text:
Is there a biological mechanism for evolution encoded into our DNA?
Throughout high school, I remember learning about Darwin's theory of evolution as if it were near-fact. But something always seemed wrong about the ideas presented.

Survival of the fittest
Random mutation
Natural Selection

All of these things seem to account for some margin of evolutionary progress, but I always remained skeptical that the extremely complex features of life could have formed from these methods alone, even after hundreds of millions of years.
Here's what I notice:
Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely.

I'm going to use this example:
Turtles on an island where shrubbery grew higher up developed longer necks, to reach the leaves.
I imagine that turtle looking up at that food, and sub-consciously wishing to get to it, constantly straining, for its entire lifetime.

It seems plausible to me that we (advanced life) could have a biological mechanism to "write" needed alterations into either our own DNA or our reproductive DNA over time, triggering the very specific evolutionary developments necessary to our survival without relying on random mutation.
My question:
Is this possible? Does any similar mechanism exist that we know of? If not, how can so many specific (advanced) evolutionary leaps be otherwise explained?

You're trying to "bootstrap" your study of this material, and there's nothing wrong with that, but grabbing an article or two would help quickly clear up some of these fallacies (e.g., "Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely").

(http://www.amazon.com/Why-Evolution-True-Jerry-Coyne-ebook/dp/B001QEQRJW/ is also a great starting point, for example)

"Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely." That's wrong--the history of life is a history of unbelievably numerous failures to develop what was needed. The great majority of all species failed to develop what would keep them alive--that is, they went extinct!  And those who did develop the needed feature often developed a "good enough" version, which is far from "precise".

@Chelonian I'll leave that line to avoid falsifying parts of answers that address it, but for the record, I agree, that was a mistake. "In many cases..." is the wording I should have used.

@jt0dd Even "in many cases..." is, though strictly true, arguably misleading. What about, "In perhaps 0.1% of cases..."? (The number of extinct species "on the internet" appears to be 99.9%, but I'm looking for a reference for it.). And of course, finding those 0.1% of cases that "worked" as reason to doubt evolution by natural selection, it is sort of like being surprised that raindrops would just happen to fall into a shot glass on a field during a long and torrential downpour.

All those turtles looking up at the bushes wouldn't "cause" them to develop longer necks/legs/whatever. What would happen is that over a long time interval small random variations in neck length would give those with longer necks a survival advantage over turtles with shorter necks, so long-necked turtles would survive and reproduce. Over time, continuing random variation in neck length would continue to favor the survival and reproduction of long-necked turtles until all the turtles on the island had longer necks. The key elements are "over time" and "small random variations".

Wow, even comments to this question are long :) Scientist really don't like teleology

This entire answer will be long, so read the short part first, then read the rest if you (or anyone else) is curious. Citations are included in the long section. I can include additional citations in the short section if needed.
Long Story Short
Your question touches on some common misconceptions about how the evolutionary process. Organisms don't "want" to evolve traits. Traits evolve through the biological processes of random mutation and natural selection.
Organisms do not "want" to evolve traits.  (Well, OK, I'd love to evolve an extra pair of hands but that is not possible.) Natural selection works by modifying existing traits. Your turtle can stare all she wants at food out of reach but she will not evolve a longer neck. Instead, natural variation exists among neck lengths of the turtles because of variation of the genes that determine features related to overall boxy size. Those individuals with longer necks may be able to get a bit more food, live a little longer, and reproduce a little more. They will pass along their genes to their offspring, so perhaps more of their offspring will also have longer necks. Over many generations, the turtles may have somewhat longer necks.
A common misconception is that the traits of organisms are precisely adapted for a specific need. They are not, for a few reasons. First, natural selection occurs relative to the current environment. Adaptations that work well in one environment may not be so useful in another environment. Environments are rarely stable over evolutionary time so traits are subject to constant change.
Next, as mentioned above, natural selection can only work on what traits are present. While an extra set of arms would be handy, I am a tetrapod. My four appendages, along with the appendages of all other tetrapods, trace back to our common ancestor. The appendages of all tetrapods are modifications of that ancestral trait.
Finally, organisms haven't "sampled" the entire realm of possible mutations and combinations of mutations. In other words, a certain mutation or set of mutations might actually be able to adaptively improve a particular trait in the current environment but, if the mutations never occur, then the improvement can never happen.
We only need to look at ourselves to realize how imperfectly adapted we are. We get bad backs and knees because our bodies weren't designed to walk upright. We evolved from quadrupedal organisms. This has happened so recently that changes in the structure of our knees and backs haven't yet evolved (and may never).  Search the internet for the "blind spot" eye test. We have a mass of blood vessels in front of the retina of our eyes, which reduces our visual accuity. We often have to have teeth pulled from our jaws because the flattening of our face (relative to our australopithicine ancestors) has shorted our jaws. We don't have as much room for our teeth but we have not evolved a reduced number of teeth.
As for human technology being able to make direct changes to our DNA to improve our adaptability, I would say no. While I do not have the ability to see into the future, the complexity of our genome, and more specifically how genes are regulated, suggests to me this would be a very daunting if not impossible task.  See the long answer below for more on regulatory genes but the gist is that a small set of regulatory genes control most of the other genes (including other regulatory genes). The interactions are extremely complex and we have a detailed understanding of very few of these interactions.  I speculate that affecting one such gene in a "positive" way is very likely to have many unintended negative consequences.
Below are some simple math and other ideas to show you how mutations can lead to the many adaptive traits that you see among the diversity of life on earth.
Long Story

how can so many specific (advanced) evolutionary leaps be otherwise explained?

Mutations occur at random throughout the genome. Most mutations will be neutral. That is, they are neither bad or good from an evolutionary viewpoint. The mutations are neutral because the genome for most organisms is non-functional. Mutations that occur in the functional regions of DNA (i.e., protein-encoding and related regions) are more likely to be detrimental (bad) because the mutation may negatively affect the function of the protein or even the ability to produce the protein.  However, some mutations are beneficial. The mutation may actually enhance the functionality of the protein or even produce new proteins.
A couple of factors have to be considered regarding mutations.  The mutation rate is very low.  For example, Kumar and Subramanian (2002) compared the DNA sequences of 5669 protein-encoding genes from 326 species of mammals.  Their results suggested that the average mutation rate among mammals is 2.2 x 10$^{-9}$ per base pair (bp) per year.  This means that, on average, a point mutation has changed each DNA nucleotide position in the mammalian genome slightly more than twice (2.2 times) every billion (10$^9$) years. That's a lot of time!
However, this same rate occurs in every individual in the population, so you have to consider the population sizes of the organisms. So, let's do a simple exercise. Consider a species like the rock pocket mouse or another small mammal that has a very short generation time. For this simple example, let's assume the generation time is one year. That means that the mutation rate of 2.2 x 10$^{-9}$ per bp per year would then correspond to 2.2 x 10$^{-9}$ mutations per bp per generation. Generation time is important because new mutations are inherited only through reproduction.
Assume the average mammalian diploid genome is about 6 billion (6 x 10$^9$) nucleotides in size. The number of heritable mutations that occur in a single offspring is
$$(6 \times 10^9) \times (2.2 \times 10^{-9}) = 13.2.$$
Next, assume that about 2.5% of the mammalian genome is composed of functional, transcribed sequences that may affect the phenotype (the traits of the organism). That means that, of all the mutations that occur in every offspring every generation, about 2.5% could potentially affect the phenotype.  That is,
$$13.2 \times 0.025 = 0.33.$$
Still a small number.  But, now we have to account for population size. Small mammals, like mice and voles, generally have large population sizes.  Assume that the population of rock pocket mice contains 100,000 reproducing individuals. If so, then
$$0.33 \times 100,000 = 33,000,$$
which is the number of new heritable mutations that could occur in the population. Most of these mutations will be detrimental and removed from the population by natural selection but, if even a small fraction of these new mutations are beneficial, then natural selection can cause these beneficial mutations to increase rapidly in frequency in the population during future generations.
In humans, Nachman and Crowell (2000) estimated that the average mutation rate was 2.5 x 10$^{-8}$ mutations per bp per generation (not year), by comparing the genomes of humans and chimps. If we assume the same genome size and effective human population size of 500,000 individuals, then applying the same math suggests that 1,875,000 new mutations that potentially affect phenotype occur in the human population every generation. Again, only some of these will be beneficial but that is still the possibility of a number of new beneficial mutations. In evolutionary terms, a mouse or human generation is the blink of an eye.
How long would it take for a beneficial mutation to spread through a population? That depends on two things. How beneficial is the mutation (called the strength of selection, s) and the population size? To estimate how long it would take for a beneficial mutation to spread through a population, we can use the formula,
$$t = \frac{2}{s}\mathrm{ln}(2N_e),$$
where $t$ is time in generations, $s$ is the strength of selection, and $N_e$ is the effective population size (number of reproducing individuals). For the strength of selection, let's assume $s=0.01$, which is weak but positive natural selection. Going back to our rock pocket mice with $N_e = 100,000$, then the beneficial mutation would be spread throughout the population in only 2441 generations (remember, we're talking evolutionary time so 2000 years is nothing). If $N_e = 10,000$, the mutation spreads in only 1981 generations.  If we increase the strength of selection t 0.2, then the times are 122 and 99 years for population sizes of 100,000 and 10,000 years, respectively.
These "back of the napkin" calculations show just how quickly even weakly beneficial mutations can appear and spread throughout a population. Yet, this doesn't include other types of mutations like gene duplications that can also allow new proteins to evolve. For example, human ability to see red colors is due to a simple gene duplication (Nathans et al. 1996 and references therein). This duplication also explains the common form of red-green colorblindness.
Whew!
There's yet more to our mutational story. Consider humans and chimps, which are nearly identical from a genetic standpoint (between 96-99% depending on how you calculate it) yet they appear very different.  If humans and chimps diverged from their common ancestor within the past five million years, how could they differ so much? This question was initially posted by [King and Wilson (1975)]. They argued that mutations to structural proteins (like those that compose bones and muscles) would not be enough to explain the phenotype differences between humans and chimps. The proposed that regulatory genes are the key to understanding the big differences. Regulatory genes are those that control other genes, by turning them on or off and other important functions. Changes to the regulatory genes can cause fairly rapid changes to the phenotype.
This understanding has led to the broad (and fascinating) field of evolutionary developmental biology. This field focuses on how mutations in regulatory genes associated with development (from embryo to adult) have had a long-term evolutionary impact. The field is rich with examples, but one cool one is associated with duck feet and bat wings. Let's begin with the embryo. Most vertebrate embryos have membranes between the digits (fingers and toes) during an early stage of development. For most vertebrates, the membranes are lost later in development. The small flaps of skin you have between your fingers are the remnants of your embryonic membranes.
A set of regulatory genes called BMPs (and a couple of others) are responsible for causing the loss of the membrane in vertebrates. However, through different sets of mutations, the BMPs are not able to function in duck feet and bat hands. Thus, they both end up with membranes between their digits (Weatherbee et al. 2006).  Thus, two different mutations block the same set of developmental genes, leading to novel adaptations in two very different types of vertebrates. One final example is the evolution of bird feathers from scales. As you may know, birds are evolved from dinosaurs. It turns out that bird feathers and alligator scales (alligators are birds closest living relative) use the same regulatory genes to develop. The genes are BMP2 and SHH (sonic hedgehog for fans of the old computer game) (Harris et al. 2002). Other regulatory genes underlie the different types of feathers, like downy feathers and flight feathers (Harris et al. 2002).
Literature Cited
Harris, M.P. et al. 2002. Shh-Bmp2 Signaling module and the evolutionary origin and diversification of feathers. Journal of Experimental Biology 294: 160-178.
King, M.-C. and A.C. Wilson. 1975. Evolution at two levels in humans and chimpanzees. Science 188: 107-116.
Kumar, S. and S. Subramanian. 2002. Mutation rates in mammalian genomes. Proceedings of the National Academy of Sciences USA 99: 803-808.
Nachman, M.W. and S.L. Crowell. 2000. Estimate fo the mutation rate per nucleotide in humans. Genetics 156: 297-304.
Weatherbee, S.D. et al. 2006. Interdigital webbing retention in bat wings illustrates genetic changes underlying amniote limb diversification. Proceedings of the National Academy of Sciences USA 103: 15103-15107,

I've asked many (hundreds of) questions on stack exchange, and time and time again, people have raised the bar, amazing me at how far they were willing to go to teach me every aspect of a question that I had asked. This one just took the lead. Thank you for your time.

@jt0dd You're welcome. I'm glad you found the answer helpful.

"Traits evolve through the biological processes of random mutation and natural selection."
Could you show us some evidences for this claim?

About your question
This kind of very basic question has the drawback to need a very long answer. In consequence, your question might get some close vote. I'll do my best to help but you might want to look at some source of information as an introduction to evolutionary biology. A book eventually or Khan academy maybe.
Darwin's evolution theory
The expression "Darwinian evolution theory" easily yield to misunderstanding because Darwin was probably the most important scientist (and one of the first if not the first) to develop evolution theory but not the only one. Evolution theory is not anymore Darwin's evolution theory.
What is Natural Selection? Lewontin Recipe
You list:
- Survival of the fittest
- Random mutation
- Natural Selection

It is a list of different concepts that might be present in evolutionary biology but its nothing like a recipe for evolution to occur. This list I think already shows some point you misunderstood about evolution. The Lewontin recipe is a good way in order to understand what is natural selection and when it occurs. The Lewontin recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such a situation, natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.
What is evolution?
Evolution is not only natural selection. It is for example very important to consider random events. One of them is mutation, another is genetic drift (I am not trying to list every parameter that influence evolution but only to give you a sense of why natural selection is different than evolution with a goal of explaining why a trait that is needed do not necessarily appear). Both mutations and genetic drift explain why a species will not necessarily be perfectly adapted to its environment.
Mutations
In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen than other but in any case, the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, a phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is totally wrong. You may be surprised by the level of adaptation of life but this does not mean that what they needed was created with the purpose to help these individuals surviving but it only means that random mutations occur, most of them are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to rise in frequency in the population.
Genetic drift
If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why a small population undergo a more random change in frequency of their genes that are big population.
Therefore, when you say that you noticed that Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely is wrong. You only noticed that species has some level of adaptiveness if I can say so. It is very hard to imagine what new mutation would be beneficial of a given individual in a population but there are in reality many mutations that are beneficial that has never occurred or that has disappeared because of genetic drift. Also, as it is implied in the Lewtontin recipe different individuals have different traits yielding to different reproductive success. If you do not consider mutations that have never occurred but only to sites in the genome that are polymorphic (where different variants exist in the population), then it is worth knowing that any single individual carries quite a lot of deleterious variants. These deleterious mutations explain many genetic diseases. No, we are not perfect.
About your question again
Hope that helps a bit. But I would need days in order to explain further what evolution is. It is a bit field in biology. Your question is a bit too broad and as I said at the beginning you should seek some information by yourself and come back to this site with a question that can be more quickly answered.
Hope that helps!

Taking out of its context the statement mutations occur randomly makes little sense. What I meant above is that the probability of that a given mutation has a particular effect is independent from the need of the lineage or if you prefer independent from what will cause a higher fitness for the carrier. If you can clarify what exactly you want evidence for, please just open a new post and ask your question.

To be accurate I did not say in my above comments that mutations occur independently from environmental changes because the sentence mutations occur independently is unclear. Typically, the mutation rate might be affected (adaptively and not adaptively) by environmental changes. If you are able to ask an accurate question, then please just do so in another post.

Here are two references (among many others). Mutation rate is affected adaptively by stressors (Stress-induced mutagenesis in bacteria. Note that most examples I have heard of so far concern increase in mutation rate in plants as a bet-hedging strategy) and radioactivity (one type of environmental change) affects the mutation rate (Radiation-induced mutation rate).

You will be banned because you fail to follow the rules. Asking tons of follow-up (and eventually unclear) questions in the comments is also not following the rules. I will not answer further questions in the comments unless your comments are more on-topic.

I am sorry but IMO, you are extremely opinion-based, know little to nothing to evolutionary biology and yet think you can disprove some of its statements. Please just take an introductory course to evolutionary biology (as I already suggested a number of times) and stop harassing us with your unclear and never ending comments. I am flagging your last comment (although I would have preferred flagging some other comments of your that are have now been deleted). Sorry and good luck in your seek for knowledge.

Comments are not for asking questions that were not within the scope of the original question. Just open a new post. And as a general advice (that I already gave you a few times), you should try to understand what evolutionary biology is about before trying to disprove it. Just take an introductory class to evolutionary biology.

"Comments are not for asking questions that were not within the scope of the original question."
I'm asking about your answer to the question.
I think it's pretty legit to do so as long as it makes sense(which I believe is the case).

To the moderator, why did you delete my penultimate comment?

Short answer version:

It seems plausible to me that we (advanced life) could have a
  biological mechanism to "write" needed alterations into either our own
  DNA or our reproductive DNA over time, triggering the very specific
  evolutionary developments necessary to our survival without relying on
  random mutation.

No, it's not.  Despite what your feelings tell you, despite what you wish the case might be, there is no evidence in molecular biology to suggest that such a mechanism exists, there is no evidence that such a mechanism is required to explain the different phenotypes we see.

That does answer my question in the most direct way, however I'll give the correct answer to the one which shows extreme effort and detail, with excellent explanations. Thank you for this, nonetheless.

I agree that the longer answers are more detailed and more useful, but one has to admit that it is hard to give a detailed description of a mechanism that does not exist.

I was not criticizing this answer, only explaining that I thought the more detailed one was more deserving of the reward. However, +1.

Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely.

This statement is clearly false. The dinosaurs didn't develop what they needed, did they?
It turned out that on this occasion, the mammals happened to be best adapted to the conditions at the time, just as the fish had managed to get the upper hand over the large arthropods and the ammonites previously.
In hindsight many of nature's solutions seem wonderfully elegant, but they were arrived at by luck under intense pressure to survive. The fact that our eye is designed with blood vessels on the front of the optical surface instead of the back is an example of a design that could have been done better if thought out from scratch. There are many vestigial features from previous generations which persist, even though they are no longer needed. Notice that flatfish hatch with eyes on opposite sides of their head and one eye then migrates to be on the same side as the other, and whale embryos that have teeth which have disappeared by the time they are born, etc.
Natural selection is a combination of lucky mutations which happen to fit in with the prevailing conditions. It's a tough world out there. Even the plants are strangling each other, as can be seen on this video: https://www.youtube.com/watch?v=aNjR4rVA8to
The turtle didn't have much time to stare longingly at the leaves he couldn't reach. Some other turtle with a slightly longer neck came and ate them. And he got bigger and stronger and fought with the first turtle so he got to mate with all the females. And so the next generation of turtles had longer necks than the last.
It's easy to forget, with our comfortable lives, what a struggle nature is. The reason for this is that humans as a species have developed the most devastating weapon of all: cooperation. Compared to most other organisms, we treat other individuals of the same species pretty well (most of the time) and we actually teach each other how to do things. While some other species cooperate among individuals, humans have taken this to a whole new level. As a result, we have been able to eradicate many species which pose a threat to us and bring many other species which are useful to us under control.
If you want to know why this didn`t happen before: humans evolved from an ape-like creature that, due to changes in its environment, came down out of the trees and started walking on the ground. This creature then had its hands free to use tools, and by sheer chance this combination of factors made a bigger brain advantageous, so this creature (which was already social, like apes but unlike octopi, one of the few other creatures blessed with the ability to perform complex manipulations) became even more intelligent and began to educate its offspring in how to control its environment.
There is nothing in biology which enables the mutation of genes to be directed. Finally, human technology has developed to the point where it may be possible to modify genes directly. However, there are significant ethical issues regarding the use of this technology. The termination of an "imperfect" human is frowned upon because it is considered that all members of the species should be given the best chance to survive. Besides, it is not at all clear if there is really ever such thing as a "defective" gene. For example carriers of the gene responsible for sickle cell anaemia have increased resistance to malaria.
Anyway, long before humans were able to manipulate genes directly, they were able to produce massive changes in the phenotype of dogs in a remarkably small number of generations. There is a breed of dog adapted to every possible use. An unfortunate consequence is that the gene pool in each breed is rather small, leading to breed-specific illnesses. If these breeds were left alone it would take many generations for mutations to allow their genotypes to diversify again. And who knows what the final animal would look like?

It seems plausible to me that we (advanced life) could have a biological mechanism to "write" needed alterations into either our own DNA or our reproductive DNA over time, triggering the very specific evolutionary developments necessary to our survival without relying on random mutation.

There is no evidence for such a mechanism, and it is very unclear how a mutation could be proved beneficial without being tested in the environment. What there is, is a way of mixing and matching genes, so that the best ones can propagate throughout the population. Unicellular organisms do this by a variety of means. For multicellular organisms the way of doing is sexual reproduction.
The cost of this is enormous. Look at a flowering plant. That flower has evolved exclusively to enable pollination, typically by insects. In some cases, virtually all the plant's energy goes into making that flower and relatively little into making the actual seeds. Plants do have a particular problem exchanging genes because they do not move about. Stationary animals, such as the barnacle, also have similar problems. The barnacle solves this by having a "penis" several times longer than its body length so that it can copulate with its neighbour without moving from its spot. In humans, fully half the population is male and therefore unable to bear offspring.
Asexual reproduction is far more efficient at producing offspring but does not enable the interchange of genes. The offspring are clones of their parent and therefore have the same genetic strengths and weaknesses. Asexual reproduction does exist, even in some animals, but exclusively asexual reproduction would preclude the spread of beneficial mutations. That's why organisms invest so much energy in sex.
Aphids are a good example of an animal that reproduces both sexually and asexually. At the boom times of the year, aphids reproduce asexually and are actually born as already pregnant females! When the availability of food slows down, they switch to the slower, sexual reproduction system with males and females.
In many animals, males must demonstrate their good health in order to be able to mate with the females (who are choosy, because they have to take the cost of bearing the young.) In many large herbivorous mammals, this is done by males fighting. Male birds often display their health by elaborate plumage, the classic example being the peacock. It is debatable whether such a conspicuous waste of resources is really beneficial to the species, but the females have evolved to select males in this way. In some fish, there is only one male in a group, and when something happens to him, the biggest healthiest female actually changes sex to become a male.
So, if an organism were able to program its own genes, why invest so much energy in sexual reproduction?

In answer to the final question, the answer is because it feels good. :)

@MikeTaylor indeed, even now that we can make babies in a test tube, I can't see the old way going out of fashion.

The answer provided by Mike Taylor is just perfect and complete.
However, I'd like to add some thoughts of my own in a more colloquial style:

Survival of the fittest is not always true. There is also "survival of the luckiest" (e.g. the fittest is showing off in the beach with the other turtles and is struck by lightning).
Reproduction is not that simple and many times the female mates with several mates (apart from the fittest one) and a paternal test should be procured.
Mutation changes are not always gradual (i.e. the turtles might develop a long neck in just one generation).
Mutations don't always lead to a phenotype change. Sometimes, depending of the environment, the phenotype change doesn't occur. For example, the turtles might only grow a long neck if the live in a sunny island.
Not all mutations are beneficial and not all beneficial mutations have an impact on survival (e.g. many actors/actresses are not very tall although they reproduce successfully).

In my opinion there are many shades of grays in between the ideas behind evolution.
The features of the "fittest" are sometimes lost by random reasons as the listed above, and the features of the "less fitted" are sometimes transmitted.
And finally, sometimes, an organism develops (or is developing) a mechanism to alter the genes directly (e.g. human beings). Where would that lead? Does evolution mean something anymore?

"I imagine that turtle looking up at that food, and sub-consciously
  wishing to get to it, constantly straining, for its entire lifetime.
It seems plausible to me that we (advanced life) could have a
  biological mechanism to "write" needed alterations into either our own
  DNA or our reproductive DNA over time, triggering the very specific
  evolutionary developments necessary to our survival without relying on
  random mutation."

That is a pre-Darwin idea of evolution called "inheritance of acquired characteristics" or Lamarckism after it's creator French natural philosopher Jean-Baptiste Lamarck. Lamarck postulated that given the use of tissues altered those tissues e.g. lifting weights makes muscles bigger, then an organisms descendants would benefit if everything the parent's tissues "learned" could be passed on.
There are actually epigenetic factors in cells that selectively turn genes on or off or otherwise modify their use generation to generation. But this is not evolution because the genes are always there, ready to be used if needed and no new information is ever created.
The flaws in Lamarckism are that, even if the mechanism existed to transmit acquired characteristics, how would it know what characteristics led to what outcome? How could it distinguish positive changes from negative ones?
Most fatally, how could an organism evolve a system that was not related to an existing behavior? For the turtle to stretch its neck, it must desire to eat the leaves and exert effort to do so. How did it acquire the behavior of desiring to eat the leave in the first place? Going forward, if the plants it does eat goes away, how would it ever find another food source? It wouldn't desire to eat inedible plants so it would never exert itself to do so and would never pass that exertion on to it's young.
The hiccup in your understanding of Darwinism is that you've got it backwards. Species don't find solutions and evolve. It's not something species do. It's something that happens to species, a force from the outside. It's not analogous to humans setting down to consciously solve a problem.
Darwin was originally going to use the analogy of "wedging" instead of "natural selection." He wanted to emphasize that it was the environment squeezing in on species that formed them. (Today we think of wedges largely for their splitting power but in but in Darwin's day, if you wanted to compress something you used a wedge hammered in from the side. It was a common tool that performed the same jobs as jacks and hydraulics do today.) But he went with the anthropomorphic analogy of nature being an animal breeder selecting for traits for reproductive success and a lot of misunderstandings followed.
Evolution is not random. Only variations themselves are random. The selection of them is not. It's like shooting dice. The fall of the dice is random but only certain values of dice are winning number and are "selected." The same mutation might show up in every generation for millions of years but produce no change until the environment changes to make the mutation useful.
Species have no existence independent from their environment. The environment squeezes them into a specific form, one that best satisfies the demands of the Second Law of thermodynamics. If the environment doesn't change, then the organism won't either. From that perspective, adaptation is about as amazing as a rock rolling downhill. (That would look pretty fantastic if you didn't know about gravity.)
Imagine you had never seen clay and never seen molding. Your walk along a stream bank lined with clay. Walking one way you pass a blank stretch of clay. After you pass, a leaf falls into the claw and creates a near perfect imprint before being blown away. When you return past that spot, it looks like the clay has somehow altered itself, against all probability, into an exact mirror duplicate of a leaf. How you might wonder, could the clay possibly know how to exactly duplicate the shape of a leaf?
But the clay did nothing. The clay did not alter to fit the leaf, the force of the falling leaf altered the clay.
Likewise, species do not evolve themselves, they are evolved by external forces. Species seem to miraculous fit their ecological niches but, just like the clay, did nothing to shape themselves to the niche. Just as the clay will be passively shaped by the pressure of molding, species have no choice but to assume the forms they do.
It's not survival of the fittist but survival of the fitted.

To add to the previous answers that treat specifically of the biological Darwinism, there is also Universal Darwinism which postulates that evolution is a natural phenomenon that appears when a set of conditions and constraints are present. And indeed, it has successfully been applied to a number of fields (see below the quote), which seems to imply that evolution is not a property of the evolving individuals (as you implied) but a property of the system where the individuals evolve (as long as the individuals satisfy a few special properties, namely variation and heredity, see below).
Here's the definition from Wikipedia:

At the most fundamental level, Charles Darwin's theory of evolution states that organisms evolve and adapt to their environment by an iterative process. This process can be conceived as an evolutionary algorithm that searches the space of possible forms (the fitness landscape) for the ones that are best adapted. The process has three components:

variation of a given form or template. This is usually (but not necessarily) considered to be blind or random, and happens typically by mutation or recombination.
selection of the fittest variants, i.e. those that are best suited to survive and reproduce in their given environment. The unfit variants are eliminated.
heredity or retention, meaning that the features of the fit variants are retained and passed on, e.g. in offspring.

After those fit variants are retained, they can again undergo variation, either directly or in their offspring, starting a new round of the iteration. The overall mechanism is similar to the problem-solving procedures of trial-and-error or generate-and-test: evolution can be seen as searching for the best solution for the problem of how to survive and reproduce by generating new trials, testing how well they perform, eliminating the failures, and retaining the successes.
The generalization made in "universal" Darwinism is to replace "organism" by any recognizable pattern, phenomenon, or system. The first requirement is that the pattern can "survive" (maintain, be retained) long enough or "reproduce" (replicate, be copied) sufficiently frequently so as not to disappear immediately. This is the heredity component: the information in the pattern must be retained or passed on. The second requirement is that during survival and reproduction variation (small changes in the pattern) can occur. The final requirement is that there is a selective "preference" so that certain variants tend to survive or reproduce "better" than others. If these conditions are met, then, by the logic of natural selection, the pattern will evolve towards more adapted forms.
Examples of patterns that have been postulated to undergo variation and selection, and thus adaptation, are genes, ideas (memes), neurons and their connections, words, computer programs, firms, antibodies, institutions, quantum states and even whole universes.

Also, you may be interested in some terminology associated with this theory, for example for John Maynard Smith an individual that can evolve in an evolvable system is called a Unit of evolution [1]. This shows how much abstract and generalizable evolution can be.
[1]: Fernando C, Vasas V, Szathmáry E, Husbands P (2011) Evolvable Neuronal Paths: A Novel Basis for Information and Search in the Brain. PLoS ONE 6(8): e23534. doi: 10.1371/journal.pone.0023534

There are indeed massive evolutionary control systems integrated into DNA. They constitute the major force for efficient change in living beings.
Random DNA mutations are not as beneficial as controlled ones, you can see random single gene mutations at work in medical books: Anemia, cancer, cheese smelling sweat, no sweat glands, skin conditions, scales, brittle bones, lactose tolerance, These are all examples of mutations of single proteins and single growth hormones and so on.
Instead of random DNA mutations, life-forms control their rate of change and types of variations in very efficient ways, changes in color, longer and shorter bones/arms/legs which you can see in humans, physical maturation times, length and quantity of hair, all these things are safe for an animal to have lots of genetic variation with. Changes in bone length vary more than 10 percent in a single generation of humans, but changes like lactose tolerance occur only every 100ds of generations. Therefore there are hundreds of genes for controlling growth hormones as it's selection-important. If color changes become important to an animal, for example, birds, fish, and butterflies, then hundreds of genes are devoted to color. If color is not important, for example, northern and snow animals, then few gene changes are devoted to color, The many Color genes of a tropical animal would go dormant very fast if it were exposed to snowy conditions.
It makes sense for DNA to favor developments that encourage reproduction and survival in variable settings, and indeed DNA is supercharged to deliver mostly useful morphological and chemical changes in large numbers. Plants, conversely, need to change their chemicals alot to attract and repel animals, whereas animals do not need to attract other animals for food, only to defend themselves, that one reason why animals have a lot less chemical variety than plants. Only Chinese use animals for medicine, and there are few aspirins and sedatives derived from animals. Animals cannot produce powerful random chemicals because their nervous system hormones and cell walls are less robust than cellulose cells and plant hormones. Otherwise, animals would have more variable smell and taste, but all mammals taste similar.
It's the same with computer evolution. If you tell a computer program to vary DNA randomly or to create life-forms randomly, it will have epileptic, disorganised animals that flop around, roll around, hit walls, and that is not what animals do to evolve. If you equip a computer evolution program with DNA tool kits copied from nature, you will much faster have meaningful animals... i.e. simple locomotive insects. If you tell the computer to use sinusoidal limb movements like fish fins, millipede legs, insect legs, using nerve impulses, and to create metameric life forms, you will have alot more success than just adding limbs onto random parts of the body, using random pattern nerve impulses and so on.
It's not an easy thing to study, as it is very complex. I would love some statistics and journals regarding types of evolutionary changes that are prevalent in different life-forms.

Can you please add some references to your answer?

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

authors: Bob Jarvis - Слава Україні


text:
Why has our nose evolved with the nostrils facing down?
For most animals, the whole bottom of their face sticks out and they have a snout with a mouth and nose at the end.  But humans have a flat face and just a nose that sticks out.  We used to have the whole face sticking out, but our jaws got smaller and smaller.  Because our noses still needed space to do their job, they had to stay sticking out.  People who come from very cold areas have bigger noses than people from where it is hot, so they can warm the air up more.
Why has our nose evolved with the nostrils facing down? Is it because we were water animals, and that would help with water coming in?

I don't quit understand how your introduction addresses your question...I may not understand your question. But very quickly I would tend to think that if the nostrils where facing the sky we would probably experiencing much discomfort when raining! Also, we probably tend to smell things that are located under our nose rather than above our nose.

@Remi.b Haha that would be a good evolutionary joke, think of monkey that has nostrils down, there are none. It makes sense that we have extruding noses, but why nostrils are down?

Which mammal has its nose upwards?

@TheLastWord Consider it a joke, An elephant when he is pointing its trunk up.

@TheLastWord The hippopotamus has nostrils pointing upward so they can breathe while mostly submerged. The blowhole of whales and dolphins are the nostrils. They're clearly directed upward.

I have not been able to find any studies that look specifically at the genetic mechanism for nose development. I certainly do not know but I'll offer up two hypotheses.
My first hypothesis is that the elongated nose is a remnant of the elongated lower face of our ancestral species, as you note in your answer. Take a look at this brief YouTube video (1:17 long, the part relevant to this answer begins at 33 seconds) of a time-lapse composite showing the develop of the human face. Our face develops as two separate halves that meet together in the middle. That's what creates the philtrum under our nose.
Watch the especially carefully from the 54 second mark to 1 minute mark. Note that our nostrils are pointing directly forward and the overall region looks somewhat like a pig snout. The mouth is vertical aligned with the front of the nose. The overall face is much more rectangular and the eyes are on the sides of the face.
Then, the face begins to become rounder and flatten. The eyes move to the front of the face and the recesses our our eye sockets recede. The lower face below the nose recedes, becoming flatter. The only part that does not recede is the nose area. The flattening of the lower face may actually cause the nostrils to turn downward.  Our nose does not develop outward from a flat face but instead is left behind as the rest of the face flattens.  This would be my initial thought as the primary reason for the shape of the nose and direction of the nostrils.
My second hypothesis (and honestly independent of the comment by @Remib) is related to our sense of smell and taste. Although our ability to detect flavors is a complex process, the primary sense involved is smell (Shepherd 2006). Therefore, downward-pointing nostrils are located directly above the mouth so we get a good smell of the food just before it enters the mouth, perhaps enhancing our flavor-sensing ability.

Shephered, G.M. 2006. Smell images and the flavour system in the human brain. Nature 444: 316-321.

Note that these two hypotheses are not mutually exclusive. The downward pointing nostrils may be a remnant of our facial development but provides an (adaptive?) advantage for flavour perception.

Wouldn't it rain in ur nose if they were the other way?

We would have just invented baseball caps sooner. :)

@MikeTaylor True. :D

Ive found that the study of this feature, the nose is far from complete.Although we see the evolution of other mammals and their faces has a great deal to do with there ability to survive different enviornments I believe it , our snozz is a genetic mutation in which allows us the ability to go from nonaquatic to aquatic with out needing a snorkel. ?.by defying why we have this thing on our face......some so large some so small I dont believe to have much to do with ancestial deviation of the jaw but the defying feature of the human race.....thank you

Could you point to the source please.

Marc Verhaegen, Putte, Belgium
New Scientist 2782 p 69 Lastword 16 October 2010

Why do humans evolve external noses that don’t seem to serve any
  useful purpose – our smelling sensors are inside the head. Our nose is
  vulnerable to damage, and the majority of primates and other mammals
  manage with relatively flat faces. Traditional explanations are that
  the nose protects against dry air, hot air, cold air, dusty air,
  whatever air, but most savannah mammals have no external noses, and
  polar animals such as arctic foxes or hares tend to evolve shorter
  extremities including flatter noses (Allen’s Rule), not larger as the
  Neanderthal protruding nose.
The answer isn’t so difficult if we simply consider humans like other
  mammals.
An external nose is seen in elephant seals, hooded seals, tapirs,
  elephants, swine and, among primates, in the mangrove-dwelling
  proboscis monkeys. Various, often mutually compatible functions, have
  been proposed, such as sexual display (in male hooded and elephant
  seals or proboscis monkeys), manipulation of food (in elephants,
  tapirs and swine), a snorkel (elephants, proboscis monkeys) and as a
  nose-closing aid during diving (in most of these animals). These
  mammals spend a lot of time at the margins of land and water. Possible
  functions of an external nose in creatures evolving into aquatic ones
  are obvious and match those listed above in many cases. They can
  initially act as a nose closure, a snorkel, to keep water out, to dig
  in wet soil for food, and so on. Afterwards, these external noses can
  also become co-opted for other functions, such as sexual display
  (visual as well as auditory) in hooded and elephant seals and
  proboscis monkeys.
But what does this have to do with human evolution?
The earliest known Homo fossils outside Africa – such as those at
  Mojokerto in Java and Dmanisi in Georgia – are about 1.8 million years
  old. The easiest way for them to have spread to other continents, and
  to islands such as Java, is along the coasts, and from there inland
  along rivers. During the glacial periods of the Pleistocene – the ice
  age cycles that ran from about 1.8 million to 12,000 years ago – most
  coasts were about 100 metres below the present-day sea level, so we
  don’t know whether or when Homo populations lived there. But coasts
  and riversides are full of shellfish and other foods that are easily
  collected and digested by smart, handy and tool-using “apes”, and are
  rich in potential brain-boosting nutrients such as docosahexaenoic
  acid (DHA).
If Pleistocene Homo spread along the coasts, beachcombing, wading and
  diving for seafoods as Polynesian islanders still do, this could
  explain why Homo erectus evolved larger brains (aided by DHA) and
  larger noses (because of their part-time diving). This littoral
  intermezzo could help to explain not only why we like to have our
  holidays at tropical beaches, eating shrimps and coconuts, but also
  why we became fat and furless bipeds with long legs, large brains and
  big noses.

Copying and editing an entire swath of an article is discouraged - please try to answer a question by using your own words and try to synthesize something from multiple sources. -1

As well as the concern over copy-pasting, this seems to be a support of the long-debunked "aquatic ape" hypothesis, coming from a source (New Scientist) that is notorious for its unsupported and over-hyped claims.

source: Stack Exchange

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

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

sort: votes


text:
What is the importance of hydrogen bonds in water? and other questions:
These are extremely simple questions — basic biology — but I would like to make sure that the way I have answered is at the very least correct.

Hydrogen bonds are very weak, so how is it possible that they are so important in the properties of water? Hydrogen bonds in water provide many characteristic benefits to water: cohesion (holding water molecules together), high specific heat (absorbing heat when breaking, releasing heat when forming; minimizing temperature change), high heat of vaporization (several hydrogen bonds must be broken in order to evaporate water), lower density of ice (molecules in ice are spaced farther apart), and solubility (polar molecules are attracted to ions and polar compounds, making them soluble in water).
Why do we feel cooler immediately after we go swimming than we do after we have fully dried off? We feel cooler immediately after we go swimming than we do after we have dried off because it takes a lot of heat to evaporate water; however, once we dry off we remove much of the water from our skin, and the water is evaporated much more quickly.
If water were non-polar, would our temperature heat up less quickly or more quickly if we went outside on a hot day? Why? More quickly. Because hydrogen bonds within water slow down the movement of molecules and allow for water to have a very high specific heat.

General chemistry questions are off-topic on Biology.SE, but instead should be asked at [chemistry.se].

You are saying what hydrogen bonds are doing, not why are they able of such achievements, despite being so weak. Their strength is in numbers. At room temperature, fully one fifth of the water molecules are engaged in four bonds with other water molecules, while the remainder forms two such bonds. (More detail at http://www1.lsbu.ac.uk/water/hbond.html ). In contrast, hydrogen sulfide forms essentially no hydrogen bonds with other hydrogen sulfide molecules, despite significant similarity between oxygen and sulfide. The difference in size between oxygen and sulfur makes the former much more electronegative. I could go on with other hydrogen compounds, but the fact that answers your first question is: each water molecule is involved in a series of bonds with other water molecules, on an unequaled scale.

Also, hydrogen bonds are stronger, pickier about distance and angle than the alternatives available to other molecules (dipole-dipole, van der Waals etc.) So even if they seem feeble, and even if the alternatives were as plentiful as hydrogen bonds, the latter would still be more capable of tying up molecules.

The effect of water drying (which comes after swimming, but also after sweating, bathing, or cleaning oneself with a hot oshibori) is caused by water evaporation. Each state transition, including that from liquid water to air-borne vapors, is a heat-consuming phenomenon. When skin dries, the heat to turn water into vapors has to come from somewhere. In perspiration's case, it is one's body.

Note that cooling down while water evaporates is not only something we feel, but a physical reality, occurring even in innate systems. For example, Amazon forests and Sahara are similarly close to the Equator, but the former is cooler than the latter, in part because heat it receives is in part used up to evaporate water.
Your answer was good.

Again, you are right. Were water non-polar, it would have lower latent heat, or, in lay terms, it would evaporate without much heat consumption. Were sweat made of a non-polar liquid, it will fail to consume heat when evaporating, leaving one to warm up sooner / faster.

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


text:
Propensity Score for amino acid
What is the meaning of propensity score of amino acid? How is it calculated? (I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

As a simplified response:
Propensity score is used to predict protein secondary structure. It is derived from looking at the aa residue of the accessible surface of the protein and also the interface which enables interactions between other proteins.
The equation is as follows:
Propensity= [probability of the residue in the interface / probability of the residue on the surface]
where,
prob of the residue in the interface = [number of amino acids in the interface / total number of amino acids of any type of interface]
and,
prob of the residue on the surface =  [number of surface amino acids / total number of surface amino acids]
Check out this PLOS paper for an example. PLoS One. 2014; 9(5): e97158.


text:
Collective name for the X- and Z-chromosomes
Chromosomes are grouped as sex chromosomes or autosomes, with the X, Y, Z and W all falling in to the former category. The Z and X are present both in the homogametic and heterogametic sexes, and the Y and W only in the heterogametic sex.
Is there a collective name for the chromosomes in such groupings (X/Z & Y/W)?
I want to talk about Z- and X- (and analagous) chromosomes in general. Rather than having to write "The X-chromosome, and analagous chromosomes such as the Z-, are present in both sexes...." I'd like to say "The blank chromosomes are present in both sexes...."

I can suggest one for Y/W- meiomorphic : Smaller in size. Heteromorphic is anyways used for dissimilar sex chromosomes.

I'm not aware of collective names but you could define one for the purpose of your paper. Inspired by @WYSIWYG you could try macro- and micro/meio- prefixes. I don't know if those terms would apply broadly to your needs.

majo- prefix means greater.. But majomorphic sounds weird. Macro/micro also seem fine (but macro/micro are not comparative prefixes). You can actually ask this in a Greek/Latin forum :P

@WYSIWYG yes this is a good Greek and Latin question

I think you can safely use the terms heterogametic (Y/W) and homogametic (X/Z) chromosomes, meaning that a heterogametic chromosome is the chromosome which makes one of the sexes heterogametic (i.e. defines the difference between the two types of gametes of the respective sex).
These terms applied to chomosomes do have some usage in the literature, e.g. in this article.

heterogametic/homogametic is used only in the diploid sense. What else could be an appropriate name for the gene-rich/deficient of the sex chromosomes?

@WYSIWYG: 1) How many cases of sex-chromosomal sex determination in haploid organisms are known? Or do you mean something else? 2) I don't know. By the way, the differences between the two (or three) sex chromosomes are not always pronounced to such a degree as observed in mammals.

you mistook me.. I meant it is said in reference to the genotype of the sex rather than the chromosome itself

@WYSIWYG My point was that the same terms can be also applied to chromosomes. E.g.: "... the heterogametic chromosome (Y or W) has repeatedly lost many genes ..." (p. 1646).

I just tried a search of major and minor sex chromosomes and found a paper here by Judith Mank who refers to the X and Z as the Major Sex Chromosomes and Y and W as the Minor Sex Chromosomes.

I will therefore refer to the W and Y as minor sex chromosomes, and
  will use the term major sex chromosomes in reference to the X and Z.
  These terms are based on abundance and do not refer in any way to size
  (discussed below) or relative effect. In fact, the effect of the minor
  sex chromosomes is, in many ways, anything but minor.

I think I will go with this naming as the hetero-/homogametic chromosomes distinction could become confusing in the context I am using it (Talking about expression of the X/Z in the homogametic and heterogametic sex).
EDIT:
Further I think it is wrong because, while "heterogametic chromosome" would be somewhat suitable for Y/W chromosomes, to call the X and Z the homogametic chromosome is wrong because the X/Z can be present in both a homogametic sense (in females/males respectively) and a heterogametic sense (paired with a Y or W).
Calling the X/Z the homogametic chromosome implies that it is only present in homogametic sexes no less than "minor sex chromosome" might imply a minor role for the Y.
Another suggestion could be to call the Y/W chromosomes the sex-limited chromosomes, but then the question of what to call the X/Z remains... non-limited? shared? sex-unlimited?
Or recombining and non-recombining sex chromosomes.

I'm not a fan of this usage since the mechanism of function varies so widely and the major/minor distinction implies something about the functional role of the two types.

@JackAidley that's why I put in the Mank clarification "the effect of the minor sex chromosomes is, in many ways, anything but minor."

I agree with @JackAidley regarding meaning but at least you have precedence to cite and it appears to suit your needs.

I am also not a fan but did not downvte

@JackAidley Thanks for your input so far, please see the edits..

@MikeTaylor Thanks for your input so far, please see the edits..

@caseyr547 Thanks for your input so far, please see the edits..

While your point about hetero/homo is valid, I think that it's likely to be a more readily understood and less confusing term than major/minor.

Regarding the meio/majo or micro/macro suggestion, I do not think it is the way to go for the following reasons:

Micro and macro-chromosomes are terms already used in species such as chicken whose genomes combine very small and big chromosomes
Although this is more the exception than the rule, bear in mind that sometimes the Y chromosome is bigger than the X chromosome (e.g. in S. latifolia)

As for the initial question, I do not know of a term the X/Z - Y/W groups. What comes to my mind is the term sex-restricted sex chromosome for the Y/W (as it is normally present only in one sex) although it does not seem to be widely used according to Google.
You could also oppose them as recombining vs non recombining sex chromosome which would hold true for most heteromorphic sex chromosomes (if we do not take PAR into consideration). It might be confusing as some persons would think you speak about the pair and not the individual chromosome. However, it seems to be used in the literature.
I checked one of my manuscript on the topic and we used X/Z when needed.
Edit: first sentence clarified.

instead of size sex chromosomes should be classified by their gene content.

I did not say we should classify by size (my second bullet point clearly shows this is not a general rule). Gene content of any of their property (e.g. recombination, segregation,...) is definitely a better way to go.

Not you. I was saying in general (after considering your example)

Based on answers and discussion so far and my own searches, I think there is no widely understood and used term for grouping the X/Z and W/Y chromosomes. You could coin your own term or pluck one from obscurity in the literature, however, I think you would probably be better off not doing so and simply writing X/Z and W/Y wherever you need to refer to the grouping.

I've mentally decided to start using WYsomes (pronounced why-somes) and ZXsomes (pronounced zicks-somes) for collective use.  Of course, I'm not trying to publish a paper. :)


text:
It is possible for person with AIDS be negative for HIV antibodies?
I'm just curious as there was a bit controversy around this topic. It is possible for person with AIDS be negative for HIV antibodies?
As of 1989, the CDC reported that 5% of all U.S. AIDS patients who had been tested for HIV to that time were HIV-negative. No figures have been reported by the CDC since 1989.
If so, how it's possible?
See:

Unexplained CD4+ T-Lymphocyte Depletion in Persons Without Evident HIV Infection -- United States at Centers for Disease Control and Prevention

You need to decide what you want to know. The paper you link talks about patients wihich have a low CD4+ count, but are not positive for HIV. So you want to know how this happens? Or do you want to know if it is possible for someone who is HIV positive (and has developed AIDS, which is the latest stage of the infection) to not develop antibodies against HIV?

Yes, how it's possible that they were HIV-negative or in general if there are any other more recent studies. More information, then better.

Ur question is still pretty confusing to me. Could you please edit it. Your question speaks about something and the comment you posted talks about something else.

There is no need to downvote this question. I can still be clarified but nothing further.

The main question is as in the title, if it's possible for person to be HIV-free. Based on CDC report it seems it is possible, but somehow this is not considered as a fact. So I just wonder why is that.

If you're looking for support for your "HIV doesn't cause AIDS" conspiracy theory, you're in the wrong place. This paper doesn't mean what you think it means, it isn't evidence for your conspiracy theory like you think it is.

I don't see anything bad in asking the question. If the paper doesn't mean what I think, then you can elaborate/explain further. I'm not biologist, therefore I ask.

@Mad Scientist: If you'll keep down-voting by not explaining the questions/inaccuracies, then I assume you don't know, then you should ignore the question and leave it for the people who know the answers. By not answering the question and closing them, you just keeping the people in the dark, therefore promoting the conspiracy theories, and not people who just ask. BTW. I'm not looking for "HIV doesn't cause AIDS" theories, just answers.

Depends on the sensitivity of the antibody detection kit

@WYSIWYG: Did they use bad antibody detection kits in the past?

perhaps they were not very sensitive.. There is always a scope for improvement

Usually an antibody test against HIV is positive three month after the infection. Before this time a test can only be done with molecular biology methods as PCR. However, it is possible, that patients which have definitely been tested in an early phase using molecular biology methods and which afterwards receive a antiretroviral therapy (ART) that these patients do not develop high serum levels of antibodies, as the virus titer in the blood is not high enough for a sufficient reaction and thus stay undetected by the tests. This has been improved, so that the kits are supposed to have a higher sensitivity now. See these papers for more details:

Seroreversion in subjects receiving antiretroviral therapy during
acute/early HIV infection.
The effects of early antiretroviral therapy and its discontinuation
on the HIV-specific antibody response.

I haven't found any papers on the decline of HIV-antibodies in AIDS (which is the late stage of the disease), but if they do, this is probably due to the effects of the infection on the immune system.
Low counts in CD4 positive T cells (which are usually associated with an HIV infection) can also occur with other diseases. See these papers (especially the first, as this is a review which contains a lot of further references):

Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections,
malignancies, and autoimmune diseases.
Decreased CD4 and increased CD8 counts with T cell activation is
associated with chronic helminth infection.
Acquired immunodeficiency without evidence of HIV infection: national
retrospective survey.

Sure, it is possible in the late stages of AIDS. Once the immune system is pretty much wiped out, the person has AIDS and is unable to produce HIV antibodies. There is nothing left of the immune system to produce antibodies of any sort.
https://www.ncbi.nlm.nih.gov/pubmed/18649337
This is why DNA based HIV detection system using quantitative PCR is better. It is not dependent on an immune response that is being destroyed by HIV.


text:
Are retroviruses cytotoxic?
There are typically hundreds of retroviruses found in healthy human beings.
Are retroviruses then cytotoxic? (In other words, are they able to kill or damage other cells).

Can you please expand your question? Actually I am not sure what you are asking.

Hundreds of retroviruses are normally found in healthy human beings. So the question is, if retroviruses are cytotoxic or it depends on the classification? Should the question  'Does all retroviruses are cytotoxic?' would be more clear? Or 'which'?

Re-phrased the question to opposite, so I think it's more clear.

The word cytotoxic in your question probably came from 'cytotoxic t cell'. Programmed cell death induced by a cytotoxic t cell is responsible for cytotoxicity, not the retrovirus itself.

Wiki says that cytotoxicity is the quality of being toxic to cells, so it's not only refered to T cells as far as I understand, but to all other natural killer cells. Please correct me if I'm wrong.

As you point out human beings (and other organisms) have hundreds of retroviruses and many can be seen in the human genome, some of which appear to be the remains of deactivated viruses, others which may be active.   Most retroviruses are not pathogenic - they don't cause disease.
This is because many retroviruses replicate slowly, budding and secreting from the cell surface in small numbers without killing their host cell.
There are several disease-causing retroviruses.  Human T-cell Leukemia Virus (HTLV) can cause T-cells to replicate in an uncontrolled fashion, resulting in leukemia.  This is not a necessary result for HTLV to replicate, but it is a result of viral infection as viral replication tweaks the cell machinery to replicate.
While it's not clear exactly how, Human Immunodeficiency Virus (HIV) kills its hosts cells.  Unfortunately HIV's hosts are CD4 immune cells.  The fact that sporadic replication of HIV can cause all host immune cells to die entirely makes HIV a pathogen.
Disease is usually thought of as a lack of adaptation of a pathogen and host: viruses do better if they do not kill their host.  Both these cases are possibly not the future for either virus: either could adapt to reproduce without causing a disease. Or they might have already , having spun off some strains into the pool of quiet retroviruses medical science does not concern itself with.

I'm going to down vote your answer you shouldn't hav +5 with 0 on the question

This answer gives a good background for how retro viruses may differentially damage biological function. The word cytotoxic in the question wasn't appropriate for the relationship between a cell and a virus.

@caseyr547 The upvote for the answer only says something about the quality of the answer. So even if the question doesn't make much sense it can still be possible that the answer is good. What is the case here.


text:
Synthesis of Fatty Acids Longer than 16 Carbons
I understand that the human body when performing Fatty Acid Synthesis can synthesize only until C16 (palmitate). However the ER has desaturases and elongases. I know that desaturases are used to add double bonds, but do humans have elongases to add even more Carbons to a double bond? If so, then this would mean that the human body can synthesize fats longer than C16?
Lets take a hypothetical case and say that humans have both desaturases and elongases. Would it be feasible to add double bonds to palmitate via desaturases, then add more carbons to the chain via elongases and then add more double bonds via desaturases? This way, the resulting fatty acid will have an increased length and more unsaturated character (i.e. more double bonds than the prescribed 4 that humans can add at positions 4, 5, 6, and 9)?

This is a fine question

Short Answer: Yes.
Long Answer: See this article:

The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found in Escherichia coli. These reactions are performed by fatty acid synthase II (FASII), which in general contain multiple enzymes that act as one complex. FASII is present in prokaryotes, plants, fungi, and parasites, as well as in mitochondria.
In animals, as well as some fungi such as yeast, these same reactions occur on fatty acid synthase I (FASI), a large dimeric protein that has all of the enzymatic activities required to create a fatty acid. FASI is less efficient than FASII; however, it allows for the formation of more molecules, including "medium-chain" fatty acids via early chain termination.
Once a 16:0 carbon fatty acid has been formed, it can undergo a number of modifications, resulting in desaturation and/or elongation. Elongation, starting with stearate (18:0), is performed mainly in the ER by several membrane-bound enzymes. The enzymatic steps involved in the elongation process are principally the same as those carried out by FAS, but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.

Another article from NCBI states:

Primers for several mouse, rat, and human elongases have been reported elsewhere.

...and cites here for this:

Fatty acid elongases and desaturases play an important role in hepatic and whole body lipid composition. We examined the role that key transcription factors played in the control of hepatic elongase and desaturase expression...In conclusion, these studies establish a role for PPARalpha, LXR, SREBP-1, ChREBP, and MLX in the control of hepatic fatty acid elongase and desaturase expression and lipid composition.

Indeed, humans do synthesize stearic acid (C18) in their body; mainly liver and adipose tissue. See this article:

Fatty acid biosynthesis from acetyl-CoA takes place primarily in the liver, adipose tissue, and mammary glands of higher animals. Successive reduction and dehydration reactions yield saturated fatty acids up to a 16-carbon chain length. Stearic acid is synthesized by the condensation of palmitoyl-CoA and acetyl-CoA in the mitochondria, and oleic acid is formed via a mono-oxygenase system in the endoplasmic reticulum.

Now, would it be feasible or not to synthesize unsaturated fatty acids is a matter of debate. Maybe this could be helpful in this matter.


text:
Applying Constraint Programming to sequence alignment/analysis
My Masters program is focused on formal methods such as SAT solving and constraint programming. I am interested in applying such techniques to problems in sequence alignment and sequence analysis, areas that have been dominated by statistical methods.
So can you give me examples of some research problems suitable to be approached as constraints satisfaction problems?
Note: By constraint programming I also include more flexible paradigms like weighted constraint programming, where a solution may violate some of the constraints.

Do you mean optimization? In any case I guess you either have to state your problem clearly and what you want to do. Moreover, this question is not really suitable for this forum. You can ask this in CS-SE.

I mean a problem that can be modeled by specifying a set of constraints and specifying relations between these constraints. Optimization is a special case and is more related to weighted constraints problem (then we are optimizing for a minimum violation weight)

As for asking this on CS-SE: I disagree, my question is not about constraint programming. It is about what problems in bioinformatics (in particular sequence alignment) can be tackled as a constraints problem. The people who would know this best are people working in biology.

First read how local and global alignment differ from each other. Then decide an objective function, i.e. how to measure the similarity between two sequences? Maybe use Hamming distance? Or Levenshtein distance? After this the optimization part probably comes out quite naturally.
Be sure to check the existing softwares. Easy things have been tried out already. (And by the way, for some reason biologists call n-grams as k-mers.)

Well, I am in the middle of project on using HMMs for alignment, and have read the basics. But the problems I have read about (aligning two sequences for functional analysis and allowing for nucleotide insertion/deletion) does not seem to be suitable for modelling with constraints. So I am asking to see if there are other problems that might be better suitable for that.

The closest thing I've seen that may be suitable for constraints approach is the use to transformational grammar for long-distance dependencies. But even there I am not very sure it can be framed as CSP.

Try reading this article: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0018093#pone-0018093-g003 Any help?

Thanks, maybe. One will have to look at the systems/tools mentioned in the article to see if there are any that are constraints-based (rather than statistics based) or at least incorporate constraints in some way.If so then that would be a good candidate for constraints programming project.


text:
How many Type II restrictions enzymes are currently available (commercially)
How many Type II restrictions enzymes are currently available (commercially) for purchase as of the date of this posting (September 1, 2014)

A lot. Why do you need to know? It would be very difficult to inventory every enzyme from every manufacturer out there...

I'm  an exercise for UGR studentS and was trying to stress the diversity out there with an accurate number. Figured this would be a tough one. NEB has always been the most pioneering company for these but I know they don't own all the patents.

This question appears to be off-topic because it is basically a "shopping-list" question, see Why are “shopping list” questions bad? and Q&A is Hard, Let’s Go Shopping!.

This question appears to be off-topic because it is not about biology per se, is extremely difficult to answer, and has no use whatsoever to the users of this website (and it seems very little use to the OP as well)

I disagree @Raoul ! Respectfully. If one is planning a cloning experiment a comprehensive list is the very thing he/she needs. This ? Explores just that. This is one of the most diverse enzymes in nature as well, knowledge about which ones have had their synthesis mastered and an appreciation if that is  perfectly relevant I believe. You can find the reason for this question above, for education.  I don't think it's an answer is impossible either. I will remove the date from the question but I figured it would allow future readers to easily gauge the accuracy of any answers.

@rhill45 I did not mean any disrespect. It may be that I have a skewed point of view, not being a fundamentalist. I however suggest not to remove the date, since its presence makes your question more compliant with site policies.

A quick look in REBASE finds 15999 type II restriction enzymes of which 616 are listed as having suppliers. Obviously some of these will share recognition and cut sites.

The Restriction Enzymes section at Biocompare is likely not comprehensive, but short of contacting every single molecular biology company and merging all their inventories into a master list, it's probably the best you can do on short notice. They currently list 289 uniquely-named enzymes, but I'm not enough of an expert to say how many are similar in activity/recognition sequence, or whether they might also be known by other names not currently listed. For your purposes, however, it'd probably be enough to tell your students that there are on the order of 300 common commercially-available enzymes. Hope this helps.

downvoter care to comment?

Because of the extreme complexity and quite easy synthesis and customization of proteins this question is unanswerable. That is to say there is such a great number of potential enzymes from any set domain or with the functionality there of that no one is able to fathom the depth even when restricted to current availability.

honestly i'm not surprised people dont think that custom enzymes are readily available but its sad someone would -1 because of it


text:
Where to find the corrected BLOSUM matrices?
I was looking at this paper which talks about the miscalculations in the BLOSUM matrices and how the "wrong" BLOSUM62 matrix performs better than the corrected version. I was trying to find the corrected version they talk about to experiment with, but the link they list in the paper appears dead.
Does anyone know where I can find the corrected matrix that the authors talk about?  (preferably a version listing frequencies rather than scores)

Either write to them asking for the files or see the images in the supplementary info (fig 4-5). They could have at least made it as a table; unfortunately you have to manually type it out.

Okay, I emailed Dr. Mark Styczynsk (one of the authors) to ask about a link to the matrix. Here are the links he gave me:
http://web.mit.edu/bamel/blosum/revised_blosum.c
http://web.mit.edu/bamel/blosum/original_blosum.c
http://web.mit.edu/bamel/blosum/RBLOSUM64 (isentropic with BLOSUM62)
http://web.mit.edu/bamel/blosum/RBLOSUM62 (not isentropic, but it's 62)
The first link is to the c code to generate the corrected BLOSUM. According to Mark, just replacing the original c file in the original BLOSUM tarball with the revised c file can generate the corrected matrix for any of the BLOSUMs (30, 50, 92). Haven't yet tried that myself.

Your question made it difficult to understand what you are looking for so I hope these two links will provide you with the desired data.
0. A source link to the paper in question and its supplementary file.
1. What blast is currently using.
2. What the math calls for.


text:
How do tight junctions in stratified squamous epithelia affect nutrient supply?
In histology we know that epithelium tissue isn't vascularized so it takes the nutrition from Lamina propia (CT) via diffusion and in other hand we know all epithilial cells have tight junction which inhibits the flow of substance so how can it diffuse nutrients between themselves because of the tight junction how can they distribute nutrients, same way in capillaries which are endothelium  how interstitial fluid passes throw endothelial cells because of thier tight junction?

Most epithelial cell layers a thin so that is not a problem. The epithelial layer of the skin gets less nutrients the further their distance to the basal layer is and eventually these cells die and form the horny layer of out skin.

Tight junctions function to occlude the baso-apical flow of small molecules. However, tight junctions do not always completely seal a cell's lateral surface. In addition to regulating diffusion, tight junctions promote cell polarity. Establishment of polarity and prevention of water loss are the major roles of tight junctions in stratified squamous epithelia.
In simple epithelia, transcytosis allows the flow of molecules through a cell with tight junctions. However, stratified squamous cells do not use transcytosis for nutrient supply.
In the stratum granulosum, skin cells lose their nuclei and become non-viable. In the stratum lucidum, an oily layer is produced by exocytosis.
It is the loss of nuclei, organells, production of an oily layer at the stratum granulosum and lucidum that contributes most to the death of skin cells, not the limits of nutrient diffusion.


text:
What is the expected effect of pH on the activity of a fungal pectinase?
I am working on an enzyme assay for a fungal pectinase.I assayed the enzyme in different buffers from pH 1-12.5 However,the enzyme has good activities starting from pH1-10.5.
Is it possible to have enzyme activity over such a broad range of pH?

Can you tell us which pectinase you are using? Besides that, is the activity the same over this pH range or does it vary? Can you show a curve of the activity plotted against the pH?

Could you also give more details of methodology and controls - pectin can be hydrolysed non-enzymatically at low and high pH.

I actually doubt that the pectinase has such a broad pH range in which it works optimally. Searching the web I found two figures which support my doubts:

The first is from an article ("Immobilization of pectinase by adsorption on an alginate-coated chitin support") which compares the activity of native and immobilized pectinase under different conditions. The second is from the datasheet of a company which sells the enzyme. Both show an activity over 50% roughly between pH 3.5 and 5.5 but not at higher or lower pH values.

I extracted the enzyme from 48 hours actinomycete culture ( submerged fermentation) the methodology I used is miller DNSA method


text:
Localization of B and T cell
What does localization of B-Cell mean?? "Localization of B and T cell in allergens may not coincide". What does this statement mean? (I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

Can you tell us, where this statement originates?

What is the source of the statement? Is this really an exact quotation?

http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1  this book

I think the reason you are having trouble discerning the statement is because it doesn't really make much sense, nor is it in my opinion sufficiently explained in the paper. The sentences preceding the it give a little explanation as to what the author may be getting at:

So far, 1500 allergenic structures have been identified. Online allergen databases and allergy prediction tools are being used to find cross-reactivity between known allergens. Localization of B and T cells in the allergen may not coincide.

During an exaggerated immune response (allergy) the lymphocytes (B and T) will localize (travel or accumulate at) to the site of the antigen (allergen).
If I could guess I would say the author is stating that data has shown that no immune response is taking place (data generated by assessing the accumulation of lymphocytes near the allergen), despite the fact that these online allergen predictors say that an immune response should be generated.
The statement in my opinion moves to discredit these online allergen predictors.
I did look over some of the rest of the manuscript, and found two other ambiguities within.
The author does cite another paper in your sentence that may shed more light on this:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2686541/?report=reader
An overview of it provided little clarity however.
I fear that only  a crystal ball or this question addressed to the senior author may answer your question with complete certainty:
Dr. Rajat Kumar De
Professor
Machine Intelligence Unit
Indian Statistical Institute
203 Barrackpore Trunk Road, Kolkata 700108, India.

"Localization of B and T cell in allergens may not coincide".
That sentence is written poorly, it confuses more than inform.
What the author means is: The epitopes that B cells and T cells can recognize are not the same in one particular allergen.
We have to remember that almost all allergens are proteins and proteins are made up of aminoacids, and that's what make up epitopes.
For one same particular structure or say, an allergen, the T cell can only recognize LINEAR epitopes whereas the B cell can recognize LINEAR or CONFORMATIONAL epitopes (that is, they recognize a 3d-like structure and not just a sequence of aminoacids).
What I always tell my students so they can grasp the concept is that the T cells are able to "see" a photograph of a chair to recognize it. While a B cell can do that and even more it can actually "see" a chair for what it is.

Welcome. Please add resources to your material so that others can background read on your material.


text:
If someone were to die on the moon, would their body decay?
I heard that the footprints of Neil Armstrong are still there, so I was wondering if someone were to die there, would they remain preserved, too?
If not how long would it take for them to decay?

i think this question suits more for skeptics.se

why? don't you believe in decay Agha?

Are you asking about if an astronaut died in their spacesuit or an unprotected body?

@shigeta.. I don't think it is opinion based... It is answerable but clearly there is no effort shown in the question. I consider this a homework.

@WYSIWYG I know what you mean,  Just hoping stronger users like yourself can help the newer users with edits.... good writing is hard and its particularly hard in science. On the other hand science is in need of stronger public relations.

Related questions on Space Exploration: http://space.stackexchange.com/q/5666/5963, http://space.stackexchange.com/q/308/5963

I am assuming in spacesuit here, on the face (lit side) of the moon. Bodily degradation involves much more than external fungi and bacteria.
Cells that receive no oxygen or nutrients die. We talk of such tissue death as dry gangrene when it affects extremities, such as fingers, feet, etc. However, we also recognize gangrenous bowel, etc. which results in tissue necrosis.
Such necrotic cell death is the consequence of acute disruption of cellular metabolism, leading to ATP depletion, ion dysregulation, mitochondrial and cellular swelling, activation of degradative enzymes, plasma membrane failure and cell lysis [1]
Lysis is messy and wet. Combined with the fluids in our bodies, what one would end up with is a mushy, smelly degraded body, not a preserved body. For a while, anaerobic bowel bacteria would flourish (which smell terrible).
Add to this the extremes of temperature (253° F in the sun and -243° F in the dark.) The suit would have lost it's heating and cooling mechanisms, so the body would alternately spend 14 days in the heat and 14 days in the freezing cold depending exactly where it was (lets say the equator of the moon.) These freeze/bake cycles would further contribute to degradation through ice crystal formation and thawing.
Eventually, because there was no new substrate, degradation would come to a halt, but I'm not sure at what stage this would be. I assume, though, there would be a vast difference between a mummified body (done by dehydration) and a body left to degrade in a spacesuit.
[1] The mitochondrial permeability transition in cell death: a common mechanism in necrosis, apoptosis and autophagy, John J. Lemasters et. al, Biochimica et Biophysica Acta 1366 (1998) 177-196

I wonder if the body would 'pop' the spacesuit by putting too much pressure on the suit by boiling in the heat. What does a partially decayed then autoclaved body look like?

@Resonating - Space suit as pressure cooker. :-O

Decay is a process where the body is digested by bacteria, fungi and other living things.
The moon has no known biological processes and while its possible for some microorganisms to survive in space, I think its generally understood that the lunar surface would not support life in a significant way, especially if the body is in vacuum.
Other processes would definitely take place. Mummification can result from the body dehydrating and direct exposure to solar radiation will also break down the corpse, but it will mostly leave the body intact.

So, essentially no but to some extent yes? :)

so essentially no :)  mummification is more of a form of preservation, as opposed to decay

I think the body would undergo decay. While it is true that the moon does not contain living organisms capable of decaying a dead human body, the human body itself contains huge load of bacteria→ on skin surface and gut which will continue to grow.
The aerobic bacteria will die out as soon as oxygen is removed which is very soon. The anaerobic bacteria will continue to grow and proliferate till substrate (dead human body) will cease to exist. This will be regulated as anongoodnurse has pointed out by the heat and light.
Further, the infectious status of the dead person will also matter. Any fungal infection can alter the rate of decay.


text:
Is greed an evolved trait?
I am not a biologist, but I am fascinated by evolution.
I was watching the news this morning and, as so often is the case, there was a news story about a corrupt politician who was accepting bribes.
This started me thinking about how greed can become such a strong factor in one's life that it cancels out empathy for your fellow human beings.
So I was wondering--is greed an evolved trait?  Maybe some result of an evolutionary pressure to hoard food for example?

I doubt that human behaviour can be biologically explained. Something that might appear greedy to someone might not be so for others.. It is opinion based I would say...

@TheLastWord I think that many evolutionary psychologists would disagree with you. I'm not saying that I necessarily would, but there's at least a lot of scientific discussion on the topic.

There's some connection to this question, although of course 'cheating' in social insects and in human societies could be a very different thing (or, perhaps, very similar): http://biology.stackexchange.com/questions/5076/modern-reference-for-kropotkins-lazy-bees/9478#9478

@Oreotrephes So maybe then this question was better suited for http://cogsci.stackexchange.com/

I think that Sociobiology should be considered enough of a science to discuss it on biology stackexchange.  It gets published in Science, hopefully that's good enough in general.

The whole point about your question is to define what is an "evolved trait"? The concept of "evolved trait" does not exist in evolutionary biology. Here are various definitions I can think of that could apply to the expression "evolved traits".
Heritable Traits
Does evolved traits mean heritable traits?
A trait may be heritable or not. See for example my answer to this post to understand what heritable mean. You may want to understand the difference between the narrow and broad sense of heritability. Greed is probably heritable as several studies showed that many personality traits are heritable. This post will maybe give you more info.
--> Greed is probably a heritable trait
Traits that evolve
Does evolved traits mean traits that can evolve?
Any (existing) biological trait evolves. Not necessarily because they are selected for or against, neither even for genetic reasons, but traits change through times. Culture changes.
--> Yes, greediness can evolve
Traits that are adaptations
Does evolved traits mean traits that are adaptations?
The concept of adaptation is not always easy to define and its definition may vary from authors to authors. Simply speaking, an adaptation might be defined as a trait that is now fixed in the population (meaning that all individuals in the population carry this trait) but when it was not fixed yet it was beneficial. Such definitions would not fit the concept of greediness if we assume there is some genetic variance for greediness. But while I am not aware of any study on the subject, a level of greediness very probably influence the fitness  (=~ reproductive success) of its carrier. If someone is extremely greedy, he might not find a mate and may fail to reproduce. On the other side, someone that is extremely generous may give everything it has up to its life and would definitely fail to reproduce. Therefore, it seems at first though that there is what we call stabilizing selection on the level of greediness.
--> It depends on the meaning of adaptation. But yes, it seems intuitive that greediness is a trait that undergoes (stabilizing) selection.

Social traits
Greediness is the kind of trait that are particularly interesting because it influences not only the fitness of its carrier but also the fitness of other individuals in the population. We say that it is a social trait and the field that study such traits is called social evolution. You'll need to get in touch with Hamilton's rule (Kin selection) and evolutionary game theory to understand more about the evolution of social traits. This post may eventually help you.

Really nice answer - I think this is a perfect example of a great response to a "I'm not a biologist, but I just wondered..." question.

this is a better answer, but would love to see a full answer to the question here on the site