can be illustrated very well using Wolpert's classic French Flag Model:

So, different concentration thresholds of the morphogen result in different patterns of gene expression. This simple system can give extremely complex results (such as yourself, for example). It gets more complex when there are multiple morphogens acting in tandem. Say morphogen1 is produced by cells on the left and morphogen2 by cells on the right, cells in the middle will have varying concentrations of both morphogens and will react accordingly:

Just about every pattern formation during development boils down to differential concentrations of diffusing morphogen molecules, it really is a wonderful example of how simple systems can give rise to extremely complex results.

On an unrelated note, this has absolutely nothing to do with evolution. At least no more so than any other biological process. If your friends do not accept evolution, I don't see how they can use this as an argument. Even if a god created humanity in his or her image as these people tend to believe, babies are still born and they still develop in the womb. As far as I know, even the most fundamentalist Christians do not believe in a mechanic god that puts babies together in the womb from some kind of IKEA kit. Even if humans sprung fully formed from the hands of this god, individual infants are still formed out of multiple cells. There is therefore a need for a mechanism that can coordinate this process, whether this mechanism evolved or was designed is irrelevant, it is still there and extremely easily observable (images taken from here):

The image above shows the locations and concentrations of various morphogens in a fruit fly embryo. You can see the concentration gradients clearly.

Just to explicitly answer "Where are the instructions?", they are in the DNA of the cells (which tell them to secrete and respond to the morphogens that terdon speaks of).  [And note terdon's point that this is just from studying cells as they exist here and now, and not related to how the cells got here.]

Wow, thanks for the detailed answer. So, if I have understood this correctly; a single cell produces these Morphogens. Morphogens are chemicals that, depending on their concentration, cause varying behaviour in surrounding cells and causes the cells to change and form different patterns. Because of the huge variations in concentration, this allows for a huge range of patterns. Is it also these Morphogens that cause the cells to bind together in the way that forms "the hand"?

@ChrisCooney Well, it's not a single cell that produces the morphogens but various groups of cells. You might want to look up Spemann's organiser for example. The rest of your analysis is pretty much correct, as for binding, that's a different issue but that too will be affected by morphogens, yes. It is the morphogens' concentration that causes one group of cells to form an index finger and another to a pinky for example.


text:
how to close a severed artery/vein?
This is a medicine-related question that I've been wondering about. I've been watching medical lectures on YouTube regarding the human body and was wondering about how surgeons treat a severed artery or vein (think Juggular or Carotid)? Specifically I was curious about what kind of tools they use and what the technique is for performing this operation.
And before anyone asks, no, I don't need to treat someone with this kind of injury :).
Thanks,
mj

They use clamps and act very very quickly.

So they clamp the blood vessel, suture it, and then release? What happens if the vessel has been damaged such that know it's going to take a while? Do they ever put in a sterile tube to join the two severed ends? Thanks for your response.

Sorry, no idea, I'm a biologist not an MD which is why I only posted an answer. Perhaps someone else here has knowledge of surgical techniques but they are not a part of biology so I wouldn't get my hopes up. Also bear in mind that this will only happen if the vessel is severed during an operation. If this happens anywhere else the chances are that the patient will be dead long before a doctor can get anywhere near them.

I likewise don't know, but here's an oddly in-depth story about a hockey player who was cut on his carotid.  The relevant point to back up @terdon is that he was clamped for about 15 minutes, which apparently isn't that long (I beg to differ...).  But anything major and for much longer will leave you dead.

I'm not really how specific an answer you are looking for, there are literally text books on the subject.  In general we contain as fast as possible, isolate, and reconnect or close depending on the options.  It's also not really correct to lump veins and arteries together as they are treated differently. Was there under a particular condition that you were curious about?  The Juggular or Carotid are not good examples of what you would normally run into in a live pt outside of surgery.

I presume that arteries in the appendages are more commonly injured? I had no condition that I was curious about, just the general question about how they splice the artery back together w/out a patient dying.

My father has had a few surgeries where they put a catheter up his femoral artery. When they're done they close up the artery and then bring in the heaviest male nurse they have to lean on the surgical site for about 20 minutes to apply pressure.

I'm going to take a shot at putting a whole lot of information into a small answer, so let me know what parts need more explanation.  To any others experienced with closure, I am certainly skipping plenty of steps and ideas in attempt to convey the general.
******A general warning that graphic surgical images are used below.******

The Setup:
You asked about "severed" jugular and carotid injuries, so we will focus on neck injuries, with a focus on insults to the R/L common carotid arteries (CCA) and the R/L internal jugular vein (IJV).  To get everyone on the same page visually, we are talking about the large blood vessels in this image:

For the sake of simplicity, we will deal with injuries that are focused directly on these vessels.  In reality, there are so many different and important tissues tightly packed in the neck that there are often many complications and multiple vessels that need to be dealt with near simultaneously.  Further, we will suppose that our patient (pt) is unlucky to have a "severed" vessel in his neck, but lucky enough to have immediate access to ATLS.
Just like you should have learned in your basic neighborhood CPR/aid class, you address the ABC's (MD's add DE): A irway, B reathing, C irculation (D isability, E xposure).  In reality when presented with a pt bleeding from the neck, you will almost always begin by applying pressure at the wound site, while you address the airway.  When I say "applying pressure" I literally mean a nurse or medic putting their fingers up against where it is bleeding and trying to stop it like a hose.
We will assume that a clear airway is established, the pt is breathing normally enough, and under general anaesthesia.  We will also give us the advantage of having the head, and to a little lesser extent body, packed down with ice.  This will give us precious time, and help prevent brain damage.  All else is presumed to be well with the pt, and all we need to do is fix the bleed in his neck.

Identifying the problem:
Now that we have our idealized pt ready to fix, the first thing you have to do is to identify where the bleed is.  Assuming you have serious bleeding, like one would come from a "severed" CCA or IJV that normally means cutting open the wound quickly and in a controlled manner.  Again, the neck is full of tissue you don't want to damage, so a anterior sternocleidomastoid incision is normally called for when you are looking for where the CCA or IJV is damaged.  As opposed to coming from the top the way we would dissect a cadaver (as in the drawing above), the sternocleidomastoid incision will give us a side view into the neck like this:

The point at this stage is to gain control of the bleed.  You don't want to just go digging in where the vessel is bleeding, because you are likely to cause more damage than help (and in this case, loose the pt).  Instead you are going to clamp above and below where the vessel is bleeding.  This will let you suck out the blood and see what's going on.  If you happen to have a large wound in a large vein, there's a chance that a clamp won't give you sufficient control of the bleeding.  In that case you have to also use a catheter to stop the bleeding (in obtaining distil control to be specific).
In our case, this means dissecting the carotid sheath.  This needs to be done very carefully so that you don't damage the vagus nerve.
You may have noticed I kept putting "severed" in quotes.  That's because it matters how the vessels are damaged.  Were they crushed or ground apart? Cut jagged or cleanly? Transverse or longitudinal?  All of these change the exact procedures into how you go forward.  Clearly a vessel that has a small tear is easier to repair than one that has been totally separated with jagged shredding from a crush injury.  Veins and arteries won't retract from the insult in the same way either, so how you find them can be a bit different.  Here is a flow chart that shows the basic decisions:

Put it back together Doc: [warning of graphic images]
You may notice that there are basically two end points for either veins or arteries: repair it or ligate it.  There are many different technical/specific ways either can be done, but those are beyond the scope of this answer.  If the sight of open wounds bothers you, note I am going to start using actual surgical photos below.
When it's possible it's better to repair the vessel.  That means that you can close the artery where it is.  If there is just a small hole, you can suture the hole closed.  With the CCA or IJV it's more likely that you are going to need a patch.  This means that you take another piece of vein or a synthetic replacement, and suture it into the hole.  I always like to tell people surgery is a lot more tailoring than most people realize (not that this is as easy as sewing fabric).  Below is an example of where a patch would be used in the CCA:
First the tear in the artery:

And after the patch has been added:

Suturing and patching can only be used to close the vessels when tension isn't needed to repair the wound.  If the laceration or severing of the vessels are such that it has come mostly (not completely) apart, but you can still get the ends together with NO tension,  end-to-end anastomosis repair can be utilized.  This means that you take the two ends, with branches if there are any at the wound, and suture them back together.
Again here is an example of the opening in the artery (popliteal):

And here it is again after end-to-end anastomosis repair:

Now let's say that you really did get the vessel cut in half.  That's a bit of bad news for you, you're going to have to ligate the vessel.  That means sewing up the end of it to close it down.  You start above the injury in arteries and below in veins, and then you tie at least three loops--many prefer five loops--down on the vein, and make a clean cut leaving at least two loops on the part staying in the body.  Then you do the same thing on the other side of the injury.  I think this is best displayed by a video, unfortunately most of the good ones I know of are not available to the public.
This video certainly not the best technique I've ever seen but it get's the idea across.  I will search for a better video as I have time.
Now if it is possible, a surgeon will try to make a graft deal with the ligation.  The first choice is a interposition graft.  This means taking a larger vein graft and connecting the two ends of the severed vessel.  You do this after making clean ends with the ligations from above.
Here we have the femoral artery prepped for an interposition graft:

And here is interposition graft in place:

In certain cases, this is not possible.  As strange as it sounds, the ligation may just be left in place, depending on where it is.

Is that all?
No, not by a long shot, but that is the basics.  There are many different techniques that can be used, with new and better ones being invented often.  For example instead of suturing, chemical cauterizing of the ligation can be used and is quicker.  That also allows the surgery to be done through a scope.  But the basics remain the same:
Stop the bleeding, gain basic access, get full control of the bleeding, obtain full exposure/access, sew up the problem, put everything back, close up, give fluids, and send them to ICU.  Even after getting everything right in surgery, the recovery can be quite difficult.

Sources and Further Reading
Note: I will try to come back with primary sources, I started from knowing what to do and searched for sources.  Here are two great sources which contain more complete information:
1) Trauma.org  This is a great site for use by actual medical professionals when addressing trauma.  They don't really cover the basics, but they do give wonderful care write ups.  Here is the relevant reference for this answer:
Karim B, 'Peripheral Vascular Trauma' trauma.org 7:3, March 2002. http://www.trauma.org/archive/vascular/PVTmanage.html
2) Acssurgery.com  Even more than Trauma.Org, this site is designed for use by clinicians.  Relevant reference:
Wisner DH, Galante JM, INJURIES TO THE NECK acssurgery.com 7:4, 2010. http://www.acssurgery.com/acssurgery/institutional/getChapterByIDHTML.action?chapId=part07_ch04&type=tab

Great answer which deserves +1, but I'm not qualified to judge if it's accurate.

@fileunderwater I linked to many sources that will say the same thing, but I will come through with line citations later.  Answers like this take long enough to write as it is.

@mj_ Let me know if this isn't covering what you wanted to know.  You mentioned tools, and I could go as deep as to the size sutures recommended, but the spirit of the question doesn't seem to call for that.

@Atl_LED My comment wasn't in any way meant as a critique, if you saw it that way, rather the opposite. It is a great and informative answer. However, since the question was specifically asking for info on how surgeons work, I just didn't feel qualified to rate the answer - therefore my comment.

I'd give a +1 just for mentioning primary survey ;)  Great answer


text:
Can Escherichia coli survive on glucose and water alone?
I am novice to biochemistry and biology in general. I am reading Lehninger Principles of Biochemistry, and I found the following sentence at the beginning of the chapter on glycolysis:

A bacterium such as Escherichia coli can obtain from glucose the carbon
  skeletons for every amino acid, nucleotide, coenzyme, fatty acid, or
  other metabolic intermediate it needs for growth.

Does this mean that E.coli can survive in a medium containing H₂O and glucose alone? E.coli can synthesize any other nutrient it needs?

This quote is not really true.  Nitrogen is necessary for all the co-enzymes and proteins to sustain life.  In order to get energy, if E coli. needs to metabolize nitogen at all as opposed to recycling it, I'd think that the bacteria would eventually all die out.

@shigeta And where can E coli find Nitrogen, in normal conditions? I assume E coli can't synthesize Nitrogen from other atoms, since that would involve nuclear reactions!

i expanded into an answer... normally E coli live in the gut and the food we eat supplies their nitrogen (and carbohydrate) needs. Its pretty hard to find an environment on earth with no nitrogen available.

The answer and comments about N and P are correct, but the quote is literally true - since it is restricted to a statement about carbon skeletons, not entire molecules.

The minimum requirement for E. coli and other bacteria to grow and survive is called minimal medium.  It's even defined at Merriam-Webster:

a medium that contains only inorganic salts, a simple carbon source (as carbon dioxide or glucose), and water

Water and glucose are pretty easy, but the source of salts may often change; regardless, you really need some potassium, phosphate, and nitrogen for amino acid synthesis.  This page has a bunch of information on bacterial growth, including some "recipes" for a few bacterial strains.  For E. coli, the classic media is M9, which over at Sigma is made of:

33.9g Na₂HPO₄.7H₂O
15g KH₂PO₄
5g NH₄Cl
2.5g NaCl

per litre of solution.

Here are some other recipes.

Yes, but no. In other words, this quote is not probably not true in the ways you'd think.  Bacteria can survive on practically nothing for long periods of time, but whether you call that life is subjective.
Nitrogen is necessary for all the co-enzymes and proteins to sustain life. In order to get energy, if E coli. needs to metabolize nitrogen to waste at all, all the bacteria would eventually all die out.  The same feat for human beings would be to add a little sugar into sewage and surviving on it.  Nobody would die right away, but its hard to call that living maybe.
Unless a medium is exchanged, E coli in a laboratory culture will start a massive die off.  When the E coli culture becomes terminal in this way, a portion of the bacteria go into stationary phases where the bacteria can survive for very long times - for months or possibly years.  So some of the bacteria would survive, but they would be dormant. You might not call this survival, but tens of thousands of bacteria are still alive and can generate colonies if transferred to fresh media.
Laboratory cultures and media are of course artificial conditions which don't reflect the environment which bacteria are adapted.  In their life cycle, they typically have other sorts of behavior and experience low nutrient conditions often enough.  Bacteria are also different in that a 99.99% die off can be considered a typical event in some cases.

It should also need some $P$ and I would guess other things like $Cl$ and $K$ too right?


text:
Is cell membrane living
We say cell wall is dead but nobody says cell membrane is dead.
Is cell membrane living or dead ? If it is not dead then why is it not included in protoplasm :

Protoplasm is the living contents of a cell that is surrounded by a
  plasma membrane.

(Source : Wikipedia)

neither the cell wall is living nor is the membrane. It is not dead either. Being a vital part of the cell it is essential for life but the concept of life doesn't apply to it.

In addition to the comment from @WYSIWYG, you must also define what aspects of the cell membrane you are talking about - only the lipid bilayer or also the embedded proteins? The latter are most definately "alive".

Also, you question seems to imply that plasma membrane is something distinct from cell membrane, when they are actually alternative names for the same thing.

Woah, @fileunderwater how are proteins living?

@terdon Which is why I wrote "alive" and not living... What I was getting at was that membrane proteins are essential for cell function and are dynamically synthesized, while the lipid molecules are more of a passive component. But I agree the comment was probably confusing.

@fileunderwater membrane lipids are also quite essential (if anything, more so than membrane prots since there is no membrane and no cell without them) and dynamically synthesized, it's just that they are not coded for by genes. Nevertheless, the enzymes needed for their production are, so lipid production is as dynamic as anything else. The cell can produce more when needed. I don't really see any difference in 'aliveness' between lipids and proteins.

It is neither living nor dead. It is simply not alive the way that any other collection of chemicals is not alive. Is salt alive or dead?
A cell's membrane consists of a collection of chemicals (mainly lipids and proteins). Individual chemicals can never be considered living or dead, any more than rocks or water can be living or dead. While the actual definition of life is tricky, everyone agrees that in order to be alive you need to (at the very least)

Somehow interact with your environment
Be able to make more copies of yourself

Therefore, the cells themselves are alive but the individual parts of the cells are not since they cannot make copies of themselves (this gets complicated when considering some organelles but never mind that here). Similarly, you are alive but your teeth are not. While you can make more of you (you can have children) your teeth cannot make more teeth.

While I agree with the basic message in your answer, I also feel that this is a bit restrictive, especially when comparing to natural language. Earlier I was also considering e.g. teeth, and wouldn't you agree that the pulp can be labeled "living tissue" while the enamel is "dead"? Along the same lines, in plants (which can reproduce clonally, so living cannot be defined at the level of the whole organism), some cells are dead (but their cell walls might still provide a function), while others are living....

[cnd:] What about the cell walls around the living cells - are those living or dead, if they have exactly the same structure as the cell walls surrounding dead cells? I realize that this is bordering on questions concerning language and philosophy, but I feel that the possibility to talk about components of organsisms as living or dead is useful. Or do you have any other terms as suggestions?

@fileunderwater I can appreciate what you are saying but I think using the term 'alive' and 'dead' is confusing since we are talking about life. I think what you are mentioning is more related to whether or not something is capable of changing or being replenished. I would suggest the terms 'static' and 'dynamic'

@vonMises I honestly think that these terms are even more confusing. Good luck trying to convince people that enamel and hair is 'static' while pulp and hair sacks are 'dynamic' - I don't see how this would improve communication, especially with laymen.

@fileunderwater it comes down to semantics. Living is not the same as alive and the opposite of living tissue is not dead tissue. Teeth are not dead and neither are rocks, they are simply not living. The point is that life needs metabolism and reproduction, things that cannot do both are not alive. The cell's membrane is not alive, the cell itself is. Your hand is not alive, despite being made of "living tissue", you are. "Living" tissue consists of cells, each of which is indeed alive, the tissue itself is not.


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What makes drosophila eyes red? and is it stable?
I have Drosophila melanogaster which I am doing an eye pigmentation assay on in the future. To do this I will dissolve the heads, 10 of them removed from frozen whole flies, in acidified ethanol for at least 48 hours (in the dark at 25 degrees) and then measure the colour of the liquid using a nanodrop. Specifically, this measures how well the liquid reflects red light, quantifying how much red pigment is in there.
I would like to know what causes the red colour in the eye and if leaving it dissolving for extended periods of time will (or is likely to) result in changes of what I measure? (ie is the material causing the redness in the eye susceptible to deterioration, which would change the colour of the liquid it is dissolving in over time)
Have any methods type papers tested this by comparing those dissolved for longer periods to those over shorter periods?

Just on a detail - a red pigment doesn't absorb red light, it absorbs light at "all other" wavelengths.

There's been a fair amount of work on this subject but a lot of it is old - see for example this 1945 paper and this 1948 paper.  That latter one in particular goes into some good stuff: color in the wildtype is due to red and brown pigments, which the authors separated by using acidic ethanol (after grinding up the flies).  Here's a 1961 paper from JSTOR that goes into a bit more detail on some of the red pigments (drosopterin, and isodrosopterin, and neodrosopterin) and looks like a good reference for some other, more basic work on Dmel eye pigmentation.  More to the point, here's a 2013 minireview on the chemical synthesis of drosopterins, which is useful mainly for referencing a lot of other work, in particular this overly detailed chapter from 1970.  That last one has tons of info about some of these pigment-causing proteins in insects.
The only particular reference to stability I could find was from that chapter, on page 144:

The simple pterines (group 2) are chemically stable under normal physiological conditions, while the substituted (groups I and 3) and conjugated pterines are unstable. Light catalysed oxydation of the polyhydroxy side chain at C-6 is a normal phenomenon. The hydrogenated pterines are extremely unstable, especially at pH 7. Tetrahydrobiopterin, for instance, is oxidized within seconds in the light, but more slowly in the dark. [sic]

Thanks @amory - I spoke to my supervisor and we'll do a mini test of it, looks like it could be something we need to consider if it is likely to be unstable. I'll post the result in a few months!

@GriffinEvo Good luck!

you never know, it may lead to the first ever Biology SE publication!


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Henrietta Lacks Cell Line - Immortality
I'm a newbie in biology and medicine. I understand that Henrietta Lacks provided the cells that formed the HeLa cell line with which much research has been done. Henrietta Lacks died of cancer. If we assume that she did not have cancer, every cell in her body could divide for an infinite period of time, and she never sustained any trauma ever, would Henrietta Lacks have been immortal?
Thanks,
mj

This doesn't seem to be a question about Biology?  Or is your question more generally, if someone's cells could "divide for an infinite period of time" would they be immortal.  HeLa cells worked in tissue culture (TC) because of her cancer, and indeed new primary cells must be "immortalized" before they can be used in TC.  https://en.wikipedia.org/wiki/Biological_immortality

I'm curious about this from a biological perspective.

Immortality does not exist and has never existed.

No, there was nothing special about Henrietta Lacks, apart from the fact that her cells have been used for so many years (without her knowledge or consent, by the way). She was not immortal, her tumor cells were. The HeLa cell line comes from her cervical cancer cells. The rest of the cells of her body were not immortal any more than yours or mine are.
Such immortality is a classic characteristic of cancer, in fact it is a hallmark of tumor cells. Normal cells die when they are told to, apoptosis (programmed cell death) is a normal part of a functioning, healthy organism. Tumors are collections of cells that replicate uncontrollably and do not do what they're told, including dying like good little soldiers.
That is why we often use tumoral cells for cultures, since they have been immortalized, it is relatively easy to keep them alive in the lab. This means, essentially, that they produce an enzyme called telomerase which lengthens telomeres. In normal cells, the telomeres get shorter with each round of mitosis and when they get shorter than a certain threshold, they are targeted for apoptosis. Cancer cells are protected from this by the telomerase and can therefore undergo many more rounds of reproduction.
So, the cells are not special because of the person they came from, they are special because they are cancer cells.

This is very interesting because I have the same understanding: "cancer cells are "immortal" in the sense of permanent division". So HeLa cells are not very specific. But sometimes, Henrietta Lacks is presented as a unique discovery. Why is that? Is it because her cells were the first to be cultivated?

@totalMongot if you have a new question, please ask it separately, but no, there was nothing unique about Ms. Lacks beyond the uniqueness of every human being. The only reason she is well known is because eher cells were used (stolen, actually, but that's another story and easily googleable) and have been used ever since.

Ok thanks, this confirms my general understanding. Any person with a cancer pathology could have provided those cells

I believe your question is unclear, but if am I am understanding the question as:

If H.L., or anyone, did not develop cancer, was never introduced to any physical insult, would they be immortal?

The answer is no, they would not.  When we talk about aging in biology, we use the technical term senescence.  Without a cancerous influence normal aging would occur, and cell division would be halted by a number of factors.  One of the best researched causes of aging is telomere shortening.
The reason that HeLa cells can be passed indefinitely is that they are immortalized.  You can only get a few passages (allowing the cells to grow out from one plate to the next) out of primary cells directly from a human.  This varies some based on the cell type, but is a good rule of thumb.  The basic rule as to how often this can be done is described as the Hayflick limit.
So no, free of cancer and all insults may mean you lead a long life, but you will most certainly not be immortal.


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What do the signs +/+ +/- mean in this image?

I don't understand what this graph is supposed to explain, especially what the signs +/+ or -/- mean. I just know it characterises some rats.

Where did you find this graph? In a book? If yes, do they give their source? This would help a lot.

No it was just a copy in an handout given in class

Diploid organisms, such as we are, generally have two copies of each gene (excepting the sex chromosomes in males).  In order to display the genotype for each, geneticists use shorthand.  When referring to a gene, + means the wildtype, which is the "normal" version, and - means that the gene is missing, often a knockout.  So a typical individual's genome for a particular gene will be +/+, a hemizygote (one copy deleted) is +/-, and a complete knockout is -/-.
The image is talking about peroxisomes, claiming that they are required for life, specifically the gene Pex5.  You can look at the graph at see that compared to the wildtype (open circles), the -/- individuals (open squares) don't make it to a normal birth weight; their lifespan is less than three days.  The +/- hemizygotes (filled circles) match the +/+ wildtype, indicating that this locus displays haplosufficiency, which means that only one functioning copy is needed for a typical phenotype.


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Large scale reverse transcription?
I need to make RNA:DNA duplexes. I can make 100 to 200 ug of mRNA through in vitro transcription, and I know how to use reverse transcription to make a cDNA library, but I have questions with this.
The mRNA I make with IVT is all poly A RNA, and the reverse transcription kit I have says to use 5ug of total RNA or 500ng of poly A RNA. I need to make at least 10ug of RNA:DNA, which is 20 times the suggested limit for poly A RNA, so a direct scale up probably isn't practical.
I can't find a literature precedent for making such large amounts of DNA through reverse transcription, everything I have found that uses RNA:DNA duplexes used short strands that were chemically synthesized and combined, my mRNA is 1800 bases long, so I can't just order an oligo, I have to make it.
EDIT : I can't comment on my own question.
The duplexes will be about 1800 bases long, it's for firefly luciferase.
Trying to make the DNA for the duplex from the original DNA template presents other issues. While it would be easy to cut it out from the plasmid, it would be double stranded, and I would have to mix with the RNA and heat it up to dissociate everything and hope that the RNA bound before the DNA strands reassociated. I also think it would complicate my controls, because it would be harder to say that any expression I see after delivering these duplexes came from the RNA and not the DNA. Of course synthesizing the DNA from the RNA could also introduce that problem.
Some crude calculations suggests that the dNTPs are the limiting reagent for a transcript this size, and that even with 5ug of mRNA I should have enough oligo dT primer for the reaction. I right now I am running reactions from 0.5 to 5ug of mRNA, 1uL of primer, and 4uL of dNTPs, to make sure I have enough. Hopefully the gel will turn out ok.
EDIT: I got the results. So far it looks like 3.0ug of mRNA works the best. It has the darkest band, and looks like the right length. Less mRNA gives fainter bands that appear too short, and more mRNA gives slightly fainter bands that appear slightly too short. Also, I ran the reaction for 2 hours instead of 1.

Can't you use the template you used to synthetize the RNA? You'd need two restriction sites to remove the parts you don't want, but using DNA to synthesize RNA and then using that RNA to synthesize DNA again seems a bit cumbersome.

how big should your RNA-DNA duplexes be ?

The best way for scaling up these kinds of reactions is to set up many reactions. Prepare a mastermix for lets say 20 reactions. You can pool them together, precipitate the RNA and dissolve to appropriate concentration in nuclease free water. Also, use gene specific primer instead of oligo-dT and don't add poly-A tails (poly-A does not affect the in-vitro stability of RNA).
As Mad Scientist already indicated, you would not need to make DNA again from RNA. Simply take 1:2 molar ratio of your IVT template dsDNA (restriction digested) and the RNA (post IVT). Heat and anneal slowly. DNA-RNA hybrids are stronger then DNA-DNA hybrids and the former is more likely to form after annealing. You can digest the unpaired strands using enzymes like mung bean nuclease.

I had almost forgotten about this question. I think we've all but abandoned this idea, RNase H seems to be a problem with RNA DNA hybrids, we paired a PolyA tailed mRNA with a 25 base oligo(dT) and dosed it to mice, completely stopped protein expression. If we used an oligo(rU) the signal was not affected, so we suspect it's RNase H cutting the polyA tail off and starting the mRNA degrdation process.


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Microscope recommendation for an amateur?
I am a mathematics student looking for a hobby and this has come up as a potential hobby. Thus I am interested in buying a high-magnification microscope that is within the limits of my budget.
My first question is, is high-magnification always better? That is, what are some examples, if any, where high-magnification isn't preferred?
Secondly, I am thinking of getting either the "OMAX 40X-2000X Digital Lab LED Binocular Compound Microscope with Built-in 1.3MP USB Camera and Double Layer Mechanical Stage". I have no idea what most of that jargon means, except that it is digital and it can magnify up to 2000x. http://www.amazon.com/40X-2000X-Binocular-Compound-Microscope-Mechanical/dp/B006MX03Q0/ref=pd_sbs_indust_4
Is there any reason I shouldn't get this microscope?

What are you trying to look at? I think without a sense of your goals, it would be hard for people here to help you with your question.

That's the question; what are then possible goals, @Oreotrephes?

Got it. I think others can answer this better than I can, but I think your first point of differentiation is going to be whether you want a "dissecting scope" which is easy to use and lets you look at things that aren't squished flat; or a "light microscope" (like the one you link to) which gives much higher magnification but for which you'd have to prepare slides. The former is great for looking in more detail at macroscopic things (e.g. living insects, whole flowers); the latter is appropriate for looking at things that are truly tiny (e.g. cells).

Why would I want to use it for macroscopic things if I can use my eyes? Also, what magnification do you need to see cells? @Oreotrephes

For anything more than about 40X you will also need a preparation laboratory and very good/expensive lighting.

Higher magnification is definitely NOT always better. Indeed, the microscope you are considering is designed for maximum magnification of 1,000x. The 2,000x is achieved by adding 20x eyepieces BUT it creates what is known as 'false magnification'. 2,000x is beyond the resolving power of a light microscope so what happens is that the image is magnified 2,000x but without a corresponding improvement in resolution. In fact, you will notice a degradation in image quality....it's like magnifying a pdf on your computer....it gets bigger but you still can't read it! And in any event, you will never use 2,000x let alone 1,000x! Read this article http://www.microscope.com/education-center/articles/false-magnification/
Second, I advise against buying an integrated digital microscope. Far better to buy a standard trinocular microscope and add a microscope camera. The reason is that the camera will be obsolete within about one year while the microscope should last a lifetime. If anything goes wrong with he camera, you will have to buy an entirely new microscope. Moreover, with separate scope/camera, you can switch cameras on the same microscope or use the camera on a different microscope. For more info read this article http://www.microscope.com/education-center/articles/digital-microscope-options/
Look for a lifetime warranty. A mechanical stage is standard and helps move the slides on the stage.
In full disclosure, I own www.microscope.com so give me a call if you would like any further assistance. You will not find false magnification or false advertising on our website!

I'm using oil immersion @Charles.

To answer your other question, you need a low power (also known as dissecting or stereo) microscope in order to see close-up views of specimens visible to the naked eye. For example, you can see a bee, but you need a stereo microscope to see the wonders of its eye. Similarly, you can see a rock or a diamond but you need a microscope to see the crystalline structure. Typical magnification ranges are 7x-45x or 50x with most work undertaken in the 20-30x range.
For viewing cells on slides, you need a high power (also known as biological or compound) microscope. Typically, these range from 40x-1,000x.


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Transfer of antibodies from mother to fetus
My questions: When does fetus begins to acquire antibodies from mother? Does it continue throughout the pregnancy?
From Wikipedia: http://en.wikipedia.org/wiki/Passive_immunity

This occurs around the third month of gestation.

From Helena Curtis Biology :

During the last month of pregnancy , the baby usually begins to acquire antibodies from its mother,....

I believe that both these sources are reliable but they contradict when the transfer of antibodies starts.

only IgG-1, 3 & 4 cross the placenta. The transfer of antibodies would start as soon as umbilical vein develops.

@WYSIWYG Yup, those are the antibodies that are transfered but I am interested in when they are transfered.

as i recall, they are actually gathered by cells and actively transported across the placental barrier.  there is an Fc receptor.  a trained immunologist might be the best person to answer this question.

Both are technically correct.  Here's a review that goes into some detail about the process: IgG Placental Transfer in Healthy and Pathological Pregnancies.  It's worth a read if you're interested in the subject.  In particular, it cites a study of immunoglobulin transport which:

demonstrated a continuous rise in IgG levels in the fetal circulation between 17 and 41 weeks of gestation. Fetal IgG concentrations were only 5%–10% of the maternal levels at weeks 17–22 but reached 50% of the maternal concentrations at weeks 28–32. The majority of IgG is acquired by the fetus during the last 4 weeks of pregnancy, and fetal IgG concentrations usually exceed maternal ones by 20%–30% at full term.

So it begins a wee bit before week 17, so definitely within the second trimester, but it is only by the third that concentrations begin to be truly meaningful.  However, most of the antibody acquired, going above the maternal level, is done in the last month.


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What are the ESSs among hawks, doves, retaliators, bully and prober retaliators?
In his book "The Selfish Gene", Richard Dawkins says that retaliator emerges as an evolutionary stable strategy. But I think dove is also a kind of retaliator and so if dove increases,  the hawks and others can exploit them.
Is retaliator an ESS? If not, which strategy is ESS?
Definitions:

hawk : They always fight hard and retreat only when injured.
doves : They merely threaten in a dignified way and never hurt anyone.

If a hawk fights a dove, dove runs away. If dove meets dove they go on posturing until one of them is tired and retreats. If a hawk meets hawk they fight until someone gets seriously injured or dies.

retaliators : A retaliator plays dove at the beginning of every fight. If opponent attacks, he attacks , if opponent behave like a dove he behaves like a dove. When 2 retaliators meet they behave like doves.
bully : A bully behave like a hawk until someone hits back. Then, he runs away.
prober retaliator : He is like a retaliator but he tries a brief escalation of the contest. He is hawk like if opponent doesn't strike back. If opponent strikes back he behave like a dove. If he is attacked he retaliates.

The pay offs: 50 for winning, 0 for losing, -100 for being seriously injured. and -10 for wasting time in a long contest.
Source: The Selfish Gene

Why would you label the dove a kind of retaliator?

Could you please describe the kind of payoff matrix in play and the definition of the different strategies (dove, hawk, retaliator)?

@fileunderwater As retaliators play like doves at the beginning of every fight and 2 doves do exactly the same thing as 2 retaliators will do when they meet.

@remi.b Sure. Will edit the question----

@biogirl But that is the whole point of the retaliator - that they behave as dove initially, but then retaliates. Doves don't retaliate (they always back down if challanged) so I dont see the point of labelling them as "...a kind of retaliator".

@biogirl Also, I think you should limit your question to one particular evolutionary game. Your question now refers to five different strategies (which can also have various payoff schemes), and to analyse all these is too much for a single question. Are you most interested in the hawk-dove-retaliator game?

@fileunderwater But when two retaliators meet they behave exactly as if two doves are meeting.

@fileunderwater I am actually interested in choosing out of all these five.

@biogirl Well, I think the question is too vague and broad. If you want to compare all five categories, you should also assign payoffs between all "encounters" more clearly, since this will ultimately determine the ESSs.

I think Dawkins answers this in the book as well.
The point was that most strategies are not stable because the "random" introduction/mutation/evolution of some alternate strategies will disrupt a population of the first strategy.
The example was a group of doves being invaded by a single hawk (the conspiracy of doves). Because the hawk does relatively better (by winning every conflict against a dove), than even after generations of entirely doves, the random addition of a hawk (say by mutation) will take hold because the hawk always wins against a dove. Whatever feature/gene that created a hawk in the pool of doves will be passed to some offspring.
If I remember correctly, the only stable case was prober-retaliator, since all others get invaded by someone else.

Yeah he has answered it in the newer editions....


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Transfer of antibodies in breast milk of humans
Why isn't the IgA secreted in breast milk digested due to proteases of the digestive system in the baby?
Wikipedia says:

The secretory component of sIgA protects the immunoglobulin from being
  degraded by proteolytic enzymes, thus sIgA can survive in the harsh
  gastrointestinal tract environment and provide protection against
  microbes that multiply in body secretions.

But what exactly does the secretory component do?  What is the secretory component?  Is IgA absorbed in the circulation of fetus? I remember reading it somewhere that it is not absorbed, at least in humans. Please answer these questions focusing more on humans. Though, information about other animals will be appreciated as well.

I haven't read it through, but maybe this might help: http://www.ncbi.nlm.nih.gov/pubmed/8292260

It is!  Here is an amazing review from 2011 that literally has all the answers.  I'm not kidding, all of them.  I would marry this review if I could.1  It also includes information on other animals.
The main takeaway is that IgA from milk is not readily absorbed by the infant body.  Secreted IgA is mainly to provide a protective coating for the mucosa while the infant is developing its own nascent immune system.  IgG passed along from the placenta (your other question) provides the main source of absorbed antibodies.  As it says in the review:

Milk sIgA is not taken up by the infant’s intestinal mucosa. In fact, gut closure in humans occurs before birth and little immunoglobulin is absorbed intact in the intestine after birth. However, the presence of sIgA in the intestinal lumen is part of the protective function of the epithelial barrier in the intestine... Secretory IgA is considered to be the primary immunoglobulin responsible for immune protection of mucosal surfaces such as the intestine.

In terms of enzymatic activity, the digestive system will in indeed chomp up the antibodies; that's part of the reason breast feeding should continue as needed.  That's okay, because there's plenty to go around:

Much of the immunoglobulin consumed in an immune milk can be expected to be partially or completely digested, however some portion of the immunoglobulin will remain intact or at least partially intact and capable of binding to an antigen.

It turns out that immunoglobulins are moderately resistant to digestion, at least more so than other milk proteins.  There's a section in there detailing some experiments where Ab was given to individuals:

In adult humans consuming a bovine whey protein concentrate, approximately 59% of IgG and IgM was detected by radial immunodiffusion from effluents from the jejunum, while 19% was detected in the ileum. These estimates of digestion of immunoglobulin compare with estimates of digestion of milk proteins in adult humans which are approximately 42% complete at the end of the jejunum and 93% complete by the end of the ileum, again underscoring the relative resistance of immunoglobulins to digestion in the gastrointestinal tract.

Digestive enzymes vary as to which antibody they prefer to digest, but at least some of them will technically digest the antibody, but still leave functional Fab fragments, which are still immunologically active and useful to the infant immune system.

1: Did I mention I love this review?  I love it.


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Nocioception (pain perception) in subcutaneous tissue
There seem to be no nocioceptors (pain and temperature sensitive nerve endings) in subcutaneous fat. there are nocioceptors and other receptors in veins running through fat, but these can be avoided. Does this mean that subcutaneous fat can be cut, or otherwise traumatised, such as with diathermy (burning) without causing pain?

No nerves no pain I guess...

"no nociceptors in subcutaneous fat"

Well nerves innervate tissue, but only the layers of skin above the hypodermis (Subcuteaneous fat layer).
You are correct.
If one was to burn below this layer they would not feel pain in that area due to having no nociceptors.
There is a great Kharn Academy video on this topic here.