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How does "be altruist to those who are similar to you" evolve?
There are many cases when people commit altruism. One is relationship. I am willing to die for 2 of my children or 8 nieces, say an evolutionary psychologist. Another is reciprocal altruism, which is just a selfish cooperation rather than true altruism.

In the 1930s J.B.S. Haldane had full grasp of the basic quantities and
  considerations that play a role in kin selection. He famously said
  that, "I would lay down my life for two brothers or eight cousins".[8]
  Kin altruism is the term for altruistic behaviour whose evolution is
  supposed to have been driven by kin selection.

Is it possible that humans may be altruists not for their 2 children or 8 nieces but to say, 1000 people that are similar to them.
If so, how does "Be altruist to 1000 of people similar to you" evolve?
Note: If the answer is negative, then we will have a hard time understanding voting. Why sacrifice your time. However, if the answer is positive that humans do love other humans "a little bit" then voting, or even suicide bombing make sense. Those humans sacrifice their little time to improve reproductive success of those who are similar to them.
Answer DOES NOT have to be about humans. If you can show me why strong/weak chimps tend to help each other or whether alpha males like one another, that'll do. Of course, naturally we would expect that leaders need followers and followers need leaders. But sometimes there are behavior that defy even this complementary nature.
Similarity does not have to be genetic. For example, fellow programmers and fellow engineers tend to be gang up.... Or does it have to be genetic?

Can you rephrase the question so that the example is not directly political? There's a valid question here, but in my opinion, it's packaged in a way that is not appropriate for this site.

I see. The problem is voting is always taking from one guy to another. It's not about common goals. I am picking the simplest sample. I suppose I can make that the other way around of middle class diligent people wanting to lower tax. The truly rich don't care about tax though. Google pays like 2% income tax or something.

Also this "altruism" toward someone not related but similar may explain suicide bombing, rather than just mere voting, for example. It explains why people are loyal to their religion, etc. I think I should have used samples in animals.

I changed the questions and the packaging. However I can't find a less political samples where I can put some math in it.

I think this article may be of interest Children, but Not Chimpanzees, Prefer to Collaborate - Rekers et al., Current Biology 2011

@JimThio My objection to this question stands. I understand that your questions stems from your political beliefs, but your examples make this question argumentative.

I've removed all the overt political stuff, that is not on-topic here, this site is about biology, and not a vehicle to promote your own political ideas.

If you make a statement like "I am willing to die for 2 of my children or 8 nieces, say an evolutionary psychologist." please provide a citation. To me it seems like you refer to some pop evo-psychology material instead of a authoritative source.

The above answers are good, but have unfortunately confused some of the concepts in the theory, I will do my best to explain.
What we are assessing is how does one behaviour evolve, links with cooperation and altruism are applications of this. The process of selection in evolution removes the the worst individuals from the gene pool, thus those with comparatively good genes survive to reproduce. With physical traits these mechanisms are well understood, with behaviour there are still multiple theories which have not been concluded but our understanding of them is reasonably complete.
Inclusive fitness is the combination of direct and indirect fitness, direct being your personal fitness, indirect being fitness gained from others. In general this is measured in terms of reproductive success (RS) (the number of offspring you successfully raise to reproductive maturity). Out of this understanding came Hamilton's Rule:

                               r.b > c

Where r is the relatedness, b is the benefit & c is the cost. In this scenario the cost is a reduction in RS, the benefit is a gain in RS. Benefits are multiplied by the relatedness to the offspring. In normal diploid organisms (Gets DNA from both parents) you are related by 0.5 (half from mother, half from father), but only related to your brother/sister's offspring by 0.25. Thus, if you have two children you have a direct fitness of 1, if your brother has two children you gain an indirect fitness of 0.5. Thus, you would prefer under normal circumstances to have your own children rather than raise your brothers.
Altruism is suffering a cost for someone else's benefit, @Winawer mentions the greenbeard theory, which rests on the assumption that if you can tell someone has the same genes as you then you know that you are related to them in someway and this will be on average be greater than to any other individual. Altruism is a behaviour, defined above, and not a specific action like giving up your own reproduction, thus it is a part of cooperation and not separate from it.
It is true that there are different forms of altruism however these are all just perspectives pertaining to the same theory. ALL behaviour is selfish, reciprocal altruism is just an example of this. Reciprocal altruism, is "If you scratch my back, I'll scratch yours" (You need help now, I may need help in the future), it is altruistic because you suffer a cost for another's benefit but it is selfish because it is still in the individual's interest to help. This is where prisoners dilemma comes in, this is basically asking the question "how do I pick the most optimal situation in this scenario?"
For simplicity, it is generally ill advised to study behaviours in humans because of the implicit bias we have in our judgment on ourselves. From political and religious associations that cloud judgment to the fact that we always strive to see ourselves differently. Also, there are all sorts of ethical difficulties in actually testing and manipulating theories on us. Thus we normally study animals to get around this. However your question specifically talks about people so I will try and answer this based on biological theory alone.
Based on the foundations above, why would someone behave altruistically to someone only 'similar' to you? The biggest difficulty is knowing that we understand all the costs and benefits involved, most of the time we only know some of them and its impossible that you can know all of them because you can't know what you don't know. Humans have effectively 'bootstrapped' behaviours which are 'for the good of society' building on from previously developed behaviours. However we are still fundamentally asking a question about Hamilton's Rule. Being seen as a part of society induces altruistic behaviour towards you (because you are seen as worth something), this is good for you and the costs associated with being altruistic are usually low. Thus you would never rationally die for 1000 unrelated individuals unless you had at least had all the children you were going to have and raised them to be independent. But you would vote, by voting you suffer a tiny cost, your time, for a huge benefit. Benefits might include:

Being seen as caring for others (altruism given to you)
Possible benefits to yourself (less tax, more support, better roads, clean air.. etc)
Possible benefits to others related to you
General good moral of your community, leading to a better life.

There could be thousands of other benefits that I can't, off the top of my head, think of. The cost is negligible and the benefit is intangible but probably higher than the cost. Relatedness isn't important (so long as it is greater than 0), if the cost is sufficiently low or the benefit is sufficiently high. I hope this has helped clarify your thinking and answer the question.
For further information:

Wikipedia is great for getting an overview of terms and definitions, but remain critical of what you could be reading.
A decent book on animal behaviour in general is: Alcock J. (2009) Animal Behaviour: An evolutionary approach. 9Th edition. Sinaur Associates.
Academic papers; if you have access to them (i.e. are an academic)

Provides the foundations
Hamilton W.D. (1963) Evolution of altruistic behaviour. The American Naturalist 97 354
Hamilton W.D. (1964) The Genetical Evolution of Social Behaviour I . Journal of Theoretical Biology 7 1
Hamilton W.D. (1964)  The Genetical Evolution of Social Behaviour II. Journal of Theoretical Biology 7 17
The current controversy mentioned in another answer is from this paper, it is widely dislike but does have some support. It is slightly off topic from from the question here, but eusociality is fundamental to our understanding of evolutionary behaviour:
Nowak M.A., Tarnita C.E. & Wilson E.O. (2010) The Evolution of Eusociality. Nature 466 1057

Very good answer. Let me read. By the way, humans related fitness with brothers and sister should be .5 not .25. It's .25 from Mom and .25 from dad.

+1 for picking that all actions are actually selfish. The thing is the genes are selfish. So how come gene "be nice to fellow programmers" evolve?

Somehow I feel that even suicide bombing (the terrorist die but others can reproduce better when free sex is illegal) is still selfish. Here the cost is actually significant. Moreover, the similarity is religion, instead of genes. I guess I didn't take into account that terrorists do get paid well (by their community standard). But some variables are still missing.

For small costs altruism it make sense. I tend to observe that people treat those who have the same religion with them as "family".

This is an important question in evolutionary biology, but you need to distinguish the biological terms 'altruism' vs 'cooperation'.
Altruism in biology means giving up your chance to reproduce so that someone else can more readily.  This is not like a gorilla troop, where only one male breeds, and the rest contribute to mutual security.  A more typical example is a honeybee or an ant, where the vast majority of the hive have no ability to reproduce at all.  This happens in animals, but is relatively rare. Its causes are currently the subject of intense debate but as far as I know, the only cases are where you do this for others who are genetically similar to you.   That logic sort of plays out as you say: "My brother has kids, why do I need to have any? I'll just help out a little bit there."
Cooperation includes forming groups for mutual safety and increased competition for food resources are why you might vote or schlep down to the DMV to get a drivers license when simply getting in your car without might be just as good most of the time.
Cooperation is incredibly common in biology.  It even happens between species.  A dolphin helps a ship navigate submerged rocks, symbiotic bacteria in our gut help us digest food, but also get enough to live and reproduce.  The benefit is always win-win in such situations.
To understand how cooperation occurs spontaneously, one of the best experiments to look at is the Prisoners Dilemma experiment.  If individuals are in a situation where you are likely to see each other again later (like a society).  The most successful ones are the ones who treat each other reasonably well, even if you do look out for less reliable types.  Why do people from Northern climates have strong hospitality traditions?  "Today you (are in trouble) tomorrow me."  As the saying goes.
There are individuals who are not cooperative, but the selection forces are positive enough that those folks will regularly disappear from the group, while more cooperative types will become more numerous.
This is a significant selective pressure that you can train robots with very simple reward mechanisms to cooperate.  http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.144.2881

+1 for mentioning prisoner dilemma, which is the real issue. In cooperation, every single individuals are better of cooperating. In voting they are better of not voting. Voting are secret anyway. Ah perhaps going to voting booth is a way to hang out with neighbors. Also the cost for voting democrat is the same with the cost for voting republican? Or perhaps humans are not entirely selfish but care about others, say by 1%? But how does care about others' reproductive success, by 1% reproduce?

thanks - ive had to go over this quite a few times in the past year - glad the question came up.

The question's a little broad, but I'll answer the question in the title:  how does "be altruist[ic] to those who are similar to you" evolve.  It turns out one way is discussed by a simple theoretical model called the "green-beard" model.  In essence, it says that a gene for altruism can spread if it produces a characteristic that can be perceived by and recognized in others (the 'green beard') and promotes altruistic behaviour towards other greenbeards.
Wikipedia has a round-up of some examples of this in action;  my general feeling from reading on this is that though it's a good idea in theory, greenbeards won't be too common in practice because of the difficulties involved in keeping out mimicry (as in many signaling systems) and because of the complexity involved in creating and maintaining all three parts of the greenbeard effect on the part of one gene.  For that reason, it's been suggested that it may be more common in smaller organisms like bacteria, where this machinery can all occur in the same cell.

This answer makes sense. It still doesn't explain why humans vote.

That question answers itself if you think about what voting really is. It's the most concise way of stating your opinion - exactly what is needed if a lot of opinions are to be assessed in a short time. It's merely a device, an idea somebody once came up with and which has since proven useful again and again. I wouldn't attach any evolutionary idea to voting (except if we're talking about memes).


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What is the number of cells in a line of a fingerprint?
I have been reading a little about the size of cells and was curious as to how small they really were.
I have noticed that on my finger, the outlines of the fingerprint are made up of thin lines. In fact, some of them are so thin that I have difficulty imagining anything thinner I can make out with the naked eye.
I have read that the naked eye has a resolution of 0.1 millimeters = 100 micrometers, whereas eukaryotic cells range in diameter of 10 - 100 micrometers.
Putting this information together, would it be reasonable to conclude that the lines on my fingers have a width ranging from 1 - 10 skin cells? Is there any satisfactory method to verify this without fancy equipment? Is it even true?
P.S.
Are there also more scientific names for these "finger lines" so that I can look it up somewhere? Googling "finger lines" brings up a lot of stuff about palm reading.

Are you just asking how large is a typical cell?

I think the scientific term is friction ridges

@Kevin More or less. But it doesn't have to be as large as "a tpyical cell". I am looking for something encountered in everyday life that I can use as a ballpark to compare with other things. I have heard stuff about how "so and so" many cells could fit in the tip of a needle, but it seems silly to think that way because a metal needle doesn't have any cells.

@math4tots I agree that the needle isn't a great size reference because the size of the tip isn't an "everyday life" kind of thing. However, I don't see why something has to be made up of cells to act as a reference for judging the size of cells. http://scaleofuniverse.com/ might be interesting to you for relating magnitudes of scale. Make sure to catch the human blood cells (~10 micrometers) between the micrometer and millimeter markers.

I am not sure that this can be accurately estimated because the outer layer of skin is ill-defined in terms of cells and cell boundaries. The outer layer or epidermis is composed of dead cells and dead cell parts that is tough and interconnected by design. Individual cells are not readily discernible.

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What is the role of acetylcholine in blood pressure regulation?
What is the role of acetylcholine in the cardiac cycle and in blood pressure regulation?

I hope this answers your question:
So the heart is an electrically excitable tissue: it pumps due to action potentials that start  from specialized heart cells called nodal cells and these nodal cells spread the action potential to surrounding heart cells. These nodal cells are found throughout the heart and they make up what's called the conducting system. These nodal cells don't need neural or hormonal input for them to spread action potentials, they have this mechanism to spontaneously start action potentials on their own called a pacemaker potential, BUT they can be influenced by neural (think sympathetic and parasympathetic) or hormonal input. These external inputs change the frequency (the pace) of the heart beat by influencing the pacemaker potential of the nodal cells.
The sympathetic nerve fibers send out epinephrine which cause the pacemaker potential to occur at a faster rate, that's why during exercise (when epinephrine is released... hopefully) the heart beats faster. Parasympathetic nerve fibers send out acetylcholine which causes the pacemaker potential to occur at a slower rate, thus slowing down the heart. What does this mean in regards to the cardiac cycle? It influences how much blood (the volume) is ejected during the cycle. The volume of blood that is ejected from the ventricles, called cardiac output (CO), which is also how many liters/min, is determined by 2 other factors: stroke volume (volume of blood ejected during each ventricle during systole) and heart rate (CO = HR x SV). And therein lies a part of the answer to your question: when heart rate decreases because of parasympathetic stimulation, cardiac output should also decrease, granted stroke volume stays constant.
I unfortunately do not know how acetylcholine affects blood pressure. I've read a paper of how acetylcholine induced relaxation in hypertensive rats, but I'm not sure of the mechanism, like how it affects systolic or diastolic BP.

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Could an animal with an open circulatory system survive in a near-zero gravity environment?
An animal such as a crayfish relies on gravity to keep its circulatory system running. If it is turned upside down, the gravity works against the system, suffocating the animal. Now if, instead of placing the animal on it's back, we were to take take it to a space station, gravity would not be working against it, and random blood flow plus capillary action should get some blood flowing. Would the animal survive this?

How does a clamfish clam?

I believe that fruit flies have been taken aboard the Space Shuttle for experiments. They survived and the adults have an open circulatory system.

Would a larger animal survive?

You'll have to dig a bit to see what is known. I vaguely recall that spiders went into orbit as well, likely to observe web-spinning behavior and characteristics. The link I provided may give you a place to poke around NASA's biology pages. If you're real serious about this, I could ask a Shuttle astronaut I know, but she is training for another mission and may not be able to provide any reply.

A list of animals sent to space also includes crickets, snails, sea urchins, brine shrimp, jellyfish, orb spider, silkworms, carpenter bees, ants (several species),hissing cockroaches, and various butterflies.


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If the xylem of a woody plant is composed of dead tissue, how does sapwood become heartwood?
If the xylem of a tree is composed entirely of dead tissue, then that means the sapwood is dead. If so, how does it transform into heartwood, and what starts the process?

I'm no expert, but I liked this question and did a quick literature search:
Xylem cells are certainly dead at maturity, and it is these cells that make up the majority of what we call wood. However, wood also contains other tissue types, some of which have live cells at maturity. From what I can glean here and here, it is ray parenchyma tissue that is responsible for many of the changes that take place during the transition from sapwood to heartwood. Ray parenchyma is formed at the vascular cambium, along with xylem, during stem secondary growth (wood formation). Ray parenchyma cells remain alive for years after the xylem cells in the sapwood die. Their functions are transporting nutrients radially in the stem, and storage of carbohydrates.
As the stem grows in diameter, there is a zone of transition from sapwood to heartwood where the ray parenchyma tissue begins to die. Before it dies, the cells undergo some metabolic changes and begin to synthesize secondary phenolic compounds (many different kinds) from stored starch or sugars. Then, as ray parenchyma cells die, they dump these phenolics into the surrounding xylem tissue, and the accumulation of these durable, decay-resistant compounds in the xylem leads to the formation of heartwood. In many hardwood trees this parenchyma death and phenolic accumulation is preceded by vessel-plugging, in which the ray parenchyma cells form balloon-like growths that block the flow of water through the xylem. So, once sapwood changes to heartwood there should be no living cells left, and the water transport capacity of its xylem is gone or greatly diminished.
There appears to be quite a bit of variability between species in when heartwood formation occurs and what triggers it. From what I could see in my brief literature search, it is all under fairly complex genetic and hormonal control that remains an area of active research. I would suggest (and speculate a bit) that the trigger has something to do with maintaining an optimum amount of sapwood as the tree grows in leaf area (which increases demand for water transport) and height (which increases demand for support, or stem diameter).


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How do the lungs act as a sieve to trap blood clots?
Does anyone know? I'm curious to find out  as my human anatomy and physiology book doesn't go into much detail on how the lungs function as such

Just as an intro...
The heart pumps deoxygenated blood from the right ventricle, through the pulmonary arteries (pic) which then eventually split into small capillary networks that surround the alveoli. The alveoli are formed by the trachea eventually branching off. So when you breathe in, the alveoli become filled with higher levels of oxygen.
The blood then becomes oxygenated and returns to the heart via the pulmonary veins to be pumped to the rest of the body.
The deoxygenated blood becomes oxygenated because there is a difference in oxygen and carbon dioxide concentration between the capillary network (O2 low / CO2 high) and the alveoli (O2 high / CO2 low) and so gas diffuses across because of the difference in concentrations (pic).

Physiology textbooks explain these mechanisms but for blood clots in particular, you'll need to check out a pathophysiology book.
Blood clots
When a blood clot travels to the lungs, it's referred to as a pulmonary embolus or PE.
Most of the time (90%), pulmonary emboli are formed in deep veins of the lower leg. These then travel to the pulmonary circulation system.
Large emboli block larger vessels - the pulmonary arteries and their branches. The smaller ones travel further into the network.
Patients can sometimes be asymptomatic and the emboli can at times resolve on its own. The extent of the severity of a PE is determined by:

how much blood flow is obstructed;
how long the embolus has been there; and
presence other underlying lung or heart disease.

There are a number of things that a PE can cause physiologically.
Reduced Gas Exchange - alveolar dead space occurs when an alveolus is ventilated, but not perfused with blood. This, along with other factors, cause varying levels of hypoxemia (lack of oxygen).
Pulmonary Infarction - in a small amount of cases loss of blood flow to lung tissue can cause tissue death. This is fairly uncommon.
Right Ventricular Failure - if there is a large enough blockage (> 50 - 60%), the pressure in the pulmonary arteries increase. Subsequently, the load on the right ventricle is higher.
So in acute cases, the ventricle hasn't had time to adapt (hypertrophy) and so the right heart can fail.
At any rate, the haemodynamic balance can be disrupted when a PE is present.
In the elderly or people with underlying disease where their lung function is already decreased, PEs can have a significantly larger effect because they can't compensate. There are many more important points related to this but hopefully this is a useful (very) basic overview.

The possible advantage of this is that if the embolism being trapped in the lungs is that it does not continue on through the left heart and into the systemic circulation, where it could cause a stroke, acute myocardial infarction (heart attack) or infarction of other vital organs.  Of course, if the pulmonary embolism affects a large portion of the the lung then this advantage is entirely negated.

I'll ask the lung experts I work with later today for a better answer. To my knowledge, the lungs, as an organ, have a very extensive capillary network that facilitates gas exchange. If blood clots become mobile in the blood stream, they can travel perfectly well in large vessels, but once they get down to a capillary, they are physically blocked from passing through. The blood clots don't have to be large in size, because the capillaries are only about 6 micrometres in diameter.

But if a blot clot gets stuck in a small capillary, won't it get occluded and prevent blood flow? I know that the lungs have a mechanism to prevent ventilation-perfusion inequality, and if a blood clot did get stuck, there would be bronchioconstriction of the airway leading to that alveolus, but  I don't see how just getting stuck in a capillary makes the lung a sieve for blood clots. I do appreciate you asking the lung experts. Thank you for answering!


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If only dicots have pith, what is the foam in the middle of cornstalks?
I've heard that the only plants that have pith are dicots, because of the shape of their vascular bundle. If that is true, what is the foam inside of the corn plants, which are monocots?

Monocots do have pith in their stems. The link even has an image of a maize stem:


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What are the evolutionary niches differentiating an apple from a pear?
So, as far as I understand (basic) evolutionary theories, diversity is generated by "niching." That is, if there is an environmental factor that hasn't been fully used by any species to "profit" off, there will be a tendency to fill up that "niche" and thus speciation occurs (not in one day of course).
I was standing in the kitchen earlier and was wondering: what is the niche that an apple fills in respect to a pear end vice versa? If I'm not mistaken they are form the same family and thus share a common ancestor (albeit I don't know if it is a "recent" ancestor).
Is it a geographical thing or do they genuinely vie for the same thing in a different way? (e.g. a pear aims to be eaten by animals that have small teeth and thus want a softer fruit, while an apple aims to be eaten by the bigger animals, that like a heartier bite).
note: I know that this question might be too speculative and too localised to be any good, but hey, some of you might just know this!

I would be very, very surprised if the current day fruit of apples and pears gives us a good indication of what the ancestral fruit was like. Remember that, like almost everything else we eat, apples and pears have been dramatically altered by artificial selection.

The ancestral apple is thought to originate in what is now Kazakhstan. See this report from the USDA on this topic. Those early apples were small and likely eaten more often by non-human species.
Pears: From Wikipedia: The genus is thought to have originated in present-day western China in the foothills of the Tian Shan, a mountain range of Central Asia, and to have spread to the north and south along mountain chains, evolving into a diverse group of over 20 widely recognized primary species. A citation for this is needed.

so they would be related only so far back in history that their differences are merely a product of very long separation in region?

Once something is cultivated for commercial purposes, it's genome is under tremendous selective pressure. As evidence, consider the origin of the tomato - small and toxic. It is bred and has been bred for very different properties over the last centuries. Apples and pears can be related at the family level, or more related than you think they are based on color, size, taste, region where grown, etc. Most pear trees survive because they are grown on quince root stocks - so differences between these species are not as great as may appear at first glance.

I chose this answer because it has the most explanatory solution: humans did it.

The Botany of Desire by Michael Pollan has a chapter on apples, where he discusses the hypothesis that apples were originally domesticated by bears. That book is a great read if this kind of topic interests you.  I'm not aware of a similar hypothesis about pears, maybe it was pandas?

I wouldn't be suprised if no one has hard data on this. In any case there is more than one answer to this question.
Niches are defined more than one way.
In the narrowest definition, the niche might be defined as the ability of the different trees to grow in different terrains or be eaten by different animals in the same environment.  I can't comment on that, but in most environments, there is in practice little difference between the two.  The classic example of this is Darwin's finches - where a single species eventually becomes many, each specializing in a specific kind of lifestyle (what they eat/where they net) on the islands of the Galapagos where they were situated.
In the broadest definition of niche, they do have a different niche because they are different species, and their differences allow them to be eaten by different people.  In their highly domesticated environs, apples and pears each have a niche defined by the fact that they are both stocked in the produce sections for people to eat as they choose.

Its worth mentioning that Darwin determined that different organisms can inhabit the same niche.  In his case he saw that on different islands of the Galapagos he saw that the finches had evolved into different species, each of which took up the role that a different bird might have back home.  so its possible that apples and pears may have substantially the same niche in their respective evolutionary histories.

Yes, people drive the current distribution of these fruit trees.


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How does the human body metabolize gasoline?
A Chinese man has been drinking gasoline to relieve his pain for 25 years. How does the human body metabolize gasoline? Also, what are the side-affects to gasoline?

Hopes the degassing tag is a bad pun

Made my day that one.

Don't discount the likelihood that the original story in your link is either completely fabricated or wildly exaggerated.

Just to add an answer to the 'how does the body process gasoline?' portion of the question, the liver and kidney would be doing most of the work of removing the stuff from the system once it was absorbed in the digestive tract.
The liver does most of the processing of toxins and their removal from the blood and would tend to do the most work in removing hydrocarbons from gasoline.  It has enzymes that oxygenate toxins (adds oxygens) which make them more soluable in the blood, usually less toxic, and also removable from the body by the liver or the kidney. In the case of gasoline the compounds are likely to be just as toxic.
The kidney works by actively filtering out excess water and mostly water soluable wastes like oxygenated hydrocarbons.  Kidney damage occurs when gasoline is ingested in excess.  This may be due to the toxicity of the gasoline, but also due to the compounds the liver is producing.
Gasoline will tend to be fat soluable too, so it will leave the system more slowly, even after being processed by the liver (benzene and toluene in gasoline will tend to become phenols which are quite toxic and fat soluable).
http://www.ncbi.nlm.nih.gov/pubmed/3379185

Gasoline toxicity through ingestions seems to be a topic where there's not a great deal of in-depth information available. I don't know how this works for chronic use, as most literature refers to acute scenarios. Either way, orally ingested, 30-50g is said to be toxic to humans while 350g can be fatal.[3].
So...
Gasoline's Constituents
A lot of components that make up gasoline are toxic to humans. This includes for example, benzene, toluene, xylene and butadiene. It's a mixture of more than 500 hydrocarbons and additives made up of:

60–70% alkanes (paraffins)
25–30% aromatics
6–9% alkenes (olefins).[2].

If you really want to know specifics about metabolism of gasoline, you can probably check out how some of the constituents are metabolised (processed) and their effects. This is because different components have varying metabolic pathways.
If you want to check this out, see Reese, et al at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1520023/pdf/envhper00383-0118.pdf.[3].
Ingestion and Toxicity
Apparently, most reported cases of toxicity from gasoline occur from inhalation or absorption through the skin (intravenous use has also been reported). Even though ingestion is a frequent occurrence, there's not much data on outcomes after oral ingestion.[1],[2]. Gasoline can however be well absorbed through the gastrointestinal tract[2].
The main target organ of gasoline toxicity is the nervous system and at high doses, this effect can cause death within minutes.[3]. However, generally, the primary cause of mortality seems to be related to gasoline's toxicity to the lungs. There are severe effects on the pulmonary system. Other effects of ingestion hasn't been as well documented.[1],[2].
It's suggested that these compounds have a direct effect on lung tissue and  disrupts gas exchange and causes fluid buildup in the lungs (pulmonary edema). This in turn causes the oxygen levels in the body to drop (hypoxemia).[2]. There are many other toxic effects on the lungs as well.
Additionally, liver damage, kidney damage, damage to blood cells, gastric ulcers and toxicity in the heart can occur.[2],[3]. Again, this is discussed in Reese, et al.
Hope that helps!

Rahman I. Gasoline ingestion: a rare cause of pancytopenia. Am J Med Sci. 2009. 338(5):433-4.
Domej W. Successful outcome after intravenous gasoline injection. J Med Toxicol. 2007. 3(4):173-7.
Reese, et al. Acute Toxicity of Gasoline and Some Additives. Environmental Health Perspectives. 1993. 115-131.

The implication seems to be gasoline disrupts membrane integrity and function.

Prolonged exposure to high concentrations of n-hexane (>1,000 ppm) has resulted in decreased sperm count and degenerative changes in the testes of rats but not those of mice.
Acute Data: Gasoline: Dermal LD50>5 ml/kg (Rabbit) LC50> 4500 ppm (Rat) Oral LD50= 18.75 ml/kg. (Rat)
Carcinogenicity: Two year inhalation studies of wholly vaporized unleaded gasoline produced increased incidences of kidney tumors in male rats and liver tumors in female mice. Follow-up studies suggest that occurrence of the kidney tumors may be linked to alpha-2-u-globulin nephropathy, and most likely unique to the male rat. Epidemiology data collected from a study of more than 18,000 petroleum marketing and distribution workers showed no increased risk of leukemia, multiple myeloma, or kidney
cancer from gasoline exposure. Unleaded gasoline has been identified as a possible carcinogen by IARC.
Because solvent extracts of gasoline exhaust particulates caused skin cancer in laboratory animals, IARC has categorized gasoline engine exhaust as a possible human cancer hazard.
Target Organ(s): A two year inhalation study of wholly vaporized unleaded gasoline producednephropathy in male rats, characterized by the accumulation of alpha-2-u- globulin in epithelial cells ofthe proximal tubules, and necrosis and hyperplasia of surrounding cells. Follow-up studies havedemonstrated that these changes are unique to the male rat. Although prolonged exposure to n-hexane, a component of gasoline, has resulted in adverse male reproductive effects in experimental animal studies, no adverse male reproductive effects were found in studies conducted with gasoline.
Developmental: No evidence of developmental toxicity was found in pregnant laboratory animals(rats and mice) exposed to up to 9,000 ppm vapor of unleaded gasoline via inhalation.
All data taken from the Material Safety Data Sheet (MSDS) from Petroleum Products Corp. See this link for more information.

Much of this answer is not relevant to the question about injesting gasoline (not inhaling it, inhaling exhaust, or being exposed to hexane); -1

-1. The question is not about n-hexane toxicity but n-hexane ADME (Absorption, Distribution, Metabolism, Escretion)

Vote up/down as you wish, but information on target organs and developmental effects does indeed give relevant information on how the body processes gasoline.


text:
What effect does vortexing have on a fluid sample that simple mechanical shaking does not?
Some protocols call for fluid samples to be mixed with a "vortexer" on the high setting.  What effect does the vortexing have on fluid samples that mechanical shaking does not?  Does it shear long molecules like DNA, for instance?
A friend is setting up a new lab and asked if vortexers were strictly necessary.  I am aware they are often called for in various protocols, but I actually don't know what specific effect the vortexing has that makes it better than manual shaking.  What do you think?

In my experience, shaking and mixing have different "dead spaces". Supposed you had an eppendorf tube and you stirred it around with a pipet tip for thirty minutes. You would have great convective mixing in the radial direction but virtually no mixing in the Z-direction. Supposed you had a very viscous fluid like PEG. If you set the tube on a shaker for an hour it will virtually not mix. The vortexer provides a very different profile of mixing.
Instances where I wouldn't use the vortexer would be for sensitive objects like DNA and cells.
(update)
We had some interesting suggestions from the FDA (since the FDA pays attention to these type of discussions). To get proper mixing, it is often not considered enough to merely swirl a tube a bunch. Their actual recommendation is to train technicians to perform a 90 degree angle arc with their forearm to generate proper force in mixing.

A single vortex is essential for any "wet-lab" for the reason bobthejoe describes. The vortex not only provides a different profile of mixing, but has the power to mix viscous fluids that would otherwise remain virtually unmixed (glycerol stocks come to mind). Vortex shakers are contra-indicated for some lab protocols (like in miniprep kits) but can be used for most mixing needs. As an aside, vortexing of DNA is safe in my experience. Genomic DNA tends to shear if precipitated and then vortexed, but plasmid DNA and oligos are fine.

Vortexing is called for when one or more of the fluid samples is more viscous than water?  For instance (as you suggest), 100% glycerol is 1000x more dynamically viscous than water, hence the need for a vortexer to mix water and glycerol well (http://www.wolframalpha.com/input/?i=viscosity%20of%20glycerol%20%2F%20viscosity%20of%20water).

Besides mixing fluids of different viscosities, are vortexers necessary for any other lab operations?

@Maccowell, doesn't mixing liquids of different viscosities describe most lab operation? I would also include suspending non-soluble mixtures.

what specific effect the vortexing has that makes it better than manual shaking

In addition to @bobthejoe's answer about viscous fluids, (manual) mechanical shaking is also less consistent and more tiresome than vortexing.
If the vortexer is always at the same speed and each sample is vortexed for the same amount of time, then the shaking step will be less variable among samples. For example, the vigor of mixing an aqueous soil suspension could potentially affect the amount of aggregate decomposition and release of molecules into the suspension (I don't have a reference for this, but it is good practice to treat replicates the same to minimize any non-treatment effect).
Manual shaking is not only less consistent, it is also tiresome - especially with larger volumes (>=10ml) and large sample sizes.


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Does age affect the frequency of flatus?
Is there any relation between age and the frequency of flatus? I often have this feeling that older people f*** more often than younger ones. Is this feeling scientifically correct?

Hi :) Medical questions here should be explaining how a treatment works rather than what it would be so I removed your last point :)

I do not have access to journals, but there is this paper claiming in its abstract that age DOES NOT play a role in flatus frequency.
Reference:  Furne JK, Levitt MD. 1996. Factors influencing frequency of flatus emission by healthy subjects. Digestive diseases and sciences 41: 1631–5.

Could be that age has an effect. As humans age three important factors, with respect to this question, change:

Diet.
Immune system flexibility and its response to even minor disturbances and infections.
Gut microbiota composition.

This seems to be going on the right track. Could you expand and maybe reference some studies? For instance, how does the gut microbial composition change (and same for the diet)?

I really can't take the time to reference any studies because these are easily found by searching the proper repositories. I have to spend my efforts analyzing our microbiome data to see how that is affected by diet - some very interesting results need to be published. Knowing what to look for should be enough assistance to Shyam to succeed in this quest.

Thanks @Larry_Parnell. I have posted an answer with a link to a paper on this.

@Larry_Parnell: no problems if you do not have time to reference it (I absolutely understand), but then this should be a comment rather than an answer.

Agree this is really a comment.


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Why can cones detect color but rods can't?
I don't know if this question applies to only humans but why can cones see much greater detail than rods? Is it possible to have a rod that can detect light intensity and color?

both useful answers!  sounds like its possible we could have an eye that is both sensitive and seeing color, though summation seems to reduce resolution as well... so to have the same resolution as our eyes, it would have to significantly bigger.

The spectral sensitivity of photoreceptors expressed is the key to color vision. See figure below for the sensitivity of three-types of cone cells (S, M, L) and rod cell (R, dashed line).

From this figure, one can say rod cells provide information about the "blue-greenness" of vision, however, despite their spectral sensitivity, it seems that in human vision rod cells do not contribute to color vision, because they are highly sensitive to intensity, and thus they are mostly saturated in their response (does not induce firing of downstream bipolar cells) during normal daylight conditions. Rod cells specialize for night vision (scotopic conditions) which is crucial for survival, and under this condition the cone cells are pretty much useless.

I would love to see some electrical recordings from cones and rods in response to various light stimuli. Do you know any paper showing that (I would assume some paper archeology would be needed for that)?

@nico I think it will look extremely similar to the graph already posted. There might be quirks because absorbency doesn't have an exactly linear relationship with polarization, but it will be nearly the same. Except, light actually inhibits the cones so mirrored along the X axis.

@nico I'd like to see electrophysiological time series for various intensity and wavelength stimulus as well. Let me know if you find any good source. :)

@Preece: I was speaking of some raw ephys data actually

I wish this chart was taught at primary schools to dispel some of the misconceptions about "primary colors".

@nico There is a large body of literature with that kind of data. King-Wai Yau, Denis Baylor, and W.A.H Rushton are good guys to look out for if you want the historical data. For example, here is a lecture by Baylor with some ephys data. This one has amazing data on the response of rods to single photons! Mike Do and King-Wai Yau have great data on the responses of photosensitive retinal ganglion cells.

Cone cells are each connected to their own neurone.  This allows them a great deal of resolution as the brain can interpret the exact position of the cone cell that was stimulated by a light photon.  However in order to improve low light vision, multiple rod cells are connected to a single neurone - this is called summation.  Whilst it does allow for an action potential to be generated in low light conditions, it greatly reduces resolution as the brain can not know precisely which rod cell was stimulated:

Rods can not detect colour as they only come in one variety - cone cells (in humans) come in a red, green and blue specific form to allow for the perception of colour by the brain due to the relative strength of these signals.

While the answers to date are correct regarding the wiring of rods and cones in the primate (specifically human) eye, they are also fundamentally wrong. Neither rods nor cones perceive color. The brain does. The rods and cones are just the receptors providing signals. The first answer in fact says this in its very last sentence.
As one answer says, during the day the rods are saturated (overstimulated) so the brain ignores them. It uses the components of the cone responses to invent the sensation "color". At night the cones are usually only weakly stimulated, so the brain sees only with the more sensitive rods, and little or no color. This is why brightly colored stars such as Betelgeuse and Rigel still appear only faintly tinged (red and blue respectively).
By the way, some primates have even better color perception than humans with four (or five) kinds of cones. It is speculated that color vision is so good in primates because of the need to judge fruit ripeness to eat. Many mammals have fewer cone types than primates.

What is an example of a pentachromatic—or even tetrachromatic—primate?

All of the above answers are great, and very informative.  But they are also technically wrong, in certain conditions. Once you understand them, you'll be able to understand this explanation of why.
The canonical answer is that cones are used for color perception in bright light and rods are used in low light. But rods have a peak color sensitivity that is very distinct from the cones (see the chart posted above).  And more importantly, there are light levels at which both rods and cones are equally functional for color perception.
This is known as the "Purkinje effect" or "Purkinje shift".  Basically, when light levels dim, your red color perception diminishes first, but your blue color perception is enhanced (or at least doesn't diminish nearly as fast).  The specific effect is that red objects get darker much faster than blue ones. But the brain isn't yet just perceiving the blue objects as a brighter gray, so it seems there is some color perception built into the brain based on the rods.
http://en.wikipedia.org/wiki/Purkinje_effect

yes you are right.. All chromophores have a wavelength range of absorption.. but Rods are not involved in color perception, it doesn't mean that they are not color-biased

It has been proved that rods do add to color vision at certain conditions, especially at mesopic vision, Purkinje effect. Further testing showed that when only rods and L cones are excited, together they produce identifiable hues, although only two monochromatic lights are being used. One very faint blue light enough for rods to react but too dim for S and M cones to react,  and one red strong enough to excite L cones, but too red to saturate rods. Rods may add some color information during phootopic vision as well, but only at low fotopic levels when rods are not being saturated yet. That part is still being investigated.
I have found this article to be very informative...
http://journal.frontiersin.org/article/10.3389/fpsyg.2014.01594/full


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Why does Rigor Mortis occur after death?
After someone dies they become stiff, this is termed Rigor Mortis and happens because the cells run out of ATP (I think). But why do the cells need it to remain flexible?

It is not flexible cells but skeletal muscle function or flexibility.

You are right that ATP is needed in relation to Rigor Mortis: This for ion pumps to maintain concentration gradients in cells. Without a constant supply of ATP to the pumps, calcium starts to diffuse from the extracellular matrix (and other intracellular compartments with high concerntations of calcium) into the sarcomere where it binds to troponin, a regulatory protein in skeletal muscles. This holds myosin the actin filaments together creating the effect of rigor mortis.

you might add that ATP is required to release the myosin heads from the actin binding sites, meaning that without ATP the contractions don't stop


text:
What is Curved DNA?
CbpA is DNA binding protein found in E. coli and binds non-specifically to curved DNA (Cosgriff et al., 2010), when the bacterium is in a static phase of growth.
The use of "curved DNA" confuses me. Is the term "curved DNA" essentially the same as "Circular DNA"?

Cosgriff, S. et al. Dimerization and DNA-dependent aggregation of the Escherichia coli nucleoid protein and chaperone CbpA. Mol. Microbiol. 77, 1289–1300 (2010).

It might be useful to link the source where you read the term, it could provide additional context that would be helpful for answering the question.

I've provided a link to the reference and unipot

I never heard of the term until today but a quick search implies that certain DNA sequences are more pliable than others. Most notable is the Widom sequence which binds to Histones. It is also noted that DNA isn't a free floating polymer but that there is also some directionality in its bend. It seems that the concept is bested explored in this review: Curved DNA.

it is not necessarily circular - the transcription factors usually require a curvature that is much greater than what a plasmid will have, and the requirement can show up on eukaryotic proteins as well.  DNA binding proteins will cause a local loop or curvature that fit the transcription factor.
The classic picture is for the Gal and Lac repressor proteins which bind 2 strands simultaneously, causing a loop in the DNA.
Reference: see fig 1 in:
http://genesdev.cshlp.org/content/3/5/606.full.pdf+html

I'm hardly an authority on this topic, but I distinctly recall an amazing report the mid-1990s of the co-crystal structure the yeast TATA binding protein in complex with DNA.  The structure shows that TBP bends the DNA axis by approximately 80 degrees, presumably in order to expose bases and improve recognition.  The structure is available at RCSB: http://www.rcsb.org/pdb/explore.do?structureId=1ytb . (Make sure you check out the Jmol view.)
Thermodynamically speaking, bending DNA would require energy. Therefore, DNA that was pre-bent (e.g., due to auxiliary binding proteins or composition bias) would improve binding.
So, I suspect that in the context DNA binding proteins, "curved" refers to the static curvature of unbound DNA or to the bending of DNA upon binding in order to facilitate recognition.


text:
(How) does coppicing fundamentally alter tree growth?
I am interested in adding the ability to model coppice tree production to a model of perennial crops (Miguez et al 2008)..
Implementing the biomass pools and allocation parameters required for tree growth is relatively straight-forward.
However, it is not clear to me if it will be necessary to account for any changes in growth form and physiology (e.g. allocation, allometry) associated with coppice management.
Are there any models that explicitly model coppice regrowth? Are there any particular issues that I should consider?

Fernando E. Miguez , Xinguang Zhu, Stephen Humphries, German A. Bollero, and Stephen P. Long. GCB Bioenergy . 2009 . Volume 1 Issue 4, Pages 282 - 296 (link)

According to Deckmyn et al (2004), the primary effect of coppice management is that the fraction of total biomass in roots is relatively higher after coppicing, and that a substantial fraction of carbon in roots (~20% of root mass) is reallocated aboveground to support shoot growth in the spring following coppicing.
Because of this large re-allocation, coppiced plants are able to grow more rapidly (and reach canopy closure sooner), than seedlings (Ceulemans et al 1996) it is important to consider that canopy closure (maximum leaf area index) occurrs more rapidly after coppicing

Deckman et al, 2004 Poplar growth and yield in short rotation coppice: model simulations using the process model SECRETS. Biomass and Bioenergy doi:10.1016/S0961-9534(03)00121-1
Ceulemans et al, 1996. A comparison among eucalypt, poplar and willow characteristics with particular reference to a coppice, growth-modelling approach Original Research Article
Biomass and Bioenergy, Volume 11, Issues 2–3, Pages 215-231 doi:10.1016/0961-9534(96)00035-9


text:
Does testosterone increase female sexual behavior?
According to my lecture notes testosterone generally increases sexual behavior.
Given that it's generally thought to be the male hormone I'm not quite sure whether they mean that it also increases sexual behavior in females.
What is the effect of testosterone on female sexual behavior?

I'll point you to this article by A. Tuiten et al.
To quickly answer your question, yes,  testosterone does have an enhancing effect on the sexual behaviour of human healthy adult females.
The (admittedly small) study indicated that after an dose of testosterone was given to the women there was found:

a statistically significantly [sic] increase in genital responsiveness (P = .04)
a statistically significant association between the increase in genital arousal and subjective reports of "genital sensations" (P = .02) and "sexual lust" (P = .01)

A time lag was reported from the administering of the dose to effects being seen of approximately 4.5 hours.

References

 Tuiten A. 2000. Time Course of Effects of Testosterone Administration on Sexual Arousal in Women. Archives of General Psychiatry 57: 149–153.

What's harder to answer is whether (or to what degree) that's due to testosterone to estrogen conversion or due to testosterone receptors.

Although male testes are responsible for huge testosterone secretion, testosterone can be produced by other organs both in males and females. So, women do have testosterone. Similarly,  estrogen is also produced in men and not only in women. In addition, both sexes produce the androgen and the estrogen receptors, so endogeneous or external testosterone will be active in women. Among other things, testosterone supplementation have been shown to be useful in clinical studies conducted on women suffering from hypoactive sexual desire.
Woodis et al., Pharmacotherapy. 2012 Jan;32(1):38-53. doi: 10.1002/PHAR.1004.

And let's not forget that testosterone can be converted into estrogen by the aromatase, so it can actually work through the estrogen receptor.

Right, and aromatase KO male mice develop steatosis, clearly indicating that estrogen is important for male liver.


text:
Is there a tool to find the action of an enzyme in a metabolic pathway?
Is there any tool to search the biochemical action of a particular enzyme in a metabolic pathway of an organism? In other words, how can I find if enzyme "E"  is involved in the metabolic pathway for organism "X".

I think the KEGG pathway database may be of some use to you.
Link is here: http://www.genome.jp/kegg/pathway.html
This a database of manually drawn pathway maps, I have used the site myself and it is very useful in determining if your enzyme is in a pathway and where it lies in it. This is assuming though, your enzyme is in the database and has been mapped.


text:
What does "nesting failure" mean?
According to the Wikipedia article on swans, swans are mostly monogamous but may sometimes separate, particularly after a "nesting failure". What "nesting failure" may mean is not entirely clear to me. Does it mean that they they have literally failed to build a physical nest? Or is it that they have failed to produce offspring? Or is it something else entirely?

Apparently it refers to the inability of nesting the eggs, because the nest was somehow destroyed, or environmental conditions were unfavourable.
I found a few examples pointing in this direction:
The Trumpeter Swan page on the Yellowstone National Park websites reports that:

Nest flooding is the primary cause of nest failure. Egg predation by coyotes, ravens, and otters does occur.

From the abstract of: Nesting Ecology of Bewick's Swans on Vaygach Island, Russia - Syroechkovsky et al., Waterbirds, 2002

Nest failure was mostly due to abandonment of nests in cold weather rather then to predation. Climatic conditions in spring are the main determinants of nesting success for swans on Vaygach Island.

From this article:
Reproductive Success of Exotic Mute Swans in Connecticut - Conover et al., The Auk, 1999 (PDF)

Egg survival was defined as the proportion of eggs in successful nests that hatched (Johnson et al. 1992). Successful nests were those from which at least one egg hatched. Egg survival is referred to by some authors as hatching rate (Willey and Halla 1972). Eggs left in the nest after incubation ceased were considered abandoned.

and

We determined the cause of failure for 33 nests: 46% were flooded, 27% were abandoned, 15% were disturbed by humans, 6% were lost to predators, and 6% failed after a parent died.

Actually, nesting failure means that nesting trial fail before offspring could even leave the nest. In case of precocial species (where chicks leave nest immediately after hatching, like swans) it means that eggs was destroyed or parents abandoned nest, as @nico point out. In case of altricial birds (offspring stay in nest) nesting failure may also mean that all nestlings died before leaving nest.
for example among House wrens (Belles-Isles & Picman 1986):

About 81%
  of nesting failures (n = 30) were due to predation (contents disappeared before the expected fledgingdate). Females abandoned seven nests, and starvation (presumably because
  of desertion by parents) accounted for one nesting failure.


text:
What's the effect of oxygen deficit on plants?
As I know all cells require oxygen. So my question is how efficiently can plants operate in no-oxygen atmosphere? Do all plants produce enough oxygen for themselves? Can they consume their own oxygen or the oxygen will be quickly lost to the air? Is there a plant that consumes more oxygen than they produce?

During the daylight, the plant is photosynthesising faster than it is respiring so there is no net uptake of oxygen (the oxygen of course being produced in the as part of the photosynthesis).
Of course, this only applies for tissues where photosynthesis is occurring.  In the roots of the plant, oxygen must always be present in the surrounding soil/growth medium for respiration.  Therefore if there is no oxygen in the roots then the root cells will be unable to produce ATP from respiration and consequently die.  This will eventually lead to the death of the entire plant as it is unable to take up nutrients due to the lack of a functioning root network.
This is the cause of plant death when soil is waterlogged - the water fills spaces in the soil that would otherwise contain air (i.e. oxygen).
Certain plants (often crop plants), rice being given as an example in the comments below, are able to survive being waterlogged and the resulting low oxygen supply. However they can only do so in the short term.  Rice plants in particular have adaptations that allow the transport of oxygen from the aerial parts of the plant down to the roots.  This does of course mean that the rice can not survive being totally submerged for an extended period of time.  Plants such as rice may have better adapted anaerobic fermentation pathways that become the main producer of ATP when aerobic respiration has arrested thus allowing them to better cope when transiently submerged than other plants.
Molecular strategies for improving waterlogging tolerance in plants

still there are plants that feel well in water-flooded environment, as rice for example.

Can you address @Anixx's point?

@Abe plants that routinely encounter saturated soils have adaptations to get O_2 to the roots.  The "knees" of Cyprus trees are an example as are the "air roots" of Mangroves.  Wetland monocots can also have hollow stems that allow them to transport air below the air-water interface.  Offhand I don't know how rice does it but adaptations to saturated soil are not uncommon.


text:
Structure of RAP Antibodies (Specifically RAP-5)
[EDIT] - Have just found not one but two papers that address my structure problem. However they concern RAP-1A, so I guess my question is now what is the difference in  structure and function of RAP-1A and RAP-5? Does anyone know of X-ray structure analysis being used to examine RAP-5?

original question
I'm a University Physics student writing a mock review article on what to me feels like a very 'un-physicsy' antibody - RAP-5.
Although my knowledge of Biology is pretty poor, research is going quite well. I've found a lot of papers from the 80s talking about conducting immunohisto(/cyto)chemistry experiments, most of them finding that RAP-5 can be used to determine whether a cell has the ras in it, so they are able to measure the percentage of cells that are neoplastic (I believe this means cancerous) and contain ras and the percentage of cells which are normal and contain ras. (the ras-gene being a proto-oncogene which on mutation can result in permanently switched on ras proteins (p21?), which results in proliferation of cells and therefore can cause tumors). This is all very nice but on first glance immunohistochemistry doesn't seem to involve a huge amount of physics (for my bio-physics assignment), apart from using an optical microscope.
I was hoping to be able focus a section of my article on the physical techniques involved in determining the structure of RAP-5. Although there seems to be plenty of literature on uses of RAP-5, I am struggling to find anything on the details on why it is able to be used in such experiments. In other words, I presume that its function is to bind on to an epitode specific to the ras protein (amino acids 10 -17 have popped up a few times) but I don't know if there is any imaging one can do to have a look at the structure and conclude 'yes this is why it binds to ras proteins and not to others'. Is there a technique that is likely to have been used to examine the structure of RAP-5? Is it's tertiary structure likely to be 'Y' shaped like other antibodies? Does it differ in structure from RAP1-4? (this book informs me that RAP1 and RAP2 have 60% sequence identity, but most sources seem to leave out RAP3-to-5, some evening telling me that the RAP family consists of RAP1A/B, RAP2A/B/C and no others!).
Also, if RAP-5 is an antibody, does this mean that it is produced in the body and gets involved in the ras protein signal pathway in order to reduce too much ras expression? (am I right in saying the amount of expression is the amount of protein the ras-gene is producing?) or is it only synthetically produced and used in experiments to measure the amount and location of ras proteins?
Also there seems to be little differentiation between the differences in the functions of each RAP. RAP-5 seems to be used quite a bit in experiments involving Ha-ras - but not exclusively. Do the different RAPs bind to different variants of ras? Ha-ras being the one unique to RAP-5.

I'm not sure is RAP5 is an antibody. Seems to be more of a transcription factor.

Also be careful with your literature search since there is both the Ras related proteins (RAP1A) and the Receptor associated protein domain (RAP/LRPAP)

Also are you sure you're not talking about RAB5c and not RAP?

it is no easy to determine the structure of rap5, but i know the related protein rap1 antibody

The confusion that you're facing is because RAP-5 is actually known as RAB5C (GENEID). The ras superfamily (review) is divided into Ras, Rho, Rab, and Rap. But the Rap GTPases are divided only into two categories, RAP1 and RAP2. On the other hand, there are multiple Rab GTPases which include RAB5A and RAB5C.
There are a few crystal structures of both Rab5A and Rab5C in both human and murine forms.
Now, for RAP-5. RAP-5 is a monoclonal murine antibody which has no relationship to the RAP family of proteins. It's probably called RAP because Spandidos and Wilkie weren't thinking clearly when they named their antibodies RAP1-5. In this case, you're probably better off looking at the antibody Y13-259 which is probably called that since its the 259th antibody they tried.
To answer your questions, specifically, very few people have attempted to get a structure since it is an antibody and everyone knows what they look like. Secondly, the antibody is produced in a mouse and added to tissue. And yes, the RAP antibodies bind to different variants of Ras. Also, no one uses RAP-5 since anti-Ras EP1125Y seems to be more popular.
If you still want a crystal structure, I would hunt down the RAP5 patent and look up the peptide sequence. From there, you can look up similar structures in the IMGT database


text:
How do insects such as crickets circulate blood through their antennae?
Some insects, like the crickets pictured below, have such slender antennae it seems no blood could fit. How do they get blood through their antennae?

Insects do not posses closed circulatory system, but a space where organs float in a fluid called hemolymph. They don't have blood vessels (but some arthropodes have pumps that act a like heart). The hemolymph allows nutrients and excretion products to diffuse, but usually doesn't serve as a means to transmit oxygen to the tissues.
In insects, the oxygen is pumped through a series of little tubes named tracheae. Trachae connect the tissue directly to the air, allowing gas diffusion efficiently.
Antennae and wings have very little metabolic needs, mainly because (in the first case) they're formed by some neurons. Movement is achieved by muscles located in the base of the antenna (where it doesn't have circulation issues). The nerve tissue has the neuron bodies located in the basis too, so the nutrients and oxygen can diffuse through the axon.

Insects primarily get oxygen through diffusion of air through their skin.  I doubt the antennae need hemolymph circulation.

References, please

the answer above this one? lol

"I doubt the antennae need hemolymph circulation." doesn't sound very scientific. Can you add references, or explain why a little better?


text:
Why don't dragonflies wings collapse?
How do dragonflies manage to fly at such high speeds without their wings collapsing? Their wings are thinner than paper, but they do not even flutter. What gives them their strength?

http://jeb.biologists.org/content/206/17/2989 N/m2

Wootton (1992) reviewed the anatomy and biomechanics of insect wings. Basically the wing is a lightweight but strong scaffolding of veins, supporting a thin membrane. The veins are composed by a sandwich of cuticle with a potential space in between. The membrane is also a double-layer but without the space.
In the venous space are is circulating hemolymph and often nerves and tracheae. The wikipedia image is pretty good:

The nerves carry sensory information and the tracheae oxygen.The hemolymph is continuous with the body and thus is able to circulate and hydrate the wing (important for maintaining flexibility). As Wootton says:

desiccation destroys both compliancy and toughness, and a dry cuticle would be mechanically disastrous

So by maintaining a flexible tissue, insects have strong and tough wings that remain light enough.


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Pedigree Probability of Autosomal Recessive Trait
Here is a pedigree:

The trait is autosomal recessive.
The question is:  What is the probability that the bottom 2 people (4 and 5) have a child with the trait?
I tried doing 2/3 * 2/3 * 2/3 *1/4 and got 2/27 but this is wrong. I thought that the probability of III 1 being a carrier is 2/3.  The probability that IV 4 is a carrier is also 2/3.  The probability that III 6 is a carrier is 2/3 and IV 5 must be a carrier.  So IV 4 and IV 5 must be carriers.  The probability that they have a child with the trait is 1/4. But I am not getting the right answer.
The right answer is 1/6.

You have now got sufficient rep to avoid new user restrictions so can post inline images yourself - you can either do this manually using markdown or there is a button on the WYSIWYG editor :)

Starting with the left hand side of the diagram:

III:2 is definitely a carrier (Tt) as one parent (II:2) is affected (tt).
III:1 is also definitely a carrier (Tt) as when mating with III:2 they produce an affected (tt) offspring (IV:1)
This means that we can work out the possibilities for IV:4 as we know the parent genotypes.  It follows the standard arrangement for two carrier parents giving the options of:

TT (1/4)
Tt (2/4 = 1/2)
tt (Normally 1/4 but in this case 0 as individual not marked as affected).

Therefore for this scenario, the probabilities for IV:4 are :

TT (1/3)
Tt (2/3)

Now if we look at the right hand side of the diagram.

IV:5 is definitely a carrier (Tt) as one of their parents (III:5) is affected.

This gives two possible Punnett squares to be examined:
|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

This gives nil affected offspring so we can disregard this option for your question (as we are ONLY looking for scenarios which produce affected individuals).
Therefore the alternative is:
|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         t |              TT                |                tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

Giving 1/4 affected offspring.
As mentioned above, in order to have affected offspring then IV:4 must be Tt.  There is a 2/3 chance of this being the case.  If this is the case, then there is a 1/4 chance of the child being tt.
Both conditions need to be true for this to happen so we multiply the fractions:
2/3 * 1/4 = 1/6


text:
Basic Amino Acid Residue Binding Mechanism to DNA
I understand that many protein DNA binding domains bind to DNA via basic residues such as Arginine and Lysine. But what is the mechanism used to bind to DNA and where on the DNA would these residues bind?

This question has no particular answer.  There are several families of DNA binding proteins, some of them bind specifically (e.g. restriction enzymes like EcoRI which binds to and cuts GAATTC or transcription factors like lac repressor which binds a particular point of the e coli genome about 25 base pairs long) and some of them bind semi-specifically (e.g. zinc fingers which bind GC rich regions), others non specifically (e.g. the sliding DNA clamp).
For all of these proteins, they will have a tendency to have positively charged amino acids facing the DNA because the DNA's phosphate backbone is negatively charged.  There are lots of protein motifs (like the helix turn helix motif) that fits into the major or minor groove of the DNA.  The lysine and argenine are important because they are the positively charged amino acids.  Histidine is also positively charged, but it is not as long and flexible, and doesn't seem to fit as often or as well.
http://en.wikipedia.org/wiki/DNA-binding_protein

I'd make a comment if I could, but our lab has worked with a lot of poly lysine peptides for binding DNA. In our experience, lysine works better than arginine, and both work a lot better than histidine. Histidine has a lower pka, so it tends to be less positively charged at physiological pH. As far as proteins binding to specific DNA sequence, the double helix has two grooves, major and minor. The "sides" of the base pairs are accessible through the grooves, and proteins probably recognize patterns in those grooves. An A-T pair presents a different shape than a G-C pair, and DNA binding portions of proteins can discriminate these bumps and bind to the helix.


text:
Predicting progeny of recessive mutations using recombination
I was asked this question on a test and got it wrong, but I'd like to know how to do it.  The answers are shown in the blanks below:

You are studying two recessive mutations in the fruit fly D.
  melanogaster. The red_ mutation causes flies to have red bristles
  (wild-type flies have black bristles) and the shiny- mutation causes
  flies to have shiny eyes (wild-type flies have eyes that are pebbly).
  You mate females from a true-breeding strain with red bristles and
  pebbly (wild-type) eyes to males from a true-breeding strain with
  black (wild-type) bristles and shiny eyes. F1 females are then mated
  to males that have red bristles and shiny eyes to produce F2 progeny.
If you analyzed 1000 male progeny in the F2 generation, how many flies
  of each possible phenotypic class would you expect, if:
The two traits are determined by two autosomal genes that are 15 cM
  apart:
Red bristles, pebbly eyes:_____ 425_______
Red bristles, shiny eyes: ______75____
Black bristles, pebbly eyes:____ 75_____
Black bristles, shiny eyes:____ 425______

My attempt:
So I know the 15cm=recombinants/parentals * 100 but I don't see how that formula can help.

First, the recombination equation is:
cM = recombinants/(recombinants AND parentals) * 100

Let's assign the following genotypes for clarity's sake:
RR = black bristles
Rr = black bristles
rr = red bristles
SS = pebbly eyes
Ss = pebbly eyes
ss = shiny eyes

F1 cross: rrSS x RRss = RrSs (all progeny)
F2 cross: RrSs (F1) x rrss = ?

You would have the following gametes:
Parent 1, RrSs = RS, Rs, rS, rs
Parent 2, rrss = rs, rs, rs, rs

Draw your punnet square and you get the following genotypes of the offspring.
So your GENOTYPES of your F2 cross will be RrSs, Rrss, rrSs, rrss
Let's translate those to phenotypes.
RrSs: black pebbly (parental)
Rrss: black shiny (recombinant)
rrSs: red pebbly (recombinant)
rrss: red shiny (parental)

Now let's look at recombination frequency.
15cM = (recombinants/(recombinants+parentals)*100
recombinants/(parentals+recombinants) = 15/100

This tells you for every 15 recombinants, you have 85 parentals. If you scale this up to 1000, that's 150 recombinants for every 850 parentals.
Your 150 recombinants comes from 75 black/shiny and 75 red/pebbly.
Your 850 parentals ceoms from 425 black/pebbly and 425 red/shiny.
Anyways that was my attempt which appears to be directly opposite to what your answer key says. Did you copy it down correctly?


text:
How long does it take for E. coli to shift feedstocks?
With our fermentations we're noticing that it takes an appreciable amount of time for E. coli (K12 variant) to change from being metabolically streamlined on amino acids to being metabolically streamlined to glucose.
How long does it take for such microorganisms to adjust to a new feedstock?

This must depend upon the conditions in question, but I think it would not be very long.
The length of a generation for e coli can be 12 minutes or 24 hours, so that gives some idea of a typical time.
I did find this interesting case in the literature. They found that even as you subject e coli to minimal nutrients they are expressing genes that prepare them for a richer nutrient mix.  The bacteria are primed for a flood of carbohydrates succinate or amino acids.
This study incubated the e coli overnight before taking their readings, so this puts an upper bound of about 12 hours.  The implication is that if you are moving the bacteria to rich media it might be just a short time before they are in log phase growth.
In practice moving from LB plates to log phase growth is usually just like 4 hours.  This paper interestingly shows that cold adapted E coli moving to other media react in a few hours, but can show behavioral changes days out.
I would say that 4 hours might be a typical expectation. 12 is typically used in the literature.


text:
What do we know about the Last Universal Common Ancestor (LUCA)?
All life on Earth (bacteria, archaea, eukarya) is thought to have evolved from a common ancestor, or last universal common ancestor (LUCA). What do we know about the characteristics of LUCA based upon extant life?

Wikipedia's article does a pretty fair job of summarizing the likely nature of the LUCA.

Seems rather broad at the moment. Perhaps one should constrain the question?

Carl Woese has much to say on this subject, including:

“The ancestor cannot have been a particular organism, a single
  organismal lineage. It was communal, a loosely knit, diverse
  conglomeration of primitive cells that evolved as a unit, and it
  eventually developed to a stage where it broke into several distinct
  communities, which in their turn become the three primary lines of
  descent [bacteria, archaea and eukaryotes].”

There is a 2000 Scientific American article by W.F. Doolittle that discusses much of Woese's (and others') work understanding this question.
Also, see a couple of Woese articles here and here.


text:
Can any plant regenerate missing tissue?
I have not yet found a plant that, when an insect eats a hole in one of its leaves, it can regenerate the lost tissue. Many plants will grow a new stem if the old one is cut, but it is not a perfect regeneration, and has no likeness in form to the previous stem. Are there any plants that can, even to a degree, regenerate missing tissue?

Essentially the answer is yes, except that your qualification "but it is not a perfect regeneration, and has no likeness in form to the previous stem." is confusing me - I would consider all stems from a single plant to share a likeness in form. No, they won't be identical, but neither is a regenerated limb identical to a lost limb.

How about the leaves?

same for leaves, I used stem as an example

So if I punch a hole in a leaf, it can regenerate the missing tissue?

it will generate a new leaf

But can it regenerate the missing tissue?

@David I know that plants can sprout new stems, and sometimes new leaves. I am a gardener. But I haven't yet found a plant that can replace a missing structure exactly. Like regenerating the tissue lost if I punch a hole in the leaf.

Most portion of leaf is made up of 'permanent tissue'-s like parenchyma, sclerenchyma etc. so due to lack of any meristematic activity, the hole would not become filled up. However such 'fill-up' and 'joining' process seen in some cases such as Grafting. (https://en.wikipedia.org/wiki/Grafting)

In general, plant cells only undergo differentiation at special regions in the plant known as meristems. Two of the primary types of meristem are the root apical meristem (at the tips of roots) and the shoot apical meristem (at shoot tips)^. Within the shoot apical meristem the plant cells divide and begin to differentiate into different cell types (such as different cells of the leaf, or vascular cells). Later growth (of, say, a leaf) is largely a result of cell expansion (although cell division does still occur, but drops off as the leaf expands). Therefore, if you punch a hole in a leaf, it probably won't be filled in because the cells in that leaf have finished growing and dividing.
However, as a shoot grows, more meristems are created. These are found in the axillary buds, just above where the leaf meets the stem. The meristems in the axillary buds can grow to form branches. Different plants obviously make different numbers of branches, but there is a common control mechanism known as apical dominance, where the meristem at the tip of the shoot suppresses the growth of the lower axillary buds. This is why a shoot with no branches can be made to grow branches by cutting off the tip (gardeners often do this to make "leggy" plants more bushy).
All of that was a long explanation to say, no, a plant doesn't normally^^ regenerate in the sense of filling in cells that have gone missing. However, if you cut off a shoot, the next remaining bud might begin to grow and, in a sense, replace the part that was lost. In that case, an existing bud is recruited to form a new branch and replace lost functionality, but I wouldn't say that qualifies as regenerating missing tissue.
^There are other types of meristem as well.
^^If you torture plant cells enough you can force them to become "stem cells" and thereby make an entirely new plant, but this is rare in nature.

One can tear the bark off a woody plant around the entire circumference of the stem/bole. If covered by a moisture barrier until the residual cambium cells form and epiderm, the phloem and bark will be regenerated. Furthermore, at the top of this girdling of a stem, enough auxin will accumulate to make cambium cells become stem cells and the form root initials. If surrounded with a moist medium, roots will grow (layering) - in a sense, regenerating roots, Rooting cuttings would be a more literal example of tissue regeneration analogous to a salamander regenerating a limb.


text:
Can fruit tissue be cultured and grown independent from the plant?
Can fruit tissue be grown in a tissue culture as is done to other plant tissues? From the answer to this question, I learned that fruit is alive. Could it be possible to manufacture fruit products without plants, using this method?

Plants are not a strong suit for me, but in general the answer is yes.  What I know mostly comes from animal tissue, so someone may have a better answer than I...
Botanists have been cloning plants from cuttings for thousands of years.  More recently, propagation from cell lines around for much longer than for animals.  Entire plants can often be grown from a plate of cells.  So you can grow roots or an entire plant from cells right now, but I can't find any mention of anyone trying to grow fruit without the rest of the plant, and there might not be any research for this.  Let me explain why this may be...
Bioengineering animal tissue and organ growth has been an intensive area of research for the past 15 years or so.  In some cases, such as the growth of skin or liver, the technology has proven to be exceptionally valuable and useful.
Using plastics with biological growth factors attached and 3D printing, even more complex organs such as bladders and tracheas can be grown from the patients own cells, which avoids the problems of rejection and the complexities of donor matching.
More recently growing muscle tissue in an animal free culture has been tried, which would relieve some of the environmental and ethical problems of raising meat animals.
All this has been driven by a strong cost-benefit payoff.  A transplanted organ is highly valuable and improving that process and making organs more broadly available for patients has a high economic value.  The more often the structure is related to the tissue around, the more structurally complex, the more difficult it is to imagine growing that organ independently of the host organism (brain and eyes come to mind).  Other transplant worthy tissue cultures look quite promising.
Right now, it seems as if plant fruit like an apple or a kiwi might be difficult/expensive to grow in the lab as opposed to just picking them off the tree.  I think that growing a banana pulp or an apple sauce might be possible, though.  Who knows what we might be doing in 50 years or more though?


text:
What conditions are necessary for HPL (human pancreatic lipase) to activate?
What conditions are necessary for human pancreatic lipase to activate? Is there an optimal temperature or pH? How quickly does it take effect?

Check this out: http://www.123helpme.com/view.asp?id=123079

There are several different lipases, you might want to specify which one you're interested in. It might help to add your motivation for asking this question, so that we might better understand what exactly you are looking for.

@Danielδ Oh my. That is almost exactly the experiment I did the other day, except I got no results. I'm wondering if my lipase was kind of smurfed.

@MadScientist I was using a 10% lipase solution; that was all the information about the kind of lipase that I was given.

Which lipase do you have in mind? From which organism(s)? There are over 90 lipase genes in the human genome.

Doesn't lingual lipase have an optimal pH  around 4 - 5? That's why it can still continue its catalytic activity even in the stomach...

I wasn't aware that most lipases needed any activation at all.  wikipedia says it is secreted from the pancreas in active form.  It might be pH dependent because its a digestive enzyme, but most lipases are....

If a lipase did not need activation, there is the risk that it would digest membrane constituents before compartmentalization and secretion. I'd expect most lipases to have a signal peptide, which needs to be cleaved prior to activation.

The protein referred to in the question is encoded by gene PNLIP, pancreatic lipase. From this annotation of the protein, I see that there is a signal peptide from amino acids 1 to 16. Thus, this signal peptide must be cleaved before the protein can be active in its digestion of emulsified triacylglyerides.
A paper describes the structural changes induced in human pancreatic lipase by lowering the pH. The secondary structure of the enzyme is stable within a pH range of 3.0 to 6.5. At this pH, a reversible opening of the lid controlling the access to the active site was observed. So, there is another aspect of activation - pH and the ability to open the enzyme lid so that the fat molecule enters the active site.


text:
What evolutionary explanations are there for death?
I know death and cancer doesn't hurt humans' reproductive success. It's not helping either.
Why do we die? Why dying humans (all of us) are common? What's the point of dying?

Not everything has an evolutionary advantage...

Cancer does hurt human's reproductive success; and evolution does fight with it.

Most cancers are post-reproductive, so fitness (strictly speaking) is 0 at that point.

This is kind of relevant to a senescence question on SE I was just came across.
A book referred to in that question, Geriatric Medicine: An Evidence Based Approach by Cassel, said biologists argue that senescence is an evolutionary byproduct rather than a bestowed advantage and is probably a result of "interaction of many genes with the environment".

@nico is correct, and he's not likely saying so with any religious zeal... for example, genetic drift is a powerful evolutionary force that has no obvious "advantage" per se. I've edited your title to remove that suggestion. but +1 anyway since it's an interesting question.

This post is very much related to your question and the answers offer a good overview of the reasons to the question "why we age? why we die?"

If there was no death,the experienced older people among animals and humans would be more successful ,so the was no progress chance for the young and the animals couldn't transfer their gen and there wouldn't happen any mutation.

An organism that spends a great deal of energy and resources protecting itself from a very rare form of damage will be out competed by ones that do not but instead spend those resources increasing its chances of mating or on its offspring.

Death is not only for humans. All 'complicated enough' organisms die (with a notable exception of Hydra, though you may argue when it comes to the complexity). It is is easier to create a new organism from scratch than to repair both internal factors (free radicals, metabolic by-products, ...) and external (physical damage, exposure to toxins, ...).
Underlying causes of death actually can be evolutionary beneficial. For example, shortening of telomeres offers protection against cancer (on a cellular level), but also bounds lifespan.
So actually they may be evolutionary competition (within the same species) of young and old. Mutations helping young but harming older may be preferred to the opposite ones.

Who is to say that having living Humans isn't hurting our reproductive success? Older non-reproducing humans cost the human network valuable resources and take up a sizeable portion of our living niche. Metabolically unstreamlined aged organisms are certainly not the most efficient and could potentially get in the way of better suited young'uns.

It's naive group-selection argument. Like "I'd sacrifice myself when I get old so that others could produce more children". But if one would live longer and help his own grandchildren - he would spread his genes better even if it would hurt the society.

@MartaCz-C: how does helping grandchildren spread genes? The only way for an old person to continue spreading his/her own gene is to have kids which would actually be bad.

@nico if person X have even 15 children but non of them have their own children through their lifespan, then genes of person X did not spread at all. One of measures of fitness is number of grandchildren.

@MartaCz-C: sure, but my question is about "helping his own granchildren". The fact of helping them in no way means you are spreading your own genes. The fact of having granchildren means you spread your own genes in the past which... well is the purpose of reproduction.

@nico Helping your relatives spread their genes is equal to spreading your own genes (if you multiply your effort in helping others by the percentage of consanguinity). That's what I mean but maybe I use wrong terminology.

+1 for effort. Flawed because it underestimate gene selfishness.

From a systemic point of view, if we wish to evolutionarily induce our descendants (descendants of the current human race on the whole) to live longer lives, we would need to pro-create later.
If the whole of human race enforced a statute that prohibits pro-creation before the age of 40, then two pronged dynamics would happen

only adults fit enough to pro-create after 40 would produce off-springs.
only off-springs born to parents older than 40 who are fit enough would survive.

Since, there is a high tendency of abnormality and low survival of off-springs born to parents of older ages, absence of resource contention and genetic dynamics would encourage the initial propagation of the rare few fit off-springs.
Hence, unnatural "natural selection" would encourage the propagation of humans of longer life-spans. Perhaps, a natural disaster or viral outbreak could discourage humans from pro-creating before age 40. Perhaps, high rates of abortion. So long as the human race does not die out due to such restrictions. Perhaps, to the satisfaction of conspiracy lovers, a secretive organisation carries out a plan every 100K years to raise the bar for child-bearing age.
Therefore, it might be less of a question of advantage and more of the effects of motivation. That current status where

high motivation for humans to pro-create early in life.
low motivation for humans to have more children as they wise-up by being tired of raising kids too early.

Therefore, since no such secret organisation exists, there is infinitesimally little motivation for the existence of a "super-virus" type of humans to exist.
There is no motivation for super-humans to exist, because the distribution of life-spans have crowded out the food and survival resources of any possible primeval super-human.

Do you have proof of your first part in your answer? I know it holds for fruit flies, but that doesn't mean it holds for humans.

There is no evolutionary advantage to dying.
So you question should be rephrased as to why organism die at all? Why hasn't evolution come up with an immortal animal that lives forever?
Well nature has actually done that https://en.wikipedia.org/wiki/Turritopsis_dohrnii Behold the immortal jellyfish.
So if we do have immortal jellyfish.. why aren't there immortal mice?
A possible answer is because mice get eaten by cats (and wolves, foxes, owls, toads, humans, etc) The idea goes like this... there is no point having genes that makes you immortal if the probability of you being eaten within 1 year approaches 100%. In fact, in such a situation, you would want genes that will allow you to have as many babies as possible before that one year is up, even if those genes result in your death (ie cancer from cells that are growing too fast in that rush to be an adult, heart problem, muscle degeneration, poor immune system.. because the body has redirected all energy from repair to reproduction). Such a trade off is worth while, as you aren't going to be alive long enough to see the downside of those bad genes.
So if this idea is correct... if an animal has fewer predators (or none at all), the animal would live longer. And yes, we actually do see such examples.
A famous example are the Opossums of Sapelo Island. The Possums were isolated on a predator free island 9000 years ago and now live 25%-50% longer than their mainland cousins. The difference is hereditary.
https://books.google.com/books?id=yYwHDAAAQBAJ&pg=PT62&lpg=PT62&dq=Sapelo+Island+opossum+long+lived&source=bl&ots=4AHZcnd8_L&sig=9Wgka1-bVl1xzJTX2F-AJhF0Y-g&hl=en&sa=X&ved=0ahUKEwi506Kq7_7QAhUI6YMKHS3FBQ84ChDoAQgZMAA#v=onepage&q=Sapelo%20Island%20opossum%20long%20lived&f=false
Another possible example is that between bats and mice. Both are small animals of similar weight. And in general the smaller the animal, the faster it breeds and the shorter its life span. Bats are a noted exception from this the rule. Bats live a very long life span or their mass. Lifespan in the wild rangers from 10 years to 40 years depending on species. Compare that to 1 year for a mouse. The difference? Not metabolism... Not mass.. Not climate. But predators. Mice have many predators. Bats very few.

One key concept to bear in mind is "mutational load".  Over time, individuals accumulate mutations - for example, older fathers pass on more mutations than younger ones.  Undesirable mutations need to be removed by natural selection each generation at at least the same rate as they accumulate, or a "mutational meltdown" occurs.  The length of time between generations needs to be set so that the number of mutations purged by deaths is equal to the number that are introduced by mutation.  Here is a rather interesting study providing some evidence for this point of view.
Note that infertility is "lethal" in genetic terms, so this concept in and of itself does not explain why a woman who passes menopause needs to die at any age.  It seems easy to add further speculation here, so I'll leave that to the reader.

The evolutionary explanation is quite simple. Without death, evolution couldn't take place in the first place at all.
Who knows that jellyfish are immortal? Did they continuously evolve from one cell (without reproduction)? I don't think so. Who knows if today present jellyfish were already alive 1000 000 years ago (i.e. without parents)? I think this is the case for any living creature.
That's why telomeres get shorter and shorter when growing older. In the case of cancer, these telomeres stay the same with each division of the parent cell, so it grows wildly. Which all species would probably do so too.

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