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Why has grey hair evolved?
A vast majority of humans get at least some grey hair as they age. As far as I know this applies to both genders and all races. Presumably this means that at least some grey haired humans have noticeable reproductive advantage, or maybe they had it in the recent past.
Theoretically, because this feature is so prevalent, there must be a strong evolutionary pressure to keep it. Am I right? If so, what is it?

gray hair happens after the optimal reproductive window period so after that window there is no selection pressure to eliminate it.

i would think that showing age will prevent less viable offspring, so it might be adaptive.  not everyone believes in such social adaptations though

There was a discussion on Reddit a while ago, and the general opinion was that other primates and even dogs show gray hair if they live long enough. That puts your question on the wrong premises.

@NickSandor can you share a link to that reddit discussion?

http://www.reddit.com/r/askscience/comments/hm3k2/what_is_the_evolutionary_reason_for_grey_hair/ I wasn't sure I am allowed to link to competition.

New development: http://www.bbc.com/news/health-35687287

@Bez Men are usually still fertile after they grey, and so are many women. I agree that this is a lack of selection pressure to avoid it, but I don't buy specifically that argument without citation.

Thus, the question is not "what makes hair grey"?

Presumably this means that at least some grey haired humans have
  noticeable reproductive advantage, or maybe they had it in the recent
  past.

No it doesn't.  Natural selection is not that strong, it doesn't optimize every single possible physical trait towards maximum reproducing.
And as others have mentioned, having lots of grey hair usually happens after reproduction is over.  Historically, lots of women did a lot of reproducing before they had any grey hair.

This seems to be almost completely correct, but some grey-haired men could still be reproducing.

"it doesn't optimize every single possible physical trait" emphasizing this in the study of evolution would eliminate much of the confusion.

Grey hair is one of many age related traits. Other traits showing a positive correlation with age include Parkinson's, cancer, and Alzheimer's. There are two key theories as to why age-related disease & decline occurs. But the key message is just because something evolves, it doesn't mean it's advantageous.
First of all is mutation accumulation (MA) theory. This theory basically suggests that as we age there is less likelihood that selection can remove the alleles that cause genetically determined aging. If we consider something like cancer, which is clearly deleterious it becomes clearer, though grey hair may be deleterious (reduces fitness) it is at least less obvious. If a cancer has early onset, affects people aged 10, then it is highly unlikely to spread through a population because those carrying the allele are unlikely to reproduce. If a cancer has late onset, causing cancer at 60 years old, then there is a much lesser chance it will affect reproductive success - most 60 year olds don't have more children in the future. In the case of MA the effect of selection is weak if a trait reduces survival post-reproduction. The same could be true of grey hair, even if it is costly it's arrival late in life is not that surprising.
The other theory is antagonistic pleiotropy (AP) which suggests that genes which improve fitness might reduce survival. For example, the genes that cause cancer at age 60 might also make you better at attracting mates, fertilising, and raising offspring. In this case it would be beneficial to carry the cancer gene (from an evolutionary perspective). I think there is some evidence (but can't find it right now) that grey hair is associated with higher fitness, in that case it could be that grey hair has evolved directly because of sexual selection (people might prefer silver haired partners) or because of AP - grey haired people are better at other fitness related things because of pleiotropy.
So to answer your question: direct selection is not necessarily the reason that grey hair has evolved, it could be because of mutation accumulation or pleiotropic gains associated with the genes affecting grey hair.
You can read more about these theories of aging in this answer and for references.

I do not think there is a reproductive advantage in gray hair - it's the other way around:
Normal colored hair has a reproductive advantage.
But it also has a cost in terms of substances needed to build it.
I make the assumption here that grey hair - which is often also more sparse - has a lower cost in terms of material.
I think we are investing the cost for the part of the live that is exposed to direct evolutionary reproductive pressure.
Later, we do not longer invest the cost.
That makes sense if we assume that hair becoming gray is a process of degradation.
It is not supported by an investment, but by the absence of an investment, following from absence of evolutionary pressure.

Can you elaborate how grey hair of same thickness "has a lower cost in terms of material"?

Oh yes, I notice I did not say that, I was thinking not of general mass, but of substances/elements that are scarce in the body, (and may be neede elsewhere). But as I wrote that is an assumption, not validated.

I think grey hair does have an evolutionary advantage related to Vit D. Vit D is crucial to life and severe deficiency may lead to death. The main source of this vitamin is the production in skin cells through exposure to UV light.
As you might know, humans who live in colder climates with limited sun exposure lost the pigmentation in their skin. This is to allow more UV rays to reach the deeper layers of skin to produce Vit D. Humans living in sunny areas had the opposite need as their skin pigmentation is protective against skin cancer, and it still allows enough UV rays to produce Vit D in sunny areas. This is why people with pigmented skin living in cold climates are recommended to take Vit D oral supplements, and why people with less pigmentation in hot climates are more vulnerable to skin cancer.
Grey hair allows more UV rays to reach the skin due to the lack of pigmentation in the hair. Humans in general need more Vit D as they age and start becoming vulnerable to osteoporosis and fractures. This explains why grey hair commonly starts at age 40-50 when the bones start to become increasingly weaker.

Welcome to Biology.SE. Could you add some references or additional evidence to your answer? I do not think this answer is correct; people at age 40-50 do not substantially (at least before recent times) contribute to the next generation and selection will thus have a hard time on such a phenotype (as has been mentioned in the comments) ...

Although I agree with the idea that a useful trait at old age has a weaker effect on natural selection, this weaker effect can't be entirely disregarded. Older people do contribute to improve the next generation's survival chances in many ways other than directly passing their genes. A parent who manages to survive till age 60 can support their offspring longer than a parent who dies at 40. The offspring of a parent who had them at age 38 and died age 50 have less chances of survival than if the same parent died at 70.

Please give (cp. AlexDelarge's comment) some reference: how does black, brown, red hair relate to the colour of white in respect of uvc or uva radiation.

My theroy is that gray hair allowed a predator to pick out the weak one in the group and focus on it as a possible food source allowing the younger ones to escape and survive.
Gray hair is also a signal to a potential mate that you might not be providing young healthy genes.
Both of these could have allowed our species of human to succeed over others.


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Why do we suddenly forget things, like PIN or phone numbers, that we've known for years?
Is it common to forget a 4 or 5 numeric code which has been used extensively for months and well remembered?
There's an article on the guardian describing this phenomenon and by the number of comments it seems quite common yet no scientific aspect trying to solve the mistery.
Is it some common phenomenon of the brain? Some erasing of irrelevant numeric things happening during sleep?

Forgetfulness is a common phenomenon that tends to increase with age. It usually affects short term memories but it can affect long term ones too. Here are some possible causes which I quote from Healthline (the full list available at that link):

sleep deprivation
use of alcohol or drugs and some prescription medications
lack of oxygen to the brain
migraine

It can happen at any age and it is normal if (quoting Deane Alban, Memory Loss: When It’s Normal and When It’s Serious):

Are you overworked and stressed out? Are you eating poorly? Are you on a low-fat diet or skipping meals to lose weight?  Do you struggle with insomnia? Do you drink too much?
If you answer “yes” to any of these questions, it’s likely you are losing your memory because your lifestyle is catching up with you.

You mention loss during sleep in your question. Sleep affects memories (see WebMD and Wikipedia):

deprivation of sleep leads to memory loss
during sleep brain selects relevant information gathered during the day and turns it into memories
certain stages of sleep improve memories

source: Stack Exchange

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How do small birds survive the winter?
I live in a region with cold winters (ca. -40 C) and many quite small birds (sparrows, crows, ducks) stay for the winter.
How can the birds survive this?
As I understand it, smaller bodies will be less able to produce and retain heat. Despite this, birds seem to cope much better than humans, sitting in the cold all winter and even swimming in cold water. In comparison, humans lose mobility in their muscles when cold, and can suffer severe frostbite causing them to lose fingers, toes, or limbs from relatively short exposure to the same conditions.
What specific adaptations allow birds to cope so well in these conditions?

Are you actually seeing these species where you live during winter? Birds tend to be migratory. Feathers and fats tend to make fairly good insulators though. They would need a food source and some form of shelter. But I would assume if you do not see them in the winter, then they have migrated towards the equator.

Also, if it is actually water, then it is greater than 0°C, so the water may actually be warmer than the air temp. And like I said above, fat and feathers make for good insulation.

@AMR: yes, I actually see them. Maybe there are less birds than in summer, but there definitely are many. I know they should migrate, but for some reason they don't really always do that.. idk, the migration thing seems broken, I see really many birds in winter in the city. Yeah, they can find heat sources in the city, but still they spend quite much time just wandering around in the cold. Good point about the water temperature.. Idk how, but sometimes, when it's -20C, some parts of the city channels are not iced, probably someting warms the water..

@AMR: also - what about their legs? They are in no way protected... still their muscules and joints do not suffer, they can just as easy grip to their sitting place, like a branch or a wire..

The coldest water is around 0 Celsius. Beyond that it's ice.

@ott-- yes, right. I guess I wanted to say that as water is more dense than air, it's thermal conductivity is also higher, and it would draw heat more eagerly than air. Same as a metal usually feels colder although it's of the same temperature as everything else around.

Which birds,  many birds have very different responses and adaptations to winter.

Not even close to a full answer, so I'll only post a comment. Here you can read about a cold adaptation of the circulatory system in bird legs that allows a heron to keep standing in icy cold water and be fine.

During cold weather, birds will go into torpor where they will reduce their metabolic rate to conserve energy over the night. This burns fewer calories and maintains fat reserves that help insulate them from cold temperatures. Behaviorally, many bird species will roost communally to share heat among each other.

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Why are the genomes of Humans 99.5% the same?
Human's DNA sequence is said to be roughly 99.5% equal. As far as I understand, this means that if I walked up to you and compared our DNA, the sequence of base pairs would be 99.5% the same.
My question is: Why is there only 0.5% variation in our DNA? I can think of two reasons:

For some reason, the other 99.5% (roughly) is locked in place. These sections, if changed, either result in us not being 'human', or simply get some sort of genetic disease and so aren't very good mutations.
There hasn't been enough time. I remember hearing that all humans have a common ancestor some long time ago. If that's the case, perhaps over time only about 0.5% of our DNA has had time to randomly mutate, and if we wait a really really really long time, more and more of our DNA will mutate, and we will become 'less like each other'.

Or am I completely misunderstanding the situation? I didn't take biology in high school so answers should be simple please.

A complete answer will need to go quite in depth into the field of population genetics and it will take time to give the introductory knowledge necessary. But shortly, the answer is definitely not 1. and is pretty close to 2 :)

@Remi.b Thanks for quick insight, would you happen to know where I could get online resources to start learning about population genetics? (or anything that might help me understand this better)

It is a little frustrating to receive as answer "just learn more", but you can find book recommendations in population genetics here. You might first want to follow an introductory course to evolutionary biology such as Understanding Evolution (free online ressource).

@JoshuaLin I am not sure if you are notified to edits to answers. I made some substantial additions to my answer to provide more detail, to hopefully address different details of your question,

In a genome that is 3 billion base pairs, a difference of 0.5% works out to a difference of 15 million bases. When a single base change can change the amino acid sequence of a protein, that can add up to a huge amount of diversity, which is what we see over the nearly 8 billion humans on the planet, and the 99.5% sameness is why we are linked together so closely as a species.
How can the lack of diversity be explained?

Nothing in Biology Makes Sense Except in the Light of Evolution.

The above quote was made by the evolutionary biologist Theodosius Dobzhansky. What this basically means is that you need to take a look at your question from the perspective of evolution and natural selection.
The first thing you need to note is that there is evidence to suggest that modern humans went through a population bottleneck. What that means is that at a certain point in our history, there were very few individual members of our species alive and this can account for the "lack" of diversity that we see in our genome. The number that is quoted is as low as 10,000 individuals left alive after the supereruption of the Toba volcano about 75 thousand years ago.
That means that there were very few mating pairs left, and that significantly reduced the genetic diversity of our species. This is known as Founder Effect.

Founder effects
A founder effect occurs when a new colony is started by a few members of the original population. This small population size means that the colony may have:

reduced genetic variation from the original population.
a non-random sample of the genes in the original population.

So if we use an average of 20 to 25 years per human generation, we are only looking at about 3,000 to 4,000 generations since there were maybe only a few thousand breeding pairs of humans. Contrast that with bacteria which can go through three to four thousand generations in less than a week, and you can begin to get a feel for why there is so much sequence homology (sameness) in the human genome. See Bottlenecks and founder effects at UC Berkley's Understanding Evolution site for more information.
You also should understand that any changes that are deleterious will be under strong selective pressure. This may not mean that the organism may not survive to reproduce, in may just mean that on average, they may be less successful; fewer offspring that have fewer offspring in comparison to the rest of the population. At some point that lineage may go extinct, either because the change makes it very difficult to survive, or the offspring make less desirable mates and eventually don't get the opportunity to reproduce.
Any changes that disrupt a vital gene will likely be fatal and will lead to spontaneous abortion or if the mutation was sustained in a sperm, then the inability of that sperm to survive to fertilize an egg, so the sperm that was heavily mutated may just never make it to the egg. The average number of sperm in a single human ejaculation is about 250 million. And yet only a single sperm makes it to fertilize the egg, and that is assuming that a fertilization event takes place. There is an incredible amount of selection that goes on in the act of procreation, even before we get to development.
Why the 99.5% to 0.5% figure might be misrepresentative of the population as a whole.
Another thing that you will want to think about is how the 0.5% to 99.5% number was arrived at. The referenced in the question links to a Wikipedia article Human Genetic Variation. The reference provided for this was from a New York Times article about J. Craig Venter, In the Genome Race, the Sequel Is Personal - Wade, Nicholas. September 4, 2007. The quote that is references in Wikipedia is:

Biologists had estimated that two individuals would be identical in 99.9 percent of their DNA, but the true figure now emerges as much less, around 99.5 percent, Dr. Scherer said.

The 0.5% figure is provided as a quote from Stephen W. Scherer, who was a coauthor of this paper, The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007. DOI: 10.1371/journal.pbio.0050254. From that paper the following quote is found:

Inclusion of insertion and deletion genetic variation into our estimates of interchromosomal difference reveals that only 99.5% similarity exists between the two chromosomal copies of an individual and that genetic variation between two individuals is as much as five times higher than previously estimated.
- The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

So at the very least, the statement was made in a peer reviewed article. However there are some problems with this.
The first is the method of the paper. It looks at a single human genome, that of Dr. Venter, and is used to draw the conclusion of 0.5% difference between any two individuals. And the comparison is made based on the analysis of differences between Dr. Venter's maternal chromosomes and paternal chromosomes. Let's look at what the problems might be here:

It is a huge leap of statistical faith to assume that a single genome is representative of the nearly 8 billion genomes out there.
Dr. Venter's genealogy is English on both parental lineages. We have to remember that there was another population bottleneck in middle ages Europe caused by outbreaks of cholera and the Black Death. This fact may imply that Dr. Venter's lineages are genetically close and that if his lineage were more diverse, say Indigenous Oceanian and English, they may have found a much higher percent difference between maternal and paternal chromosomes.

The donor's three-generation pedigree is shown in Figure 1A. The donor has three siblings and one biological son, his father died at age 59 of sudden cardiac arrest. There are documented cases of family members with chronic disease including hypertension and ovarian and skin cancer. According to the genealogical record, the donor's ancestors can be traced back to 1821 (paternal) and the 1700s (maternal) in England. Genotyping and cluster analysis of 750 unique SNP loci discovered through this project support that the donor is indeed 99.5% similar to individuals of European descent (Figure 1B), consistent with self-reporting.
- The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

Dr. Venter is male. The Y-chromosome was problematic to sequence, and you cannot really do a comparison between it and the X-chromosome. How would the genome of a woman compare?

The Y chromosome is 59% covered by the one-to-one mapping due to difficulties when producing comparison between repeat rich chromosomes. In addition, the Y chromosome is more poorly covered because of the difficulties in assembling complex regions with sequencing depth of coverage only half that of the autosomal portion of the genome. The X chromosome coverage with HuRef scaffolds is at 95.2%, which is typical of the coverage level of autosomes (mean 98.3% using runs). However it is clear that the X chromosome has more gaps, as evidenced by the coverage with matches (89.4%) compared with the mean coverage of autosomes using matches (97.1%). The overall effects of lower sequence coverage on chromosomes X and Y are clearly evident as a sharp increase in number of gaps per unit length and shorter scaffolds compared to the autosomes (Figure 3). Similarity between the sex chromosomes is another source of assembly and mapping difficulties. For example, there is a 1.5-Mb scaffold that maps equally well to identical regions of the X and Y chromosomes and therefore cannot be uniquely mapped to either (see Materials and Methods and Figure 3). From our one-to-one mapping data, we are also able to detect the enrichment of large segmental duplications 10 on Chromosomes 9, 16, and 22, resulting in reduced coverage based on difficulties in assembly and mapping (Table S3).
- The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

There is another thing that you need to remember and that is the history of the Human Genome Project. Dr. Venter developed a new method of sequencing and became a commercial competitor to the International Human Genome Sequencing Consortium project. While the International Human Genome Sequencing Consortium project beat out Dr. Venter's enterprise(8), it's approach, to use an amalgamation of the DNA of many donors, some of whom had their DNA included and some who did not, to preserve anonymity, Dr. Venter circumvented this by performing the sequencing on his own DNA. When his team was beat out by the International Human Genome Sequencing Consortium, he doubled-down, invested more time and effort and came up with the sequence put forth in this paper, which had a higher degree of resolution than previous efforts. The paper is making an argument for the value of their technique over the techniques being used by the International Human Genome Sequencing Consortium and is trying to make a claim of the superiority of their method. The data being presented is likely factual, but because of this history you have to look at the paper, the methods, and the motives behind it.
It is only 15.5 years since we had a full draft of a Human Genome Project produced by the International Human Genome Sequencing Consortium. In order to sequence that genome samples were taken from a few hundred individuals. Small stretches of the DNA were sequenced and then all of those pieces were put together in computer. That means that there was a lot of averaging that happened. So by default, the most prevalent base in the population of volunteers at every position was chosen. That means that that should be representative for the rest of the population as well.
When we make statements about comparisons in datasets as large as the human genome, more often than not we are looking at known, small subsets of the genome, and we are extrapolating by statistical methods based on that fact. One thing you learn as you read science papers, and not just science news articles, is that you always need to look at their materials and methods to determine how they arrived at their data and headline numbers. It is often quoted that we have only a 1.5% difference between Humans and Chimpanzees, however when you look at those papers the comparisons were done only on areas of the genomes that lined up well. That isn't to say that there isn't a remarkable degree of similarity between us and our nearest living evolutionary relative, it is just that there is more to the story than the headline.
Also, we don't have that many full genomes sequenced to compare to one another, as a percentage of the 8 billion people alive today. While we have representations from most a vast majority of the ethnic groups identified, we may be missing families with novel lineages.
Another thing that you need to think about is that many of the areas in the human genome are repeats and structural elements that do not encode for genes of affect gene expression. Things like telomeres, which protect the ends of chromosomes, and centromeres which are the attachment points on chromosomes that make sure that the are distributed properly into newly divided cells. These elements tend to stay the same because the proteins that bind to them require that sequence specificity in order to function properly, so those are regions were almost every ones DNA will be the same, and not just between humans. These elements often are very similar in most vertebrates.
We also need to consider structural RNAs. These molecules have functions within the cell that require that there sequences be highly conserved (unchanged). Ribosomal RNAs, Transfer RNAs, Small Nuclear RNAs all rely on their specific sequence to fold properly in order to perform their task in the cell. A single base change can change the folding of these elements and as a result they will loose their function, which means those cells won't be able to produce proteins properly which means that the cells will die. If this is happening in germline cells, then they are not going to be involved in fertilization so any mutations there will be passed on.
I could go on and on, but the take away is that it isn't surprising that there is very little sequence diversity on a percentage bases within the human species, but there are many caveats to that fact as well.
Edit: Significant edits to add relevant, referenced information to back up answer.

I want to create more accounts so I can upvote this answer more.

@Nathan I appreciate the sentiment, I am simply glad you found it informative.

I would like to comment that out of the 150 million differences only a tiny fraction change protein sequence in a meaningful way. First, because protein coding sequences are 1.5% of the genome. Second, a random amino acid change in a protein is very unlikely to have a functional effect. Third, because changes that affect function may potentially be selected against. So the actual number of functional differences much smaller (I am guessing ~100000 or less).

@Bitwise I think you should read that paragraph again. I don't say that it leads to 150 million changes, I say that because only a single base change can change an amino acid sequence, that can add up to a significant difference. The point was that you need very few differences to come up with a large amount of variety between individuals. What you are saying about functional change isn't quite right. You can have a "Silent" mutation in a gene, but if it is such that the tRNA is encoded at a factor of 10 or 100 less that the original tRNA, then you can kill the protein even with no aa change.

@AMR I did not say you are wrong, I just wanted to clarify for readers that even if there are 150 million differences, only a very tiny fraction are actually meaningful. I considered proteins because that is what you mentioned, but there are many other types of changes that can be functional (e.g. in regulatory regions). Still, even if you consider all of these, the vast majority of differences will not have any effect.

@Bitwise The OP is a High School student that hasn't taken Biology. I agree that there are many more places such as promoters and enhancers, splice donor / acceptor sites that can affect functionality, but as we don't usually teach that to first year undergrads, I was only pointing out what someone with a casual understanding may know. Their question is from the perspective that 0.5% is not a lot of variation, they use "only", and I was trying to say to them that that is more than enough to provide uniqueness to 8 billion individuals.

@AMR: It's some time ago, but why would you bring up a sentence like "You also should understand that any changes that are deleterious will be under strong selective pressure." after talking about bottlenecks? After bottlenecks selection (be it purifying, positive or balancing) in general is quite weak and has low efficacy in reducing deleterious variants. Of course both purifying selection and drift reduce variation (and therefore contribute to the low genetic diversity among humans) , but this might still lead to misinterpretations ...


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What is genomic imprinting?
What is a  genomic imprint? How does genomic imprinting take place?
If I say that "this" allele is maternally imprinted does it mean that the allele of the gene is passed only by the mother? If a pedigree is given, how can we identify whether the trait is paternally imprinted or maternally imprinted?
Please try to explain all this in as simple words as possible.

Is this a homework question? If so, please tag it accordingly.

Have you read the wikipedia entry for genomic imprinting?

@Biogirl here is a new review paper all about genomic imprinting http://www.nature.com/nrg/journal/v14/n9/pdf/nrg3543.pdf?WT.ec_id=NRG-201309

**** "What is a genomic imprint? How does genomic imprinting take place?"**

Genomic imprinting is an epigenetic mechanism  of inheritance which allows genes to be expressed differently depending on which parent they come from. This means it is modification of the genome, or changes what the genome produces, without changing the nucleotide (DNA) sequence. The result of imprinting in diploid organisms is that one of the two alleles is silenced.  This page provides a good overview of imprinting.
Two major mechanisms are proposed called DNA methylation and histone modification though others may yet be discovered. DNA methylation silences a gene by adding methyl groups to nucleotides (it modifies the nucleotide but not the sequence) which affects how they are expressed, whilst the exact mechanism is unknown (at least I can't find one on scholar) it does appear to be a key factor in some cancer growths. Genes can also be silenced by histone modification, binding a gene to histones reduces its activity, ie it produces less product.
Genomic imprinting was first described in Mealy Bugs (or at least this is one of the first described) which silence half of their genome in males. Whilst females are fully diploid, the male is also diploid but one half of the genome is silenced, making them effectively haploid. This is done by turning one half of the genome heterochromatic.

****"If I say that "this" allele is maternally imprinted does it mean that
  the allele of the gene is passed only by the mother? If a pedigree is
  given, how can we identify whether the trait is paternally imprinted
  or maternally imprinted?"**

Specific control of a gene, rather than entire chromosomes described above, is only known in plants and some mammals. In this case, when a gene is imprinted, the gene is silenced. An example is Igf2 in mice described in the below diagram which is maternal imprinting (ie the mothers allele is silenced). When the mother has a mutant allele and the father a normal allele and normal offspring is produced. When the male passes on the Igf2 mutant the offspring is mutant because the mother's normal copy was imprinted.

The Igf2 gene can be seen in the above diagram. This is the one of the
  first evidences of genomic imprinting discovered. In the first part of
  the diagram a mutant gene trying to make the mouse offspring dwarf is
  passed from the mother. It can be seen that the mouse is not dwarf
  because the allele for size in this mouse is an imprinted. The
  maternal allele is not expressed, so the dwarf trait is not expressed
  in the offspring, only the normal size trait from the father is. In
  the second part of the diagram the father passes on the mutant gene
  and therefore all the offspring will be dwarf because the size trait
  is completely dependent on the paternal allele, which in this case is
  dwarf. - Creating Variation

The page this diagram and quote comes from also has a good section on genomic imprinting.

It is incorrect to say that a trait is imprinted, although the phrase is often used.  I will simplify this by talking about just two chromosomes.  A mammal will have one chromosome from mother and one that is nearly identical inherited from the father.  The genes on each chromosome typically have an equal likelihood of being expressed.  An imprinted allele creates silencing on one chromosome and gene expression from solely the other parent. There are many more complexities and Wikipedia is a great source as well as Geneimprint http://www.geneimprint.com/site/what-is-imprinting
See the link regarding Parental Imprinting, the definition is concise.
http://groups.molbiosci.northwestern.edu/holmgren/Glossary/Definitions/Def-M/molecular_imprinting.html

So if I say maternal imprinting , does it mean the maternal allele has been silenced ?

No, it means that whatever imprinting was effected, it came on the maternal gene. It could have been silenced, activated, or something more complicated.


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Insect identification, Chennai, India
Could someone tell me what the species of this beautiful insect is? Location: Chennai, India.

Thank you!

To me, it looks like a Lepidoptera from the Sphingidae family (Hawk moths). It is similar to species in Hemaris and might belong to this genus.
One similar species from this genus (found in India) is Hemaris tityus, but the moth in your picture doesn't look exactly like this particular species. Another similar species is Hemaris saundersii, which is found in and around India.

(Hemaris tityus, pic from wikipedia)

Thank you. I will try to find the exact species by going through Wikipedia. Thanks again!

As suggested by @fileunderwater this moth belongs to the Sphingidae. It is Cephonodes hylas the Coffee bee hawkmoth, aka the pellucid hawk moth or Coffee clearwing. It is a largely distributed moth, found from the Middle east to Autralia.
Glass wings are not very common among butterflies. Research has shown that the glass wings of this species act like a sort of invisibility cloak, as explained in this article and this blog

https://en.m.wikipedia.org/wiki/Cephonodes_hylas


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Reasons why people say that AIDS/HIV doesn't exist
It's been recurrent when I hear people saying that AIDS doesn't exist. When I ask why, they give weird reasons like HIV is a virus created to control economy and to develop medicine, etc. Also when I try to watch videos on youtube about people that are infected with this virus, I see a lot of comments saying that AIDS is a lie and some of them base their opinions on a documentary called House of Numbers. So I would like to know scientific reasons if this a myth, or why this is true.

Ultimately I suspect that those people are just terrified of getting HIV, so they invent or accept these conspiracy theories in order to not lose the one thing in their lives that can make them happy. There's nothing scientific about it.

Well, the fact that there is an ENORMOUS amount of scientific evidence in favour of the fact that HIV is the pathogenic agent causing AIDS and that there is zero proof of the contrary seems to be a good starting point... Anyway this has been discussed here: http://skeptics.stackexchange.com/questions/10435/is-hiv-the-cause-of-aids Now, the reasons why a restrict amount of (delusional) people say the contrary are probably that they do not really understand how immunology works, but feel like they should have a say on it anyway.

@nico - despite people's efforts to the contrary, science is not a democracy (see the global warming "debate"). Just because a lot of people have an opinion doesn't mean it's right, or even deserves to be seriously discussed...

@MattDMo: I am not speaking of opinions. I am speaking of a large amount of scientific literature. Surely, in science you can never say something is true, but the current body of knowledge (see the large amount of refs in the Skeptics.SE link or this NIAID page) is in support of the current theory. So, until proof of conspiracy arise, or until a better explanation of the current experimental data is found, we can say HIV causes AIDS.

@nico - I completely agree with you - I was more speaking to the OP's mention of "opinions"

@MattDMo: oh, sorry, I didn't notice you were referring to that :)

I think no one can really deny the existence of HIV or AIDS, just a search on google scholar will show >1,500,000 hits for each of those terms, and ask (hopefully any) doctor and they will say it does, though AIDS denialists do debate whether HIV causes AIDS. This paper explains the process of HIV causing AIDS. Further, AIDS denialists have not offered up well supported alternatives as to how AIDS arises without HIV being involved.
I think however that there is more debate fuelled by conspiracy theorists as to how the disease came about. This article from TIME magazine on conspiracy theories is a short piece about it, there are two main conspiracy theories:
1) The west invented the disease to "decimate the African population."
2) The US government invented the disease in the 70's and injected gay men to stop the spread of homosexuality.
You should read this section on the critical response to the film House of Numbers, it seems to be thought that the film was driven by funding wishing to promote conspiracy theory and interviews were edited in such a way as to help portray that message.
Caution, the following is my own personal opinion ;)

To most these seem like pretty outlandish claims and most people do ignore them - apart from anything, placing blame on someone won't stop the continuing spread of this horrendously devastating disease so the conspiracies are quite pointless. I personally think these conspiracies are driven by the uneducated, the scared, and those who want to "bring down the man & corporate/capitalist western society led by a powerful minority" etc..

Back to the science: The people who discovered the disease (Dr. Robert Gallo of the National Cancer Institute and Dr. Luc Montagnier of the Pasteur Institute in Paris) along with the majority of the scientific community say:

"the virus jumped from monkeys to humans some time during the 1930s"

Molecular analysis of the genetic sequence for the virus supports the theory that the jump from apes to humans was around 1920-1930. Some other studies support the jump being made around this time though some estimate it to be a little earlier, this is due to estimated rates of mutation being used to calibrate molecular clocks.
I recommend taking a look at AIDStruth.org and more specifically start with this page (thanks for the link @MattDMo) if you have watched House of Numbers.

I seem to recall hearing recently that the jump could have been as early as the late 1800s, I just wish I could remember where. Knowing my viewing/listening habits, it was probably NPR/PBS...

@MattDMo There are a few papers which show it generally to be around the late 1800's-early 1900's. The uncertainty comes from the model used I believe, to do with rates of mutation and calibration of the molecular clock.

OK, thanks, I'll look into it further. BTW, you might want to link to this page on aidstruth.org which specifically refutes "House of Numbers" and many of the denialist claims it makes.

@GriffinEvo Thank you so much for all the references and the information. I've never been interested in biology at all but now these sort of "existencial" questions arise quite often in my head. In the overall I can deduce then that people is being mislead and confused for some reason. In my case, as an ordinary person, meaning I have almost no information about these sort of things, this documentary makes me feel totally confused and sad about manipulation of science, the government and the economical system in general.

Unfortunately there are definitely people who can deny it and believe it wholeheartedly.  Christine Maggiore is a good example.  She had AIDS, transmitted it to her infant daughter via breastfeeding, refused proper treatment for her daughter (which led to the daughter's death) then refused proper treatment for herself, ultimately leading to her own death.  It's sad, but there genuinely are people who absolutely believe that HIV/AIDS isn't real.

I'm not sure if I should be posting this as an answer, but I think a very approachable and accurate account of the history of HIV can be found from Dinis de Sousa et al..  I agree with what has been posted above.  On the theory that a picture is worth a thousands words, you might also introduce skeptics to the cryo-electron microscopy images of the virus (searching cryo-EM HIV will pull up plenty).
That said, hard skeptics would likely want discount the thousands of publications, studies, and plain old researchers who have studied the virus (myself included).
Also, for the record, viruses that are "created" by humans artificially in a lab do exist, practically by definition.  I, and a great many others, make viruses with markers that make them easier to measure or see (such as fluorescent proteins).  But given the time that HIV entered humanity, it seems highly unlikely that anyone had the technology, let alone the will, to engineer the virus as a bioweapon.  Certainly SIV predates HIV, but the technology to make such modifications (or even of the basic players and genetics) to make a recombinant/chimeric virus simply didn't exist.
It is the unfortunate truth that viruses have been used as weapons of terror and warfare against various populations (I could get into examples but that seems off topic).  But the historical examples we have of this are all surrounding existing viruses.
To the question of people made to make money (not withstanding all of the above), it is certainly not for lack of trying that we don't have an vaccine for HIV.  There are a lot of complications (extremely rapid mutation and escape mutants, reservoirs of virus, direct infection of cells from your immune system, etc etc).  And it shouldn't be seen as though HIV is the long lasting human virus we need a vaccine for (Herpes and RSV just two good examples).  You would stand to make a lot of money if you could successfully make a vaccine to any of the pathogens.  And a LOT of people are trying.  The US government alone is spending a lot of money on HIV/AIDS.  Having a successful vaccine could actually SAVE a good deal of money.


text:
Effect of sex-ratio on the effective population size
As stated on this wikipedia article, the effective population size $N_e$ when the sex ratio differs from $\frac{1}{2}$ is
$$N_e = \frac{4N_mN_f}{N_m+N_f}$$
I understand the biased sex-ratio decreases the effective population size and the formula is quite simple. However, I would fail to prove that this formula is right.
Can you demonstrate to me that $N_e = \frac{4N_mN_f}{N_m+N_f}$ is true?

The reason that an unequal sex ratio affects the effective population size is because offspring are produced by one male and one female parent, and an unequal sex ratio increases the rate at which genetic drift will occur.

"...the smaller number of males still contributes half of the genes in the next generation..."

In other words, assuming the male population is smaller, the genes passed on by the males/fathers are sampled from a smaller population than that of females/mothers. As you know, smaller populations are more prone drift.
Imagine the classic drift example with a bag of blue and red marbles, but have the parental generation with an unequal number of marbles in either bag.
Hartl & Clark illustrate (see figure 4 here) the relationship between sex-ratio and effective population size, where a sex ratio of 1:9 gives an effective population size of around 36% the actual size (given by $100 \times (N_e/N)$). This means that the rate of inbreeding and drift in the focal population is equivalent to that of an idealised population which is 0.36 times the census size of the focal population.
$$N_e = \frac{4N_mN_f}{N_m+N_f} = \frac{4 \times 1 \times 9}{1 + 9} = 3.6$$
The population is diploid and dioecious; each parent carries two genes, and each parent must be replaced within the population so each pair must produce two offspring. Consider the case where $N_m = N_f = 1$ (and thus $N = N_e = 2$). The number of genes in this population is four. Therefore, to maintain the same population size, four genes must be drawn from the ancestral population.

Further reading:

Hartl & Clark (Page 123-124, Random Genetic Drift: Unequal Sex Ratio)
Conner & Hartl (Page 62, Chapter 3)

While (personally) I can't prove this mathematically, I can demonstrate it using simulation. I've written up a simulator of genetic drift in R, which can cope with unequal sex ratios.
The first four graphs are populations with $N_E = 360$ at various sex ratios ($N_M / N_F$ = 0.11, 0.33, 0.67, 1.00), for 100 replicate populations simulated over 80 generations, with an initial allele frequency of 0.2. The four simulations have different census population size, but equal effective population size, because of the sex ratio. The four groups of populations behave similarly (rates of drift are similar for the simulated populations under the various conditions).

These four use larger populations ($N \times 15$), at the same sex ratios, where $N_E = 5400$ in all cases simulated over 400 generations. Again the groups of simulations behave similarly.

Update:
I've added histograms to ease viewing of the pattern, using $P = 0.5$, for 1000 populations simulated over 25 generations, where $N_E = 360$ and census population size/sex ratio varies between simulations. This distributions are similar despite the different census population sizes.

Thank you for your answer. As stated in the post I understand the biased sex-ratio decreases the effective population size. I fail to prove that $N_e = \frac{4N_mN_f}{N_m+N_f}$ is true (while $N_e = \frac{\left(N_mN_f\right)^2}{4(N_m+N_f)}$ is wrong for example)

Hum... no it does not quite help. I am looking for a mathematical proof that $N_e=\frac{4N_fN_m}{N_f+N_m}$. In other words, I am looking for a mathematical proof that the rate of loss of heterozygosity of a population with $N_m$ males and $N_f$ females is the same as a Wright-Fisher population with $N=\frac{4N_fN_m}{N_f+N_m}$ (by the definition of the effected population size $N_e$).

@Remi.b made some edits, still I don't prove mathematically though

Wow. You definitely deserves a +1 for a al of that. Thanks

thanks - I've updated the scripts (available in the linked page) to give sex ratio rather than $N_M$ and $N_F$ and it shows it with fewer replicate populations which is a bit nicer to look at - I did 100 reps here to show the general trend (i.e. how the trajectories spread out over time) but that's quite ugly to look at


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What limits our healing speed?
Our bodies can repair quite a number of injuries very well. However, it takes time. For larger wounds, complete recovery can last many weeks. Why is this time so long, what is the most important limiting factor? The speed of cell division? I thought cell division was faster, and if necessary, cells could also be transported in the blood stream. Thrombocytes, as far as I know, are transported to the location of the emergency by the blood, and are not produced locally.
If the pure physics and chemistry allowed, for example, a 2x faster healing rate, wouldn't there be any evolutionary pressure for it?

The limiting problem is the formation of new tissue. New cells could indeed be produced faster, but forming tissue requires much more than just cells. It requires extracellular matrix to provide attachment for new cells, collagen and various other intercellular fluid components (which are secreted by fibroblasts), migration of cells. And bear in mind all of this isn't done on an open end, it needs to be done without actually at any point breaking the blood circulation system or other boundaries between tissue compartments.

One reason is simply "scale". The healing recovery is taking place on a molecular scale, and it involves a huge number of very, very tiny things. How long does it take to place all of the bricks in a brick wall (for a trivial analogy)?

Do you want speed, or accuracy. Uncontrolled cell growth is CANCER. We do not want cells growing extra fast or it is cancer. Also, it takes time to correctly sequence dna strands. Do you want fast healing with lots of scars, extra skin, some new limbs and extra tumors. It takes time to form correct cells.

The process of wound healing is pretty complicated and is much more than only cell division. The woundhealing process starts almost immediately in the moment of the injury and depending on the injury can take quite a long time. Have a look at the figure below (from the second reference), which shows the phases:

Basically this can roughly be diveded into four phases:

Hemostasis/Coagulation:

vascular constriction (blood vessel contraction)
platelet aggregation, degranulation, and fibrinformation (formation of a thrombus and closure of the wound)

Inflammation:

neutrophil infiltration
monocyte infiltration and differentiation into different kinds of macrophages
lymphocyte infiltration

Proliferation:

re-epithelialization
angiogenesis (formation of new blood vessels)
collagen synthesis (formation of new connective tissue)
formation of the extracellular matrix

Remodeling:

collagen remodeling
vascular maturation and regression

This process takes some time and can be prolonged when a wound is infected.  So I don't think there is much room to speed this up, as you need to go through all these phases. This process is also the result of extensive evolutionary processes; otherwise, such complex cooperation between different cells is not possible. For more details on the process itself, have a look at the references.

References

Factors affecting wound healing.
Cellular aspects of wound healing.

+1 just for HIPR.  You imply it, but it might be worth stating out right that remodeling is most likely to be the rate limiting step (to answer directly)

Thats possible. If there is no additional infection. Although this is not really "rate limiting" but takes time to clear.

The time needed for a wound to heal is related to the type of tissue injured and the amount of tissue that needs to be 'reconstructed.' Cell division rates are also a factor.
Healing is a complex process that involves multiple stages.

The body has to limit the damage that can result from an injury. So, first it tries to stop the bleeding and then a local inflammatory process is triggered. This inflammation will:

stop pathogens from entering the systemic circulation
'clean' the injured tissue by removing dead cells

In order to recreate the tissue, there is the need for blood which will deliver nutrients and other factors. So, fibroblasts and endothelial cells migrate in the wounded area and form temporary tissue and new blood vessels; the new tissue is called granulation tissue.
The granulation tissue allows for the formation of definitive tissue. This is the remodelling phase. Depending on the wound, the tissue that grows can either be the same as the original one or be fibrous scar tissue.

Looking at the time required by each of these steps:

should be the fastest as it relies on blood cells and factors that are already present in blood. Also, the wound itself will stimulate the local production of some cells/factors involved (inflammatory factors, vasodilator, vasoconstrictor factors.)
and 3. depend on the duration of cell-division processes, extracellular matrix formation, and vascularization. Cell division time can be slowed down by a lack of required nutrients and/or substances.  While the granulation tissue forms in almost constant time no matter the injury, the final tissue depends on what type it will be. One simple example is bone tissue versus skin.

References & Links:

Wound healing on Wikipedia
John Miller: http://physioworks.com.au/treatments-1/what-are-the-phases-of-a-soft-tissue-injury

While it's a good answer in describing how the healing of wounds works, most of this I already found on Wikipedia and other sources. I'm still curious about what actually causes it to have this speed? What physical or chemical processes are most responsible that a certain step takes 8 days instead of 8 hours?

I claim that one great limitation in our understanding of the healing process is that biologists have no understanding of the progression of disease or infection, that not enough time may be given for the body to recover, and that doctors might not understand how to help their patients recover from disease or infection.
Each patient is different, and personalised recovering plan is often important.
So, too few resources — e. g.:  the time of a doctor and/or a nurse — are offered to patients, so doctors have little time to build their understanding of the disease or injury with which their patients are dealing.
It is the patient who makes himself or herself able to recover.
But, without understanding, the recovery process is not optimal.
Healing from upper respiratory infection:
I will give one example in LOR Medicine.
Upper respiratory infections are one of the most common infections and most expensive diseases in society.
One reason is that people do not understand:

how to recover from disease
how long the common cold or flu lasts (doctors underestimate the time that it will take for their patients to heal very often.)

In nursing school, they teach students how to, among other things:

prevent reinfection
prevent acute hyaline membrane formation by elevated sleeping position (in LOR, for instance.)

There is no way to measure what the correct course of treatment is for any given patient during the course of, for example, an upper respiratory infection.
Nurses ask the patient when he or she feels their best and adjusts treatment accordingly.
So, good communication is essential in nursing.
Wound healing:
Chris and Cornelius cover some of the basic cellular processes of wound healing.
However, some big steps are still missing in regards to healing.
The primary healing of wounds is aided by:

adequate wound-edge coaptation
healing without complications
minimal scar tissue

through the cellular processes of wound healing described by Cornelius and Chris.
Secondary healing of wounds is characterized by:

wound tissue left exposed (open)
defect filled with granulation tissue
surface covering the epithelium
less functionality
possible thermal and mechanical injuries

Embryological and biochemical aspects of tissue healing
I cover here some growth factors.
If they are not present, then their absence will surely be a limitation to the healing process.

TGF - transforming growth factor
MDGF - macrophage-derived growth factor
HB-ECG - heparin-binding epidermal growth factor

Here are some other factors:

bFGF - basic fibroblast growth factor
KAF - keratinocyte-derived growth factor

Special cytokines for inflammation may later come into play.
Sources

Human skin wounds: a major and snowballing threat to public health and the economy. Sen C.K., Gordillo G.M., Roy S., Kirsner R., Lambert L., Hunt T.K., Gottrup F., Gurtner G.C., Longaker M/T. Wound Repair Regen. 2009 NovDec;17(6):763-71.
My notes during 4 years of nursing
My notes during classes of Surgery
My notes of Embryology and Surgery about the growth factors

Once again: Why the downvotes without explanation? Answers can only get better with some explanation what can/should be done.

@Chris : While I didn't vote on this answer yet, I guess it's because it is about why medics cannot treat wounds faster. The question was about the biological process itself, and not why we don't have the technology to speed it up.

@vsz: That would be a perfect comment on this topic.

I think the challenge of the case is that the main question is open and asks much more than some processes. Your body then again explains much more narrower thing about biological level. The answer should be adequate to the question in title - not only textbook answer and/or simplification what can be found in books and/or review articles. Simplification is NOT enough for practical purposes. The body is user's attempt to answer it so well as possible. Biology is not only about one process. It is a multidisciplinary field with limitations.


text:
How does geography affect morphological features of the human body
I've seen many times how a person born in one place, goes to another country for a long time, and then they start looking more like the people there, but I never found out how it works.
This report claims that second generation Japanese, born in the US are taller and heavier than those living in their native lands (there had been no intermingling of races).

To what extent do the genetic/environmental factors control human morphology ?
What factors apart from the diet can bring about such morphological differences ?

I think this needs to be referenced as an actual phenomenon in order to be answerable.

I'm searching for any relevant research documents right now, and I only find blog posts of people wondering the same thing, but the answers are only based on guesses.

@user1306322: added a reference for you.. co-incidentally someone told me about this just few hours ago :)

I think that particular instance probably reflects dietary changes more than anything else.

Geography does not typically affect the morphology of the human body.
In certain special cases, there are physiological adaptations, the most obvious being tanning and acclimatization to high altitude, but these aren't changes in body morphology.
So why the difference in children of immigrants?  This is because diet, nutrition, and disease have quite strong effects on children's growth. Kids growing up in a healthier environment with more food get bigger, and those are linked to the wealth of the community where you live.

+1 There is also cause-and-effect relation involved here: immigrants are not a random sample from the population of their original countries. One may argue about whether this translates into educationald and professional achievement, which may affect physical appearance... but teh comparisons between the average immigrants and non-immigrants are likely skewed.


text:
Can someone identify this ant?
This is one of seven ant queens I just collected yesterday morning (2015-09-21 9AM) around home.
I live in Hong Kong, at a hillside facing south. The weather was as follows (Hong Kong Observatory Daily Weather Summary, Hong Kong Observatory Daily Extract):

Mean Pressure (hPa): 1008.6
Max temp in my district: 24.2C
Min temp in my district: 28.0C
Mean dew point: 23.8C
Relative humidity: 66% - 95%
Rainfall: 16.9mm

Judging by the ridged head and the large mandibles, I'm guessing this is one of the Tetramoriums (Wikipedia, AntWeb).
The colour is dark brown. The total length from the tip of the mandibles to the tip of the abdomen is about 17mm. The length of the large wing is also 17mm. I don't know what habitat it lives in and I also don't know how the workers or soldiers look like, as I have never seen where these ant queens emerge from.
If anybody is fairly confident in identifying this species, I would also appreciate some tips about keeping it and starting a colony. I have a make-shift ant farm made out of two plastic bottles, one nested inside the other like a Russian doll. Out of the seven queens that I collected, three are already dying. A fourth one already show signs that she won't make it either.
More info
When I picked them up, they were not exactly "outdoors". The short but heavy rain was mostly over and these queens were "taking shelter" in the stairwell of my building, which is usually dim, slightly damper and cooler than outside.
Here are more pictures; these should be better because I just took these in natural daylight:

Somebody at The Ant Farm and Myrmecology Forum suggests that this is in the genus Carebara (previously Pheidologeton). After some more Google search of my own, and image comparing, I believe that this is indeed a Carebara affinis, which has previously been spotted in Hong Kong. Could somebody confirm?

I also want to commend you for providing a lot of information. However, even though I know very little about ant identification, I do know that the number/amount of bristles (setae) on head and legs, spines on the alitrunk/mesosoma and petiole as well as the number and shape of antennal segments are often used for genera and species determination, and these characters are difficult to see in your pictures. So it might be difficult to determine this to species, based on your pictures.

@fileunderwater Thanks for the tips! I'll try to get clearer pictures or count the setae, etc myself when I get home.

In my opinion you are pretty close to the exact identification.
I think it is Marauder Ant, which could be Pheidologeton diversus, but probably Carebara affinis as well.
The main feature I can gother from your pictures is Venation of wings which matches with Pheidologeton diversus venation (it would probably match with affinis as well, but I failed to find the picture):

Venation match: the combo picture of the wing from the post and the wing from the reference:

This ant is known as Hong Kong inhabitant -

Yes, I'm aware that it is also possibly a Pheidologeton diversus, renamed nowadays as Carebara diversa, if I'm not mistaken. Unfortunately, without successfully starting a colony and looking at all the different casts, it's rather hard to tell the C. diversa and C. affinis apart. IIRC from my research, the C. diversa has a more diverse range of worker sizes, ranging from super majors (with really big heads) to minors. C. diversa are also rarer than C. affinis, which makes the C. diversa highly prized as pet ants. There are even reports of sellers selling C. affinis as C. diversa knowingly.


text:
Why is there more variation in proteins than genes?
The Genome of a cell or organism is the same as that of the entire organism. However, the proteome of an organism is much greater than that of each cell (unless the organism is unicellular).
How do you account for the presence of more variation among of proteins than there are in genes?
The simple answer would be "there are more proteins than genes", but I'm more interested in why. Is it sufficient to say that during gene expression a single gene codes for multiple proteins (Alternative Splicing) and ribosomes translating mRNA to polypeptide chains (Posttranslational modification)? Could someone expand more on this?

There are several concepts to understand:

Alternative splicing

From one gene, several proteins can be constructed depending on which introns are spliced.

Tissue-specific genetic expression

Genes are differentially expressed (and differentially spliced) depending on the tissue.

Post-transcriptional modifications

Those are modifications that are made directly on the proteins (in opposition with alternative splicing which are modifications made on the RNA)

Structure of the proteins

Proteins may fold (to what we call primary, secondary, tertiary and quaternary structures) differently in different environment.

Therefore there is variance in proteome between cells although there is no variance in genome between cells (except mutations and red blood cells). Moreover, one gene sequence can give rise to many different proteins due to the processes of alternative splicing and PMT.

On a similar note: What is meant by the 'complexity' of the proteome? Why is it described "the proteome has at least two levels of complexity lacking in the genome"?

The word complexity is used with many different meanings. Here is another post that maybe interest you. Or the Wiki article I don't quite know what can be meant with this sentence: "the proteome has at least two [...]". I guess that indeed it is closely related to your question. I would suggest you to post it as another question and give a link to your article and maybe a small summary of the context in which this sentence come from.

This is according to the Wiki page regarding the proteome. Perhaps the following sentences will help: "The proteome has at least two levels of complexity lacking in the genome. While the genome is defined by the sequence of nucleotides, the proteome cannot be limited to the sum of the sequences of the proteins present. Knowledge of the proteome requires knowledge of (1) the structure of the proteins in the proteome and (2) the functional interaction between the proteins."

aha. Here is the link to the wiki page for others. Ok, so I missed this point in my answer. The proteom is indeed greater than the genome due to alternative splicing and PTM. Let me try to improve my answer (but I am slowly affraid to go into details that I might not know very well..)

@Cloud I think, by saying two levels of complexity , it means that proteins are not mere chains of amino acids they also have to have specific structure and interaction with other molecules.

To comment on the "why" question: I would say that its a relatively simple way to get a high number of proteins with more or less slight differentiations. This can include exons which are only present in special environments or cell types and so on. It saves a lot of energy for keeping all the information about every single transcript (the BNC2 gene for example can produce up to 90.000 different mRNA transcripts coding for up to 2000 different proteins of unknown function, see here) and makes the genome a lot less complex, despite the fact that we now need an also complex regulation.

90 or 90,000 mRNA Transcripts?

@TalhaIrfan If you look at the linked paper, you would see that the number 90.000 is true. I think that this is a theoretical number and less transcripts are made, but it shows the possibilities.


text:
Are there any side-effects from a mosquitoes extinction?
Suppose that we have the ability to make mosquitoes extinct, what would be the likely effects (on disease and ecosystems for example) of such extinction? Essentially, what roles in nature do mosquitoes perform?

There was actually just such an article in Nature recently.
"They don't occupy an unassailable niche in the environment," says entomologist Joe Conlon, of the American Mosquito Control Association in Jacksonville, Florida. "If we eradicated them tomorrow, the ecosystems where they are active will hiccup and then get on with life. Something better or worse would take over."

Sometimes I wonder what the editors of Nature are thinking when they publish those "pearls"...

The "or worse" is all the answer you need, I guess.

Eliminate Culicidae (mosquitoes) because some of the species transmit virus is a very bad idea. I have used the family name to make you realize there is more than 3500 species of mosquitoes and only a few are responsible for the transmission of disease or virus.
First, the male mosquitoes are important pollinators of multiple flowers (here is an example of some http://www.mosquitoreviews.com/mosquitoes-niche-pollinate.html ).
Secondly, mosquitoes are important food source for multiple predator such has bats, birds, frogs and fish. If you think it's negligible, just come down to Quebec in august and try to go naked in the wood you will see thousand of happy female mosquitoes on your skin in a minute.
Indeed, eliminating species because the have some consequence on humans is seeing the world as a simple thing. Ecosystem are complex and removing a group of animal will have consequences on the rest of the member of the ecosystem including us. Control of the population is a much better idea. Per example, in Montreal, the SOPFIM threat the sewer with larvicide (Methoprene) to control the mosquitoes population in the city. They also threat swamp close to the city. But the most efficient way to reduce mosquitoes population is by removing stagnant water (tires, plastic bag...). And cause of those effort,there are very few case of VNO in Montreal. So before causing to the extreme, educate the people about the biology of the mosquitoes and control the population.
Cheers


text:
Method to recognize the age of a firebug from the pattern on its back
Can I recognize the age of a firebug from the pattern on its back?
If yes, what pattern shows what age/stage?
Below is what I extrapolated from Wikipedia, but is there a more precise scale with more steps? (I could not find more than this with google).
Nymph: Adults:

The answer is more or less yes. Normally Firebugs (Pyrrhocoris apterus) go through 5 nymph instar stages (as do most Hemiptera), where they resemble the adults more and more as they grow. Only adults are winged and have have functional reproductive organs. This type of metamorphosis is called hemimetabolous or simple metamorphosis (in contrast to Holometabolism or complete metamorphosis). However, I cannot find a good overview of the instar stages of Firebugs to link to.
A generic overview of Heteroptera (True Bugs) can bee seen here
(from www.amnh.org/learn/biodiversity_counts):

This picture shows (at least) three instars + adults of Pyrrhocoris apterus (from http://www.projectnoah.org/spottings/17248017). The large nymph with 3 dots along the midline is the final 5th instar nymph:

However, due to hormonal disruptions there have been cases with even more nymph stages (6th and 7th instars with adult characteristics), but this is under unnatural laboratory conditions (e.g. Slama & Williams 1965 and Konopova et al. 2011). Konopova et al (2011) also has pictures of instar stages 4 & 5 (along with gene knowdown versions).

Nice referenced info. The first image would be even better if indicated the patterns too :-)

I'm sure you can find one for Firebugs in a suitable book. However, the graph I posted is a general overview of Heteroptera, which consists of >40000 species, and the growth patterns naturally differs quite alot within the taxon.


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Are there birds with knees instead of elbows?
Are there any birds whose legs fold the same way human legs do, in a knee, instead of an elbow which is what all the birds I know have?

The joint you are thinking of is not a knee, nor is it an elbow, instead it is an ankle which is bending the same way as us humans. You can see from the below diagram that the knee - the joint between the femur and tibia - is just further up the leg normally hidden by feathers.
Birds have a comparatively elongated metatarsus which gives the impression that the knee bends backwards more like an elbow, but it's just the ankle. (Image from here)

I also liked this diagram from a blogpost on a similar theme...

To follow up there appears to be no animals whose ankles bend the "wrong" way.
http://www.answers.com/Q/Which_animal_has_backward_knees
http://qi.com/infocloud/knees
http://www.ehow.com/info_12317202_birds-knees-backwards.html#page=1
Though these are far from conclusive resources. I'd guess the way knee is defined (it means something to humans but not to nature (a bit like the species being a concept which has weak biological bounds)) has something to do with that

Good point, thank you! It didn't occur to me. However, the joint I'm talking about is between Tibia and Metatarsus (ankle, right)? Are there any birds whose ankles bend backwards?

according to the blogpost mentioned above no, no tetrapods do this

@violetgirraffe edits made

+1 Nice answer. You should add a reference to the first figure thought.

Did you replace the first illustration? You shouldn't have, the other one was much larger and clearer; I can hardly read anything on this one.


text:
Calculation of saturation of carbon in surface waters
I've been looking at some journals lately that look at carbon emission from lakes where some lakes act as sources and other act as sinks. The paper that I have been looking at is
http://www3.nd.edu/~underc/east/publications/documents/Cole_94Science.pdf
where they show that lakes are sources of CO2 to the atmosphere. What are the equations that are used to determine the saturation of CO2 in surface waters?
The recent IPCC report also mentions that lakes act as sources of CO2 but does not give any indication of the equations used to come up with these values. Presumably, to determine the concentration of carbon in the surface water you need to use other measured variables such as temperature. Can anyone suggest a method for estimating this concentration ?

I imagine this would get a better response on the chemistry SE

Paragraph 2 describes their methods in detail.  If I have time I can outline it, but it might not be today... i think this is a fair biology/ecology question.  These days a fair number of biologists need to know their environmental/bio chemistry

second paragraph reads: Data were obtained from the literature and direct measurements. The value for PCO2 was calculated from ph and DIC or ANC with corrections for other variables. I am looking for the equation used for calculating PCO2 from these variables.

I agree with @shigeta this is still a biology question (I recommend asking on both biology and chemistry SE)

Take a look at Paragraph 2.
I'll outline it in more or less plain english (I hope).
for 37 lakes they used this method:
1) they took a sample of water from 0.1 to 0.25 m below the surface.  Using a thermos bottle.  This would minimize change of the gas composition of the water with a change of temperature.  The bottle was not sealed, but left out for a while in the air there at the lake (it was "equilibrated with ambient air").  If you were looking for issues you might or might not like this.
2) a sample of air 1m above the lake was taken.
3) they got a gas chromatograph to measure the CO2 in the air above the water sample, as well as in the air from above the lake.  They might have taken the readings right there at the sampling point, or not its not clear. They may have also sealed bottles up and taken them to the lab.  It sort of sounds like a point of sample measurement.
If the air above the water samples had more CO2 than the air above the lake, they called the water supersaturated as the water was emitting CO2.
This method does its best to simplify the question of whether fresh water bodies are saturated with CO2 and emitting it or if they might be absorbing it.  By not outgassing the CO2 in the water and trying to get an absolute content of CO2, they are able to get around the various organisms and minerals in the water and pH which would vary the amount of CO2 the lakes can hold.  they are just focusing on whether the water is giving off CO2.


text:
What does 'H' in BamHI stand for?
It's not explained on the wikipedia page. So if, apparently, 'H' is not relevant, why is it part of the name? And if it is relevant, why is it not explained?

These enzymes are named by the bacteria and the strain from which they are isolated. For BamHI this is Bacillus amyloliquefaciens strain H. In the beginning the enzyme was named BamI, which was later changed to BamHI.
See these two references:

Isolation of a sequence-specific endonuclease (BamI) from Bacillus
amyloliquefaciens H.
Recognition sequence of specific endonuclease BamH.I from Bacillus
amyloliquefaciens H.

The same is true for all the other restriction enzymes, so is EcoRI the first restriction endonuclease isolated from Escherichia coli strain R.


text:
How do you remove DNA/RNA from plastics?
I want to know how to make plastic containers free of DNA & RNA? this is just for knowledge

Use disposable containers like Eppendorf tubes and Falcons, that is by far the easiest way.

Lab cleaning solutions can be bought which remove/destroy nucleic acids such as this one. UV is another technique for destroying DNA. And bleach is used to remove contaminant DNA in ancient DNA studies.
Searching for a DNA/RNA lab cleaning protocol would be a good idea to - something like this.

Both the 'this one' link is not working and the 'something like this' aren't working, would you mind providing updated links?


text:
What triggers DNA to produce proteins?
What is the trigger for DNA to produce proteins or RNA?
I have found enough material to study the inner workings of the cell and DNA; but, I can't find an explanation of the mechanics the cell uses to react to its inner state or external events and in turn initiate transcription.

Maybe I don't understand the question, but the Wikipedia entry for Gene Regulation is a good place to start: http://en.wikipedia.org/wiki/Gene_regulation

@Alan Boyd: I think the question is asking what environmental signals act to recruit TF to start transcription. For instance activation of membrane receptors and so on.

This question is not easily answered as there are a multitude of factors involved in the production of proteins.  DNA - the molecule - does not "determine" when proteins will be produced.  The environment (truly environmental, extracellular, intracellular, etc.) of the organism governs this.  If you have not found enough material to satisfy your inquiries I recommend Jim Watson et. al. Molecular Biology of the Gene.  A classic.


text:
Why are some fungi poisonous?
There are many poisonous fungi in nature. For example Amanita Phalloides.
What reasons could a fungus need poison for? Some species, like venomous snakes, use poison to kill other species as prey. But what about fungi? I can't think of any purpose for poison in fungi. If poison has no real function in fungi shouldn't evolution get rid of it?

I just want to make the general point that poisons do not have to be adaptive. It is entirely possible for metabolites of one organism (e.g. fungi) to be poisonous for another organism if ingested (e.g. humans), without having been selected for because of its poisonous effect.

@fileunderwater that makes sense :)

The same reason some plants are poisonous: to stop animals from eating them.
The visible part of the fungus is called, rather misleadingly, the fruiting body. It exists to produce and spread spores and thus produce the next fungal generation. Getting eaten, rather obviously, inhibits its ability to do this. Being poisonous discourages animals from eating the fruiting body and thus permits it to complete its life cycle.

Some mycotoxins are designed to kill/weaken the host in the case of pathogenic fungi, and some others (penicillin) are designed to kill off competitors for food.

Sorry, but it is often claimed the contrary: that some mushrooms have bright colors to ATTRACT animals so that they eat them to spread spores.

@Anixx: I'm not aware of such a claim and would be interested in a source? Even if it is true I am quite certain that those mushrooms will not be poisonous.

http://biology.stackexchange.com/questions/20333/whats-the-purpose-of-colorful-mushrooms-caps

@Anixx Fungi have come up with many weird and wonderful ways of spreading spores, from being eaten as you say to mind altering neurotoxins! You're right to bring this up. But for the general nature of the question I thing a general answer is best fitting else the answer would risk going off topic perhaps...


text:
Are nucleotides at the ends of DNA stripped on aging?
I had the following understanding (now after reading a popular science article seeming wrong understanding):
DNA in (regular) cells (in human and some other organisms) are protected by telomers. Telomeres are shortened at each division. When telomeres reach zero size, nucleotides of the ends of DNA become "stripped" so that the DNA shortens a little. The shortened DNA does is not fully functional. This leads to aging of the organism.
But in a popular science article I've read that telomeres however shortened seem not to reach zero length. So the DNA nucleotides at the ends of DNA are never stripped. However shortening telomeres leads to the cell to become not divisible or even death of the cell.
So two related questions:

Are coding/regulatory nucleotides (not just telomeres) at the ends of the DNA ever stripped as a result of aging?
If they are not stripped and so the DNA itself is not damaged, how shortening telomeres may lead to aging? That is how aging can be caused by just shortening telomeres which however do not reach zero length?

There seems to be a slight confusion. Telomeres are made of nucleotides. Telomeres are not adds up at the end of the chromosome, they are the end of the chromosomes.  Telomeres are repetitive sequences. For example the repetition of the sequence TTAGGG is commonly found in telomeres in vertebrates.

I suppose you might want to rephrase your question to ask whether the chromosomes are sometimes shortened enough so that coding sequences or regulatory sequences get stripped.

Also, could you post the article you read?

@MarchHo https://med.stanford.edu/news/all-news/2015/01/telomere-extension-turns-back-aging-clock-in-cultured-cells.html

The Stanford article that you read is correct, in the sense that telomeres do not need to be completely removed by cell division before deleterious effects occur and cells start undergoing senescence.
This Nature article describes an experiment in which the minimum length of telomeres (beyond which chromosomal fusion occurs) was determined:

The critical telomere length was 12.8 repeats (of six base pairs)
  long, they found — any shorter and the chromosomes began to fuse
  together at their ends (R. Capper et al. Genes Dev.
  doi:10.1101/gad.439107; 2007). Baird suggests that without
  sufficiently long telomere caps, the cell may perceive the chromosome
  ends as broken strands of DNA and attempt to piece them together.

Therefore, we can conclude that while it is not impossible for non-telomeric nucleotides to be stripped from chromosomal ends, this generally does not happen, since cellular defense mechanisms such as non-homologous end joining (NHEJ) and microhomology-mediated end joining (MMEJ) would activate before that point, and start joining chromosomal ends together. This would then lead to issues during mitosis, which would likely halt further cell divisions.

Are you sure that the research was replicated? From what I am familiar with, human telomeres usually require somewhere between 2kb-4kb of TTAGGG repeats to prevent senescence. I thought it had to do with the ability for the telomere to loop over on itself and form a T-Loop with strand invasion into the D-loop. I thought that that chromosomal architecture is what imposes the limit, and you can get much shorter than that as still form the T-loop.


text:
How different is an introverts brain different from an extroverts?
How is an introverts brain wired differently than an extroverts? Just to give you an example. On an average, the processing that goes on in an introverts brain is greater than in an extroverts [citation needed].
What part of the brain affects personality traits such how introverted someone is? How is this part of the brain different in either it's physical entity or it's activity between extroverts and introverts?

I think we are several years away from understanding how those type of behaviours are coded in the brain...

This question might fare better on cogsci.SE.

I think you will have a better chance of getting an answer if you narrow down the question and include references for your claims.

i think you can look at an extreme case. It's called Williams-Beuren Syndrome. The patients have a deletion in 7th chromosome (q11.23) and have a highly naive and sociable behavior [there are also other markers, of course].

Do introverts have "brains"?  I think this is actually a controversial subject.  Certainly, some have highly connected networks that are somewhat analogous to a brain, but I think of brain as a uniquely vertebrate organ.


text:
What causes autism?
What causes autism?
By this I don't mean what is to blame i.e. Vaccines, Gluten or Pharmaceuticals etc.. I mean what exactly is happening in the brain to cause the autistic behaviors such as little to no communication skills, regression of skills around age 3, hand flapping etc..
I see a lot of research looking for something to blame however I see little to no research on identifying the physical causes or links (maybe I'm not using the correct search terms).

There's a significant body of anatomical research that is going on, both in neuropathology and neuroimaging, see http://www.ncbi.nlm.nih.gov/pubmed/21360830 for example.

Fragile X syndrome is a genetic disorder which is highly related to autism and is considered to be the most common single gene association with autism.
Establishing what actually happens in autistic people is difficult because it is hard to quantify someone as being autistic or not - it is common for some people to show some signs of autistic type behaviour and some people are more extreme than others - plus the symptoms are numerous:

Clinically, autism is defined by a “triad” of deficits comprising
  impaired social interaction, impaired communication, restricted
  interests, and repetitive behaviors.

Wikipedia splits the mechanisms in to two key groups, pathophysiology and neuropsychology. The pathophysiological aspects are perhaps better documented and some known correlates to autism are listed:

Excess of neurons in key brain regions
Disturbed neuronal migration during early gestation
Unbalanced excitatory–inhibitory networks
Abnormal formation of synapses and dendritic spines

Our understanding of the mechanisms causing autistic behaviours does not go much beyond this. This paper is a review of the neuroanatomic associations with autism which could, at least in part, help you to identify the physical differences linked to autism.

Here is a brand new article on autism http://www.the-scientist.com/?articles.view/articleNo/36379/title/Maternal-Antibodies-Linked-to-Autism/

It's also worth noting that conditions aren't always due to single gene mutations and their aetiology can be more complex. Autism could easily be the result of 10 different gene mutations affecting different processes during brain development (e.g. receptor trafficking, spine growth and all sorts of stuff). The same is true for loads of psychiatric conditions

I would like to asnwer this question. I will try to avoid repeating any information about possible causes of autism, which was mention here. Anyway there is new interesting information.

Autism spectrum disease (ASD) is typically diagnose from the psychological point of view. Such thing like repetitive behavior, echolilia, stimming and stuff like that. True reason why does we still diagnose ASD in this way is because we still dont know causes of this disorder.

Sleep inconsistency
Kids with ASD are well know for theirs sleep disturbance.

Polysomnography studies of ASD children showed most of their abnormalities related to rapid eye movement (REM) sleep which included decreased quantity, increased undifferentiated sleep, immature organization of eye movements into discrete bursts, decreased time in bed, total sleep time, REM sleep latency, and increased proportion of stage 1 sleep.

REM sleep is one of the two types of sleep in general. By the ontological point of view the REM sleep might provide neural stimulation. In this way good sumury provide us at wikipedia page on REM:

REM sleep prevails most after birth, and diminishes with age. According to the "ontogenetic hypothesis", REM (also known in neonates as active sleep) aids the developing brain by providing the neural stimulation that newborns need to form mature neural connections.Sleep deprivation have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, and decreased brain mass,and can result in an abnormal amount of neuronal cell death.unreliable medical source? The strongest evidence for the ontogenetic hypothesis comes from experiments on REM deprivation and the development of the visual system in the lateral geniculate nucleus and primary visual cortex.

So lack of REM sleep can be one of the many important factor to autism brain development.
Autistic microbiom
Microbiome is an ecological community of commensal, symbiotic and pathogenic microorganisms found in and on all multicellular organisms studied to date from plants to animals.

Recent studies suggest that autism is often associated with dysregulated immune responses and altered microbiota composition. This has led to growing speculation about potential roles for hyperactive immune responses and the microbiome in autism. Yet how microbiome–immune cross-talk contributes to neurodevelopmental disorders currently remains poorly understood. In this study, we report critical roles for prenatal microbiota composition in the development of behavioral abnormalities in a murine maternal immune activation (MIA) model of autism that is driven by the viral mimetic polyinosinic-polycytidylic acid. We show that preconception microbiota transplantation can transfer susceptibility to MIA-associated neurodevelopmental disease and that this is associated with modulation of the maternal immune response. Furthermore, we find that ablation of IL-17a signaling provides protection against the development of neurodevelopmental abnormalities in MIA offspring. Our findings suggest that microbiota landscape can influence MIA-induced neurodevelopmental disease pathogenesis and that this occurs as a result of microflora-associated calibration of gestational IL-17a responses.

It may not sound like something related to the neural system but now study lift up mircobiome importance.

EECs play an important role in gut chemosensing to orchestrate appropriate functional responses to a variety of stimuli ranging from nutrients, food degradation products, toxic chemicals, microorganisms and bacteria products. This complex balance between maximizing nutrient assimilation and minimizing danger to maintain optimal homeostasis is the result of the interplay of different detection systems including the distinct types of sensory receptors expressed by EECs, the variety of signaling molecules released by EECs and the targets that are activated directly and indirectly such as neighboring cells, distant targets reached via the bloodstream and neuronal pathways. Considerable progress has been made in understanding EECs relationship with neurons of the ENS and CNS and EEC bidirectional communication with the brain. There is now strong evidence that EECs can directly participate in the brain-gut axis bidirectional communication through axon-like processes or basal cytoplasmic processes. The basal processes connect EECs and neurons innervating the gut forming neuroepithelial circuits, which allow sensory transmission from the gut lumen and feedback from the brain to the gut EECs. The activation of afferent and efferent nerve pathways may be explored for the management of diseases related to feeding disorders and GI dysfunction. Alterations in the bidirectional communication between the brain and the gut are likely associated with an impairment of gut functions (e.g. intestinal secretion, motility, blood flow and afferent sensitivity). The modification of the homeostatic reflex might lead to a chronic perturbation of the gut such as visceral hypersensitivity. Therefore, a better understanding of the EEC roles and their relationship with the brain and sensory nerves is an important research target. Future studies are required to fully decipher this complex network. The direct EEC to nerve connection opens a new horizon of research and provides new tools to understand the mechanisms underlying EEC control of food intake and GI dysfunction as well as potential new therapeutic targets.

I think there more and more clues that the biggest role in development may be complexes imune reactions on brain development such as recent relation was found in homosexual brain development
Source
Devnani, P. A., & Hegde, A. U. (2015). Autism and sleep disorders. Journal of pediatric neurosciences, 10(4), 304-7.
Why We Sleep: Unlocking the Power of Sleep and Dreams book by Matthew Walker
Cutting Edge: Critical Roles for Microbiota-Mediated Regulation of the Immune System in a Prenatal Immune Activation Model of Autism
Latorre, R., Sternini, C., De Giorgio, R., & Greenwood-Van Meerveld, B. (2015). Enteroendocrine cells: a review of their role in brain-gut communication. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society, 28(5), 620-30.

Cerebral folate deficiency (CFD) has been found to be the cause of autism in as many as 75% of autism patients. Specifically, the folate uptake into the brain occurs primarily through folate receptors in the choroid plexus.
Folate receptor alpha antibodies (FRAA) in autism patients, bind to these folate receptors and block folate uptake. Folate is of course an essential nutrient for various brain functions. So one can expect numerous brain functions to be impacted by CFD.
Cerebral folate receptor autoantibodies in autism spectrum disorder
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578948/
Folinic acid (not to be confused with folic acid) has been used to treat CFD induced autism. Basically, it is a method of getting folate to the brain by an alternate pathway, that bypasses the primary path that is blocked by FRAA.
Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial
https://www.nature.com/articles/mp2016168

I know it's been about a year since you posted this but, I'm just now seeing this one... thank you!